Harvard gets record donation from Hong Kong billionaire brothers

English.news.cn   2014-09-09 10:04:52

WASHINGTON, Sept. 8 (Xinhua) — Harvard University announced Monday its school of public health has received 350-million-U.S.-dollar donation, the largest in Harvard’s history, from a charitable foundation run by Hong Kong billionaire brothers Ronnie and Gerald Chan.

The gift from the Morningside Foundation will also lead to the renaming of the School, which will be called the Harvard T.H. Chan School of Public Health, in honor of the two’s late father, the university said in a statement.

Harvard School of Public Health (HSPH) Dean Julio Frenk said the gift will focus on four global health threats: pandemics old and new, such as malaria, Ebola, cancer, and obesity; harmful physical and social environments such as those resulting from tobacco use, gun violence and pollution; poverty and humanitarian crises such as those stemming from war and natural disasters; and failing health care systems around the world.

 

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Gravity measurements confirm subsurface ocean on Saturn’s moon Enceladus

California Institute of Technology
 
This illustration depicts the possible interior of Enceladus based on Cassini’s gravity investigation. At high southern latitudes, a regional water ocean is shown sandwiched between an icy outer shell and a low density, rocky core. Cassini Imaging Science Subsystem images were used to depict the surface geology and the plumes.

In 2005, NASA’s Cassini spacecraft sent pictures back to Earth depicting an icy Saturnian moon spewing water vapor and ice from fractures, known as “tiger stripes,” in its frozen surface. It was big news that tiny Enceladus — a mere 500 kilometers in diameter — was such an active place. Since then, scientists have hypothesized that a large reservoir of water lies beneath that icy surface, possibly fueling the plumes. Now, using gravity measurements collected by Cassini, scientists have confirmed that Enceladus does in fact harbor a large subsurface ocean near its south pole, beneath those tiger stripes.

“For the first time, we have used a geophysical method to determine the internal structure of Enceladus, and the data suggest that indeed there is a large, possibly regional ocean about 50 kilometers below the surface of the south pole,” says David Stevenson, the Marvin L. Goldberger Professor of Planetary Science at Caltech and an expert in studies of the interior of planetary bodies. “This then provides one possible story to explain why water is gushing out of these fractures we see at the south pole.”
Continue reading “Gravity measurements confirm subsurface ocean on Saturn’s moon Enceladus”

Creating indestructible self-healing circuits

Contact: Brian Bell bbell2@caltech.edu 626-395-5832 California Institute of Technology

Caltech engineers build electronic chips that repair themselves

PASADENA, Calif.—Imagine that the chips in your smart phone or computer could repair and defend themselves on the fly, recovering in microseconds from problems ranging from less-than-ideal battery power to total transistor failure. It might sound like the stuff of science fiction, but a team of engineers at the California Institute of Technology (Caltech), for the first time ever, has developed just such self-healing integrated chips.

      IMAGE:   Some of the damage Caltech engineers intentionally inflicted on their self-healing power amplifier using a high-power laser. The chip was able to recover from complete transistor destruction. This image was…Click here for more information.

 

The team, made up of members of the High-Speed Integrated Circuits laboratory in Caltech’s Division of Engineering and Applied Science, has demonstrated this self-healing capability in tiny power amplifiers. The amplifiers are so small, in fact, that 76 of the chips—including everything they need to self-heal—could fit on a single penny. In perhaps the most dramatic of their experiments, the team destroyed various parts of their chips by zapping them multiple times with a high-power laser, and then observed as the chips automatically developed a work-around in less than a second.

“It was incredible the first time the system kicked in and healed itself. It felt like we were witnessing the next step in the evolution of integrated circuits,” says Ali Hajimiri, the Thomas G. Myers Professor of Electrical Engineering at Caltech. “We had literally just blasted half the amplifier and vaporized many of its components, such as transistors, and it was able to recover to nearly its ideal performance.”

The team’s results appear in the March issue of IEEE Transactions on Microwave Theory and Techniques.

Until now, even a single fault has often rendered an integrated-circuit chip completely useless. The Caltech engineers wanted to give integrated-circuit chips a healing ability akin to that of our own immune system—something capable of detecting and quickly responding to any number of possible assaults in order to keep the larger system working optimally. The power amplifier they devised employs a multitude of robust, on-chip sensors that monitor temperature, current, voltage, and power. The information from those sensors feeds into a custom-made application-specific integrated-circuit (ASIC) unit on the same chip, a central processor that acts as the “brain” of the system. The brain analyzes the amplifier’s overall performance and determines if it needs to adjust any of the system’s actuators—the changeable parts of the chip.

Interestingly, the chip’s brain does not operate based on algorithms that know how to respond to every possible scenario. Instead, it draws conclusions based on the aggregate response of the sensors. “You tell the chip the results you want and let it figure out how to produce those results,” says Steven Bowers, a graduate student in Hajimiri’s lab and lead author of the new paper. “The challenge is that there are more than 100,000 transistors on each chip. We don’t know all of the different things that might go wrong, and we don’t need to. We have designed the system in a general enough way that it finds the optimum state for all of the actuators in any situation without external intervention.”

Looking at 20 different chips, the team found that the amplifiers with the self-healing capability consumed about half as much power as those without, and their overall performance was much more predictable and reproducible. “We have shown that self-healing addresses four very different classes of problems,” says Kaushik Dasgupta, another graduate student also working on the project. The classes of problems include static variation that is a product of variation across components; long-term aging problems that arise gradually as repeated use changes the internal properties of the system; and short-term variations that are induced by environmental conditions such as changes in load, temperature, and differences in the supply voltage; and, finally, accidental or deliberate catastrophic destruction of parts of the circuits.

The Caltech team chose to demonstrate this self-healing capability first in a power amplifier for millimeter-wave frequencies. Such high-frequency integrated chips are at the cutting edge of research and are useful for next-generation communications, imaging, sensing, and radar applications. By showing that the self-healing capability works well in such an advanced system, the researchers hope to show that the self-healing approach can be extended to virtually any other electronic system.

“Bringing this type of electronic immune system to integrated-circuit chips opens up a world of possibilities,” says Hajimiri. “It is truly a shift in the way we view circuits and their ability to operate independently. They can now both diagnose and fix their own problems without any human intervention, moving one step closer to indestructible circuits.”

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Along with Hajimiri, Bowers, and Dasgupta, former Caltech postdoctoral scholar Kaushik Sengupta (PhD ’12), who is now an assistant professor at Princeton University, is also a coauthor on the paper, “Integrated Self-Healing for mm-Wave Power Amplifiers.” A preliminary report of this work won the best paper award at the 2012 IEEE Radio Frequency Integrated Circuits Symposium. The work was funded by the Defense Advanced Research Projects Agency and the Air Force Research Laboratory.

Geologists: Groundwater extraction caused earthquake in Spain

By Agence France-Presse Sunday, October 21, 2012 21:05 EDT

A damaged building is pictured in Lorca, southeastern Spain, after a 5.2 magnitude earthquake in 2011. (AFP)

Massive extraction of groundwater helped unleash an earthquake in southeastern Spain last year that killed nine people, injured at least 100 and left thousands homeless, geologists said on Sunday.

The finding adds a powerful piece of evidence to theories that some earthquakes are human-induced, they said.

Seismologists were surprised by the May 11, 2011 earthquake which happened two kilometres (1.2 miles) northeast of the city of Lorca.

The quake struck in the Eastern Betics Shear Zone, one of Spain’s most seismically active regions, where there has been a large number of moderate-to-large temblors over the last 500 years.

But the May event was unusual because it was so devastating and yet so mild — only 5.1 magnitude — in terms of energy release.

Researchers led by Pablo Gonzalez of the University of Western Ontario in Canada probed the mystery.

Reporting in the journal Nature Geoscience, they found that the quake occurred at a very shallow depth, of just three kilometres (1.8 miles), so the shockwave swiftly reached the surface with little to dampen it on the way.

The quake also happened on a complex but dormant fault that ripped open after water had been extensively pumped out of a neighbouring aquifer, causing a domino effect of subterranean stresses, they said.

Gonzalez’ team first used ground-radar imaging by the European satellite Envisat to build a map of how terrain around Lorca changed before and after the quake.

The picture confirmed that the event had occurred on the so-called Alhama de Murcia fault, which slipped between five and 15 centimetres (two and six inches).

They then investigated the Alto Guadalentin Basin, an aquifer lying just five kms (three miles) south of the fault, where they found widespread evidence of subterranean subsidence from water extraction.

Between 1960 and 2010, the level of groundwater from this aquifer fell by at least 250 metres (812 feet), according to records from local wells.

A computer model put together by the team suggests what happens: lowering of the water table caused part of the crust, located next to the Alhama de Murcia fault, to break.

This led to an “elastic rebound” of the crust that in turn cranked up horizontal pressure on the fault, bringing it that much closer to rupture.

The investigation adds to anecdotal evidence that human activities, ranging from exploration for shale gas, quarrying and even water reservoirs, can cause quakes.

“Our results imply that anthopogenic [man-made] activites could influence how and when earthquakes occur,” said the study.

In a commentary, Jean-Philippe Avouac, a geologist at the California Institute of Technology (Caltech) said water extraction at Lorca probably accelerated a natural process of stress accumulation rather than unleashed the earthquake by itself.

Even so, “the consequences are far-reaching,” said Avouac.

He pointed to carbon storage, a still-experimental technique in which carbon dioxide from a fossil-fuel power station is pumped into underground caverns rather than released to the atmosphere, where it would add to global warming.

“For now, we should remain cautious of human-induced stress perturbations, in particular those related to carbon dioxide sequestration projects that might affect very large volumes of crust,” said Avouac.

“We know how to start earthquakes, but we are still far from being able to keep them under control.”

http://www.rawstory.com/rs/2012/10/21/geologists-groundwater-extraction-caused-earthquake-in-spain/

 

UCLA/Pitt scientists uncover virus with potential to stop pimples in their tracks

Contact: Elaine Schmidt eschmidt@mednet.ucla.edu 310-794-2272 University of California – Los Angeles Health Sciences

Going viral to kill zits

Watch out, acne.  Doctors soon may have a new weapon against zits:  a harmless virus living on our skin that naturally seeks out and kills the bacteria that cause pimples.

The Sept. 25 online edition of the American Society for Microbiology’s mBio publishes the findings by scientists at UCLA and the University of Pittsburgh.

“Acne affects millions of people, yet we have few treatments that are both safe and effective,” said principal investigator Dr. Robert Modlin, chief of dermatology and professor of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA.  “Harnessing a virus that naturally preys on the bacteria that causes pimples could offer a promising new tool against the physical and emotional scars of severe acne.”

The scientists looked at two little microbes that share a big name:  Propionibacterium acnes, a bacterium thriving in our pores that can trigger acne; and P. acnes phages, a family of viruses that live on human skin.  The viruses are harmless to humans, but programmed to infect and kill the aforementioned P. acnes bacteria.

When P. acnes bacteria aggravate the immune system, it causes the swollen, red bumps associated with acne.  Most effective treatments work by reducing the number of P. acnes bacteria on the skin.

“We know that sex hormones, facial oil and the immune system play a role in causing acne, however, a lot of research implicates P. acnes as an important trigger,” explained first author Laura Marinelli, a UCLA postdoctoral researcher in Modlin’s laboratory.  “Sometimes they set off an inflammatory response that contributes to the development of acne.”

Using over-the-counter pore cleansing strips from the drugstore, the researchers lifted acne bacteria and the P. acnes viruses from the noses of both pimply and clear-skinned volunteers.

When the team sequenced the bacteriophages’ genomes, they discovered that the viruses possess multiple features – such as small size, limited diversity and the broad ability to kill their hosts – that make them ideal candidates for the development of a new anti-acne therapy.

“Our findings provide valuable insights into acne and the bacterium that causes it,” observed corresponding author Graham Hatfull, Eberly Family Professor of Biotechnology, professor of biological sciences at the University of Pittsburgh and a Howard Hughes Medical Institute researcher.  “The lack of genetic diversity among the phages that attack the acne bacterium implies that viral-based strategies may help control this distressing skin disorder.”

“Phages are programmed to target and kill specific bacteria, so P. acnes phages will attack only P. acnes bacteria, but not others like E. coli,” added Marinelli.  “This trait suggests that they offer strong potential for targeted therapeutic use.”

Acne affects nearly 90 percent of Americans at some point in their lives, yet scientists know little about what causes the disorder and have made narrow progress in developing new strategies for treating it.  Dermatologists’ arsenal of anti-acne tools — benzoyl peroxide, antibiotics and Accutane – hasn’t expanded in decades.

“Antibiotics such as tetracycline are so widely used that many acne strains have developed resistance, and drugs like Accutane, while effective, can produce risky side effects, limiting their use,” explained coauthor Dr. Jenny Kim, director of the UCLA Clinic for Acne, Rosacea and Aesthetics.  “Acne can dramatically disfigure people and undermine their self-esteem, especially in teens.  We can change patients’ lives with treatment.  It’s time we identified a new way to safely treat the common disorder.”

The research team plans to isolate the active protein from the P. acnes virus and test whether it is as effective as the whole virus in killing acne bacteria. If laboratory testing proves successful, the researchers will study the compound’s safety and effectiveness in combating acne in people.

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The study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R21AR060382, R01 AR053542 and F32AR060655) at the National Institutes of Health in Bethesda, Md.

Additional coauthors included Sorel Fitz-Gibbon, Megan Inkeles, Shawn Cokus, Matteo Pellegrini and Jeffrey F. Miller, all of UCLA; former UCLA researchers Clarmyra Hayes and Anya Loncaric, now of the California Institute of Technology and Solta Medical, respectively; and  Charles Bowman, Daniel Russell and Deborah Jacobs-Sera of the University of Pittsburgh.

The Clinic for Acne, Rosacea and Aesthetics at the UCLA Division of Dermatology at the David Geffen School of Medicine offers comprehensive care for acne and rosacea, as well as the scarring and discoloration that can result from these conditions.  The clinic’s goal is to educate the public and help patients develop habits leading to healthy skin.  Current research projects include studying the effect of Vitamin-D on immune response to acne, the effect of Omega-3 fatty acids on acne and its treatment, and the use of a mobile device application for acne management.  To schedule an appointment, call (310) 825-6911

Intestinal bacteria promote — and prevent — inflammatory bowel disease

2008 – re-post for filing

Contact: David Cameron
david_cameron@hms.harvard.edu
617-432-0441
Harvard Medical School

BOSTON, Mass. (May 28, 2008)—Scientists search for drug candidates in some very unlikely places. Not only do they churn out synthetic compounds in industrial-scale laboratories, but they also scour coral reefs and scrape tree bark in the hope of stumbling upon an unsuspecting molecule that just might turn into next year’s big block buster. But one region that scientists have not been searching is their guts. Literally.

Now, a team of researchers at Harvard Medical School, Brigham and Women’s Hospital, and the California Institute of Technology have demonstrated that a molecule produced by bacteria in the gut’s intestinal microflora can eliminate symptoms of inflammatory bowel disease (IBD), a condition that includes Crohn’s disease and ulcerative colitis, in animal models.

“Given the sheer number of bacteria in the gut, the potential for discovering new molecules that can treat a whole range of these diseases is promising,” says Dennis Kasper, co-lead author on the study, professor of medicine and microbiology and molecular genetics at Harvard Medical School, and director of the Channing Laboratory at Brigham and Women’s Hospital.

The study will appear as the cover story in the May 29 issue of Nature.

Scientists have known for many decades that the mammalian gut is an ecosystem teeming with approximately 1,000 different species of bacteria, species as distinct from the host as a single-cell amoeba in pond scum. Rather than causing disease, these bacteria are responsible for protecting against infection and aiding digestion. An increasing number of scientists also suspect that recent increases in asthma and even certain food allergies are caused by disruptions in the delicate balance of this intestinal ecosystem.

In 2005, Kasper and Sarkis Mazmanian, then a postdoc in Kasper’s lab and now an assistant professor of biology at the California Institute of Technology, discovered that a species of intestinal bacteria called Bacteroides fragilis could restore immune system balance in mice that were bred to lack intestinal bacteria. A particular product of B. fragilis, a sugar molecule called polysaccharide A (PSA), recovered the equilibrium of a certain subclass of immune system cells (called Th1 and Th2) whose levels became skewed when bacteria in the gut were absent. The researchers referred to PSA as a “symbiosis factor,” one that established a beneficial link between bacteria and mammals. This was the first study in which such a link was demonstrated.

Interestingly, when the study was completed, Kasper and Mazmanian found in these mice an abundance of immune system cells that were known to protect against colitis and Crohn’s disease. In the current report, the groups decided to expand these findings and explore potential links between PSA and inflammatory bowel disease.

When immunocompromised mice with a specific pathogen-free microbiota were given an intestinal bacterium called Helicobacter hepaticus, they soon developed “rip roaring” IBD, according to Kasper. However, when Helicobacter was combined with B. fragilis, the mice were fine. Further experiments revealed that PSA—the special sugar molecule—was the key factor in preventing IBD. In fact, when mice were given Helicobacter combined with PSA purified from B. fragilis bacteria, they showed no symptoms of IBD.

“But then the key question was, if PSA was essential for preventing these animals from coming down with either colitis or Crohn’s, how did it do it”” says Kasper. “What was the mechanism””

The answer came by studying a subset of interleukins, that is, molecules secreted by immune cells.

Previous studies had shown that two particular interleukins, called IL-17 and IL-23, promote intestinal inflammation and are present at high levels in IBD patients. Here, while the researchers found IL-17 and IL-23 in the guts of animals who had received Heliobacter alone, these interleukins were absent from animals who had also received both PSA-producing B. fragilis and purified PSA.

“We realized that something in PSA must be preventing the inflammation that causes colitis and Crohn’s, which would explain the reduction in IL-17 and IL-23,” says Kasper.

This hunch brought the researchers to consider a third interleukin, IL-10. The opposite of IL-17 and IL-23, IL-10 is anti-inflammatory and had previously been shown to protect against experimental colitis.

The researchers once again administered Helicobacter and PSA-active B. fragilis (the combination that had previously led to healthy mice), only this time they included an antibody that blocked IL-10. As a result, the mice all came down with IBD.

“This demonstrated for us the mechanism by which PSA protects against IBD,” says Kasper.

Indeed, the researchers deduced that PSA prompts immune system cells to secrete IL-10, which in turn suppresses the inflammation caused by IBD. In other words, PSA is an anti-inflammatory.

This research should encourage people (including many scientists) to consider the vast potential for beneficial contributions to human health by “good” bacteria. And what’s more, “This is the first time that a beneficial molecule produced by intestinal bacteria has been shown to work therapeutically in an animal model,” says Mazmanian.

The researchers caution that these findings do not promise any near-term treatments for IBD. “PSA might do the same thing in humans, and it might not,” says Kasper.

However, the mechanism that they’ve discovered should persuade scientists and drug manufacturers to consider new sources for expanding the drug pipeline.

“There is currently no effort to develop molecules that are naturally made by bacteria to use therapeutically,” continues Mazmanian. “This study opens up that possibility.”

 

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Full citation:
Nature, May 29, 2008, 453 (7195), 620-624
“A microbial symbiosis factor prevents intestinal inflammatory disease”
Sarkis K. Mazmanian(1), June L. Round(1) & Dennis L. Kasper(2,3)

1-Division of Biology, California Institute of Technology, Pasadena, California.
2-Channing Laboratory, Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts
3-Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts

Harvard Medical School (http://hms.harvard.edu/hms/home.asp) has more than 7,500 full-time faculty working in 11 academic departments located at the School’s Boston campus or in one of 47 hospital-based clinical departments at 18 Harvard-affiliated teaching hospitals and research institutes. Those affiliates include Beth Israel Deaconess Medical Center, Brigham and Women’s Hospital, Cambridge Health Alliance, Children’s Hospital Boston, Dana-Farber Cancer Institute, Forsyth Institute, Harvard Pilgrim Health Care, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Children’s Center, Immune Disease Institute, Massachusetts Eye and Ear Infirmary, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Schepens Eye Research Institute, Spaulding Rehabilitation Hospital, and VA Boston Healthcare System.

Brigham and Women’s Hospital (http://www.brighamandwomens.org/) is a 747-bed nonprofit teaching affiliate of Harvard Medical School and a founding member of Partners HealthCare, an integrated health care delivery network. BWH is committed to excellence in patient care with expertise in virtually every specialty of medicine and surgery. BWH is an international leader in basic, clinical and translational research on human diseases, involving more than 860 physician-investigators and renowned biomedical scientists and faculty supported by more than $416 M in funding. BWH is also home to major landmark epidemiologic population studies, including the Nurses’ and Physicians’ Health Studies and the Women’s Health Initiative.