Prostate cancer is 5 different diseases

Public Release: 29-Jul-2015

Cancer Research UK

Cancer Research UK scientists have for the first time identified that there are five distinct types of prostate cancer and found a way to distinguish between them, according to a landmark study* published today in EBioMedicine.

The findings could have important implications for how doctors treat prostate cancer in the future, by identifying tumours that are more likely to grow and spread aggressively through the body.

The researchers, from the Cancer Research UK Cambridge Institute and Addenbrooke’s Hospital, studied samples of healthy and cancerous prostate tissue from more than 250 men.

By looking for abnormal chromosomes and measuring the activity of 100 different genes linked to the disease they were able to group the tumours into five distinct types, each with a characteristic genetic fingerprint.

This analysis was better at predicting which cancers were likely to be the most aggressive than the tests currently used by doctors – including the PSA test** and Gleason score. But, the findings need to be confirmed in clinical trials with larger groups of men.

Study author Dr Alastair Lamb, from the Cancer Research UK Cambridge Institute, said: “Our exciting results show that prostate cancer can be classified into five genetically-different types. These findings could help doctors decide on the best course of treatment for each individual patient, based on the characteristics of their tumour.

“The next step is to confirm these results in bigger studies and drill down into the molecular ‘nuts and bolts’ of each specific prostate cancer type. By carrying out more research into how the different diseases behave we might be able to develop more effective ways to treat prostate cancer patients in the future, saving more lives.”

Prostate cancer is the most common cancer in men in the UK, with around 41,700 cases diagnosed every year. There are around 10,800 deaths from the disease each year in the UK.

Professor Malcolm Mason, Cancer Research UK’s prostate cancer expert, said: “The challenge in treating prostate cancer is that it can either behave like a pussycat – growing slowly and unlikely to cause problems in a man’s lifetime – or a tiger – spreading aggressively and requiring urgent treatment. But at the moment we have no reliable way to distinguish them. This means that some men may get treatment they don’t need, causing unnecessary side effects, while others might benefit from more intensive treatment.

“This research could be game-changing if the results hold up in larger clinical trials and could give us better information to guide each man’s treatment – even helping us to choose between treatments for men with aggressive cancers. Ultimately this could mean more effective treatment for the men who need it, helping to save more lives and improve the quality of life for many thousands of men with prostate cancer.”

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For media enquiries contact the Cancer Research UK press office on 020 3469 8300 or, out of hours, on 07050 264 059.

Notes to editor:

*Ross-Adams et al. Integration of copy number and transcriptomics provides risk stratification in prostate cancer: a discovery and validation cohort study. EBioMedicine. DOI: 10.1016/j.ebiom.2015.07.017.

This work was funded by Cancer Research UK with support from Prostate Cancer UK.

**http://www.cancerresearchuk.org/about-cancer/type/prostate-cancer/about/screening-for-prostate-cancer

About Prostate Cancer UK and Men United

  • Men deserve better. Men United is Prostate Cancer UK’s movement for everyone who believes that men are worth fighting for, to help us beat prostate cancer and keep friendships alive. Some 230,000 people have engaged with Men United since 2014.
  • This summer Men United has tons of fun ways for people to see their mates, from bike rides, sponsored walks, BBQs and quiz nights – all whilst doing something great for Prostate Cancer UK.
  • Search Men United, or visit prostatecanceruk.org/menunited
  • Prostate Cancer UK works to get men in all areas of the country the early detection, effective diagnosis and better treatments that will beat this disease.
  • Prostate cancer is the most common cancer in men. More than 10,000 men die every year from this male-only disease, and 330,000 men are living with and after prostate cancer in the UK.
  • Anyone with concerns about prostate cancer can contact Prostate Cancer UK’s Specialist Nurses in confidence on 0800 074 8383 or via the online Live chat, instant messaging service: http://www.prostatecanceruk.org. The Specialist Nurse phone service is free to landlines and open from 9am to 6pm Monday to Friday with late opening until 8pm on Wednesdays.

About Cancer Research UK

  • Cancer Research UK is the world’s leading cancer charity dedicated to saving lives through research.
  • Cancer Research UK’s pioneering work into the prevention, diagnosis and treatment of cancer has helped save millions of lives.
  • Cancer Research UK receives no government funding for its life-saving research. Every step it makes towards beating cancer relies on every pound donated.
  • Cancer Research UK has been at the heart of the progress that has already seen survival in the UK double in the last forty years.
  • Today, 2 in 4 people survive their cancer for at least 10 years. Cancer Research UK’s ambition is to accelerate progress so that 3 in 4 people will survive their cancer for at least 10 years within the next 20 years.
  • Cancer Research UK supports research into all aspects of cancer through the work of over 4,000 scientists, doctors and nurses.
  • Together with its partners and supporters, Cancer Research UK’s vision is to bring forward the day when all cancers are cured.

For further information about Cancer Research UK’s work or to find out how to support the charity, please call 0300 123 1022 or visit http://www.cancerresearchuk.org. Follow us on Twitter and Facebook.

Chemical derived from broccoli sprouts shows promise in treating autism

At special request I am posting our video from our other operating site, Here.

– Most of those who responded to sulforaphane showed significant improvements by the first measurement at four weeks and continued to improve during the rest of the treatment. After 18 weeks of treatment, the average ABC and SRS scores of those who received sulforaphane had decreased 34 and 17 percent, respectively, with improvements in bouts of irritability, lethargy, repetitive movements, hyperactivity, awareness, communication, motivation and mannerisms.
– Zimmerman adds that before they learned which subjects got the sulforaphane or placebo, the impressions of the clinical team — including parents — were that 13 of the participants noticeably improved. For example, some treated subjects looked them in the eye and shook their hands, which they had not done before. They found out later that all 13 had been taking sulforaphane, which is half of the treatment group.
* Sulforaphane treatment of autism spectrum disorder PNAS 10 2014 Continue reading “Chemical derived from broccoli sprouts shows promise in treating autism”

A cure or treatment for Cystic Fibrosis ? Delta-F508 defect is corrected with Curcumin


They found that the Delta-F508 defect is corrected in tissue culture and in mouse model systems by curcumin, the component that gives the spice turmeric its bright yellow color. In cultured cells, the CFTR protein moved to the surface of the cells, and in CFTR mice, the nasal and rectal epithtlia regained nearly normal function.

There has been no follow up research since 2006

*Science 304: 600-602 ( April 23 2004)

http://healthresearchreport.me/2012/07/24/researchers-show-cystic-fibrosis-defect-in-mice-corrected-with-turmeric-extract/

Vitamin E in front line of prostate cancer fight

Public release date: 18-Oct-2010 – EEV- Reposted at request from the HRR site

– Survival rates of the world’s most common cancer might soon be increased with a new vitamin E treatment which could significantly reduce tumour regrowth.

– “Previous clinical trials using another vitamin E constituent to inhibit prostate cancer development were unsuccessful, but these trials did not use the vitamin E constituent γ-T3,” he said.

–  in animal trials, γ-T3 completely inhibited tumour formation in more than 70 per cent of the mice implanted with prostate cancer cells and fed the vitamin E constituent in water. In the remaining cases, tumour regrowth was considerably reduced, while tumours reformed in 100 per cent of the control group.

Chemical structure of tocotrienols. α: R 1 = R...
Chemical structure of tocotrienols. α: R 1 = R 2 = R 3 = CH 3 ; β: R 1 = R 3 = CH 3 , R 2 = H; γ: R 1 = H, R 2 = R 3 = CH 3 ; δ: R 1 = R 2 = H, R 3 = CH 3 . (Photo credit: Wikipedia)

– existing chemotherapy and hormonal therapy treatment of prostate cancer was insufficient because it failed to kill off the prostate cancer stem cells

– the research team have discovered a particular form of T3, called gamma-tocotrienol (γ-T3), can successfully kill off the prostate cancer CSCs Continue reading “Vitamin E in front line of prostate cancer fight”

Subclinical deficiencies of vitamin C and D have each been linked to psychological abnormalities

Public release date: 23-Sep-2010 HRR: Requested Repost

– Patients administered vitamin C had a rapid and statistically and clinically significant improvement in mood state

“About one in five acute-care patients in our hospital have vitamin C levels so low as to be compatible with scurvy,”

Happy Smiley Face from Urine Samples

Subclinical deficiencies of vitamin C and D have each been linked to psychological abnormalities

Simple treatment may counteract widespread problem of subnormal vitamin levels in acute-care patients Continue reading “Subclinical deficiencies of vitamin C and D have each been linked to psychological abnormalities”

The symphony of life, revealed

 

A new imaging technique captures the vibrations of proteins, tiny motions critical to human life

             IMAGE:   Using a new imaging technique they developed, scientists have managed to observe and document the vibrations of lysozyme, an antibacterial protein found in many animals. This graphic visualizes the vibrations…

Click here for more information.     

BUFFALO, N.Y. — Like the strings on a violin or the pipes of an organ, the proteins in the human body vibrate in different patterns, scientists have long suspected.

Now, a new study provides what researchers say is the first conclusive evidence that this is true.

Using a technique they developed based on terahertz near-field microscopy, scientists from the University at Buffalo and Hauptman-Woodward Medical Research Institute (HWI) have for the first time observed in detail the vibrations of lysozyme, an antibacterial protein found in many animals.

The team found that the vibrations, which were previously thought to dissipate quickly, actually persist in molecules like the “ringing of a bell,” said UB physics professor Andrea Markelz, PhD, wh0 led the study.

These tiny motions enable proteins to change shape quickly so they can readily bind to other proteins, a process that is necessary for the body to perform critical biological functions like absorbing oxygen, repairing cells and replicating DNA, Markelz said. Continue reading “The symphony of life, revealed”

Long-term use of common heartburn and ulcer medications linked to vitamin B12 deficiency

Contact: Cyrus Hedayati chedayati@golinharris.com 415-318-4377 Kaiser Permanente

OAKLAND, Calif. — Long-term use of commonly prescribed heartburn and ulcer medications is linked to a higher risk of vitamin B12 deficiency, according to a new study published in the Journal of the American Medical Association. Continue reading “Long-term use of common heartburn and ulcer medications linked to vitamin B12 deficiency”

Vitamin D Decreases Pain in Women with Type 2 Diabetes and Depression

Continue reading “Vitamin D Decreases Pain in Women with Type 2 Diabetes and Depression”

Probiotic therapy alleviates autism-like behaviors in mice

Contact: Deborah Williams-Hedges mr@caltech.edu 626-395-3227 California Institute of Technology

Autism spectrum disorder (ASD) is diagnosed when individuals exhibit characteristic behaviors that include repetitive actions, decreased social interactions, and impaired communication. Curiously, many individuals with ASD also suffer from gastrointestinal (GI) issues, such as abdominal cramps and constipation.

Using the co-occurrence of brain and gut problems in ASD as their guide, researchers at the California Institute Technology (Caltech) are investigating a potentially transformative new therapy for autism and other neurodevelopmental disorders.

Continue reading “Probiotic therapy alleviates autism-like behaviors in mice”

Micronutrient supplements reduce risk of HIV disease progression and illness

Contact: Maydel Santana-Bravo santanam@fiu.edu 305-348-1555 The JAMA Network Journals

Long-term (24-month) supplementation with multivitamins plus selenium for human immunodeficiency virus (HIV)-infected patients in Botswana in the early stages of disease who had not received antiretroviral therapy delayed time to HIV disease progression, was safe and reduced the risk of immune decline and illness, according to a study appearing in the November 27 issue of JAMA.

“Micronutrient deficiencies, known to influence immune function, are prevalent even before the development of symptoms of HIV disease and are associated with accelerated HIV disease progression. Micronutrient supplementation has improved markers of HIV disease progression (CD4 cell count, HIV viral load) and mortality in clinical trials; however, these studies were conducted either in the late stages of HIV disease or in pregnant women,” according to background information in the article.

Marianna K. Baum, Ph.D., of Florida International University, Miami, and colleagues examined whether specific supplemental micronutrients enhance the immune system and slow HIV disease progression during the early stages of the disease in antiretroviral therapy (ART)-naive adults. They randomized 878 HIV patients to supplementation with daily multivitamins (B vitamins and vitamins C and E), selenium alone, multivitamins with selenium, or placebo for 24 months. The vitamins (vitamins B, C and E, and the trace element selenium) are nutrients essential for maintaining a responsive immune system. Selenium may also have an important role in preventing HIV replication.

Participants receiving the combined supplement of multivitamins plus selenium had a lower risk compared to placebo of reaching a CD4 cell count 250/µL or less (a measure that is consistent with the standard of care in Botswana for initiation of ART at the time of the study). This supplement also reduced the risk of a combination of measures of disease progression (CD4 cell count ≤ 250/µL, AIDS-defining conditions, or AIDS-related death, whichever occurred earlier).

“This evidence supports the use of specific micronutrient supplementation as an effective intervention in HIV-infected adults in early stages of HIV disease, significantly reducing the risk for disease progression in asymptomatic, ART-naive, HIV-infected adults. This reduced risk may translate into delay in the time when the HIV-infected patients experience immune dysfunction and into broader access to HIV treatment in developing countries,” the authors conclude.

The researchers add that their “findings are generalizable to other HIV subtype C-infected cohorts in resource-limited settings where the provision of ART is being scaled up, rolled out, or not yet available to all in conditions similar to those in Botswana at the time of this study.”

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(doi:10.l001/jama.2013.280923; Available pre-embargo to the media at http://media.jamanetwork.com)

Editor’s Note: This study was funded by the National Institute on Drug Abuse. All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported

A touch of garlic helps kill contaminants in baby formula

Media Release | November 25, 2013

garlic 770

Two compounds derived from garlic may help contaminants in baby formula, says a UBC study. Photo: Rüdiger Wölk, Münster/Wikimedia Commons.

Garlic may be bad for your breath, but it’s good for your baby, according to a new study from the University of British Columbia.

The study, recently published in Applied and Environmental Microbiology, is the first to identify two compounds derived from garlic – diallyl sulfide and ajoene – that significantly reduce the contamination risk of Cronobacter sakazakii in the production of dry infant formula powder.

Continue reading “A touch of garlic helps kill contaminants in baby formula”

Most ignored medical breakthroughs ( Part 1 ) Please share or Repost Freely

This is part 1 of the most ignored medical breakthroughs since I started accumulating research. There is far more research that never made any of the major media outlets. Healthcare does not need to be scary nor expensive if science not profit were held in a higher esteem.

Please share this list…It can make a significant difference in more ways than one.. 😉

Ralph Turchiano

 

LSUHSC research finds combo of plant nutrients killed 100% of sample breast cancer cells

Contact: Leslie Capo lcapo@lsuhsc.edu 504-568-4806 Louisiana State University Health Sciences Center

New Orleans, LA – A study led by Madhwa Raj, PhD, Research Professor in Obstetrics and Gynecology at LSU Health Sciences Center New Orleans and its Stanley S. Scott Cancer Center, has found that a super cocktail of six natural compounds in vegetables, fruits, spices and plant roots killed 100% of sample breast cancer cells without toxic side effects on normal cells. The results, which also revealed potential treatment target genes, are published in the November 2013 issue of The Journal of Cancer.

Continue reading “LSUHSC research finds combo of plant nutrients killed 100% of sample breast cancer cells”

Discovery of brain activity in severely brain injured patients who ‘wake up’ with sleep drug

Contact: Jennifer Gundersen jeg2034@med.cornell.edu 646-317-7402 Weill Cornell Medical College

Pattern of brain activity points to possible neural circuit switched on by drug and may identify other patients who could respond

NEW YORK (November 19, 2013) — George Melendez has been called a medical miracle. After a near drowning deprived his brain of oxygen, Melendez remained in a fitful, minimally conscious state until his mother, in 2002, decided to give him the sleep aid drug Ambien to quiet his moaning and writhing. The next thing she knew, her son was quietly looking at her and trying to talk. He has been using the drug ever since to maintain awareness, but no one could understand why Ambien led to such an awakening.

Continue reading “Discovery of brain activity in severely brain injured patients who ‘wake up’ with sleep drug”

Resveratrol a Natural Compound Mitigates Effects of Methamphetamine Abuse

Nov. 19, 2013

Story Contact(s):  Jeff Sossamon, sossamonj@missouri.edu, 573-882-3346

COLUMBIA, Mo. – Studies have shown that resveratrol, a natural compound found in colored vegetables, fruits and especially grapes, may minimize the impact of Parkinson’s disease, stroke and Alzheimer’s disease in those who maintain healthy diets or who regularly take resveratrol supplements. Now, researchers at the University of Missouri have found that resveratrol may also block the effects of the highly addictive drug, methamphetamine.

Continue reading “Resveratrol a Natural Compound Mitigates Effects of Methamphetamine Abuse”

Bitter melon extract may have potential to fight head and neck cancer

Contact: Riya V. Anandwala ranandwa@slu.edu 314-977-8018 Saint Louis University

ST. LOUIS – Extract taken from an Asian vegetable may have therapeutic qualities to treat head and neck cancer, a Saint Louis University researcher has found.

Continue reading “Bitter melon extract may have potential to fight head and neck cancer”

Can Certain Herbs Stave Off Alzheimer’s Disease?

 

 

ST. LOUIS — Enhanced extracts made from special antioxidants in spearmint and rosemary improve learning and memory, a study in an animal model at Saint Louis University found.

“We found that these proprietary compounds reduce deficits caused by mild cognitive impairment, which can be a precursor to Alzheimer’s disease,” said Susan Farr, Ph.D., research professor geriatrics at Saint Louis University School of Medicine.

Farr added, “This probably means eating spearmint and rosemary is good for you. However, our experiments were in an animal model and I don’t know how much — or if any amount — of these herbs people would have to consume for learning and memory to improve. In other words, I’m not suggesting that people chew more gum at this point.”

Farr presented the early findings at Neuroscience 2013, a meeting of 32,000 on Monday, Nov. 11. She tested a novel antioxidant-based ingredient made from spearmint extract and two different doses of a similar antioxidant made from rosemary extract on mice that have age-related cognitive decline.

She found that the higher dose rosemary extract compound was the most powerful in improving memory and learning in three tested behaviors. The lower dose rosemary extract improved memory in two of the behavioral tests, as did the compound made from spearmint extract.

Further, there were signs of reduced oxidative stress, which is considered a hallmark of age-related decline, in the part of the brain that controls learning and memory.

“Our research suggests these extracts made from herbs might have beneficial effects on altering the course of age-associated cognitive decline,” Farr said. “It’s worth additional study.”

The research, which was supported by the VA Medical Center in St. Louis, was conducted in conjunction with Kemin Industries, which manufactures specialty ingredients for vitamin/dietary supplements or that can be added to food to enhance its nutritional and health benefits.

Established in 1836, the School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: infectious disease, liver disease, aging and brain disease, cancer and heart/lung disease.

Inflammatory skin damage in mice blocked by bleach solution, Stanford study finds

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center

STANFORD, Calif. — Processes that age and damage skin are impeded by dilute bleach solution, according to a new study by researchers at the Stanford University School of Medicine.

The study was conducted on mice. But if shown to work similarly in humans, the inexpensive, widely available household chemical could provide a new way to treat skin damage caused by radiation therapy, excess sun exposure or aging.

Dilute bleach baths have been used for decades to treat moderate to severe eczema in humans, but it has not been clear until now why they work. “Originally it was thought that bleach may serve an antimicrobial function, killing bacteria and viruses on the skin,” said Thomas Leung, MD, PhD, an instructor in dermatology at Stanford and a pediatric dermatologist at Lucile Packard Children’s Hospital. “But the concentrations used in clinic are not high enough for this to be the sole reason. So we wondered if there could be something else going on.”

Leung is the lead author of the study, which will be published online Nov. 15 in the Journal of Clinical Investigation. Seung Kim, MD, PhD, professor of developmental biology and a Howard Hughes Medical Institute investigator, is the study’s senior author.

“Dr. Leung relentlessly followed his hunch that an antimicrobial effect of dilute bleach wasn’t the whole story,” Kim said. “And his work has revealed new mechanisms for targeting inflammatory pathways with this versatile small molecule. It has also identified new possible clinical applications.”

Leung and his colleagues knew that many skin disorders, including eczema and radiation dermatitis, have an inflammatory component. When the skin is damaged, immune cells rush to the site of the injury to protect against infection. Because inflammation itself can be harmful if it spirals out of control, the researchers wondered if the bleach (sodium hypochlorite) solution somehow played a role in blocking this response.

To find out, they homed in on a molecule called nuclear factor kappa-light-chain-enhancer of activated B cells, or NF-kB, which is known to play a critical role in inflammation, aging and response to radiation. When activated by signaling molecules, it enters the cell’s nucleus and binds to DNA to control gene expression. When inactive, it is sequestered in the cytoplasm, away from the DNA.

Leung wondered if there could be a link between the effect of the dilute bleach solution and NF-kB’s role in skin. He exposed human keratinocytes, or skin cells, to 0.005 percent bleach for one hour before treating them with a signaling molecule that normally activates NF-kB function. He found that exposure to the solution blocked the expression of two genes known to be regulated by NF-kB. The effect was reversible, however — waiting 24 hours after the bleach treatment restored NF-kB’s ability to activate expression of the target genes.

Further investigation divulged how this happens.

“We found that the bleach solution oxidizes and inhibits an activator necessary for NF-kB to enter the nucleus, essentially blocking NF-kB’s effect,” Leung said. When the researchers mutated the activator to be oxidation-resistant, NF-kB’s gene targeting activity was unhindered.

Next, the researchers turned to potential clinical applications. Radiation dermatitis is a common side effect of radiation therapy for cancer. While radiation therapy is directed at cancer cells inside the body, the normal skin in the radiation therapy field is also affected. Radiation therapy often causes a sunburn-like skin reaction. In some cases, these reactions can be quite painful and can require interrupting the radiation therapy course to allow the skin to heal before resuming treatment. However, prolonged treatment interruptions are undesirable.

“An effective way to prevent and treat radiation dermatitis would be of tremendous benefit to many patients receiving radiation therapy,” said Susan Knox, MD, PhD, associate professor of radiation oncology and study co-author.

Leung and his colleagues tested the effect of daily, 30-minute baths in bleach solution on laboratory mice with radiation dermatitis. They found that the animals bathed in the bleach solution experienced less severe skin damage and better healing and hair regrowth than animals bathed in water.

They then turned their attention to old — but healthy — laboratory mice.

“Multiple research studies have linked increased NF-kB activity with aging,” Leung said. “We found that if we blocked NF-kB activity in elderly laboratory mice by bathing them in the bleach solution, the animals’ skin began to look younger. It went from old and fragile to thicker, with increased cell proliferation.” The effect diminished soon after the dilute-bleach baths were stopped, indicating that regular exposure is necessary to maintain skin thickness.

The researchers are now considering clinical trials in humans, and they are also looking at other diseases that could be treated by dilute-bleach baths. “It’s possible that, in addition to being beneficial to radiation dermatitis, it could also aid in healing wounds like diabetic ulcers,” Leung said. “This is exciting because there are so few side effects to dilute bleach. We may have identified other ways to use hypochlorite to really help patients. It could be easy, safe and inexpensive.”

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Other Stanford co-authors of the study were Lillian Zhang, a life sciences research assistant; senior researcher Jing Wang, MD; and research associate Shoucheng Ning, MD, PhD.

The study was supported by the Dermatology Foundation, the National Institutes of Health (training grant DK007217-38) and the Howard Hughes Medical Institute.

Information about Stanford’s Department of Dermatology, which also supported the work, is available at http://dermatology.stanford.edu.

The Stanford University School of Medicine consistently ranks among the nation’s top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children’s Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.

Print media contact: Krista Conger at (650) 725-5371 (kristac@stanford.edu) Broadcast media contact: M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)

Scientists report human dietary supplement cures lab animals infected with human intestinal parasite ( Hookworm )

Contact: Preeti Singh psingh@burnesscommunications.com 301-280-5722

Bridget DeSimone bdesimone@burnesscommunications.com 301-280-5735

Burness Communications

Preliminary success using ‘probiotics’ against hookworms raises hope for treating afflictions that burden 1.5 billion and cause stunting, development delays in children

WASHINGTON, D.C. (November 15, 2013) — Laboratory animals fed a modified version of a common human dietary supplement were completely cured of intestinal worms that belong to a family of parasites that currently infect 1.5 billion people, or almost one quarter of the world’s population, according to new research presented today at the annual meeting of the American Society of Tropical Medicine and Hygiene (ASTMH).

“We need to replicate the results in other animals and also in humans, but this is an important development in our effort to find a safe, affordable and effective way to confront a major global health problem,” said Raffi Aroian, PhD, principal investigator of a team of scientists at the University of California, San Diego who are seeking new treatments for a variety of parasitic worms known as “soil-transmitted helminths” or STHs.

While rarely fatal, STHs and other intestinal worms are leading contributors to disease in school-age children in low-income countries and are viewed by many experts as among the most burdensome of the world’s “neglected tropical diseases” or NTDs.

The study conducted by Aroian’s team focused on hookworms, common STHs that are found in soil that has been contaminated with human feces. Hookworms can linger in the intestines for years, where they feed on blood and tissue, robbing their hosts of iron and protein and interfering with absorption of critical nutrients. They frequently cause stunting and cognitive delays in infected children. They also can have long-term effects on educational achievement and productivity.

Currently, the only drugs available to treat hookworms in humans were originally developed to combat parasites that infect farm animals. Aroian said they are only partially effective against the range of intestinal parasites that infect humans. There is also evidence of reinfections occurring rapidly after treatment and low levels of efficacy in some places.

At the ASTMH meeting, Aroian’s colleague Yan Hu, PhD reported findings from a study in which hamsters were deliberately infected with hookworms. The hamsters were later divided into two groups. One group received a common strain of the bacteria Bacillus subtilis, which is often marketed as a “probiotic”—a dietary supplement consumed as a pill or added to food that is intended to promote digestive health. It also is the key ingredient in a popular Japanese fermented soybean dish called Natto. The other group received the same probiotic, except the researchers modified it to express a protein derived from a closely related bacterium, Bacillus thuringiensis or Bt, which is known to be safe in humans but potentially lethal to intestinal worms.

“Five days after we administered the bacteria, we examined the animals’ intestines,” Hu said. “We found no worms in the animals that received the modified probiotic, while those that did not receive the modified probiotic remained infected.”

Hu said the next step will be to conduct tests in different types of animals and against different types of STHs. If the probiotic continues to perform well against multiple intestinal parasites and is shown to be safe, then researchers would consider testing in humans, she said.

The research is supported by grants from the Bill & Melinda Gates Foundation and the National Institutes of Health.

“While the research has yet to move beyond tests in animals, the human health burden is so immense and the solutions so few that it’s gratifying to see progress being made toward finding new treatments for intestinal worm diseases,” said ASTMH President David H. Walker, MD. “It shows that new investments in neglected tropical diseases are inspiring creative solutions for the more than a billion people in need.”

Aroian said the overall goal of the work is to produce a treatment for intestinal worms that is safe, effective and affordable in the world’s poorest countries, where hookworms and other STHs do the most damage.  “This probiotic is a food-grade bacterial product that can be easily produced in large quantities in a simple fermenter, and it can be manufactured in a form that has a long shelf-life,” he said. “It could be well-suited to providing the cheap, mass treatment we need to substantially reduce the burden of this disease.”

Aroian said Bt is attractive because it is a well-understood, natural substance for controlling plant pests that is believed to be safe for animals and humans. It is frequently sprayed on organic crops and is mainly lethal to insects in their larva stage. Bt also is a bacteria used in genetically engineered corn and soybean to endow the crops with resistance to plant pests.

Aroian said that while the modified probiotic under development in his lab should be safe to consume, if it proves to be an effective intervention for intestinal worms it would be marketed as a treatment, not as a dietary supplement.

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About the American Society of Tropical Medicine and Hygiene ASTMH, founded in 1903, is a worldwide organization of scientists, clinicians and program professionals whose mission is to promote global health through the prevention and control of infectious and other diseases that disproportionately afflict the global poor.

Compound stymies polyomaviruses and Ricin in lab tests

Contact: David Orenstein david_orenstein@brown.edu 401-863-1862 Brown University

A team of scientists reports that a small molecule compound showed significant success in controlling the infectivity and spread of three polyomaviruses in human cell cultures. To date there has been no medicine approved to treat such viruses, which prey on transplant recipients, people with HIV, and others whose immune systems have been weakened.

The compound, known by the abbreviated name “Retro-2,” was able to protect the vast majority of cells in cultures when it was administered even after infection began. According to results published this week in the journal mBio, 12 days of treatment with Retro-2 kept 90.5 percent of cells free from JC Polyomavirus, 89 percent of cells clear of the BK Polyomavirus, and 84 percent of cells protected from the SV40 polyomavirus. Infection rates and virus production were much higher among cells in cultures that were similarly infected, but left untreated as controls.

That the compound gained the upper hand on viruses that had a head start is a key advance, said Brown University biologist Walter Atwood, corresponding author of the paper. Other substances have defeated the viruses only if they were used to pre-treat cells before any infection.

“But that’s not reality,” Atwood said. “The reality is that someone is already infected with the virus. Whenever in the past we first infected the cells with the virus and then came in with the drug, we’ve never been successful in being able to stop the spread of the virus. This drug is successful at that.”

Brown University has a patent filed on the use of the compound against pathogen infections. The research also involved a team of scientists at Yale University led by Professor Daniel DiMaio.

An ‘ER’ medicine

Retro-2 appears to work by blocking the ability of polyomaviruses to sneak around host cells by hijacking the workings of the intracellular protein transportation hub: the endoplasmic reticulum (ER).

Christian Nelson, a Brown postdoctoral researcher currently visiting at Yale, first thought to study Retro-2 after reading a 2010 paper in Cell showing that it blocks certain toxins, including ricin, from working through the ER. Ricin and polyomaviruses have been thought to operate similarly. The compound also did not appear to be toxic to the mice in that study.

“There are a lot of viruses that use these trafficking mechanisms,” Atwood said.

So the team bought some Retro-2 from Chembridge, a company that makes vast libraries of small molecule compounds for scientists to study, and pitted it against the polyomaviruses.

The researchers tested it in several ways, including with both kidney cells and brain cells because those are the tissues in the body where they can cause disease. Retro-2 appeared effective in protecting the various cells, as long as it was present within several hours of infection.

“When this causes disease in people there’s progressively more and more cells infected,” Nelson said. “If we can identify infection early, a treatment could help to stop that progression.”

Improving the chemistry

Atwood and Nelson acknowledge that they aren’t yet sure exactly how Retro-2 blocks the viruses in the ER, but thanks to a team of collaborating chemists, they do know what chemical structure makes the drug effective.

Brown chemistry Professors Jason Sello and Paul Williard and graduate student Daniel Carney studied the compound’s chemical structure. In efforts to prepare Retro-2, Sello and Carney found that the last step in the synthesis yielded not only the reported structure but also a form called a dihydroquinazolinone (DHQ). The DHQ was the apparent result of a “cyclizing” reaction of Retro-2 that gives it a different chemical structure.

Further experiments identified the exact structure of the DHQ form and showed that it was the form that matched what Atwood and Nelson had found to be effective in the lab.

This detailed understanding of the compound is helping Sello and his team improve the drug further.

“A critical part of any drug development program is the unambiguous assignment of the structure of the lead compound,” Sello said. “With knowledge of the Retro-2 structure, we have been rationally preparing analogs that have improved pharmacological properties.”

###

In addition to Atwood, Sello, Nelson, Carney, Willard and DiMaio, other authors on the paper are Aaron Derdowski, Gretchen Gee, and Bethany O’Hara of Brown; and Alex Lipovsky of Yale.

The National Institutes of Health, the National Science Foundation and Johnson & Johnson supported the research. Some research occurred in Brown’s Leduc Bioimaging Facility and Genomics Core, as well as in Yale’s Cooley lab.

Study is the first to show higher dietary acid load increases risk of diabetes ( Up to 56% Increased Risk )

Contact: Dr Guy Fagherazzi Guy.FAGHERAZZI@gustaveroussy.fr 33-142-116-140 Diabetologia

A study of more than 60 000 women has shown that higher overall acidity of the diet, regardless of the individual foods making up that diet, increases the risk of type 2 diabetes. The study, the first large prospective study to demonstrate these findings, is published in Diabetologia, the journal of the European Association for the Study of Diabetes (EASD), and is by Dr Guy Fagherazzi and Dr Françoise Clavel-Chapelon, Center for Research in Epidemiology and Population Health, INSERM, Paris, France, and colleagues.

A western diet rich in animal products and other acidogenic foods can induce an acid load that is not compensated for by fruit and vegetables; this can cause chronic metabolic acidosis and lead to metabolic complications. Most importantly from a blood-sugar control perspective, increasing acidosis can reduce the ability of insulin to bind at appropriate receptors in the body, and reduce insulin sensitivity. With this in mind, the authors decided to analyse whether increased acidosis caused by dietary acid loads increased the risk of type 2 diabetes.

A total of 66,485 women from the E3N study (the French Centre of the European Prospective Investigation into Cancer and Nutrition, a well-known ongoing epidemiological study) were followed for new diabetes cases over 14 years. Their dietary acid load was calculated from their potential renal acid load (PRAL) and their net endogenous acid production (NEAP) scores, both standard techniques for assessing dietary acid consumption from nutrient intake.

During follow-up, 1,372 new cases of incident type 2 diabetes occurred. In the overall population, those in the top 25% (quartile) for PRAL had a 56% increased risk of developing type 2 diabetes compared with the bottom quartile. Women of normal weight (BMI of 25 and under) had the highest increased risk (96% for top quartile versus bottom) while overweight women (BMI 25 and over) had only a 28% increased risk (top quartile versus bottom). NEAP scores showed a similar increased risk for higher acid load.

The authors say: “A diet rich in animal protein may favour net acid intake, while most fruits and vegetables form alkaline precursors that neutralise the acidity. Contrary to what is generally believed, most fruits such as peaches, apples, pears, bananas and even lemons and oranges actually reduce dietary acid load once the body has processed them. In our study, the fact that the association between both PRAL and NEAP scores and the risk of incident type 2 diabetes persisted after adjustment for dietary patterns, meat consumption and intake of fruit, vegetables, coffee and sweetened beverages suggests that dietary acids may play a specific role in promoting the development of type 2 diabetes, irrespective of the foods or drinks that provide the acidic or alkaline components.”

They conclude: “We have demonstrated for the first time in a large prospective study that dietary acid load was positively associated with type 2 diabetes risk, independently of other known risk factors for diabetes. Our results need to be validated in other populations, and may lead to promotion of diets with a low acid load for the prevention of diabetes. Further research is required on the underlying mechanisms.”

How zinc starves lethal bacteria to stop infection

Contact: Dr Christopher McDevitt christopher.mcdevitt@adelaide.edu.au 61-449-823-946 University of Adelaide

Australian researchers have found that zinc can ‘starve’ one of the world’s most deadly bacteria by preventing its uptake of an essential metal.

The finding, by infectious disease researchers at the University of Adelaide and The University of Queensland, opens the way for further work to design antibacterial agents in the fight against Streptococcus pneumoniae.

Streptococcus pneumoniae is responsible for more than one million deaths a year, killing children, the elderly and other vulnerable people by causing pneumonia, meningitis, and other serious infectious diseases.

Published today in the journal Nature Chemical Biology, the researchers describe how zinc “jams shut” a protein transporter in the bacteria so that it cannot take up manganese, an essential metal that Streptococcus pneumoniae needs to be able to invade and cause disease in humans.

“It’s long been known that zinc plays an important role in the body’s ability to protect against bacterial infection, but this is the first time anyone has been able to show how zinc actually blocks an essential pathway causing the bacteria to starve,” says project leader Dr Christopher McDevitt, Research Fellow in the University of Adelaide’s Research Centre for Infectious Diseases.

“This work spans fields from chemistry and biochemistry to microbiology and immunology to see, at an atomic level of detail, how this transport protein is responsible for keeping the bacteria alive by scavenging one essential metal (manganese), but at the same time also makes the bacteria vulnerable to being killed by another metal (zinc),” says Professor Bostjan Kobe, Professor of Structural Biology at The University of Queensland.

The study reveals that the bacterial transporter (PsaBCA) uses a ‘spring-hammer’ mechanism to bind the metals. The difference in size between the two metals, manganese and zinc, causes the transporter to bind them in different ways. The smaller size of zinc means that when it binds to the transporter, the mechanism closes too tightly around the zinc, causing an essential spring in the protein to unwind too far, jamming it shut and blocking the transporter from being able to take up manganese.

“Without manganese, these bacteria can easily be cleared by the immune system,” says Dr McDevitt. “For the first time, we understand how these types of transporters function. With this new information we can start to design the next generation of antibacterial agents to target and block these essential transporters.”

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The research has been funded by the Australian Research Council and the National Health and Medical Research Council.

Media Contact:

Dr Christopher McDevitt Research Fellow Research Centre for Infectious Diseases School of Molecular and Biomedical Science The University of Adelaide Mobile: +61 449 823 946 christopher.mcdevitt@adelaide.edu.au

Professor Bostjan Kobe Professor of Structural Biology Australian Infectious Diseases Research Centre School of Chemistry & Molecular Biosciences The University of Queensland Phone : +61 7 3365 2132 b.kobe@uq.edu.au

Robyn Mills Media Officer The University of Adelaide Phone: +61 8 8313 6341 Mobile: +61 410 689 084 robyn.mills@

Acid levels in the diet could have profound effects on kidney health

Contact: Kurtis Pivert kpivert@asn-online.org 202-699-0238 American Society of Nephrology

Atlanta, GA (November 9, 2013)—Three new studies suggest that controlling dietary acid intake could help improve kidney health. Results of these studies will be presented at ASN Kidney Week 2013 November 5-10 at the Georgia World Congress Center in Atlanta, GA.

A diet rich in wheat flour and animal protein produces an acidic environment in the body that worsens with age as kidney function declines. This acid load can be detrimental to a variety of tissues and processes. Research suggests that consuming more fruits and vegetables—which are highly alkaline—may help counteract these effects.

In a new study, a team led by Nimrit Goraya, MD (Texas A&M College of Medicine) investigated whether consuming fruits and vegetables can protect the kidney health of individuals with hypertensive nephropathy, a condition in which damage to the kidneys occurs due to high blood pressure. In this study, 23 hypertensive patients received extra dietary fruits and vegetables, 23 patients received an oral alkaline medication, and 25 patients received nothing. One year later, kidney injury progressed in patients who received no intervention, but kidney health was preserved in those receiving fruits and vegetables or oral alkaline medication.

In another study, Eiichiro Kanda, MD, PhD (Tokyo Kyosai Hospital) and his colleagues investigated the role of dietary acid levels in chronic kidney disease (CKD) progression. The retrospective study analyzed data from 249 CKD patients in Japan. High acid levels were linked with accelerated kidney function decline, and patients with elevated acid levels had an increased risk of CKD progression compared with patients with low acid levels. The findings suggest that monitoring and control of dietary acid levels are necessary for the prevention of CKD progression.

Another study led by Deidra Crews, MD, FASN (Johns Hopkins University School of Medicine) looked to see whether the effect of dietary acid on risk of kidney failure differed by race in a group of 159 non-Hispanic black and 760 non-Hispanic white CKD patients who had an annual household income below 300% of the federal poverty guideline. Participants were taking part in the 1999-2004 National Health and Nutrition Examination Survey. Overall, 12.4% of participants (38.3% whites and 61.7% blacks) developed kidney failure during an average of 6.4 years of follow up. Blacks had higher acid levels than whites. They also had a 3-fold higher risk of developing kidney failure compared with whites after adjusting for factors such as age, sex, and caloric intake. Increased acid levels were more strongly associated with kidney failure among blacks than among whites. The findings indicate that among CKD patients with low socioeconomic status, the detrimental effect of high dietary acid levels on progression to kidney failure appears to be greater for blacks than for whites.

###

Highlights

  • In patients with hypertensive nephropathy, kidney health was preserved in those consuming extra fruits and vegetables, which are highly alkaline.
  • In patients with chronic kidney disease, those with high dietary acid levels experienced accelerated kidney function decline.
  • In chronic kidney disease patients with low socioeconomic status, the detrimental effect of high dietary acid levels on progression to kidney failure was greater for blacks than for whites. 

Studies:

“Fruits and Vegetables or Oral NaHCO3 Prevent Progression of Kidney Injury in Stage 1 CKD Due to Hypertensive Nephropathy.” (Abstract FR-PO816)

“Dietary Acid Load Is Associated with Chronic Kidney Disease Progression in Elderly Patients.” (Abstract TH-PO243)

Disclosures: Masumi Ai receives research funding from MSD, Co., and Kyowa-Kirin, Co. Masayuki Yoshida receives research funding and honoraria from Astra Zeneca, Novartis, Pfizer, MSD, and Bayer.

“Race, Dietary Acid Load and Risk of ESRD among Low Income Americans with CKD.” (Abstract SA-OR050)

Disclosures: Deidra C. Crews is a consultant for The Boston Consulting Group and receives honoraria from the National Institute on Aging and National Institutes of Health. Hal Morgenstern is a consultant for the Arbor Research for Collaborative Health. Rajiv Saran receives research funding from the Renal Research Institute, Forest Research Institute, and Arbor Research Collaborative for Health; and honoraria from Otsuka. Neil R. Powe receives honoraria from ABIM, ASN, Robert Wood Johnson Foundation, Vanderbilt University, Commonwealth Fund, Informed Medical Decision Making Foundation. The authors report funding from the Department of Defense.

ASN Kidney Week 2013, the largest nephrology meeting of its kind, will provide a forum for 14,000 professionals to discuss the latest findings in renal research and engage in educational sessions related to advances in the care of patients with kidney and related disorders. Kidney Week 2013 will take place November 5 – 10, 2013 in Atlanta, GA.

The content of this article does not reflect the views or opinions of The American Society of Nephrology (ASN). Responsibility for the information and views expressed therein lies entirely with the author(s). ASN does not offer medical advice. All content in ASN publications is for informational purposes only, and is not intended to cover all possible uses, directions, precautions, drug interactions, or adverse effects. This content should not be used during a medical emergency or for the diagnosis or treatment of any medical condition. Please consult your doctor or other qualified health care provider if you have any questions about a medical condition, or before taking any drug, changing your diet or commencing or discontinuing any course of treatment. Do not ignore or delay obtaining professional medical advice because of information accessed through ASN. Call 911 or your doctor for all medical emergencies.

Founded in 1966, and with more than 14,000 members, the American Society of Nephrology (ASN) leads the fight against kidney disease by educating health professionals, sharing new knowledge, advancing research, and advocating the highest quality care for patients.

Vitamin C could ease muscle fatigue in chronic obstructive pulmonary disease patients

Contact: Donna Krupa dkrupa@the-aps.org American Physiological Society

Bethesda, Md. (Nov. 7, 2013)—Chronic obstructive pulmonary disease—a health problem in which the lungs lose their inherent springiness, making it progressively harder to breathe—can have a dramatic effect on the ability to exercise and even perform simple activities of daily life because of the disease’s fallout effects on skeletal muscles. Several factors have been implicated in these muscle problems. These include loss of fitness from inactivity, problems with the part of cells that convert fuel to energy caused by the COPD itself, and oxidative stress, a phenomenon in which cells and tissues become damaged by unstable molecules called free radicals that harm other molecules in domino-like chain reactions. Some research suggests that easing oxidative stress could improve skeletal muscle function.

To test this idea, researchers led by Matthew J. Rossman of the George E. Whalen VA Medical Center and the University of Utah gave COPD patients intravenous (IV) infusions of vitamin C, a powerful antioxidant that can combat oxidative stress, or saline as a placebo before the patients performed knee extension exercises and underwent neuromuscular function tests. Their findings show that IV infusions of vitamin C can improve skeletal muscle fatigue in COPD patients, further implicating the role of oxidative stress in the skeletal muscle problems that accompany this disease.

The article is entitled “Ascorbate Infusion Increases Skeletal Muscle Fatigue Resistance in Patients with Chronic Obstructive Pulmonary Disease“. It appears in the online edition of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, published by the American Physiological Society.

Methodology

The researchers worked with 10 COPD patients. Each patient performed a set of knee extension exercises, receiving either an IV infusion of saline or an IV infusion of vitamin C before the set, but both the study volunteers and the researchers monitoring the exercises didn’t know which infusion the volunteers received. Two to three days later, the volunteers performed a second set of knee exercises after receiving the other type of infusion. Before and after they performed these exercises, the study subjects had blood drawn to test for antioxidant levels. Immediately after the exercises, the researchers measured a variety of other factors, including the volunteers’ breathing and heart rate, blood pressure, feelings of exertion of breathlessness, and blood flow.

Results

The researchers found that during exercises, patients had significantly less muscle fatigue after receiving vitamin C and breathed better and slower. After vitamin C infusions, the volunteers also had significantly higher blood antioxidant activity than when they received only saline. Additionally, vitamin C infusions lowered their resting blood pressure and blood flow.

Importance of the Findings

These findings suggest that IV infusions of antioxidants, such as vitamin C, can curb the skeletal muscle fatigue that plagues COPD patients. They also provide further evidence that oxidative stress plays a critical role in the skeletal muscle dysfunction that many COPD patients experience. They suggest that antioxidants could eventually be used as a treatment for these problems.

“Targeting oxidative stress with some form of antioxidant therapy in a clinical setting may represent an important therapeutic avenue for patients with COPD,” they write.

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Study Team

In addition to Matthew J. Rossman, the study team also includes Ryan S. Garten, J. Jonathan Groot, Van Reese, Jia Zhao, Markus Amann, and Russell S. Richardson, all of the George E. Whalen VA Medical Center and the University of Utah.

Physiology is the study of how molecules, cells, tissues, and organs function in health and disease. Established in 1887, the American Physiological Society (APS) was the first US society in the biomedical sciences field. The Society represents more than 11,000 members and publishes 14 peer-reviewed journals with a worldwide readership.

NOTE TO EDITORS: To schedule an interview with a member of the research team, please contact Donna Krupa at dkrupa@the-aps.org, @Phyziochick, or 301.634.7209. The article is available online at http://bit.ly/1bZiW5W.

Higher chocolate consumption associated with lower levels of total fat—fat deposits all over the body—and central—abdominal—fat, independently of whether or not subjects are physically active, and of their diet

Scientists at the University of Granada have disproved the old idea that chocolate is fattening, in a study reported this week in Nutrition

 

The study—possibly the most comprehensive to date—included 1458 European adolescents aged between 12 and 17 years

University of Granada researchers from the Faculty of Medicine and the Faculty of Physical Activity and Sports Sciences have scientifically disproven the old belief that eating chocolate is fattening. In an article published this week in the journal Nutrition, the authors have shown that higher consumption of chocolate is associated with lower levels of total fat (fat deposited all over the body) and central fat (abdominal), independently of whether or not the individual participates in regular physical activity and of diet, among other factors.

The researchers determined whether greater chocolate consumption associated with higher body mass index and other indicators of total and central body fat in adolescents participating in the HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) study. This project, financed by the European Union, studies eating habits and lifestyle in young people in 9 European countries, including Spain.

 

Independent of diet and physical activity

The study involved 1458 adolescents aged between 12 and 17 years and results showed that a higher level of chocolate consumption associated with lower levels of total and central fat when these were estimated through body mass index, body fat percentage—measured by both skinfolds and bioelectrical impedance analysis—and waist circumference. These results were independent of the participant’s sex, age, sexual maturation, total energy intake, intake of saturated fats, fruit and vegetables, consumption of tea and coffee, and physical activity.

As the principle author Magdalena Cuenca-García explains, although chocolate is considered a high energy content food—it is rich in sugars and saturated fats—“recent studies in adults suggest chocolate consumption is associated with a lower risk of cardiometabolic disorders”.

In fact, chocolate is rich in flavonoids—especially catechins—which have many healthy properties: “they have important antioxidant, antithrombotic, anti-inflammatory and antihypertensive effects and can help prevent ischemic heart disease”.

Recently, another cross-sectional study in adults conducted by University of California researchers found that more frequent chocolate consumption also associated with a lower body mass index. What’s more, these results were confirmed in a longitudinal study in women who followed a catechin-rich diet.

The effect could be partly due to the influence of catechins on cortisol production and on insulin sensitivity, both of which are related with overweight and obesity.

 

Calorie impact is not the only thing that matters

The University of Granada researchers have sought to go further and analyse the effect of chocolate consumption at a critical age like adolescence by also controlling other factors that could influence the accumulation of fat. The research, which is both novel and, perhaps, the largest and best-controlled study to date, is the first to focus on the adolescent population. It includes a large number of body measures, objective measurement of physical activity, detailed dietary recall with 2 non-consecutive 24-hour registers using image-based software, and controls for the possible effect of a group of key variables.

In Nutrition, the authors stress that the biological impact of foods should not be evaluated solely in terms of calories. “The most recent epidemiologic research focuses on studying the relation between specific foods—both for their calorie content and for their components—and the risk factors for developing chronic illnesses, including overweight and obesity”.

Despite their results, the authors insist that chocolate consumption should always be moderate. “In moderate quantities, chocolate can be good for you, as our study has shown. But, undoubtedly, excessive consumption is prejudicial. As they say: you can have too much of a good thing”.

The University of Granada researchers stress that their findings “are also important from a clinical perspective since they contribute to our understanding of the factors underlying the control and maintenance of optimal weight”.

 

 

Reference: Association between chocolate consumption and fatness in European adolescents Magdalena Cuenca-García, Jonatan R. Ruiz, Francisco B. Ortega, Manuel J. Castillo Nutrition (2013). http://dx.doi.org/10.1016/j.nut.2013.07.011

chocolate

 

In the photo, the University of Granada researchers who have published this article. From left to right, Jonatan R. Ruiz, Magdalena Cuenca-García, Manuel J. Castillo and Francisco B. Ortega. Dr Ruiz and Dr Ortega currently work in the Department of Physical and Sports Education (Faculty of Physical Activity and Sports Sciences), and Dr Cuenca-García and Dr Castillo work in the Department of Physiology (Faculty of Medicine).

Corresponding author: Magdalena Cuenca-García Department of Physiology Faculty of Medicine University of Granada Telephone: +34 958 24 3540 E-mail address: mmcuenca@ugr.es

Study links intestinal bacteria to rheumatoid arthritis

Contact: Craig Andrews craig.andrews@nyumc.org 212-404-3511 NYU Langone Medical Center / New York University School of Medicine

Findings suggest bacterial disturbances in the gut may play a role in autoimmune attacks on the joints, point the way to novel treatments and diagnostics

Researchers have linked a species of intestinal bacteria known as Prevotella copri to the onset of rheumatoid arthritis, the first demonstration in humans that the chronic inflammatory joint disease may be mediated in part by specific intestinal bacteria. The new findings by laboratory scientists and clinical researchers in rheumatology at NYU School of Medicine add to the growing evidence that the trillions of microbes in our body play an important role in regulating our health.

Using sophisticated DNA analysis to compare gut bacteria from fecal samples of patients with rheumatoid arthritis and healthy individuals, the researchers found that P. copri was more abundant in patients newly diagnosed with rheumatoid arthritis than in healthy individuals or patients with chronic, treated rheumatoid arthritis. Moreover, the overgrowth of P. copri was associated with fewer beneficial gut bacteria belonging to the genera Bacteroides.

“Studies in rodent models have clearly shown that the intestinal microbiota contribute significantly to the causation of systemic autoimmune diseases,” says Dan R. Littman, MD, PhD, the Helen L. and Martin S. Kimmel Professor of Pathology and Microbiology and a Howard Hughes Medical Institute investigator.

“Our own results in mouse studies encouraged us to take a closer  look at patients with rheumatoid arthritis, and we found this remarkable and surprising association,” says Dr. Littman, whose basic science laboratory at NYU School of Medicine’s Skirball Institute of Biomolecular Medicine collaborated with clinical investigators led by Steven Abramson, MD, senior vice president and vice dean for education, faculty, and academic affairs; the Frederick H. King Professor of Internal Medicine; chair of the Department of Medicine; and professor of medicine and pathology at NYU School of Medicine.

“At this stage, however, we cannot conclude that there is a causal link between the abundance of P. copri and the onset of rheumatoid arthritis,” Dr. Littman says. “We are developing new tools that will hopefully allow us to ask if this is indeed the case.”

The new findings, reported today in the open-access journal eLife, were inspired by previous research in Dr. Littman’s laboratory, collaborating with Harvard Medical School investigators, using mice genetically predisposed to rheumatoid arthritis, which resist the disease if kept in sterile environments, but show signs of joint inflammation when exposed to otherwise benign gut bacteria known as segmented filamentous bacteria.

Rheumatoid arthritis, an autoimmune disease that attacks joint tissue and causes painful, often debilitating stiffness and swelling, affects 1.3 million Americans. It strikes twice as many women as men and its cause remains unknown although genetic and environmental factors are thought to play a role.

The human gut is home to hundreds of species of beneficial bacteria, including P. copri, which ferment undigested carbohydrates to fuel the body and keep harmful bacteria in check. The immune system, primed to attack foreign microbes, possesses the extraordinary ability to distinguish benign or beneficial bacteria from pathogenic bacteria. This ability may be compromised, however, when the gut’s microbial ecosystem is thrown off balance.

“Expansion of P. copri in the intestinal microbiota exacerbates colonic inflammation in mouse models and may offer insight into the systemic autoimmune response seen in rheumatoid arthritis,” says Randy S. Longman, MD, PhD, a post-doctoral fellow in Dr. Littman’s laboratory and a gastroenterologist at Weill-Cornell, and an author on the new study. Exactly how this expansion relates to disease remains unclear even in animal models, he says.

Why P. copri growth seems to take off in newly diagnosed patients with rheumatoid arthritis is also unclear, the researchers say. Both environmental influences, such as diet and genetic factors can shift bacterial populations within the gut, which may set off a systemic autoimmune attack. Adding to the mystery, P. copri extracted from stool samples of newly diagnosed patients appears genetically distinct from P. copri found in healthy individuals, the researchers found.

To determine if particular bacterial species correlate with rheumatoid arthritis, the researchers sequenced the so-called 16S gene on 44 fecal DNA samples from newly diagnosed patients with rheumatoid arthritis prior to immune-suppressive treatment; 26 samples from patients with chronic, treated rheumatoid arthritis; 16 samples from patients with psoriatic arthritis (characterized by red, flaky skin in conjunction with joint inflammation); and 28 samples from healthy individuals.

Seventy-five percent of stool samples from patients newly diagnosed with rheumatoid arthritis carried P. copri compared to 21.4% of samples from healthy individuals; 11.5% from chronic, treated patients; and 37.5% from patients with psoriatic arthritis.

Rheumatoid arthritis is treated with an assortment of medications, including antibiotics, anti-inflammatory drugs like steroids, and immunosuppressive therapies that tame immune reactions. Little is understood about how these medications affect gut bacteria. This latest research offers an important clue, showing that treated patients with chronic rheumatoid arthritis carry smaller populations of P. copri. “It could be that certain treatments help stabilize the balance of bacteria in the gut,” says Jose U. Scher, MD, director of the Microbiome Center for Rheumatology and Autoimmunity at NYU Langone Medical Center’s Hospital for Joint Diseases, and an author on the new study. “Or it could be that certain gut bacteria favor inflammation.”

The researchers plan to validate their results in regions beyond New York, since gut flora can vary across geographical regions, and investigate whether the gut flora can be used as a biological marker to guide treatment. “We want to know if people with certain populations of gut bacteria respond better to certain treatment than others,” says Dr. Scher. Finally, they hope to study people before they develop rheumatoid arthritis to see whether overgrowth of P. copri is a cause or result of autoimmune attacks.

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In addition to researchers from the NYU School of Medicine, investigators from Memorial Sloan Kettering Cancer Center and from the Harvard School of Public Health contributed to the study.  Funding for this research comes from the National Institutes of Health, the Howard Hughes Medical Institute, and the American Gastroenterological Association.

About NYU Langone Medical Center:

NYU Langone Medical Center, a world-class, patient-centered, integrated academic medical center, is one of the nation’s premier centers for excellence in clinical care, biomedical research, and medical education. Located in the heart of Manhattan, NYU Langone is composed of four hospitals—Tisch Hospital, its flagship acute care facility; Rusk Rehabilitation; the Hospital for Joint Diseases, the Medical Center’s dedicated inpatient orthopaedic hospital; and Hassenfeld Pediatric Center, a comprehensive pediatric hospital supporting a full array of children’s health services across the Medical Center—plus the NYU School of Medicine, which since 1841 has trained thousands of physicians and scientists who have helped to shape the course of medical history. The Medical Center’s tri-fold mission to serve, teach, and discover is achieved 365 days a year through the seamless integration of a culture devoted to excellence in patient care, education, and research. For more information, go to http://www.NYULMC.org, and interact with us on Facebook, Twitter, and YouTube.

New wonder cure for killer flu originates from the humble turnip ( H1N1 & H7N9 )

A DRINK derived from a vegetable has been hailed as a breakthrough in the search for a cure for flu.

Published: Wed, November 6, 2013

Flu could soon be banished by a landmark scientific discovery
 

Flu could soon be banished by a landmark scientific discovery [GETTY: Pic posed by model]

 

  When a particular strain of Lactobacillus brevis is eaten by mice, it has protective effects against influenza

Naoko Waki

Scientists believe it could revolutionise the way the killer virus is tackled.

They discovered that a strain of bacteria in pickled turnip, a dish popular in Japan, boosts immunity to the virus. Experts are already ­carrying out human trials on a probiotic drink which contains the powerful new ingredient.

The development comes as a leading British expert has warned that the UK is facing one of the worst winter flu tolls for years, with up to 4,000 deaths.

If the research proves effective, a huge number of lives could be saved by people protecting themselves with a probiotic drink, similar to those drunk daily to boost good bacteria in the gut.

flu, flu cures, flu jabs, winter flu, summer flu, dieting to beat flu, easy flu cures, flu symptoms, turnip beats flu, japanese turnips, super foods,

 

Japanese turnips are hailed as the new health wonder [ALAMY]

Japanese scientists discovered that the bacteria Lactobacillus brevis found in a pickled turnip called suguki protected mice exposed to flu.

The bacteria increased the production of immune system moleclues, including flu-specific antibodies. In mice, the effects were powerful enough to prevent infection by the highly contagious H1N1 swine flu. Scientists at research company Kagome believe there could also be protection against the deadly H7N9 strain which has recently emerged in China.

While suguki fans hail its protective powers, it is unknown why the bacteria protects against flu, but it was found to be extremely tolerant to acidic stomach juices.

It is not known whether the same effects will be seen in humans but scientists are hopeful they have found the next superfood.

flu, flu cures, flu jabs, winter flu, summer flu, dieting to beat flu, easy flu cures, flu symptoms, turnip beats flu, japanese turnips, super foods,

Scientists warn this year could be the worst for flu deaths [GETTY: Pic posed by model]

Study author Naoko Waki, writing in science journal Letters of Applied Microbiology, said: “When a particular strain of Lactobacillus brevis is eaten by mice, it has protective effects against influenza.”

The research concluded: “Continual intake of (the drink) for 14 days prior to influenza virus infection alleviated symptoms such as loss of body weight and deterioration in observational physical conditions induced by the infection.”

Ms Waki said further studies are needed to confirm initial findings. Human trials are now under way.

Last month, virologist Professor John Oxford, of Queen Mary University in London, said Britain had “got away with it” recently and predicted this would be the worst winter for flu deaths for years.

He warned doctors and other health staff to improve the shockingly low levels of flu jabs among their ranks, which greatly increases the chances of flu spreading.

Many Britons have limited immunity after several years of relatively low-level outbreaks.

Analysts at Datamonitor Healthcare are forecasting that 10.5 million people will get flu this winter. The virus is most deadly to the elderly and very young.

 

http://www.express.co.uk/news/health/441374/New-wonder-cure-for-killer-flu-originates-from-the-humble-turnip

Oligomeric proanthocyanidin ( Grape Seed Extract ) suppresses the death of retinal ganglion cells

Contact: Meng Zhao
eic@nrren.org
86-138-049-98773
Neural Regeneration Research

 

 

The death of retinal ganglion cells is a hallmark of many optic neurodegenerative diseases such as glaucoma and retinopathy. Oxidative stress is one of the major reasons to cause the cell death. A latest study, published in the Neural Regeneration Research (Vol. 8, No. 25, 2013), has shown that grape seed extract can protect retinal ganglion cells against oxidative stress-induced apoptosis. In this study, Prof. Kwok-Fai So, an academician of Chinese Academy of Sciences, and Prof. Daxiang Lu from Jinan University, China show that oligomeric proanthocyanidin, enriched in grape seeds, has a protective effect on retinal ganglion cells against oxidative stress-induced injury, as confirmed by using both RGC-5 cell lines and retinal explant culture. These findings imply a potential application of oligomeric proanthocyanidin in the clinical treatment of many neural diseases, from glaucoma, ischemia to neurodegenerative disease.

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Article: ” Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis,” by Hui Wang1, 2, Chanjuan Zhang1, 2, Dan Lu1, 2, Xiaoming Shu1, Lihong Zhu1, 2, Renbing Qi1, Kwok-Fai So2, Daxiang Lu1, Ying Xu2 (1 Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of China, Jinan University School of Medicine, Guangzhou 510632, Guangdong Province, China; 2 GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, Guangdong Province, China)

Wang H, Zhang CJ, Lu D, Shu XM, Zhu LH, Qi RB, So KF, Lu DX, Xu Y. Oligomeric proanthocyanidin protects retinal ganglion cells against oxidative stress-induced apoptosis. Neural Regen Res. 2013;8(25):2317-2326.

Contact:

Meng Zhao
eic@nrren.org
86-138-049-98773
Neural Regeneration Research
http://www.nrronline.org/

Full text: http://www.sjzsyj.org/CN/article/downloadArticleFile.do?attachType=PDF&id=704

How does ursolic acid induce neural regeneration after sciatic nerve injury? ( In Apples / Rosemary )

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

Ursolic acid (chemical name 3-hydroxy-12- ursen-28-oic acid) is a triterpenoid extracted from natural plant-based drugs, and has anti-oxidative, anti-inflammatory, anti-apoptotic, and anti-scarring effects, and it regulates the immune system and promotes the repair of injured neurons.However, no reports have explored its role in peripheral nerve injury. A recent study by Prof. Jiajun Chen and team from China-Japan Union Hospital of Jilin University, China established mouse models of sciatic nerve injury through unilateral sciatic nerve complete transection and microscopic anastomosis. The successfully generated model mice were treated with 10, 5, or 2.5 mg/kg ursolic acid via intraperitoneal injection. This study, published in the Neural Regeneration Research (Vol. 8, No. 27, 2013), is the first to demonstrate a role of ursolic acid in repair and regeneration following peripheral nerve injury. Ursolic acid promoted the regeneration of injured nerve myelin sheaths and reconstructed muscular functions. All experimental findings provide favorable evidence for the application of ursolic acid following peripheral nerve injury.

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Article: ” Ursolic acid induces neural regeneration after sciatic nerve injury” by Biao Liu1, Yan Liu1, Guang Yang1, Zemin Xu1, Jiajun Chen2 (1 Department of Hand Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China; 2 Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China)

Liu B, Liu Y, Yang G, Xu ZM, Chen JJ. Ursolic acid induces neural regeneration after sciatic nerve injury. Neural Regen Res. 2013;8(27):2510-2519.

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/

Full text: http://www.sjzsyj.org/CN/article/downloadArticleFile.do?attachType=PDF&id=724

Food additive may prevent spread of deadly new avian flu

Contact: Sharon Parmet sparmet@uic.edu 312-413-2695 University of Illinois at Chicago

A common food additive can block a deadly new strain of avian influenza virus from infecting healthy cells, report researchers at the University of Illinois at Chicago College of Medicine in the online journal, PLOS ONE.

The compound, in wide use as a preservative, binds to a part of the flu virus that has never been targeted by any existing antiviral drug, raising hopes for its effectiveness against multi-drug-resistant flu viruses.

“The recent H7N9 outbreak in China this past March had a mortality rate of more than 20 percent,” says Michael Caffrey, associate professor of biochemistry and molecular genetics at UIC. That strain, which is new, is already showing resistance to the majority of existing drugs used to treat it, Caffrey said. Preventing an outbreak that could lead to mass casualties would be difficult with the current arsenal.

“The need to develop new antiviral therapeutics now is crucial,” he said.

Flu viruses enter host cells using a special protein called hemagglutinin, which acts as a “key” that opens receptors on the cell surface. If hemagglutinin is disabled, the virus is locked out and can’t infect cells.

UIC researchers, led by Caffrey, found that the FDA-approved food additive tert-butyl hydroquinone sticks to a specific region on the hemagglutinin molecule. The additive, he said, “attaches to the Achilles’ heel of the virus—a loop-shaped portion of hemagglutinin necessary for binding to cells, making cell infection impossible.”

The loop on the hemagglutinin molecule represents a new therapeutic target, since existing drugs don’t go after it, Caffrey said.

“Any drugs that focus on the hemagglutinin loop would be totally novel to flu viruses, and so resistance, if developed, would still be a long way off.”

Caffrey and his colleagues were looking at a different class of viruses when the first outbreak of the H7N9 virus was reported in China last spring.

“Tert-butyl hydroquinone was known to have virus-blocking effects for H3 viruses,” he said. “So when the H7N9 outbreak occurred, we thought we’d see if it had any effect on H7 viruses.”

Using a novel technique, the researchers fused the hemagglutinin of the H7N9 virus to a less dangerous virus in order to study it safely. They found that tert-butyl hydroquinone was able to prevent the virus from infecting human lung cells in the lab.

The researchers are now looking for ways to enhance tert-butyl hydroquinone’s ability to prevent infection. One way might be to add it to poultry feed. Keeping the virus from spreading in chickens could reduce the likelihood of it jumping to humans, Caffrey said. While the compound is used in a variety of foods as a preservative and stabilizer, questions remain regarding its safety if consumed in very high doses.

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Coauthors on the PLOS ONE paper, all of UIC, are graduate student Aleksandar Antanasijevic; postdoctoral researcher Han Cheng; Duncan Wardrop, associate professor of chemistry; and Lijun Rong, associate professor microbiology and immunology.

Coffee consumption reduces risk of liver cancer / By over 40%

Contact: Aimee Frank media@gastro.org 301-941-2620 American Gastroenterological Association

Bethesda, MD (Oct. 22, 2013) — Coffee consumption reduces risk of hepatocellular carcinoma (HCC), the most common type of liver cancer, by about 40 percent, according to an up-to-date meta-analysis published in Clinical Gastroenterology and Hepatology, the official clinical practice journal of the American Gastroenterological Association. Further, some data indicate that three cups of coffee per day reduce liver cancer risk by more than 50 percent.

“Our research confirms past claims that coffee is good for your health, and particularly the liver,” said Carlo La Vecchia, MD, study author from the department of epidemiology, Istituto di Ricerche Farmacologiche “Mario Negri,” and department of clinical sciences and community health, Università degli Studi di Milan, Italy. “The favorable effect of coffee on liver cancer might be mediated by coffee’s proven prevention of diabetes, a known risk factor for the disease, or for its beneficial effects on cirrhosis and liver enzymes.”

Researchers performed a meta-analysis of articles published from 1996 through September 2012, ultimately studying 16 high-quality studies and a total of 3,153 cases. This research fills an important gap as the last meta-analysis was published in 2007, and since then there has been data published on more than 900 cases of HCC.

Despite the consistency of results across studies, time periods and populations, it is difficult to establish whether the association between coffee drinking and HCC is causal, or if this relationship may be partially attributable to the fact that patients with liver and digestive diseases often voluntarily reduce their coffee intake.

“It remains unclear whether coffee drinking has an additional role in liver cancer prevention,” added Dr.  La Vecchia. “But, in any case, such a role would be limited as compared to what is achievable through the current measures.”

Primary liver cancers are largely avoidable through hepatitis B virus vaccination, control of hepatitis C virus transmission and reduction of alcohol drinking. These three measures can, in principle, avoid more than 90 percent of primary liver cancer worldwide.

Liver cancer is the sixth most common cancer in the world, and the third most common cause of cancer death. HCC is the main type of liver cancer, accounting for more than 90 percent of cases worldwide. Chronic infections with hepatitis B and C viruses are the main causes of liver cancer; other relevant risk factors include alcohol, tobacco, obesity and diabetes.

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Learn more about liver cancer in AGA’s patient brochure, “Understanding Cirrhosis of the Liver”.

About the AGA Institute

The American Gastroenterological Association is the trusted voice of the GI community. Founded in 1897, the AGA has grown to include 17,000 members from around the globe who are involved in all aspects of the science, practice and advancement of gastroenterology. The AGA Institute administers the practice, research and educational programs of the organization. http://www.gastro.org.

About Clinical Gastroenterology and Hepatology

The mission of Clinical Gastroenterology and Hepatology is to provide readers with a broad spectrum of themes in clinical gastroenterology and hepatology. This monthly peer-reviewed journal includes original articles as well as scholarly reviews, with the goal that all articles published will be immediately relevant to the practice of gastroenterology and hepatology. For more information, visit http://www.cghjournal.org.

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UWM researchers help reveal how specific wavelengths of light can heal

Contact: Chukuka Enwemeka enwemeka@uwm.edu 414-229-4712 University of Wisconsin – Milwaukee

Light as medicine?

Multiple sclerosis (MS) causes progressive paralysis by destroying nerve cells and the spinal cord. It interrupts vision, balance and even thinking.

On a suggestion from a colleague, Jeri-Anne Lyons decided to test how the disease responded to a radical therapy – exposure to a certain wavelength of light called near-infrared (NIR).

“Never in a million years did I think it would help,” says Lyons, an associate professor of biomedical sciences at the University of Wisconsin-Milwaukee (UWM), who studies the role of the immune response in MS.

But it did. In rodent models, early MS-like symptoms were treated with exposure to NIR light for a week, alternating with a week of no light. The clinical condition of the mice improved.

Professor Janis Eells, who shared the idea with Lyons, had the same initial reaction after she used NIR therapy on rats to treat blindness caused by poisoning, a condition thought to be permanent. Repeating experiments again and again, she found that certain doses of NIR light allowed lab animals to regain their sight.

Scientists have known for years that certain wavelengths of light in certain doses can heal, but they are only now uncovering exactly how it works, thanks in large part to three UWM faculty researchers, including Chukuka S. Enwemeka, dean of UWM’s College of Health Sciences who is internationally known for his work in phototherapy.

Enwemeka researches the effects of both NIR and blue light in the visible range on healing wounds. Among his discoveries is that some wavelengths of blue light can clear stubborn infections – even MRSA, the antibiotic-resistant “superbug” form of Staphylococcus aureus.

Together, the UWM cluster has found that NIR and blue light repair tissue in dramatically different ways, but both act on the same enzyme in the cell’s energy supply center: the mitochondria.

The studies have revealed key information about managing the effects of aging and disease.

A bodyguard

So how is light accomplishing such wonders?

In applying NIR light therapy to MS, Lyons has identified the right timing and dose. But she’s also dug deeper, analyzing the effect the light had on the activities of the animal’s genes. It turns out, molecules that would make the disease worse were weakened after exposure to the light, and the ones responsible for improvement were strengthened.

Eells says NIR light acts on the mitochondria and a particular enzyme, cytochrome C oxidase, to stimulate cell repair.

Light can do all that?

“We’re not talking about white light [all wavelengths in the visible spectrum combined] as treatment, but only certain wavelengths, at a certain intensity, for a certain amount of time,” says Lyons. “Like ingested medication, it’s all about the dose.”

Determining the best wavelength of light for phototherapy is a difficult task. Studies show that 670 nanometer (nm) and 830 nm light are beneficial, but 730 nm is not. The other difficult task is determining the appropriate dose and dose regimen for delivering the light.

Promising leads

Even more exciting is phototherapy’s potential to improve a host of other degenerative diseases. Damaged mitochondria lead to a rise in destructive “free radicals,” which play a key role in aging and cancer.

“It’s why we try to put antioxidants into our diets,” says Lyons, “to fight that process.”

One source of free radicals comes from the inflammation caused by the body’s immune response. The researchers have found that after an injury or illness triggers the immune response, NIR light resets the mitochondria so they function normally again.

“NIR reduces inflammation,” says Eells. “If you can tone down the inflammation in an eye disease like retinitis pigmentosa, you slow the progression of the disease.”

A similar observation with inflammation occurred in a study on recalcitrant bedsores, she adds. Wounds treated with phototherapy healed two and a half times more quickly than untreated wounds.

“Chronic non-healing wounds are ‘stuck’ in the inflammatory phase of wound healing” The light removes that obstacle,” says Eells.

She has been working with Tim Kern at Case Western Reserve in treating an animal model of diabetic retinopathy with NIR light, which has been shown to slow progression and reduce the severity of the condition.  Kern hopes to initiate a clinical trial in the near future.

A killer

NIR light heals by ensuring that cytochrome oxidase binds with oxygen to turn on protectors and stimulate cell metabolism. Blue light, on the other hand, causes a toxic environment when the immune response has been triggered. That poisonous effect hastens healing of topical wounds by killing bacteria that cause infection.

The question is, “What gives light in the longer wavelength its antibiotic effect?”

Enwemeka’s studies suggest that blue light also acts on the mitochondrial enzyme site, but allows cytochrome oxidase to bind with nitric oxide, a free radical that is elevated in the immune response. It’s a pairing that poisons the invader.

This theory is still unproven, but the therapy has achieved undeniable results in the lab with antibiotic-resistant MRSA. Enwemeka demonstrated that one dose of irradiation killed as much as 92 percent of two pervasive strains of MRSA.

He is working to improve that success rate by getting the light to penetrate deeper in order to finish off the few colonies that survive irradiation.

Limited availability

Enwemeka is leading a research effort in Brazil and at UWM that he hopes will ultimately lead to clinical use of NIR and blue light in the U.S. for the treatment of wounds.

In the six years since he was asked to test the effects of blue light on MRSA, he says, research on the topic has picked up. But currently, the U.S. Food and Drug Administration (FDA) has not sanctioned the use of blue light in treating wounds, or NIR light for conditions other than wounds and pain.

With so much success, why isn’t phototherapy being used more widely?

“It’s considered alternative therapy in Western medicine. It seems too simple for people to accept,” says Lyons.

What the FDA is waiting for, says Enwemeka, is confirmation from a large-scale clinical study before approving phototherapy for a wider variety of ailments. It’s something Enwemeka and Harry Whelan, a UWM alumnus and physician-researcher at the Medical College of Wisconsin, are determined to accomplish.

“To see people who have not had relief see their wounds heal and not return,” says Enwemeka of the Brazilian patients who have benefited from therapy, “is very touching.”

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Additional study: Photobiomodulation Induced by 670 nm Light Ameliorates MOG35-55 Induced EAE in Female C57BL/6 Mice: A Role for Remediation of Nitrosative Stress

KA Muili, S Gopalakrishnan, JT Eells, JA Lyons

PLoS ONE 8(6): e67358. doi:10.1371/journal.pone.0067358  [2013]

Breast milk protein may be key to protecting babies from HIV infection

DURHAM, N.C. – A substance in breast milk that neutralizes HIV and may protect babies from acquiring HIV from their infected mothers has been identified for the first time by researchers at Duke Medicine.

The protein, called Tenascin-C or TNC, had previously been recognized as playing a role in wound healing, but had not been known to have antimicrobial properties. The discovery could lead to potential new HIV-prevention strategies.

Reporting in the journal Proceedings of the National Academy of Sciences during the week of Oct. 21, 2013, the researchers describe how the TNC protein in breast milk binds to and neutralizes the HIV virus, potentially protecting exposed infants who might otherwise become infected from repeated exposures to the virus.

“Even though we have antiretroviral drugs that can work to prevent mother-to-child transmission, not every pregnant woman is being tested for HIV, and less than 60 percent are receiving the prevention drugs, particularly in countries with few resources,” said senior author Sallie Permar, M.D., Ph.D., assistant professor of pediatrics, immunology and molecular genetics and microbiology at Duke. “So there is still a need for alternative strategies to prevent mother-to-child transmission, which is why this work is important.”

Worldwide in 2011, an estimated 330,000 children acquired HIV from their mothers during pregnancy or birth, or through breastfeeding according to UNICEF. As international health organizations have set a goal of eliminating mother-to-child infections, researchers have worked to develop safe and affordable alternatives to antiretroviral therapy that can be used to block HIV transmission to infants.

Permar and colleagues focused on breast milk, which has long been recognized as having some protective quality that inhibits mother-to-child transmission despite multiple daily exposures over months and even years of nursing. Earlier studies had identified some antiviral properties in breast milk, but the majority of the HIV-neutralizing activity of breast milk remained unexplained. More recent studies pointed to a large protein that had yet to be identified.

In their study, the Duke team screened mature milk samples from uninfected women for neutralizing activity against a panel of HIV strains, confirming that all of the detectable HIV-neutralization activity was contained in the high molecular weight portion. Using a multi-step protein separation process, the researchers narrowed the detectable HIV-neutralization activity to a single protein, and identified it as TNC.

“TNC is a component of the extracellular matrix that is integral to how tissues hold themselves together,” Permar said, noting that co-author Harold Erickson, Ph.D., professor of cell biology at Duke, was among the first to identify and describe TNC in the 1980s. “This is a protein involved during wound healing, playing a role in tissue repair. It is also known to be important in fetal development, but its reason for being a component of breast milk or its antiviral properties had never been described.”

Further analysis described how TNC works against HIV by blocking virus entry. The protein is uniquely effective in capturing virus particles and neutralizes the virus, specifically binding to the HIV envelope. These properties provide widespread protection against infection.

“It’s likely that TNC is acting in concert with other anti-HIV factors in breast milk, and further research should explore this,” Permar said. “But given TNC’s broad-spectrum HIV-1-binding and neutralizing activity, it could be developed as an HIV-prevention therapy, given orally to infants prior to breastfeeding, similar to the way oral rehydration salts are routinely administered to infants in developing regions.”

Permar said TNC would also appear to be inherently safe, since it is a naturally occurring component of breast milk, and it may avoid the problem of HIV resistance to antiretroviral regimens that complicate maternal/infant applications.

“The discovery of the HIV inhibiting effect of this common protein in breast milk provides a potential explanation for why nursing infants born to HIV-infected mothers do not become infected more often than they do,” said Barton F. Haynes, M.D., director of the Duke Human Vaccine Institute. “It also provides support for inducing inhibitory factors in breast milk that might be even more protective, such as antibodies, that would completely protect babies from HIV infection in this setting.”

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In addition to Permar, co-senior author was S. Munir Alam. Other authors include Genevieve G. Fouda, Frederick H. Jaeger, Joshua D. Amos, Carrie Ho, Erika L. Kunz, Kara Anasti, Lisa W. Stamper, Brooke E. Liebl; Kimberly H. Barbas, Tomoo Ohashi, M. Arthur Moseley, Hua-Xin Liao and Harold P. Erickson.

The study was funded by the Doris Duke Charitable Foundation Clinical Scientist Development Award; Duke University School of Medicine; Center for HIV/AIDS Vaccine Immunology; and the National Institute of Allergic and Immunologic Diseases (U19 AI067854) (K08AI087992) (CA047056).

Compound derived from vegetables shields rodents from lethal radiation doses

Contact: Karen Mallet km463@georgetown.edu Georgetown University Medical Center

WASHINGTON — Georgetown University Medical Center researchers say a compound derived from cruciferous vegetable such as cabbage, cauliflower and broccoli protected rats and mice from lethal doses of radiation.

Their study, published today in the Proceedings of the National Academy of Sciences (PNAS) suggests the compound, already shown to be safe for humans, may protect normal tissues during radiation therapy for cancer treatment and prevent or mitigate sickness caused by radiation exposure.

The compound, known as DIM (3,3′-diindolylmethane), previously has been found to have cancer preventive properties.

“DIM has been studied as a cancer prevention agent for years, but this is the first indication that DIM can also act as a radiation protector,” says the study’s corresponding author, Eliot Rosen, MD, PhD, of Georgetown Lombardi Comprehensive Cancer Center.

For the study, the researchers irradiated rats with lethal doses of gamma ray radiation.  The animals were then treated with a daily injection of DIM for two weeks, starting 10 minutes after the radiation exposure.

The result was stunning, says Rosen, a professor of oncology, biochemistry and cell & molecular biology, and radiation medicine. “All of the untreated rats died, but well over half of the DIM-treated animals remained alive 30 days after the radiation exposure.”

Rosen adds that DIM also provided protection whether the first injection was administered 24 hours before or up to 24 hours after radiation exposure.

“We also showed that DIM protects the survival of lethally irradiated mice,” Rosen says. In addition, irradiated mice treated with DIM had less reduction in red blood cells, white blood cells and platelets — side effects often seen in patients undergoing radiation treatment for cancer.

Rosen says this study points to two potential uses of the compound. “DIM could protect normal tissues in patients receiving radiation therapy for cancer, but could also protect individuals from the lethal consequences of a nuclear disaster.”

Rosen and study co-authors Saijun Fan, PhD, and Milton Brown, MD, PhD, are co-inventors on a patent application that has been filed by Georgetown University related to the usage of DIM and DIM-related compounds as radioprotectors.

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This work was supported by U.S. Public Health Service Grants (CA104546 and CA150646), a grant from the Center for Drug Discovery at Georgetown University, and other Georgetown funding.

About Georgetown University Medical Center

Georgetown University Medical Center (GUMC) is an internationally recognized academic medical center with a three-part mission of research, teaching and patient care (through MedStar Health).  GUMC’s mission is carried out with a strong emphasis on public service and a dedication to the Catholic, Jesuit principle of cura personalis — or “care of the whole person.”  The Medical Center includes the School of Medicine and the School of Nursing & Health Studies, both nationally ranked; Georgetown Lombardi Comprehensive Cancer Center, designated as a comprehensive cancer center by the National Cancer Institute; and the Biomedical Graduate Research Organization, which accounts for the majority of externally funded research at GUMC including a Clinical and Translational Science Award from the National Institutes of Health

Multivitamins with minerals may protect older women with invasive breast cancer

Contact: Deirdre Branley sciencenews@einstein.yu.edu 718-430-3101 Albert Einstein College of Medicine

October 9, 2013 — (BRONX, NY) — Findings from a study involving thousands of postmenopausal women suggest that women who develop invasive breast cancer may benefit from taking supplements containing both multivitamins and minerals. The new research, published today in Breast Cancer Research and Treatment, found that the risk of dying from invasive breast cancer was 30 percent lower among multivitamin/mineral users compared with nonusers.

“Our study offers tentative but intriguing evidence that multivitamin/mineral supplements may help older women who develop invasive breast cancer survive their disease,” said Sylvia Wassertheil-Smoller, Ph.D., lead author of the study and distinguished university professor emerita of epidemiology and population health at Albert Einstein College of Medicine of Yeshiva University.

Multivitamin/mineral supplements are the most commonly consumed dietary supplements among U.S. adults. They usually contain 20-30 vitamins and minerals, often at levels of 100 percent of U.S. Recommended Dietary Allowances or less, and the usual label recommendation is to take them daily.

The research was conducted as part of the Women’s Health Initiative Clinical Trials and the Women’s Health Initiative (WHI) Observational Study. Combined, the two studies include data from 161,608 postmenopausal women ages 50 to 79 when they first joined the study. These women were enrolled at 40 clinical centers throughout the United States during the years 1993-1998.

The current study focused on 7,728 participants who were diagnosed with invasive breast cancer during the WHI and were followed for an average of seven years after their diagnosis. Invasive breast cancer is defined as cancer that has spread outside the membrane of the milk glands or ducts and into the breast tissue. Two common types of invasive breast cancer are invasive ductal carcinoma and infiltrating lobular carcinoma.

After enrolling in the WHI and during repeated follow-up visits, all participants provided extensive information about their health including whether or not they had taken a multivitamin/mineral supplement at least once a week during the prior two weeks.

About 38percent of the 7,728 women who developed invasive breast cancer during the WHI were using the supplements. The vast majority were taking the supplements before their breast-cancer diagnosis. A comparison of mortality rates revealed that women with invasive breast cancer who took multivitamin/mineral supplements were 30 percent less likely to die from their cancers than women with invasive breast cancer who hadn’t taken the supplements.

Could differences between the multivitamin/mineral users and nonusers account for this finding? The researchers looked at many possible confounding factors including additional supplements that the women took, their smoking status, education, race/ethnicity, weight, depression, alcohol use, physical activity, age at breast cancer diagnosis, and diabetes. The association between regular use of multivitamin/mineral supplements and reduced risk of death persisted even after these factors were taken into account.

“Controlling for these other factors strengthens our confidence that the association we observed – between taking multivitamin/mineral supplements and lowering breast-cancer mortality risk among postmenopausal women with invasive breast cancer – is a real one,” said Dr. Wassertheil-Smoller, who also holds the Dorothy and William Manealoff Foundation and Molly Rosen Chair in Social Medicine Emerita. “But further studies are needed to confirm whether there truly is a cause-and-effect relationship here. And our findings certainly cannot be generalized to premenopausal women diagnosed with invasive cancer or to other populations of women.”

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The paper is titled “Multivitamin and Mineral Use and Breast Cancer Mortality in Older Women with Invasive Breast Cancer in the Women’s Health Initiative.” Dr. Wassertheil-Smoller is the principal investigator of the WHI at Einstein. Other authors of the study at Einstein are  Aileen McGinn, Ph.D., and Gloria Ho, Ph.D., and additional co-authors are affiliated with the following centers: University of Oklahoma Health Science Center, Los Angeles Biomedical Research Institute, University of Tennessee Health Science Center, Stony Brook University School of Medicine, University of Massachusetts Medical School, Fred Hutchinson Cancer Research Center, Stanford Prevention Research Center, University of Alabama School of Medicine at Birmingham, Brigham and Women’s Hospital and the University of Arizona Cancer Center.

The WHI is sponsored by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health.

About Albert Einstein College of Medicine of Yeshiva University

Albert Einstein College of Medicine of Yeshiva University is one of the nation’s premier centers for research, medical education and clinical investigation. During the 2013-2014 academic year, Einstein is home to 734 M.D. students, 236 Ph.D. students, 106 students in the combined M.D./Ph.D. program, and 353 postdoctoral research fellows. The College of Medicine has more than 2,000 full-time faculty members located on the main campus and at its clinical affiliates. In 2013, Einstein received more than $155 million in awards from the NIH. This includes the funding of major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Its partnership with Montefiore Medical Center (http://www.montefiore.org/), the University Hospital and academic medical center for Einstein, advances clinical and translational research to accelerate the pace at which new discoveries become the treatments and therapies that benefit patients. Through its extensive affiliation network involving Montefiore, Jacobi Medical Center–Einstein’s founding hospital, and five other hospital systems in the Bronx, Manhattan, Long Island and Brooklyn, Einstein runs one of the largest residency and fellowship training programs in the medical and dental professions in the United States. For more information, please visit http://www.einstein.yu.edu and follow us on Twitter @EinsteinMed.

NAC ( N-Acetyl Cysteine ) amino acid offers a potential therapeutic alternative in psychiatric disorders

Contact: Sonja Mak s.mak@update.europe.at 43-140-55734 European College of Neuropsychopharmacology

This press release is in support of a presentation by Professor Michael Berk on Monday Oct. 7 at the 26th ECNP Congress in Barcelona, Spain

BARCELONA, SPAIN (7 October 2013) – Improved understanding of the roles of inflammation and oxidative stress in psychiatric disorders has generated new leads in the search for novel therapies. One such investigative compound currently in clinical trials is an amino acid, N-Acetyl Cysteine (NAC), which appears to reduce the core symptoms of bipolar disorder, schizophrenia, depression, autism and cravings in addictions including cocaine, cannabis abuse and cigarette smoking.

At the start of the decade of the brain, in the early 1990s, there was great hope that a flurry of new treatment discoveries would eventuate. In contrast, today, most pharmaceutical companies have a drying psychiatry and neurology pipeline and many have exited the field entirely. “One of the factors has been an over reliance on typical monoamine pathways as targets for drug discovery,” said Professor Michael Berk, Chair in Psychiatry at Deakin University, Geelong, Australia.

Professor Berk pointed out that the situation regarding new drug development for psychiatric problems was best summarised by former National Institute for Mental Health Director, Steven Hyman: “drug discovery is at a near standstill for treating psychiatric disorders such as schizophrenia, bipolar disorder, depression and common forms of autism.”

Beyond the monoamine-based drugs, neuroscience has elucidated an array of other important pathways that are involved in most major psychiatric disorders, for example schizophrenia and both unipolar and bipolar depression. According to Professor Berk, there is now an incontrovertible evidence base that these disorders share inflammation and oxidative stress as part of their disease physiology. In addition, associated pathways including reduction in proteins that stimulate neuronal growth (neurotrophins), and increased cell death (apoptosis), as well as energy generation in organelles called mitochondria are intimately involved. “This understanding provides an entirely new set of treatment targets.”

The amino acid, NAC, seems to have multiple effects on all these pathways: it boosts glutathione, which is the body’s major antioxidant defence; has anti-inflammatory properties; enhances levels of nerve cell growth proteins and the growth of new neurons; and reduces cell death pathways. It also appears to reduce dysfunction of mitochondria.

These molecular effects of NAC have been investigated in a series of clinical trials, which show that NAC reduces the core symptoms of schizophrenia including negative symptoms such as improved apathy, social interaction and motivation. It also appears to reduce depression in people with bipolar disorder and at this meeting, new data on its role in unipolar major depression was presented. Furthermore, there is intriguing evidence that it reduces cravings in a number of addictions including cocaine, cannabis and cigarette smoking. “Apart from nausea, it appears to be relatively free of problematic side effects,” said Professor Berk.

In addition to NAC, a range of other compounds that target similar pathways, particularly inflammation, seem to have therapeutic potential. These include aspirin, cyclooxygenase (COX) inhibitors, statins, omega-3 fatty acids and even some anti-diabetic agents such as pioglitazone. “Capitalising on our understanding of inflammation and oxidative stress in major psychiatric disorders appears to give us an entirely new range of potential treatments for these common, severe and disabling conditions,” said Professor Berk.

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Contact

Michael Berk Chair in Psychiatry at Deakin University Geelong, Australia  Email: MIKEBE@BarwonHealth.org.au

ECNP Press Office

For all enquiries, please contact:

Sonja Mak  Update Europe GmbH  Tigergasse 3/5  1080 Vienna, Austria  T: +43 1 405 5734  F: +43 1 405 5734-16  E-mail: s.mak@update.europe.at

About ECNP

The European College of Neuropsychopharmacology (ECNP) is an independent scientific association dedicated to translating advances in the understanding of brain function and human behaviour into better treatments and enhanced public health. ECNP organises a wide range of scientific and educational activities, programmes and events across Europe, promoting exchange of high-quality experimental and clinical research and fostering young scientists and clinicians in the field. The annual ECNP Congress attracts around 4,000-7,000 scientists and clinicians from across the world to discuss the latest advances in brain research in Europe’s largest meeting on brain science.

Disclaimer: Information contained in this press release was provided by the abstracts’ authors and reflects the content of the studies. It does not necessarily express ECNP’s point of view.

Component of citrus fruits found to block the formation of kidney cysts

Contact: Tanya Gubbay tanya.gubbay@rhul.ac.uk 01-784-443-552 Royal Holloway, University of London

A new study published today in British Journal of Pharmacology has identified that a component of grapefruit and other citrus fruits, naringenin, successfully blocks the formation of kidney cysts.

Known as polycystic kidney disease, this is an inherited disorder which leads to the loss of kidney function, high blood pressure and the need for dialysis. Few treatment options are currently available.

The team of scientists from Royal Holloway University, St George’s, University of London and Kingston University London used a simple, single-celled amoeba to identify that naringenin regulates the PKD2 protein responsible for polycystic kidney disease and as a result, blocks formation of cysts.

“This discovery provides an important step forward in understanding how polycystic kidney disease may be controlled,” said Professor Robin Williams from the School of Biological Sciences at Royal Holloway.

“In the study, we have demonstrated how effective the amoeba Dictyostelium is in the discovery of new treatments and their targets. Having previously applied the same method of testing in our work into epilepsy and bipolar treatments, it is clear that this new approach could help us reduce reliance on animal testing and provide major improvements.”

To test how this discovery could apply in treatments, the team used a mammalian kidney cell-line, and triggered the formation of cysts in these cells. They were then able to block the formation of the cysts by adding naringenin and saw that when levels of the PKD2 protein were reduced in the kidney cells, so was the block in cyst formation, confirming that the effect was connected.

Dr Mark Carew, from the School of Pharmacy and Chemistry at Kingston University, said: “Further investigation is underway to understand the action of naringenin at the molecular level. This work will entail looking at the function of the PKD2 protein as a cell growth regulator.”

“Indeed, this study provides a good example of how chemicals identified in plants can help us develop new drugs for the treatment of disease,” added Professor Debbie Baines from St George’s, University of London.

“Autosomal dominant polycystic kidney disease affects between 1 in 10 people on dialysis and 1 in 8 with a kidney transplant. Kidney Research UK welcomes this publication that may provide hope for a future new treatment for polycystic kidney disease, alongside its own on-going research focusing on tackling this common genetic kidney disease,” said Elaine Davies, Head of Research Operations at Kidney Research UK.

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The research was funded by a SWan (SouthWest London Academic Network) research grant.

Niacin, the fountain of youth

The vitamin niacin has a life-prolonging effect, as Michael Ristow has demonstrated in roundworms. From his study, the ETH-Zurich professor also concludes that so-called reactive oxygen species are healthy, not only disagreeing with the general consensus, but also many of his peers.

             Fabio Bergamin
Roundworms live longer when fed the food supplement niacin (inverted microscopic photo). (Photo: Michael Ristow / ETH Zurich)

       Roundworms live longer when fed the food supplement niacin (inverted microscopic photo). (Photo: Michael Ristow / ETH Zurich)       <!– (mehr Bilder) –>

Who would not want to live a long and healthy life? A freely available food supplement could help in this respect, scientists from ETH Zurich have demonstrated in roundworms. Vitamin B3 – also known as niacin – and its metabolite nicotinamide in the worms’ diet caused them to live for about one tenth longer than usual.

As an international team of researchers headed by Michael Ristow, a professor of energy metabolism, has now experimentally demonstrated, niacin and nicotinamide take effect by promoting formation of so-called free radicals. “In roundworms, these reactive oxygen species prolong life,” says Ristow.

“No scientific evidence for usefulness of antioxidants”

This might seem surprising as reactive oxygen species are generally considered to be unhealthy. Ristow’s view also contradicts the textbook opinion championed by many other scientists. Reactive oxygen species are known to damage somatic cells, a condition referred to as oxidative stress. Particular substances, so-called antioxidants, which are also found in fruit, vegetables and certain vegetable oils, are capable of neutralising these free radicals. Many scientists believe that antioxidants are beneficial to health.

“The claim that intake of antioxidants, especially in tablet form, promotes any aspect of human health lacks scientific support,” says Ristow. He does not dispute that fruit and vegetables are healthy. However, this may rather be caused by other compounds contained therein, such as so-called polyphenols. “Fruit and vegetables are healthy, despite the fact that they contain antioxidants,” says the ETH-Zurich professor. Based on the current and many previous findings he is convinced that small amounts of reactive oxygen species and the oxidative stress they trigger have a health-promoting impact. “Cells can cope well with oxidative stress and neutralise it,” says Ristow.

Substance mimics endurance sport

In earlier studies on humans, Ristow demonstrated that the health-enhancing effect of endurance sports is mediated via an increased formation of reactive oxygen species – and that antioxidants abolish this effect. Based on the present study, he concludes that niacin brings about a similar metabolic condition to exercise. “Niacin tricks the body into believing that it is exercising – even when this is not the case,” says Ristow. Such compounds are known as “exercise mimetics”.

The researchers conducted their experiments on the model organism Caenorhabditis elegans. This worm, which is merely one millimetre in length, can be easily maintained and has a lifespan of only a month, making it the ideal model organism for ageing research.

Also relevant for humans

The results of the study may also be of relevance for humans, says Ristow. After all, the metabolic pathway initiated by niacin is very similar in roundworms and higher organisms. Whether niacin has similar effects on the life expectancy of mice is the subject of Ristow’s current research. Previous studies also suggest a health-enhancing effect of niacin in humans with elevated blood cholesterol levels.

Niacin and nicotinamide have been approved as dietary supplements for decades. Ristow could easily envisage the substances being used broadly for therapeutic purposes in the future. A whole series of foods naturally contain niacin, including meat, liver, fish, peanuts, mushrooms, rice and wheat bran. Whether nutritional uptake is sufficient for a health-enhancing or lifespan-extending effect, however, remains to be demonstrated, says Ristow.

Disputed impact of enzymes

The latest study on the effects of niacin and nicotinamide is based on a particular class of enzymes, the sirtuins, which convert niacin into nicotinamide. Moreover, they are also involved in gene regulation, helping to down regulate the activity of certain genes. Until today, scientists have been disputing whether sirtuins have a life-prolonging impact.

Ristow and his team’s work now suggests that the activity of sirtuins actually prolongs life in roundworms. According to the study, however, the life-prolonging effect is not down to gene regulation, as has often been supposed in the past. Instead, the effect is due to the conversion of niacin into nicotinamide. Studying genetically modified roundworms that were unable to convert nicotinamide into certain other metabolic products, the scientists did not observe any lifespan extension, even after overexpression of sirtuins, which otherwise lead to an increased life expectancy.

Literature reference

Schmeisser K et al.: Role of Sirtuins in Lifespan Regulation is Linked to Methylation of Nicotinamide. Nature Chemical Biology, 2013, Advance Online Publication, doi: 10.1038/nchembio.1352

MS reversed in mice / Single dose ( Calcitriol ) Vitamin D followed by Vitamin D supplements

Contact: Colleen Hayes cehayes@wisc.edu 608-263-6387 University of Wisconsin-Madison

Mouse studies reveal promising vitamin D-based treatment for MS

MADISON — A diagnosis of multiple sclerosis (MS) is a hard lot. Patients typically get the diagnosis around age 30 after experiencing a series of neurological problems such as blurry vision, wobbly gait or a numb foot. From there, this neurodegenerative disease follows an unforgiving course.

Many people with MS start using some kind of mobility aid — cane, walker, scooter or wheelchair — by 45 or 50, and those with the most severe cases are typically bed-bound by 60. The medications that are currently available don’t do much to slow the relentless march of the disease.

In search of a better option for MS patients, a team of University of Wisconsin-Madison biochemists has discovered a promising vitamin D-based treatment that can halt — and even reverse — the course of the disease in a mouse model of MS. The treatment involves giving mice that exhibit MS symptoms a single dose of calcitriol, the active hormone form of vitamin D, followed by ongoing vitamin D supplements through the diet. The protocol is described in a scientific article that was published online in August in the Journal of Neuroimmunology.

“All of the animals just got better and better, and the longer we watched them, the more neurological function they regained,” says biochemistry professor Colleen Hayes, who led the study.

MS afflicts around 400,000 people nationwide, with 200 new cases diagnosed each week. Early on, this debilitating autoimmune disease, in which the immune system attacks the myelin coating that protects the brain’s nerve cells, causes symptoms including weakness, loss of dexterity and balance, disturbances to vision, and difficulty thinking and remembering. As it progresses, people can lose the ability to walk, sit, see, eat, speak and think clearly.

Current FDA-approved treatments only work for some MS patients and, even among them, the benefits are modest. “And in the long term they don’t halt the disease process that relentlessly eats away at the neurons,” Hayes adds. “So there’s an unmet need for better treatments.”

While scientists don’t fully understand what triggers MS, some studies have linked low levels of vitamin D with a higher risk of developing the disease. Hayes has been studying this “vitamin D hypothesis” for the past 25 years with the long-term goal of uncovering novel preventive measures and treatments. Over the years, she and her researchers have revealed some of the molecular mechanisms involved in vitamin D’s protective actions, and also explained how vitamin D interactions with estrogen may influence MS disease risk and progression in women.

In the current study, which was funded by the National Multiple Sclerosis Society, Hayes’ team compared various vitamin D-based treatments to standard MS drugs. In each case, vitamin D-based treatments won out. Mice that received them showed fewer physical symptoms and cellular signs of disease.

First, Hayes’ team compared the effectiveness of a single dose of calcitriol to that of a comparable dose of a glucocorticoid, a drug now administered to MS patients who experience a bad neurological episode. Calcitriol came out ahead, inducing a nine-day remission in 92 percent of mice on average, versus a six-day remission in 58 percent for mice that received glucocorticoid.

“So, at least in the animal model, calcitriol is more effective than what’s being used in the clinic right now,” says Hayes.

Next, Hayes’ team tried a weekly dose of calcitriol. They found that a weekly dose reversed the disease and sustained remission indefinitely.

But calcitriol can carry some strong side effects — it’s a “biological sledgehammer” that can raise blood calcium levels in people, Hayes says — so she tried a third regimen: a single dose of calcitriol, followed by ongoing vitamin D supplements in the diet. This one-two punch “was a runaway success,” she says. “One hundred percent of mice responded.”

Hayes believes that the calcitriol may cause the autoimmune cells attacking the nerve cells’ myelin coating to die, while the vitamin D prevents new autoimmune cells from taking their place.

While she is excited about the prospect of her research helping MS patients someday, Hayes is quick to point out that it’s based on a mouse model of disease, not the real thing. Also, while rodents are genetically homogeneous, people are genetically diverse.

“So it’s not certain we’ll be able to translate (this discovery to humans),” says Hayes. “But I think the chances are good because we have such a broad foundation of data showing protective effects of vitamin D in humans.”

The next step is human clinical trials, a step that must be taken by a medical doctor, a neurologist. If the treatment works in people, patients with early symptoms of MS may never need to receive an official diagnosis.

“It’s my hope that one day doctors will be able to say, ‘We’re going to give you an oral calcitriol dose and ramp up the vitamin D in your diet, and then we’re going to follow you closely over the next few months. You’re just going to have this one neurological episode and that will be the end of it,'” says Hayes. “That’s my dream.”

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Nicole Miller nemiller2@wisc.edu 608-262-3636

Foot Cream Kills HIV by Tricking Cells to Commit Suicide

Ciclopirox is currently approved by the FDA as a topical antifungal cream (Credit: Fougera) A common drug that dermatologists turn to treat nail fungus appears to come with a not-so-tiny side effect: eradicating HIV .

CNET

Ciclopirox is currently approved by the FDA as a topical antifungal cream.

A common drug that dermatologists turn to treat nail fungus appears to come with a not-so-tiny side effect: eradicating HIV.

In a study performed at Rutgers New Jersey Medical School, not only does the drug Ciclopirox completely eradicate infectious HIV from cell cultures, but unlike today’s most cutting-edge antiviral treatments, the virus doesn’t bounce back when the drug is withheld. This means it may not require a lifetime of use to keep HIV at bay.

The same group of researchers had previously shown that Ciclopirox — approved by the FDA and Europe’s EMA as safe for human use to treat foot fungus — inhibits the expression of HIV genes in culture. Now they have found that it also blocks the essential function of the mitochondria, which results in the reactivation of the cell’s suicide pathway, all while sparing the healthy cells.

The researchers said that one aspect of HIV that makes it particularly persistent, even in the face of strong antiviral treatments, is its ability to disable a cell’s altruistic suicide pathway — which is typically activated when a cell is damaged or infected. In other words, infected cells that would normally commit suicide to spare healthy cells no longer pull any altruistic kamikaze missions. Ciclopirox tricks these cells back into their old ways with a double negative, disabling the disabling of the suicide pathway.

It’s obviously still going to take clinical trials on humans to study the safety and efficacy of Ciclopirox as a potential topical HIV treatment, but the fact that it’s already deemed safe for one type of human use could make the regulatory process faster than usual.

In fact, the researchers note that another FDA-approved drug now thought to help subdue HIV, called Deferiprone, skipped studies in animals and went straight from tests in culture to a phase I human trial in South Africa, possibly paving the way for other FDA-approved drugs to move faster through the study phases. (Unlike Ciclopirox, which is approved for topical treatment, Deferiprone is FDA- and EMA-approved for systemic use, meaning it effects more than just one part of the body.)

The new findings on Ciclopirox appear in the current issue of the journal PLOS ONE.

CNET ©2013 CBS Interactive Inc., a CBS Company. All rights reserved. Used by permission.

http://www.scientificamerican.com/article.cfm?id=foot-cream-kills-hiv-by-tricking-ce-2013-09

Could dog food additive prevent disabling chemotherapy side effect?

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine

Johns Hopkins researchers find, in mice, that common preservative may thwart pain and damage of peripheral neuropathy

Working with cells in test tubes and in mice, researchers at Johns Hopkins have discovered that a chemical commonly used as a dog food preservative may prevent the kind of painful nerve damage found in the hands and feet of four out of five cancer patients taking the chemotherapy drug Taxol.

The Food and Drug Administration-approved preservative, an antioxidant called ethoxyquin, was shown in experiments to bind to certain cell proteins in a way that limits their exposure to the damaging effects of Taxol, the researchers say.

The hope, they say, is to build on the protective effect of ethoxyquin’s chemistry and develop a drug that could be given to cancer patients before taking Taxol, in much the same way that anti-nausea medication is given to stave off the nausea that commonly accompanies chemotherapy. While half of Taxol users recover from the pain damage, known as peripheral neuropathy, the other half continue to have often debilitating pain, numbness and tingling for the rest of their lives.

“Millions of people with breast cancer, ovarian cancer and other solid tumors get Taxol to treat their cancer and 80 percent of them will get peripheral neuropathy as a result,” says Ahmet Höke, M.D., Ph.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and director of the Neuromuscular Division. “They’re living longer thanks to the chemotherapy, but they are often miserable. Our goal is to prevent them from getting neuropathy in the first place.”

A report on Höke’s research is published online in the Annals of Neurology.

Höke and his team knew from previous experiments that adding Taxol to a nerve cell line growing in a petri dish would cause neurodegeneration. In a series of experiments, they set out to hunt for compounds that might interrupt the degenerative process by adding Taxol to nerve cells along with some 2,000 chemicals — one at a time — to see which, if any, could do that.

Ethoxyquin did so, Höke says, apparently by making the cells resistant to the toxic effects of the Taxol.

Once they identified ethoxyquin’s effects, they gave intravenous Taxol to mice, and saw nerves in their paws degenerate in a couple of weeks. But when they gave ethoxyquin to the mice at the same time as the Taxol, it prevented two-thirds of the nerve degeneration, which Höke says would have a big impact on quality of life if the same effects were to occur in humans.

Specifically, Höke and his team discovered that molecules of ethoxyquin were binding to Hsp90, one of the so-called heat shock proteins that cells defensively make more of whenever they are stressed. Hsp90 acts as a cell’s quality control officer, determining whether a protein is properly formed before sending it out where it is needed.  When ethoxyquin binds to Hsp90, two other proteins — ataxin-2 and Sf3b2 — can’t bind to Hsp90. When they can’t bind, the cell senses that these two proteins are flawed, so they are degraded and their levels in the cell diminished.

Höke says his team is not certain why too much of those two proteins appears to have a negative effect on nerves, but reducing their levels clearly appears in their studies to make cells more resistant to Taxol toxicity.

Höke and his colleagues are looking into whether this medication could also make nerves more resistant to damage in peripheral neuropathy caused by HIV and diabetes, two other major causes of the pain. A previous study, Höke says, showed that ataxin-2 may cause degeneration in motor neurons in a rare form of ALS, commonly known as Lou Gehrig’s disease, suggesting that ethoxyquin or some version of it might also benefit people with this disorder.

Twenty to 30 million Americans suffer from peripheral neuropathy. Höke says it’s a “huge public health issue” that doesn’t get much attention because it is not fatal.

Höke’s team is hoping to conduct safety studies with ethoxyquin in animals in advance of possible testing in people. He says that while too much ethoxyquin is thought to be potentially harmful to dogs, the needed dose for humans would likely be 20-to-30-fold lower than what is found in dog food. Ethoxyquin was developed in the 1950s as an antioxidant, a compound to prevent pears and other foods from becoming discolored and spoiling.

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Other Johns Hopkins researchers involved in the study include Jing Zhu, Ph.D.; Weiran Chen, M.D.; Ruifa Mi, M.D., Ph.D.; Chunhua Zhou, B.S.; and Nicole Reed, M.S.

The research was supported by the Foundation for Peripheral Neuropathy, Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (R01 NS43991) and Johns Hopkins Brain Science Institute.

For more information about Höke, click here.

Johns Hopkins Medicine (JHM), headquartered in Baltimore, Maryland, is a $6.5 billion integrated global health enterprise and one of the leading health care systems in the United States. JHM unites physicians and scientists of the Johns Hopkins University School of Medicine with the organizations, health professionals and facilities of the Johns Hopkins Hospital and Health System. JHM’s mission is to improve the health of the community and the world by setting the standard of excellence in medical education, research and clinical care. Diverse and inclusive, JHM educates medical students, scientists, health care professionals and the public; conducts biomedical research; and provides patient-centered medicine to prevent, diagnose and treat human illness.  JHM operates six academic and community hospitals, four suburban health care and surgery centers, and more than 30 primary health care outpatient sites. The Johns Hopkins Hospital, opened in 1889, was ranked number one in the nation from 1990 to 2011 by U.S. News & World Report.

Johns Hopkins Medicine Media Relations and Public Affairs Media Contacts:

Stephanie Desmon 410-955-8665; sdesmon1@jhmi.edu

Helen Jones 410-502-9422; hjones49@jhmi.edu

Disarming HIV With a “Pop”

PHILADELPHIA,          September 19, 2013

The DAVEI molecule is comprised of two main pieces: Membrane Proximal External Region (MPER), which attaches to the viral membranes, and cyanovarin (CVN), which binds to the sugar coating of the virus’s protein spike.

Pinning down an effective way to combat the spread of the human immunodeficiency virus, the viral precursor to AIDS, has long been a challenge for scientists and physicians, because the virus is an elusive one that mutates frequently and, as a result, quickly becomes immune to medication. A team of Drexel University researchers is trying to get one step ahead of the virus with a microbicide they’ve created that can trick HIV into “popping” itself into oblivion.

Its name is DAVEI – which stands for “Dual Action Virolytic Entry Inhibitor”- and it can pull a fast one on HIV. DAVEI was invented and tested by scientists from Drexel’s College of Engineering; School of Biomedical Engineering, Science and Health Systems; and College of Medicine, and is the latest in a new generation of HIV treatments that function by specifically destroying the virus without harming healthy cells.

“While several molecules that destroy HIV have recently been announced, DAVEI is unique among them by virtue of its design, specificity and high potency,” said Dr. Cameron Abrams, a professor in Drexel’s College of Engineering and a primary investigator of the project.

A team co-led by Abrams and Dr. Irwin Chaiken in the Department of Biochemistry and Molecular Biology in Drexel’s College of Medicine, and including Dr. Mark Contarino and doctoral students Arangassery Rosemary Bastian and R. V. Kalyana Sundaram, developed the chimeric recombinantly engineered protein – that is, a molecule assembled from pieces of other molecules and engineered for a specific purpose, in this case to fight HIV. Their research will be published in the October edition of the American Society for Microbiology’s Antimicrobial Agents and Chemotherapy.

The idea behind DAVEI was to design a molecule that hijacks the virus’s fusion machinery, the tools it uses to attach to and attack a healthy cell, and tricks the virus into destroying itself. HIV invades a healthy cell by first attaching via protein “spikes” that then collapse to pull viral and cell membranes together, fusing them and allowing the genetic contents of the virus to enter the healthy cell. The cell is rewired by the viral genetic material into producing more viruses instead of performing its normal function, which, in the case of cells infected by HIV, involves normal immunity. AIDS is the result.

“We hypothesized that an important role of the fusion machinery is to open the viral membrane when triggered, and it follows that a trigger didn’t necessarily have to be a doomed cell,” Abrams said. “So we envisioned particular ways the components of the viral fusion machinery work and designed a molecule that would trigger it prematurely,” Abrams said.

The team designed DAVEI from two main ingredients. One piece, called the Membrane Proximal External Region (MPER), is itself a small piece of the fusion machinery and interacts strongly with viral membranes. The other piece, called cyanovirin, binds to the sugar coating of the protein spike. Working together, the MPER and cyanovirin in DAVEI “tweak” the fusion machinery in a way that mimics the forces it feels when attached to a cell.

“For lack of a better term, DAVEI ‘tricks’ the virus into ‘thinking’ it is about to infect a healthy cell, when, in fact, there is nothing there for it to infect,” Abrams said. “Instead, it releases its genetic payload harmlessly and dies.”

Chaiken’s lab has extensively studied the molecular mechanisms of HIV-1 envelope protein interactions and structure-based design of agents that fight HIV. The researchers produced DAVEI using recombinant protein engineering and used HIV-1 pseudoviruses to demonstrate that it can physically rupture and irreversibly inactivate the virus particles.

“DAVEI and other new-generation virolytic inactivators open up an important opportunity to develop a topical microbicide to block the transmission of HIV, and at the same time provide lead ideas to discover treatment strategies for people who are already infected,” Chaiken said. “Our hope is that determining the structural driving forces of both inhibitors and viral entry machinery that enable spike inactivation will help to advance molecular designs with increased power, specificity and clinical potential for both prevention and treatment.”

 

News Media Contact

Britt Faulstick

News Officer, University Communications

britt.faulstick@drexel.edu Phone: 215-895-2617 Mobile: 215-796-5161

Ed Federico

Media Relations Manager, Drexel University College of Medicine

edward.federico@drexelmed.edu Phone: 215-255-7331

– See more at: http://drexel.edu/now/news-media/releases/archive/2013/September/DAVEI-HIV-molecule/#sthash.7eofB5q4.dpuf

Can vitamin B supplements help stave off stroke? ( 7% reduction in 6 months )

Contact: Rachel Seroka rseroka@aan.com 612-928-6129 American Academy of Neurology

MINNEAPOLIS – New evidence suggests that taking vitamin B supplements may help reduce the risk of stroke. The research appears in the September 18, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Previous studies have conflicting findings regarding the use of vitamin B supplements and stroke or heart attack,” said author Xu Yuming, with Zhengzhou University in Zhengzhou, China. “Some studies have even suggested that the supplements may increase the risk of these events.”

For the research, scientists analyzed 14 randomized clinical trials with a total of 54,913 participants. All of the studies compared B vitamin use with a placebo or a very low-dose B vitamin. Participants were then followed for a minimum of six months. There were 2,471 strokes throughout the studies, all of which showed some benefit of taking vitamin B.

Vitamin B lowered the risk of stroke in the studies overall by seven percent. However, taking supplements did not appear to affect the severity of strokes or risk of death from stroke.

Folic acid, a supplemental form of folate (vitamin B9), which is often found in fortified cereals, appeared to reduce the effect of vitamin B. Researchers did not find a reduction in stroke risk for vitamin B12.

“Based on our results, the ability of vitamin B to reduce stroke risk may be influenced by a number of other factors such as the body’s absorption rate, the amount of folic acid or vitamin B12 concentration in the blood, and whether a person has kidney disease or high blood pressure,” said Yuming. “Before you begin taking any supplements, you should always talk to your doctor.”

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To learn more about stroke, please visit http://www.aan.com/patients.

The American Academy of Neurology, an association of more than 26,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy.

For more information about the American Academy of Neurology, visit http://www.aan.com or find us on Facebook, Twitter, Google+ and YouTube.

Media Contacts: Rachel Seroka, rseroka@aan.com, (612) 928-6129 Michelle Uher, muher@aan.com, (612) 928-6120

Designer Molecule Causes AIDS Virus to Destroy Itself

A scanning electron micrograph shows HIV particles infecting a colorized human H9 T cell. (Credit: NIAID) FILE PHOTO

A scanning electron micrograph shows HIV particles infecting a colorized human H9 T cell. (Credit: NIAID) FILE PHOTO

by Jessica Berman

Researchers have designed a synthetic molecule that tricks the AIDS virus into destroying itself. The compound, called DAVEI, was developed by researchers at Philadelphia’s Drexel University and causes the deadly pathogen to eject its contents before it can infect human cells.

The AIDS virus uses protein spikes on its surface to fuse to healthy cells. Once attached, the microbe inserts its genetic material, turning the cells into little factories that crank out thousands of copies of HIV.

But DAVEI hijacks the virus, mimicking its interaction with immune system cells. DAVEI binds to the pathogen’s outer coat, triggering a firing mechanism that breaches the wall of the AIDS virus, according to Irwin Chaiken, a researcher in the Department of Biochemistry and Molecular Biology at Drexel’s College of Medicine.

Explaining how DAVEI works, Chaiken said, “so that the contents that are inside the virus that are small enough to go through the pores will go through the pores and leak out. And at that point, the virus shrinks and it becomes inactivated.”

DAVEI was designed by Cameron Abrams, a professor of engineering at Drexel. Abrams envisions using the synthetic agent in a microbicide, a cream or gel that women can use vaginally to protect themselves from contracting the disease from their HIV-infected partners.

“And so this we think this would benefit primarily populations in sub-Saharan Africa where male-to-female transmission is very high rate, young women are being infected at a very high rate. That’s extremely detrimental to those societies,” said Abrams.

Abrams also says DAVEI might be used someday as a treatment for those who are HIV positive by destroying infected cells.

“In an active infection in an individual, there are cells that are continuously producing virus. And if those cells could be destroyed before they produce a lot of virus that obviously would be very good,” Abrams pointed out.

Researchers say much more work needs to be done with DAVEI and compounds like it before actual anti-HIV therapies could be developed. An article on the manmade molecule was published in the October edition of Antimicrobial Agents and Chemotherapy.

 

http://www.voanews.com/content/designer-molecule-causes-aids-virus-destroy-itself/1753479.html

New study discovers copper destroys highly infectious norovirus

 

Ref: 13/162

10 September 2013

Sarah Warnes and Professor Bill Keevil

Scientists from the University of Southampton have discovered that copper and copper alloys rapidly destroy norovirus – the highly-infectious sickness bug.

Worldwide, norovirus is responsible for more than 267 million cases of acute gastroenteritis every year. In the UK, norovirus costs the National Health Service at least £100 million per year, in times of high incidence, and up to 3,000 people admitted to hospital per year in England.

There is no specific treatment or vaccine, and outbreaks regularly shut down hospital wards and care homes, requiring expensive deep-cleaning, incurring additional treatment costs and resulting in lost working days when staff are infected. Its impact is also felt beyond healthcare, with cruise ships and hotels suffering significant damage to their reputation when epidemics occur among guests.

The virus is highly infectious and can be contracted from contaminated food or water, person-to-person contact, and contact with contaminated surfaces, meaning surfaces made from copper could effectively shut down one avenue of infection.

The study, which was designed to simulate fingertip-touch contamination of surfaces, showed norovirus was rapidly destroyed on copper and its alloys, with those containing more than 60 per cent copper proving particularly effective.

Copper alloys have previously been shown to be effective antimicrobial surfaces against a range of bacteria and fungi. The Southampton research reported rapid inactivation of murine norovirus on alloys, containing over 60 per cent copper, at room temperature but no reduction of infectivity on stainless steel dry surfaces in simulated wet fomite and dry touch contamination. The rate of inactivation was initially very rapid and proportional to the copper content of alloy tested. Viral inactivation was not as rapid on brass as previously observed for bacteria but copper-nickel alloy was very effective.

One of the targets of copper’s antimicrobial activity was the viral genome and a reduced number of the gene for a viral encoded protein, VPg (viral-protein-genome-linked), which is essential for infectivity, was observed following contact with copper and brass dry surfaces.

Lead author Sarah Warnes, from the Centre for Biological Sciences at the University of Southampton, says: “The use of antimicrobial surfaces containing copper in clinical and community environments, such as cruise ships and care facilities, could help to reduce the spread of this highly infectious and costly pathogen.

“Copper alloys, although they provide a constant killing surface, should always be used in conjunction with regular and efficient cleaning and decontamination regimes using non-chelating reagents that could inhibit the copper ion activity.”

Co-author Professor Bill Keevil, from the University’s Institute for Life Sciences, adds: “Although the virus was identified over 40 years ago, the lack of methods to assess infectivity has hampered the study of the human pathogen.

“The virus can remain infectious on solid surfaces and is also resistant to many cleaning solutions. That means it can spread to people who touch these surfaces, causing further infections and maintaining the cycle of infection. Copper surfaces, like door handles and taps, can disrupt the cycle and lower the risk of outbreaks.”

The study ‘Inactivation of norovirus on dry copper alloy surfaces’ is published in the latest issue of the journal PLOS ONE.

Previous laboratory studies by the University of Southampton have described the rapid death of bacterial, fungal and viral pathogens such as MRSA on copper alloy surfaces and also prevention of antibiotic resistance horizontal gene transfer between pathogens.

For more information and scientific references, visit http://antimicrobialcopper.com/

Oral nutritional supplements demonstrate significant health and cost benefits

Contact: Kim Modory 847-938-4696 Fleishman-Hillard, Inc.

Analysis of more than 1 million adult hospital cases revealed 21 percent reduction in length of hospital stay and cost with nutritional intervention

ABBOTT PARK, Ill., Aug. 30, 2013 – Abbott (NYSE: ABT) A recent health economics and outcomes study, conducted by leading health economists and supported by Abbott, found that oral nutritional supplements provided to patients during hospitalization were associated with significant reductions in length of stay and hospitalization cost. Additionally, the 30-day readmission risk was significantly reduced for patients with at least one known subsequent readmission.

The study is being presented this weekend at the European Society for Clinical Nutrition and Metabolism (ESPEN) annual congress in Leipzig, Germany, where it will be highlighted as one of the conference’s three “Best Abstracts.” The meeting is a leading conference in clinical nutrition, bringing together participants from more than 80 countries.

The study analyzed more than 1 million adult inpatient cases in the U.S., and found that patients provided oral nutritional supplements during hospitalization benefited from:

  • 21 percent, or 2.3 day, reduction in length of stay
  • 21.6 percent, or $4,734, reduction in patient hospitalization cost 

Additionally, there was a 6.7 percent reduction in the probability of a 30-day readmission in patients who had at least one known subsequent readmission and were provided oral nutritional supplements during the previous hospitalization.

The study, which also was recently published in the American Journal of Managed Care, provides insights into the economic benefits of prescribing oral nutritional supplements to adult patients in the hospital setting.

“Patients identified as having nutritional deficiencies often face a longer and more difficult recovery process, resulting in higher health care costs and an increase in complication rates,” said Marinos Elia, MD, BSc Hon, FRCP, Professor of Clinical Nutrition and Metabolism at University of Southampton. “Research demonstrates that oral nutritional supplementation can lead to highly positive economic benefits and improved patient outcomes.”

In the study, investigators were able to determine differences in length of stay and costs by comparing hospital stays where oral nutritional supplements were prescribed to patients with similar conditions where oral nutritional supplements weren’t prescribed.

“Because oral nutritional supplements are formulated to provide advanced nutrition and calories for patients and are relatively inexpensive to provide, the sizeable savings they generate make supplementation a cost-effective therapy,” said study co-author, Tomas Philipson Ph.D., Daniel Levin Chair of Public Policy at the University of Chicago.

“In today’s outcome conscious hospital environment, Abbott is committed to delivering products that improve the quality of care for patients and also help reduce health care costs,” said Robert H. Miller, Ph.D., divisional vice president, Global R&D and Scientific Affairs for Abbott Nutrition. “In addition to the numerous retrospective studies focused on health economics and outcomes research in our pipeline, nearly all of our clinical research studies now include an economic analysis to help demonstrate a nutritional therapy’s total value proposition.”

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About the Study

The ″Impact of Oral Nutritional Supplementation on Hospital Outcomes” study is a retrospective data analysis on the effect of oral nutritional supplements on hospital economic outcomes. The study compared hospital stays where oral nutritional supplements were provided with similar hospital stays that did not provide oral nutritional supplements. The difference between length of hospital stay and cost of treatment (including supplies, labor, depreciation of equipment, etc.) were measured. The probability of 30-day hospital readmission also was calculated.

The retrospective analysis utilized information from more than one million adult inpatient cases found in the Premier Research Database from 2000 – 2010, maintained by the Premier healthcare alliance – representing a total of 44 million hospital episodes from across the United States or approximately 20 percent of all inpatient admissions in the United States. The full sample consisted of adults 18 years and older and focused on oral feeding interventions only. The matched sample ultimately included: 1,160,088 total episodes (oral nutritional supplements episodes N= 580,044 and non-oral nutritional supplements episodes N=580,044), where propensity score matching and instrumental variables were used to address potential bias due to non-random selection.

About Abbott Nutrition

For more than 85 years, Abbott Nutrition has been developing and marketing science-based nutritional products to support the growth, health and wellness of people of all ages. Internationally recognized brands include the Similac® brand of infant formulas; the Gain® brand of growing-up milks; the PediaSure® brand of complete and balanced nutrition for children; and the Ensure® brand of complete and balanced nutrition for adults.

The company is a leader in nutritional products clinically shown to address the distinct dietary needs of people with serious health conditions or special nutrient requirements, such as the Glucerna® brand of nutrition shakes and bars for people with diabetes.

About Abbott

Abbott is a global healthcare company devoted to improving life through the development of products and technologies that span the breadth of healthcare. With a portfolio of leading, science-based offerings in diagnostics, medical devices, nutritionals and branded generic pharmaceuticals, Abbott serves people in more than 150 countries and employs approximately 70,000 people.

Visit Abbott at http://www.abbott.com and connect with us on Twitter at @AbbottNews.

Novel Chinese herbal medicine JSK improves spinal cord injury outcomes in rats

Contact: Daphne Watrin d.watrin@iospress.nl 31-206-883-355 IOS Press

Findings published in Restorative Neurology and Neuroscience

Amsterdam, NL, August 19, 2013 – A new study published in Restorative Neurology and Neuroscience demonstrates that Chinese herbal medicine Ji-Sui-Kang (JSK), given systemically for three weeks after injury in rats, improved locomotor function, reduced tissue damage, and preserved the structure of neural cells compared to control rats. The report also includes data showing that JSK may first act to reduce inflammation and cell apoptosis and death, and boost local oxygen supply while, later on, it appears to restore function and promote tissue regeneration.

Although Chinese herbal medicines have traditionally been used for a variety of ailments, the rationale for their use relies more on anecdotal evidence than the results of modern-day controlled experiments.

“A number of anecdotal reports from Chinese medicine practitioners indicate that treatment with a novel herbal formulation, JSK, for periods of one week or three months improved functional recovery,” explains co-lead investigator Shucui Jiang, MD, PhD, head of the Hamilton NeuroRestorative Group at McMaster University in Hamilton, Ontario, Canada. “Our present study provides an important and necessary foundation for further studies of JSK.”

In this study rats began JSK treatment immediately after undergoing spinal cord injury. Within 7 days, hindlimb locomotor function was significantly better in JSK-treated rats compared to those receiving only saline. JSK-treated rats continued to have better motor function than controls throughout the 21-day test period and treated animals appeared to support their weight better and have more coordinated movements.

When the investigators looked at histological samples of the spinal cord, they found that the architecture of the spinal cord was better preserved in JSK-treated animals and the size of the injured area was significantly smaller 7 days after injury. JSK-treated animals also showed more intact axons and myelin in the injured areas compared to controls. Other encouraging signs were less deposition of fibrinogen in the injured areas of JSK-treated animals, a decrease in pro-inflammatory COX-2 expression, and fewer cell deaths at the lesion site (as measured by caspase-3 staining).

JSK also increased the expression of growth associated protein 43 (GAP43), a marker of neuronal development and axonal regeneration, and neuroglobulin, a protein found in cerebral neurons that is thought to help neurons survive and recover after trauma. “Our data suggest that JSK may enhance tissue recovery by reducing cell growth inhibitors and by promoting the proliferation of cells within the injured spinal cord,” says co-lead investigator Michel P. Rathbone, MD, CHB, PhD, Professor, Division of Neurology, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

Other findings suggest JSK might help protect against injury caused by damage to spinal cord blood vessels. For instance, JSK increased vascular endothelial growth factor (VEGF), a protein involved in the formation and growth of blood vessels, down-regulated clotting-associated genes, and promoted factors that contribute to vasodilation.

The authors say that JSK targets multiple biochemical and cellular pathways that may help protect against the primary traumatic injury as well as subsequent secondary injuries that evolve over time.

The authors do not disclose the complete herbal composition of JSK for proprietary reasons. Some of its ingredients include Ginseng, Rhizoma (chuan xiong), Glycyrrhizae Radix (gan cao), Paeoniae Alba Radix (bai shao) and Cinnamomi Cortex (rou gui).