Dramatic FLU virus mutations may be due to antiquated vaccine manufacturing

Dramatic FLU virus mutations may be due to antiquated vaccine manufacturing

Dramatic FLU virus mutations may be due to antiquated vaccine manufacturing

Researchers discovered that by manufacturing the vaccine through the use of chicken eggs it had the unintentional consequence of causing dramatic mutations in the H3N2 Virus. These mutations the researchers speculate resulted in a equally dramatic decline in vaccine effectiveness

Prediction of influenza vaccine effectiveness for the influenza season 2017/18 in the US [version 1; referees: 1 approved]. F1000Research 2017, 6:2067 (doi: 10.12688/f1000research.13198.1)

A structural explanation for the low effectiveness of the seasonal influenza H3N2 vaccine  (doi: /10.1371/journal.ppat.1006682)

Folic acid deficiency can affect the health of great, great grandchildren

Contact: Genevieve Maul gm349@admin.cam.ac.uk 44-012-237-65542 University of Cambridge

Deficiencies associated with spina bifida, heart defects and placental abnormalities

Folic acid deficiency can cause severe health problems in offspring, including spina bifida, heart defects and placental abnormalities. A study out today reveals that a mutation in a gene necessary for the metabolism of folic acid not only impacts the immediate offspring but can also have detrimental health effects on the next several generations. The new research, which also sheds light on the molecular mechanism of folic acid (also known as folate) during development, was published today in the journal Cell.

“Although our research focused on genetic mutations which disrupts the break down and metabolism of folic acid, we believe that folic acid deficiency in the diet would have a similar multi-generational impact on health,” said Dr Erica Watson from the Centre for Trophoblast Research at the University of Cambridge, who led the study.

The detrimental effects of folic acid deficiency on development are quite well known. As a result, many countries, to include Canada and the US, have implemented folate fortification programmes which require folic acid to be added to cereal products. However, until now, very little was known about how folic acid deficiency caused the diverse range of health problems in offspring.

“Fortification programmes have reduced the risk of health effects but not eliminated them completely,” said Dr Watson. “Based on our research, we now believe that it may take more than one generation to eliminate the health problems caused by folate deficiency.”

The researchers, from the Universities of Cambridge and Calgary, used mice for the study as they metabolize folic acid very similarly to humans and because folic acid deficiency or mutations in the same genes required to break down folic acid in humans result in similar developmental abnormalities and diseases in mice. This enabled the researchers to explore how the molecular mechanism of folic acid deficiency impacted development, thereby causing health problems.

For the study, the scientists used mice in which a gene called Mtrr was specifically mutated. The gene is key to the normal progression of the folic acid cycle and, when mutated, it results in abnormal folic acid metabolism causing similar effects to dietary folic acid deficiency. The researchers found that when either the maternal grandmother or the maternal grandfather had this Mtrr mutation, their genetically normal grandchildren were at risk of a wide spectrum of developmental abnormalities. These developmental abnormalities were also seen in the fourth and fifth generations of mice.

Through another experiment which involved transferring the embryo from the third generation into a normal healthy female mouse, they discovered that these developmental abnormalities were not passed down genetically. Instead, the serious defects were the result of epigenetic changes which had been inherited.

Epigenetics is a system which turns genes on and off. It occurs when chemicals, such as methyl groups, bind to the DNA at specific locations to control which genes are expressed and when they are expressed. (Interestingly, the folic acid cycle is required to make sure that the cell has enough methyl groups for normal gene expression.) Epigenetic inheritance refers to the passing of these epigenetic marks from one generation to the next – despite the epigenome, for the most part, being ‘wiped clean’ after each generation.

The researchers hypothesize that, for a yet unknown reason, some of these abnormal epigenetic marks caused by the Mtrr mutation may escape this normal erasure and are inherited by the next generation. If these abnormal epigenetic marks that regulate genes important for development are inherited, then these generations may develop abnormalities as a result of the wrong genes being turned on or off.

“It surprised us to find that the great, great grandchildren of a parent who has had a folic acid deficiency could have health problems as a result – suggesting that the ‘sins of your maternal grandparents’ can have an effect on your development and your risk for disease,” said Dr Watson.

“More importantly, our research shows that disease in general can be inherited through epigenetic means rather than genetic means, which has huge implications for human health. Environmental factors that influence epigenetic patterns – e.g., diet, epigenetic disruptors in the environment such as chemicals, etc. – may also have long term, multigenerational effects.”

###

For additional information please contact:

Genevieve Maul, Office of Communications, University of Cambridge Tel: direct, +44 (0) 1223 765542, +44 (0) 1223 332300 Mob: +44 (0) 7774 017464 Email: Genevieve.maul@admin.cam.ac.uk

Notes to editors:

  • The paper ‘Mutation in Folate Metabolism Causes Epigenetic Instability and Transgenerational Effects On Development’ will be published in the 26 September edition of Cell

     

  • Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge 

     

  • To view a video of the researchers explaining their study, please go to: http://www.youtube.com/watch?v=Dlfg49sjo3U

Scientists to make mutant forms of new bird flu to assess risk

Source: Reuters – Wed, 7 Aug 2013 05:00 PM

Author: Reuters

 

* Controversial research sparked previous security fears

* Flu experts say it is critical to prepare for threat

* New H7N9 bird flu strain has killed 43 people so far

* Outbreak currently controlled, may return in autumn

By Kate Kelland, Health and Science Correspondent

LONDON, Aug 7 (Reuters) – Scientists are to create mutant forms of the H7N9 bird flu virus that has emerged in China so they can gauge the risk of it becoming a lethal human pandemic.

The genetic modification work will to result in highly transmissible and deadly forms of H7N9 being made in several high security laboratories around the world, but it is vital to prepare for the threat, the scientists say.

The new bird flu virus, which was unknown in humans until February, has already infected at least 133 people in China and Taiwan, killing 43 of them, according to the latest World Health Organization (WHO) data.

Announcing plans to start the controversial experiments, leading virologists Ron Fouchier and Yoshihiro Kawaoka said H7N9’s pandemic risk would rise “exponentially” if it gained the ability to spread easily among people.

And the only way to find out how likely that is, and how many genetic changes would need to take place before it could happen, is to engineer those mutations in laboratory conditions  and test the virus’s potential using animal models, they said.

“It’s clear this H7N9 virus has some hallmarks of pandemic viruses, and it’s also clear it is still missing at least one or two of the hallmarks we’ve seen in the pandemic viruses of the last century,” Fouchier told Reuters in a telephone interview.

“So the most logical step forward is to put in those (missing) mutations first.”

Writing in the journals Nature and Science on behalf of 22 scientists who will carry out various aspects of the H7N9 work, Fouchier said because the risk of a pandemic caused by a bird flu virus exists in nature, it was critical for risk-mitigation plans to study the likely mutations that could make that happen.

This kind of science is known as “gain of function” (GOF) research. It aims to identify combinations of genetic mutations that allow an animal virus to jump to humans and spread easily.

By finding the mutations needed, researchers and health authorities can better assess how likely it is that a new virus could become dangerous and if so, how soon they should begin developing drugs, vaccines and other scientific defences.

Yet such work is highly controversial. It has fuelled an international row in the past two years after it was carried out on another threatening bird flu virus called H5N1.

BIOTERRORISM FEARS

When Fouchier, of the Erasmus Medical Centre in Rotterdam, The Netherlands, and Kawaoka, at the University of Wisconsin in the United States, announced in late 2011 they had found how to make H5N1 into a form that could spread between mammals, the U.S. National Science Advisory Board for Biosecurity (NSABB) was so alarmed that it took the unprecedented step of trying to censor publication of the studies.

The NSABB said it feared details of the work could fall into the wrong hands and be used for bioterrorism. A year-long moratorium on such research followed while the World Health Organisation, U.S. security advisers and international flu researchers sought ways to ensure the highest safety controls.

The laboratory Fouchier will be working in is known as a  BSL3 Enhanced lab (Bio-Safety Level 3), the highest level of biosecurity that can be achieved in academic research.

“Nature is the biggest threat to us, not what we do in the lab. What we do in the lab is under very intense biosecurity measures,” he said. “There are layers upon layers of layers of biosafety measures such that if one layer might break there are additional layers to prevent this virus ever coming out.”

Fouchier conceded that GOF research has been “under fire” recently. “One of the accusations against the flu community was that we were not transparent enough about what experiments were being done, and why and how they were being done,” he said. “We’re trying to pre-empt such accusations this time.”

The H7N9 bird flu outbreak currently appears under control with only 3 new human cases in May after 87 in April and 30 in March. Experts say this is largely thanks to the closure of many live poultry markets and because of warmer weather.

Yet as winter approaches in China, many experts believe H7N9 could re-emerge, meaning the threat of a pandemic looms if it mutates to become easily transmissible between people.

The first scientific analysis of probable human-to-human transmission of H7N9 raised concern about its pandemic potential and prompted scientists James Rudge and Richard Coker of the London School of Hygiene and Tropical Medicine to warn: “The threat posed by H7N9 has by no means passed.”

Fouchier and colleagues said they hope to unravel the molecular processes behind H7N9 by manipulating its genetic material to increase virulence or induce drug resistance.

Wendy Barclay, an Imperial College London flu expert, said it would be ludicrous to shy away from such studies. “This type of work is like fitting glasses for someone who can’t see well,” she said. “Without the glasses the vision is blurred and uncertain, with them you can focus on the world and deal with it a lot more easily.”   (Reporting by Kate Kelland; editing by David Evans)

http://www.trust.org/item/20130807165536-m5jun/?source=hpbreaking

 

Health Research Report 10 JUN 2013


Topics:
Vitamin C found to kill Tuberculosis:including MDR-TB, XDR-TB by fenton reaction
Statins prevent exercise benefits and erode skeletal muscle mitochondria
Phosphatidyl Serine improve Familial Dysautonomia, Parkinsons, and IKAP protein
LED lights shown to cause Blindness

Scientists described small genetic changes that enable the H5N1 bird flu virus to replicate more easily in the noses of mammals

 

Bird flu mutation study offers vaccine clue

by  Sam Wong   08 April 2013                   

main image

 

shadow Scientists have described small genetic changes that enable the H5N1 bird flu virus to replicate more easily in the noses of mammals.

So far there have only been isolated cases of bird flu in humans, and no widespread transmission as the H5N1 virus can’t replicate efficiently in the nose. The new study, using weakened viruses in the lab, supports the conclusions of controversial research published in 2012 which demonstrated that just a few genetic mutations could enable bird flu to spread between ferrets, which are used to model flu infection in humans.

Researchers say the new findings could help to develop more effective vaccines against new strains of bird flu that can spread between humans.

“Knowing why bird flu struggles to replicate in the nose and understanding the genetic mutations that would enable it to happen are vital for monitoring viruses circulating in birds and preparing for an outbreak in humans,” said Professor Wendy Barclay, from the Department of Medicine at Imperial College London, who led the study.

“The studies published last year pointed to a mechanism that restricts replication of H5N1 viruses in the nose. We’ve engineered a different mutation with the same effect into one of the virus proteins and achieved a similar outcome. This suggests that there is a common mechanism by which bird flu could evolve to spread between humans, but that a number of different specific mutations might mediate that.”

Bird flu only rarely infects humans because the human nose has different receptors to those of birds and is also more acidic. The Imperial team studied mutations in the gene for haemagglutinin, a protein on the surface of the virus that enables it to get into host cells. They carried out their experiments in a laboratory strain of flu with the same proteins on its surface as bird flu, but engineered so that it cannot cause serious illness.

The more we understand about the kinds of mutations that will enable them to transmit between humans, the better we can prepare for a possible pandemic.– Professor Wendy Barclay

Department of Medicine

The research found that mutations in the H5 haemagglutinin enabled the protein to tolerate higher levels of acidity. Viruses with these mutations and others that enabled them to bind to different receptors were able to replicate more efficiently in ferrets and spread from one animal to another.

The results have important implications for designing vaccines against potential pandemic strains of bird flu. Live attenuated flu vaccines (LAIV) might be used in a pandemic situation because it is possible to manufacture many more doses of this type of vaccine than of the killed virus vaccines used to protect against seasonal flu. LAIV are based on weakened viruses that don’t cause illness, but they still have to replicate in order to elicit a strong immune response. Viruses with modified haemagglutinin proteins induced strong antibody responses in ferrets in this study, suggesting that vaccines with similar modifications might prove more effective than those tested previously.

“We can’t predict how bird flu viruses will evolve in the wild, but the more we understand about the kinds of mutations that will enable them to transmit between humans, the better we can prepare for a possible pandemic,” said Professor Barclay.

The research was funded by the Medical Research Council and the Wellcome Trust and published in the Journal of General Virology.

Reference

H Shelton et al. ‘Mutations in hemagglutinin that affect receptor binding and pH stability increase replication of a PR8 influenza virus with H5 HA in the upper respiratory tract of ferrets and may contribute to transmissibility.’ Journal of General Virology (2013) doi:10.1099/vir.0.050526-0

http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_8-4-2013-12-47-4

 

Are we getting more stupid? Researchers claim our intelligence is diminishing as we no longer need it to survive

By Mark Prigg

PUBLISHED:13:57 EST, 12  November 2012| UPDATED:14:10 EST, 12 November 2012

Our intelligence and behaviour requires  optimal functioning of a large number of genes, which requires enormous  evolutionary pressures to maintain.

Now, in a provocative theory, a team from  Stanford University claim we are losing our intellectual and emotional  capabilities because the intricate web of genes which endows us with our brain  power is particularly vulnerable to mutations – and these mutations are not  being selected against our modern society because we no longer need intelligence  to survive.

But we shouldn’t lose any sleep over our  diminishing brain power – as by the time it becomes a real problem technology  will have found a solution making natural selection obsolete.

Researchers say be are becoming less intelligent because we no longer need intelligence to surviveResearchers say be are becoming less intelligent because  we no longer need intelligence to survive

‘The development of our intellectual  abilities and the optimisation of thousands of intelligence genes probably  occurred in relatively non-verbal, dispersed groups of peoples before our  ancestors emerged from Africa,’ says Dr Gerald Crabtree, lead author of the  paper published today in Cell Press journal Trends in Genetics.

In this environment, intelligence was  critical for survival, and there was likely to be immense selective pressure  acting on the genes required for intellectual development, leading to a peak in  human intelligence.

But it was downhill from there on in as, from  that point, it’s likely that we began to slowly lose ground, the researchers  claim.

With the development of agriculture, came  urbanisation, which may have weakened the power of selection to weed out  mutations leading to intellectual disabilities.

The team believe we have sustained mutations harmful to our intelligence
The team believe we have sustained mutations harmful to  our intelligence

Based on calculations of the frequency with  which deleterious mutations appear in the human genome and the assumption that  2,000 to 5,000 genes are required for intellectual ability, Dr Crabtree  estimates that within 3,000 years, about 120 generations, we have all sustained  two or more mutations harmful to our intellectual or emotional  stability.

Also, recent findings from neuroscience  suggest that genes involved in brain function are uniquely susceptible to  mutations.

Dr Crabtree argues that the combination of  less selective pressure and the large number of easily affected genes is eroding  our intellectual and emotional capabilities.

But the loss is quite slow, and judging by  society’s rapid pace of discovery and advancement, future technologies are bound  to reveal solutions to the problem, Dr Crabtree believes.

He said: ‘I think we will know each of the  millions of human mutations that can compromise our intellectual function and  how each of these mutations interact with each other and other processes as well  as environmental influences.

‘At that time, we may be able to magically  correct any mutation that has occurred in all cells of any organism at any  developmental stage.

‘Thus, the brutish process of natural  selection will be unnecessary.’

Read more: http://www.dailymail.co.uk/sciencetech/article-2231924/Are-getting-stupid-Researchers-claim-longer-need-intelligence-survive.html#ixzz2C3MKs8xC Follow us: @MailOnline on Twitter | DailyMail on Facebook

Human nose too cold for bird flu, says new study ( H5N1 )

2009 study posted for filing

Contact: Lucy Goodchild
lucy.goodchild@imperial.ac.uk
44-207-594-6702
Imperial College London

Avian influenza viruses do not thrive in humans because the temperature inside a person’s nose is too low, according to research published today in the journal PLoS Pathogens. The authors of the study, from Imperial College London and the University of North Carolina, say this may be one of the reasons why bird flu viruses do not cause pandemics in humans easily.

There are 16 subtypes of avian influenza and some can mutate into forms that can infect humans, by swapping proteins on their surface with proteins from human influenza viruses.

Today’s study shows that normal avian influenza viruses do not spread extensively in cells at 32 degrees Celsius, the temperature inside the human nose. The researchers say this is probably because the viruses usually infect the guts of birds, which are warmer, at 40 degrees Celsius. This means that avian flu viruses that have not mutated are less likely to infect people, because the first site of infection in humans is usually the nose. If a normal avian flu virus infected a human nose, the virus would not be able to grow and spread between cells, so it would be less likely to damage cells and cause respiratory illness.

The researchers also found that when they created a mutated human influenza virus by adding a protein from the surface of an avian influenza virus, this mutated virus struggled to thrive at 32 degrees Celsius. This suggests that if a new human influenza strain evolved by adopting proteins from an avian influenza virus, this would need to undergo further changes in order to adapt to the conditions in the human body.

The researchers reached their conclusions by growing cells from the human airway and infecting them with different human and avian influenza viruses, including H5N1, to see how well the viruses grew and spread. The human influenza viruses grew equally well in the cells whether they were maintained at 37 degrees Celsius, our core body temperature, or at 32 degrees Celsius, the temperature of the nose. In contrast, the four avian influenza viruses tested grew well at 37 degrees Celsius but grew very slowly at 32 degrees Celsius.

When the researchers added proteins from an avian influenza virus to a human influenza virus, the human influenza virus also grew slowly and struggled to replicate at 32 degrees Celsius.

As viruses kill the cells they infect, the researchers also measured the extent of cell death in the model. This showed that at 32 degrees Celsius, far fewer cells died as a result of infection with avian influenza compared with human influenza, supporting the idea that the avian virus could not thrive at that temperature.

Professor Wendy Barclay, one of the authors of the study from the Division of Investigative Science at Imperial College London, said: “Bird viruses are out there all the time but they can only cause pandemics when they undergo certain changes. Our study gives vital clues about what kinds of changes would be needed in order for them to mutate and infect humans, potentially helping us to identify which viruses could lead to a pandemic.

“It would be impossible to develop vaccines against all 16 subtypes of avian flu, so we need to prioritise. By studying a range of different viruses in systems like this one we can look for warnings that they are already beginning to make the kinds of genetic changes in nature that mean they could be poised to jump into humans; animal viruses that spread well at low temperatures in these cultures could be more likely to cause the next pandemic than those which are restricted,” added Professor Barclay.

 

###

 

The research was funded by the Medical Research Council in the UK and by the NIH in the USA.

54th Health Research Report 14 APR 2009 – Reconstruction

Editors Top Five:

1. The new ‘epigenetics:’ Poor nutrition in the womb causes permanent genetic changes in the offspring

2. Einstein scientists propose new theory of autism

3.Soybean component reduces menopause effects

4. Omega-3 kills cancer cells

5.Aspirin and similar drugs may be associated with brain microbleeds in older adults

In this Issue:

1.Physical activity may strengthen children’s ability to pay attention

2. How probiotics can prevent disease

3. Omega-3 kills cancer cells

4. Source of major health benefits in olive oil revealed

5. Einstein scientists propose new theory of autism

6. Broccoli sprouts may prevent stomach cancer by defeating Helicobacter pylori

7. Biology of flushing could renew niacin as cholesterol drug

8. Oral contraceptives associated with increased risk of lupus

9. Soybean component reduces menopause effects

10.Vitamin D Deficiency Related to Increased Inflammation in Healthy Women, MU Study Finds

11.Parkinson’s disease medication triggers destructive behaviors

12.Aspirin and similar drugs may be associated with brain microbleeds in older adults

13.The new ‘epigenetics:’ Poor nutrition in the womb causes permanent genetic changes in the offspring

14.Low glycemic breakfast may increase benefits of working out

Health Research Report

54th Issue Date 31 MAR 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/engineeringevil

www.engineeringevil.com

Researchers Map Molecular Details That Encourage H1N1 Transmission To Humans

The 2009 H1N1 pandemic influenza virus appears to have required certain mutations in order to be transmitted to humans, according to a paper in the September Journal of Virology. The research could prove extremely valuable for efforts to predict human outbreaks.

The 2009 influenza pandemic was caused by a swine influenza virus that mutated in a way that made it transmissible among humans. The researchers, led by Hualan Chen of the Harbin Veterinary Research Institute, Harbin, China, have determined the probable details of the mutations that led to human transmission.

In this study, Chen, who is director of the National Avian Influenza Reference Laboratory at the Institute, and her collaborators have shown that two specific mutations in each of two proteins appear to be critical to transmission to, and among humans. One of those mutations, of a single amino acid in the virus’ hemagglutinin protein, gives the virus the ability to bind to human receptors, and enables transmission in mammals via droplets of respiratory fluids.

That amino acid, in the 226th slot in the protein, is glutamine. The researchers showed its importance by causing a mutation from glutamine, the amino acid in that position seen in viruses from infected humans, to argenine, as seen in swine. Working in cell cultures, the researchers showed that the switch dampened the virus’ ability to bind the human receptor, while boosting its ability to bind to the avian receptor. They showed further that the change rendered the virus non-transmissible via respiratory droplets in guinea pig models, and unable to replicate in the lungs of ferrets—results that suggest, but do not prove that the same may happen in humans.

Also in guinea pigs, changing an amino acid in the virus’ PB2 protein abolished transmission in guinea pigs via respiratory droplets, while that change, plus another single amino acid change in the hemagglutinin protein, killed such transmission in ferrets.

It gets still more convoluted. The same amino acid in the PB2 protein that enables virus transmission via respiratory droplets, which is located at position 271 in that protein, can also encourage the afore-mentioned mutation in hemagglutinin position 226 to glutamine, which enables the virus to cleave to the human receptor.

The value of all this information, says Chen, is that it provides a means for predicting outbreaks of human-transmissible H1N1.

(Y. Zhang, Q. Zhang, Y. Gao, X. He, H. Kong, Y. Jiang, Y. Guan, X. Xia, Y. Shu, Y. Kawaoka, Z. Bu, and H. Chen, 2012. Key molecular factors in hemagglutinin and PB2 contribute to efficient transmission of the 2009 H1N1 pandemic influenza virus. J. Virol. 86:9666-9674.)

Download a copy of the article at http://bit.ly/asmtip0912b

Learning faster with neurodegenerative disease

Contact: Dr. Christian Beste Christian.Beste@rub.de 49-234-322-4323 Ruhr-University Bochum

Huntington’s gene mutation carriers: Severity of the genetic mutation related to learning efficiency

People who bear the genetic mutation for Huntington’s disease learn faster than healthy people. The more pronounced the mutation was, the more quickly they learned. This is reported by researchers from the Ruhr-Universität Bochum and from Dortmund in the journal Current Biology. The team has thus demonstrated for the first time that neurodegenerative diseases can go hand in hand with increased learning efficiency. “It is possible that the same mechanisms that lead to the degenerative changes in the central nervous system also cause the considerably better learning efficiency” says Dr. Christian Beste, head of the Emmy Noether Junior Research Group “Neuronal Mechanisms of Action Control” at the RUB.

Passive learning through repeated stimulus presentation

In a previous study, the Bochum psychologists reported that the human sense of vision can be changed in the long term by repeatedly exposing subjects to certain visual stimuli for short periods (we reported in May 2011, http://aktuell.ruhr-uni-bochum.de/pm2011/pm00136.html.de). The task of the participants was to detect changes in the brightness of stimuli. They performed better if they had viewed the stimuli passively for a while first. In the current study, the researchers presented the same task to 29 subjects with the genetic mutation for Huntington’s disease, who, however, did not yet show any symptoms. They also tested 45 control subjects without such mutations in the genome. In both groups, the learning efficiency was better after passive stimulus presentation than without the passive training. Subjects with the Huntington’s mutation, however, increased their performance twice as fast as those without the mutation.

Glutamate may have paradoxical effect

Degenerative diseases of the nervous system are based on complex changes. A key mechanism is an increased release of the neurotransmitter glutamate. However, since glutamate is also important for learning, in some cases it could lead to the paradoxical effect: better learning efficiency despite degeneration of the nerve cells.

Detecting differences in brightness under aggravated conditions

In each experimental run, the subjects saw two consecutive small bars on a computer screen that either had the same or different brightness. Sometimes, however, not only the brightness changed from bar one to bar two, but also the orientation of the bar (vertical or horizontal). “Normally, the distraction stimulus, i.e. the change in orientation, draws all the attention” Christian Beste explains. “But after the passive training with the visual stimuli, the distraction stimulus has no effect at all.” The shift of attention from the non-relevant to the relevant properties of the stimulus was also visible in the electroencephalogram (EEG) in brain areas for early visual processing.

Better performance with stronger mutation

In Huntington’s disease, a short segment of a gene is repeated. The number of repetitions determines when the disease breaks out. In the present study, a greater number of repetitions was, however, also associated with higher learning efficiency. “This shows that neurodegenerative changes can cause paradoxical effects” says Christian Beste. “The everyday view that neurodegenerative changes fundamentally entail deterioration of various functions can no longer be maintained in this dogmatic form.”

###

Bibliographic record

C. Beste, E. Wascher, H.R. Dinse, C. Saft (2012): Faster perceptual learning through excitotoxic neurodegeneration, Current Biology, doi: 10.1016/j.cub.2012.08.012

Further information

Dr. Christian Beste, Institute of Cognitive Neuroscience, Department of Biological Psychology, Faculty of Psychology at the Ruhr-Universität, 44780 Bochum, Germany, Tel. +49/234/32-24323 Christian.Beste@rub.de

Click for more

Previous press release on the subjecthttp://aktuell.ruhr-uni-bochum.de/pm2011/pm00136.html.en

Editor: Dr. Julia Weiler

Breast cancer risks acquired in pregnancy may pass to next 3 generations

Contact: John Pastor jdpastor@vt.edu 540-231-5646 Virginia Tech

Chemicals or foods that raise estrogen levels during pregnancy may increase cancer risk  in daughters, granddaughters, and even great-granddaughters, according to scientists from Virginia Tech and Georgetown University.

Pregnant rats on a diet supplemented with synthetic estrogen or with fat, which increases estrogen levels, produce ensuing generations of daughters that appear to be healthy, but harbor a greater than normal risk for mammary cancer, the researchers report in today’s Nature Communications.

Although the findings have not yet been validated in humans, the study shows that environmental damage may be passed from one generation to the next not through genetic mutations, but through “epigenetic” alterations that influence how genomic information is decoded.

The research also raises hope that people who may be especially sensitive to carcinogens can be identified and novel prevention strategies can be employed before cancer strikes.

“We have shown for the first time that altered DNA methylations modulated by specific diet in normal development are heritable and transgenerational,” said Yue “Joseph” Wang, the Grant A. Dove Professor of Electrical and Computer Engineering at Virginia Tech Research Center – Arlington. “We also identified key methylation alteration sites that may be involved or responsible for increased breast cancer risk, which may serve as novel biomarkers for scientists to develop novel and targeted prevention strategies.”

The National Cancer Institute estimates that more than 226,000 women and more than 2,000 men will develop breast cancer in 2012, and nearly 40,000 people will die of the disease.

Two thirds of breast cancers that occur in families have no known genetic cause, according to Leena Hilakivi-Clarke, a professor of oncology at Georgetown Lombardi Comprehensive Cancer Center. The study shows what may be underlying the cancer are not genetic mutations, but inherited effects of maternal intake of high-fat diets and exposure to excess estrogen during pregnancy.

“It is becoming clear that the process of epigenetic signaling — which genes are expressed and which genes are silenced — is being affected by a mother’s hormonal environment during pregnancy,” said Hilakivi-Clarke, who has studied the effects of maternal diet on offspring in animals and humans for more than 20 years. “The early studies indicate in a normal pregnancy a woman may have more than 20 different estrogen levels, and the highest and the lowest all result in a healthy baby. The challenge has been to understand how something in fetal development can affect breast cancer risk more than 50 years later.”

The study was led by Sonia de Assis, a postdoctoral researcher in Hilakivi-Clarke’s laboratory at the Georgetown Lombardi Comprehensive Cancer Center at Georgetown University Medical Center.

Virginia Tech researchers developed mathematical models and machine-learning techniques to analyze the changes in DNA methylation status in the descending daughters to understand how increased cancer risk is transmitted without genetic mutation.

DNA methylation is a key process in normal development, allowing cells with the same genome to perform different functions by adding chemical groups to DNA to turn some genes on and some genes off.

Wang’s group found that the descendants with increased risk had several hundred common DNA regions that were methylated differently than in a control group, providing statistically convincing evidence that breast cancer risk can be transmitted via epigenetic means.

“Ultimately, it may be possible to undo or prevent this harmful methylation and decrease the risk of breast cancer.” Wang said. “A next step will be to study the timing of the intervention and the impacts of the methylation as it occurs in the early, middle or end of the pregnancy. The promising news is pharmacologic or other interventions may be able to reverse the harmful exposure.”

###

 

This study was supported by the American Cancer Society (116602-PF-09-018-01-CNE) and the National Institutes of Health including the National Cancer Institute (R03 CA150040, RO1 CA069065, U54 CA100970, U54CA149147, P30 CA051668 and P30 CA054174), the National Institute of Environmental Sciences (RO1 ES017594), and the National Institute of General Medical Sciences (R21 GM085665).

137th Health Research Report 07 SEP 2008

 Full Report at www.healthresearchreport.me

Editors Top Five:

 

1. Study Finds How BPA Affects Gene Expression, Anxiety; Soy Mitigates Effects

2. Vitamin B3 may offer new tool in fight against ‘superbugs’

3. Johns Hopkins team finds ICU misdiagnoses may account for as many annual deaths as breast cancer

4. Prenatal exposure to pesticide additive linked with childhood cough

5. Childhood virus RSV shows promise against adult cancer

 

 

In this Issue:

1. Vitamin B3 may offer new tool in fight against ‘superbugs’

2. How a virus might make you diabetic later in life

3. Adolescent pot use leaves lasting mental deficits

4. Nutrition tied to improved sperm DNA quality in older men

5. Energy drinks improve heart function

6. Breast milk promotes a different gut flora growth than infant formulas

7. Johns Hopkins team finds ICU misdiagnoses may account for as many annual deaths as breast cancer

8. WSU researcher documents links between nutrients, genes and cancer spread

9. Antibiotic residues in sausage meat may promote pathogen survival

10. Smoking after stroke increases death risk by 3-fold

11. The raccoon spreads dangerous diseases as it invades Europe

12. Chocolate: A sweet method for stroke prevention in men?

13. Bacterial cause found for skin condition rosacea

14. WSU researchers discover mechanism leading from trichomoniasis to prostate cancer

15. Lyme retreatment guidance may be flawed

16. Chemical exposure in the womb from household items may contribute to obesity

17. Affluent people less likely to reach out to others in times of chaos, study suggests

18. Coconut oil could combat tooth decay

19. Heavy drinking rewires brain, increasing susceptibility to anxiety problems

20. Even in normal range, high blood sugar linked to brain shrinkage

21. High doses of Vitamin D help tuberculosis patients recover more quickly

22. High levels of DDT in breast milk

23. Large Review Finds Some Evidence for “Chemo Brain” in Breast Cancer Survivors, Moffitt Cancer Center Says

24. Are restrictions to scientific research costing lives?

25. Toddlers increasingly swallowing liquid detergent capsules

26. Brainy beverage: Study reveals how green tea boosts brain cell production to aid memory

27. Children exposed to 2 phthalates have elevated risk of asthma-related airway inflammation

28. Prenatal exposure to pesticide additive linked with childhood cough

29. Nutritional supplement offers promise in treatment of unique form of autism

30. Diagnostic chest radiation before 30 may increase breast cancer risk

31. Report: Strategies to prevent noise-induced hearing loss, tinnitus in soldiers

32. Childhood virus RSV shows promise against adult cancer

33. Stress prompts some to retain as much salt as eating fries

34. Study Finds How BPA Affects Gene Expression, Anxiety; Soy Mitigates Effect

 

 

Health Technology Research Synopsis

137th Issue Date 07 SEP 2012

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/vitaminandherbstore

www.engineeringevil.com


Poxviruses defeat antiviral defenses by duplicating a gene – Engineered an E3L-deficient strain that was quickly able to increase infectious virus production by selectively increasing the number of copies of the K3L gene in its genome

Contact: Phil Sahm phil.sahm@hsc.utah.edu 801-581-2517 University of Utah Health Sciences

Study helps explain how large DNA viruses undergo rapid evolution

SALT LAKE CITY – Scientists have discovered that poxviruses, which are responsible for smallpox and other diseases, can adapt to defeat different host antiviral defenses by quickly and temporarily producing multiple copies of a gene that helps the viruses to counter host immunity. This discovery provides new insight into the ability of large double-stranded DNA viruses to undergo rapid evolution despite their low mutation rates, according to a study published by University of Utah researchers in the Aug. 17, 2012, issue of Cell.

Poxviruses are a group of DNA-containing viruses that are responsible for a wide range of diseases in both humans and animals, including smallpox. Unlike smaller RNA-containing viruses, such as those that cause influenza and HIV, which are able to evade host immune responses through rapid mutation, poxviruses have larger genomes and low mutation rates and little is known about their adaptive strategies against host defenses.

“Poxviruses encode a variety of genes that help them to counter host immune defenses and promote infection,” says Nels Elde, Ph.D., assistant professor of human genetics at the University of Utah School of Medicine and first author on the study. “Despite ample evidence that the poxvirus genome can undergo adaptive changes to overcome evolving host defenses, we still don’t know that much about the mechanisms involved in that adaptation.”

To determine mechanisms of adaptation, Elde and his colleagues studied the vaccinia virus, a type of poxvirus best known for its role as the vaccine used to eradicate smallpox.  Previous research has shown that vaccinia virus encodes two genes, known as K3L and E3L, which inhibit host defenses that normally block viral infection. In this study, Elde and his colleagues started with a strain of vaccinia virus that had been altered to delete the E3L gene and repeatedly propagated this E3L-deficient strain in human cells to see how well the virus would replicate. They found that this E3L-deficient strain was quickly able to increase infectious virus production by selectively increasing the number of copies of the K3L gene in its genome.

“This highly specific and rapid gene amplification was unexpected,” says Elde. “Our studies show that increasing K3L copy number leads to increased expression of K3L and enhanced viral replication, providing an immediate evolutionary advantage for those viruses that can quickly expand their genome.”

Elde and his colleagues also found that, in addition to K3L copy number amplification, some of the E3L-deficient vaccinia strains also acquired a mutation consisting of a single amino acid substitution in the K3L gene. Both the mutation-bearing and multicopy K3L viruses displayed improved viral fitness, or ability to replicate in the host environment, compared to wild-type vaccinia virus. The emergence of this beneficial amino acid substitution suggests that increasing K3L copy number facilitated the appearance of the variant by providing additional mutational targets, despite the virus’ otherwise low mutation rate.

“We were able to demonstrate at least two strategies by which poxviruses are able to adapt diverse mechanisms of host immunity,” says Elde. “Our observations reveal that, while poxviruses do undergo gene mutation, their first response to a new, hostile host environment can be rapid gene expansion. We also found evidence that the virus genome can contract after acquiring an adaptive mutation, thus alleviating the potential trade-off of having a larger genome, while leaving a beneficial mutation in place.”

Although smallpox was officially eradicated by the World Health Organization in 1980, concerns about the use of smallpox as a bioterrorism agent have spurred renewed interest in the study of vaccinia and other poxviruses. In addition, poxvirus infections, such as monkeypox, can be transmitted from animals to humans and the adaptive strategies of poxviruses may be relevant for other infectious organisms.

###

 

The collaborative team of researchers involved in this study included scientists from the University of Utah, the Fred Hutchinson Cancer Research Center, the University of Washington, and the Howard Hughes Medical Institute