Influenza is circulating in Africa, but virtually no information or attention is evident, says a new essay in PLoS Medicine. Maria Yazdanbakhsh and Peter Kremsner argue that the lack of adequate surveillance means that the burden of influenza in Africa is incorrectly believed to be negligible. But sporadic reports from various regions in Africa indicate that influenza is circulating and may be regularly causing epidemics Whereas in temperate areas influenza activity displays a seasonal pattern with marked peaks in the winter, influenza is present all year round throughout the tropics. The authors say that the well-established surveillance network WHO Flu Net in place in Europe and North America, provides continuous data on influenza burden and the spread of viral types and subtypes. Recent threats of pandemic influenza have prompted similar active monitoring in parts of Southeast Asia and Latin America. But the prevalence and incidence of influenza in most tropical countries especially in Africa are largely unknown, say the authors, and improved surveillance is needed. For example, the authors state, the WHO H1N1 swine flu update of May 2009 contained reports of infected patients in many countries, but none in Africa, whereas two reports in October 2009 confirmed swine flu cases from South Africa and Kenya. This indicates that "that the virus was circulating in Africa, but because of the lack of a rigorous surveillance system, it was not reported as readily."

Recent interest in “land grabs” or the international acquisition of land to produce rice is sparked by a looming threat of inadequate rice supplies. To put it simply, there is not enough rice to feed the world,” says Dr. Robert Zeigler, director general of the International Rice Research Institute (IRRI). “To meet the need and keep rice prices around US$300 a ton – which allows poor rice farmers to make some profit yet keeps rice affordable for poor rice consumers – we need to produce an additional 8–10 million tons of rice more than in the previous year for the next twenty years.” Many countries do not have the capacity to grow enough rice on their own land to meet existing or anticipated demand. To meet their needs governments or the private sector import rice and some are exploring ways to invest in rice production or rice-growing land in other countries. IRRI is not involved in any projects on land acquisition for rice production, nor does it provide advice on land acquisition, but it does find ways to help increase the overall rice supply – with a mandate to help poor rice farmers and consumers and improve environmental health.

A team of researchers, at Washington University School of Medicine, St Louis, has identified a group of 12 genetic variants in the HSPB7 gene that is associated with heart failure in humans. The research is reported in the Journal of Clinical Investigation. The team, led by Gerald Dorn, used an approach they have recently developed that allows ultra-high-throughput targeted DNA sequencing to identify genetic variation in four genes with biological relevance to heart failure. They identified in a large group of Caucasian individuals with heart failure, 129 separate genetic variants in the four genes, including 23 that seemed to be novel. Further analysis of 1117 Caucasian individuals with heart failure and 625 nonaffected Caucasians indicated that a block of 12 genetic variants in the HSPB7 gene was associated with heart failure. Confirmation of this association was provided by analysis of an independent group of individuals. The authors hope to use the same approach to identify further genetic variants associated with heart failure, a disease that is influenced by multiple genetic factors.

Researchers at Binghamton University, State University of New York, have identified three key regulators required for the formation and development of biofilms. The discovery could lead to new ways of treating chronic infections. Biofilms -- communities of bacteria in self-produced slime -- may be found almost anywhere that solids and liquids meet, whether in nature, in hospitals or in industrial settings. Biofilms are implicated in more than 80 percent of chronic inflammatory and infectious diseases caused by bacteria, including ear infections, gastrointestinal ulcers, urinary tract infections and pulmonary infections in cystic fibrosis patients, according to the Centers for Disease Control. Biofilms are difficult to eradicate with conventional antimicrobial treatments since they can be nearly 1,500-fold more resistant to antibiotics than planktonic, free-floating cells. Biofilms also pose a persistent problem in many industrial processes, including drinking water distribution networks and manufacturing.

One of the most common reasons for needing a liver transplant is liver failure or liver cancer caused by liver cell infection with hepatitis C virus (HCV). However, in nearly all patients the new liver becomes infected with HCV almost immediately. But now, Hideki Ohdan, Kazuaki Chayama, and colleagues, at Hiroshima University, Japan, have developed an approach that transiently keeps HCV levels down in most treated HCV-infected patients receiving a new liver. The researchers report their findings in the Journal of Clinical Investigation. Specifically, the team took immune cells known as lymphocytes from the donor livers before they were transplanted into the HCV-infected patients, activated them in vitro, and then injected them into the patients three days after they had received their liver transplants. Importantly, these infused cells were able to keep the HCV at bay even though the patients were taking immunosuppressive drugs to prevent their immune systems from rejecting the new livers. Despite showing clear clinical effects, the authors are planning further studies in which they will modify the protocol in an attempt to find a way to keep HCV levels down for longer and in all patients.

An instrument package developed in part by the University of Colorado at Boulder for the $2.2 billion orbiting Herschel Space Observatory launched in May by the European Space Agency has provided one of the most detailed views yet of space up to 12 billion years back in time. The December images have revealed thousands of newly discovered galaxies in their early stages of formation, said CU-Boulder Associate Professor Jason Glenn, a co-investigator on the Spectral and Photometric Imaging Receiver, or SPIRE instrument, riding aboard Herschel. The new images are being analyzed as part of the Herschel Multi-tiered Extragalactic Survey, or HerMES, which involves more than 100 astronomers from six countries. Equipped with three cameras including SPIRE, the Herschel Space Observatory was launched in May 2009 from Europe's Spaceport in French Guiana. The spacecraft -- about one and one-half times the diameter of the Hubble Space Telescope -- is orbiting nearly 1 million miles from Earth. Herschel is the first space observatory to make high-resolution images at submillimeter wavelengths, which are longer than visible and infrared light waves and shorter than radio waves. SPIRE was designed to look for emissions from clouds and dust linked to star-forming regions in the Milky Way and beyond, said Glenn. The most recent observations were made in the constellation Ursa Major, which includes the Big Dipper.

In a mouse model, scientists have discovered that alpha-cells in the pancreas, which do not produce insulin, can convert into insulin-producing beta-cells, advancing the prospect of regenerating beta-cells as a cure for type 1 diabetes. The research team, led by senior author Dr. Pedro L. Herrera of the University of Geneva, demonstrated that beta-cells will spontaneously regenerate after near-total beta-cell destruction in mice and the majority of the regenerated beta-cells are derived from alpha-cells that had been reprogrammed, or converted, into beta-cells. Using a unique model of diabetes in mice, in which nearly all of the beta-cells are rapidly destroyed, the researchers found that if the mice were maintained on insulin therapy, beta-cells were slowly and spontaneously restored, eventually eliminating the need for insulin replacement. Alpha-cells normally reside alongside beta-cells in the pancreas and secrete a hormone called glucagon, which works in opposition to insulin to regulate the levels of sugar in the blood. Alpha-cells are not attacked by the autoimmune processes that destroy beta-cells and cause type 1 diabetes. Dr. Andrew Rakeman, the Juvenile Diabetes Research Foundation (JDRF) Program Manager in Beta-Cell Therapies and who was not involved in the research, said that the breakthrough in Dr. Herrera's work is the demonstration that alpha-to-beta-cell reprogramming can be a natural, spontaneous process. "If we can understand the signals that are triggering this conversion, it will open a whole new potential strategy for regenerating beta-cells in people with type 1 diabetes," he said. "It appears that the body can restore beta-cell function either through reprogramming alpha-cells to become beta-cells or, as previously shown by others, by increasing growth of existing beta cells. This path may be particularly useful in individuals who have had the disease for a long time and have no, or very few, remaining beta cells." Interestingly, the researchers pointed out that the critical factor in sparking the alpha-to-beta-cell reprogramming was removing (or ablating) nearly all the original insulin-producing cells in the mice. In mice where the loss of beta cells was more modest, the researchers either found no evidence of beta cell regeneration (when only half the cells were destroyed) or less alpha cell reprogramming (when less than 95 percent of cells were destroyed). "The amount of beta-cell destruction thus appears to determine whether regeneration occurs. Moreover, it influences the degree of cell plasticity and regenerative resources of the pancreas in adult organisms," said Dr. Herrera. This work was published online on April 4, 2010 in Nature. The image shows three lightly stained islets of Langerhans.

Researchers at the University of Massachusetts Medical School and colleagues have discovered a critical step for blood vessel growth in zebrafish embryos, providing new insight into how vascular systems develop and offering a potential therapeutic target for preventing tumor growth, which depends on vascularization. The researchers have identified a novel microRNA-mediated genetic pathway responsible for new blood vessel growth (angiogenesis) in zebrafish embryos. The work provides new insights into how vascular systems use the forces of existing blood flow to initiate the growth of new vessels. Focusing on the development of the fifth and sixth aortic arches in the zebrafish, senior author Dr. Nathan Lawson described how the forces exerted by blood flow on endothelial cells are a critical component for expressing a microRNA that triggers new vessel development. In the early stages of development, when blood flow is present in the aortic vessels, but the vascular linkages between the two arches have yet to be established, the stimulus provided by active blood flow leads to expression of an endothelial-cell specific microRNA (mir-126). In turn, this microRNA turns on vascular endothelial growth factor (VEGF), a chemical signal produced by surrounding cells that normally stimulates angiogenesis. Thus, blood flow allows the endothelial cells to respond to VEGF by growing into new blood vessels. However, when blood flow in the aortic arches was restricted, mir-126 failed to be expressed. In the absence of this microRNA, new blood vessels were unable to develop due to a block in VEGF signaling. "We have known for over a hundred years that blood flow makes new vessels grow," said Dr. Lawson. "But we never really knew how cells in a growing vessel interpreted this signal. Our results show that miR-126 is the crucial switch that allows flow to turn on VEGF signaling and drive blood vessel growth. Because VEGF is crucial for tumor progression, not to mention a number of other vascular diseases, our findings may provide new ways to modify this pathway in these settings." One possibility, for instance, is that regulation of mir-126 could be a potential therapeutic target in limiting blood vessel development in solid cancers. This work was published online on April 4, 2010 in Nature.

"Personalized Medicine 3.0--Targeting Cancer" is a one-day conference and networking opportunity for health and industry professionals, educators, and scientists. The conference will focus on cancer--using genomic information to characterize tumors precisely and ensure the use of the most effective treatment regimens for individual patients with the fewest side effects. The organizers note that personalized medicine is poised to transform healthcare over the next several decades, and that it offers both the possibility of improved health outcomes and the potential to make healthcare more cost-effective. The conference will be held in San Francisco at San Francisco State University from 9 am to 7 pm on Tuesday, May 25, 2010. The two previous annual conferences on personalized medicine have been enormous successes and similar results are expected for this third conference. The organizers urge you to register early as space is limited and the registration fee is $249 until April 15, 2010. Registration includes a light breakfast, lunch, and a networking reception at the end of the day. Registration details and a preliminary program are available at the conference web site (http://personalizedmedicine.sfsu.edu/), as are additional details on the conference.

New results indicate that targeting a specific microRNA (miR-210) with a drug that could be used topically on the skin might offer new strategies for treating chronic wounds, which are sometimes fatal and cost the U.S. health-care system an estimated $25 billion annually. Ohio State University researchers have discovered, in a new animal study, that the presence of miR-210 in wounds with limited blood flow lowers the production of a protein (E2F3) that is needed to encourage skin cells to grow and close over the wound. In a parallel experiment using human skin cells, the researchers silenced the miR-210 with an experimental drug and saw E2F3 protein levels rise. The skin cells multiplied as a result. The research involved wounds that are ischemic, that is, they heal very slowly or are in danger of never healing because they lack blood flow and oxygen at the wound site. These types of wounds affect approximately 6.5 million patients each year, and are common complications of diabetes, high blood pressure, obesity, and other conditions characterized by poor vascular health. "When blood supply is inadequate, many things are deficient at the wound site, including oxygen. That leads to a condition called hypoxia," said Dr. Chandan Sen, senior author of the study. "We have shown that hypoxia induces miR-210, which actually blocks the ability of the cells to proliferate, a step necessary for the wound-closure process.” This research was published online on March 22, 2010 in PNAS.