Evidence of biological basis for religion in human evolution

Jan. 17, 2014 — An Auburn University researcher teamed up with the National Institutes of Health to study how brain networks shape an individual's religious belief, finding that brain interactions were different between religious and non-religious subjects.

Gopikrishna Deshpande, an assistant professor in the Department of Electrical and Computer Engineering in Auburn's Samuel Ginn College of Engineering, and the NIH researchers recently published their results in the journal, "Brain Connectivity."

The group found differences in brain interactions that involved the theory of mind, or ToM, brain network, which underlies the ability to relate between one's personal beliefs, intents and desires with those of others. Individuals with stronger ToM activity were found to be more religious. Deshpande says this supports the hypothesis that development of ToM abilities in humans during evolution may have given rise to religion in human societies.

"Religious belief is a unique human attribute observed across different cultures in the world, even in those cultures which evolved independently, such as Mayans in Central America and aboriginals in Australia," said Deshpande, who is also a researcher at Auburn's Magnetic Resonance Imaging Research Center. "This has led scientists to speculate that there must be a biological basis for the evolution of religion in human societies."

Deshpande and the NIH scientists were following up a study reported in the Proceedings of the National Academy of Sciences, which used functional magnetic resonance imaging, or fMRI, to scan the brains of both self-declared religious and non-religious individuals as they contemplated three psychological dimensions of religious beliefs.

The fMRI -- which allows researchers to infer specific brain regions and networks that become active when a person performs a certain mental or physical task -- showed that different brain networks were activated by the three psychological dimensions; however, the amount of activation was not different in religious as compared to non-religious subjects.

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'Ardi' skull reveals links to human lineage

Jan. 6, 2014 — One of the most hotly debated issues in current human origins research focuses on how the 4.4 million-year-old African species Ardipithecus ramidus is related to the human lineage. "Ardi" was an unusual primate. Though it possessed a tiny brain and a grasping big toe used for clambering in the trees, it had small, humanlike canine teeth and an upper pelvis modified for bipedal walking on the ground.

Scientists disagree about where this mixture of features positions Ardipithecus ramidus on the tree of human and ape relationships. Was Ardi an ape with a few humanlike features retained from an ancestor near in time (between 6 and 8 million years ago, according to DNA evidence) to the split between the chimpanzee and human lines? Or was it a true relative of the human line that had yet to shed many signs of its remote tree-dwelling ancestry?

New research led by Arizona State University paleoanthropologist William Kimbel confirms Ardi's close evolutionary relationship to humans. Kimbel and his collaborators turned to the underside (or base) of a beautifully preserved partial cranium of Ardi. Their study revealed a pattern of similarity that links Ardi to Australopithecus and modern humans, but not to apes.

The research appears in the Jan. 6-10 online edition of Proceedings of the National Academy of Sciences. Kimbel is director of the ASU Institute of Human Origins, a research center of the College of Liberal Arts and Sciences in the School of Human Evolution and Social Change. Joining ASU's Kimbel as co-authors are Gen Suwa (University of Tokyo Museum), Berhane Asfaw (Rift Valley Research Service, Addis Ababa), Yoel Rak (Tel Aviv University) and Tim White (University of California at Berkeley).

White's field-research team has been recovering fossil remains of Ardipithecus ramidus in the Middle Awash research area, Ethiopia since the 1990s. The most recent study of the Ardi skull, led by Suwa, was published in Science in 2009, whose work (with the Middle Awash team) first revealed humanlike aspects of its base. Kimbel co-leads the team that recovered the earliest known Australopithecus skulls from the Hadar site, home of the "Lucy" skeleton, in Ethiopia.

"Given the very tiny size of the Ardi skull, the similarity of its cranial base to a human's is astonishing," says Kimbel.

The cranial base is a valuable resource for studying phylogenetic, or natural evolutionary relationships, because its anatomical complexity and association with the brain, posture and chewing system have provided numerous opportunities for adaptive evolution over time. The human cranial base, accordingly, differs profoundly from that of apes and other primates.

In humans, the structures marking the articulation of the spine with the skull are more forwardly located than in apes, where the base is shorter from front to back and the openings on each side for passage of blood vessels and nerves are more widely separated.

These shape differences affect the way the bones are arranged on the skull base, such that it is fairly easy to tell apart even isolated fragments of ape and human basicrania.

Ardi's cranial base shows the distinguishing features that separate humans and Australopithecus from the apes. Kimbel's earlier research (with collaborator Rak) had shown that these human peculiarities were present in the earliest known Australopithecus skulls by 3.4 million years ago.

The new work expands the catalogue of anatomical similarities linking humans, Australopithecus and Ardipithecus on the tree of life, and shows that the human cranial base pattern is at least a million years older than Lucy's species, A. afarensis.

Paleoanthropologists generally fall into one of two camps on the cause of evolutionary changes in the human cranial base. Was it the adoption of upright posture and bipedality that caused a shift in the poise of the head on the vertebral column? If so, does the humanlike cranial base of Ar. ramidus confirm postcranial evidence for partial bipedality in this species? Or, do the changes tell us about the shape of the brain (and of the base on which it sits), perhaps an early sign of brain reorganization in the human lineage? Both alternatives will need to be re-evaluated in light of the finding that Ardi does indeed appear to be more closely related to humans than to chimpanzees.

"The Ardi cranial base fills some important gaps in our understanding of human evolution above the neck," adds Kimbel. "But it also opens up a host of new questions . . . just as it should!"

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Found a way around the two human proteins to get 'jumping genes' affect

Elusive 'jumping genes' law, researchers at Johns Hopkins Sydney Kimmel Comprehensive Cancer found one type of DNA to replicate two human proteins used to themselves and by using new methods to catch the Center (home), to move from place to place. Explore new frontiers as described in issue 11/21 of the cell, but they understand colonization of new areas of work to limit the risks posed by a bit of volatility like the DNA of the human genome, cell-driven jumping genes while an arms race.

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Human influence on climate clear, IPCC report says

Sep. 27, 2013 — Human influence on the climate system is clear. This is evident in most regions of the globe, a new assessment by the Intergovernmental Panel on Climate Change (IPCC) concludes.

It is extremely likely that human influence has been the dominant cause of the observed warming since the mid-20th century. The evidence for this has grown, thanks to more and better observations, an improved understanding of the climate system response and improved climate models.

Warming in the climate system is unequivocal and since 1950 many changes have been observed throughout the climate system that are unprecedented over decades to millennia. Each of the last three decades has been successively warmer at Earth's surface than any preceding decade since 1850, reports the Summary for Policymakers of the IPCC Working Group I assessment report, Climate Change 2013: the Physical Science Basis, approved on Friday by member governments of the IPCC in Stockholm, Sweden.

"Observations of changes in the climate system are based on multiple lines of independent evidence. Our assessment of the science finds that the atmosphere and ocean have warmed, the amount of snow and ice has diminished, the global mean sea level has risen and the concentrations of greenhouse gases have increased," said Qin Dahe, Co-Chair of IPCC Working Group I.

Thomas Stocker, the other Co-Chair of Working Group I said: "Continued emissions of greenhouse gases will cause further warming and changes in all components of the climate system. Limiting climate change will require substantial and sustained reductions of greenhouse gas emissions."

"Global surface temperature change for the end of the 21st century is projected to be likely to exceed 1.5°C relative to 1850 to 1900 in all but the lowest scenario considered, and likely to exceed 2°C for the two high scenarios," said Co-Chair Thomas Stocker. "Heat waves are very likely to occur more frequently and last longer. As Earth warms, we expect to see currently wet regions receiving more rainfall, and dry regions receiving less, although there will be exceptions," he added.

Projections of climate change are based on a new set of four scenarios of future greenhouse gas concentrations and aerosols, spanning a wide range of possible futures. The Working Group I report assessed global and regional-scale climate change for the early, mid-, and later 21st century.

"As the ocean warms, and glaciers and ice sheets reduce, global mean sea level will continue to rise, but at a faster rate than we have experienced over the past 40 years," said Co-Chair Qin Dahe. The report finds with high confidence that ocean warming dominates the increase in energy stored in the climate system, accounting for more than 90% of the energy accumulated between 1971 and 2010.

Co-Chair Thomas Stocker concluded: "As a result of our past, present and expected future emissions of CO2, we are committed to climate change, and effects will persist for many centuries even if emissions of CO2 stop."

Rajendra Pachauri, Chair of the IPCC, said: "This Working Group I Summary for Policymakers provides important insights into the scientific basis of climate change. It provides a firm foundation for considerations of the impacts of climate change on human and natural systems and ways to meet the challenge of climate change." These are among the aspects assessed in the contributions of Working Group II and Working Group III to be released in March and April 2014. The IPCC Fifth Assessment Report cycle concludes with the publication of its Synthesis Report in October 2014.

"I would like to thank the Co-Chairs of Working Group I and the hundreds of scientists and experts who served as authors and review editors for producing a comprehensive and scientifically robust summary. I also express my thanks to the more than one thousand expert reviewers worldwide for contributing their expertise in preparation of this assessment," said IPCC Chair Pachauri.

The Summary for Policymakers of the Working Group I contribution to the IPCC Fifth Assessment Report (WGI AR5) is available at www.climatechange2013.org or www.ipcc.ch.

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Human robot getting closer: iCub robot must learn from its experiences

Sep. 27, 2013 — A robot that feels, sees and, in particular, thinks and learns like us. It still seems like science fiction, but if it's up to UT researcher Frank van der Velde, it won't be. In his work he wants to implement the cognitive process of the human brain in robots. The research should lead to the arrival of the latest version of the iCub robot in Twente. This human robot (humanoid) blurs the boundaries between robot and human.

Decades of scientific research into cognitive psychology and the brain have given us knowledge about language, memory, motor skills and perception. We can now use that knowledge in robots, but Frank van der Velde's research goes even further. "The application of cognition in technical systems should also mean that the robot learns from its experiences and the actions it performs. A simple example: a robot that spills too much when pouring a cup of coffee can then learn how it should be done."

Possible first iCub in the Netherlands

The arrival of the iCub robot at the University of Twente should signify the next step in this research. Van der Velde submitted an application together with other UT researchers Stefano Stramigioli, Vanessa Evers, Dirk Heylen and Richard van Wezel, all active in the robotics and cognitive research. At the moment, twenty European laboratories have an iCub, which was developed in Italy (thanks to a European FP7 grant for the IIT). The Netherlands is still missing from the list. Moreover, a newer version is currently being developed, with for example haptic sensors. In February it will be announced whether the robotics club will actually bring the latest iCub to the UT. The robot costs a quarter of a million Euros and NWO (Netherlands Organisation for Scientific Research) will reimburse 75% of the costs. Then the TNO (Netherlands Organisation for Applied Scientific Research) and the universities of Groningen, Nijmegen, Delft and Eindhoven can also make use of it. Within the UT, the iCub can be deployed in different laboratories thanks to a special transport system.

Robot guide dog

The possibilities are endless, according to Van der Velde. "The new iCub has a skin and fingers that have a much better sense of touch and can feel strength. That makes interaction with humans much more natural. We want to ensure that this robot continues to learn and understands how people function. This research ensures, for example, that robots actually gather knowledge by focusing on certain objects or persons. In areas of application like healthcare and nursing, such robots can play an important role. A good example would be that in ten years' time you see a blind person walking with a robot guide dog."

Nano-neural circuits

A recent line of research that is in line with this profile is the development of electronic circuits that resemble a web of neurons in the human brain. Contacts have already been made to start this research in Twente. In the iCub robot, this can for example be used for the robot's visual perception. This requires a lot of relatively simple operations that must all be performed in parallel. This takes a lot of time and energy in the current systems. With electronic circuits in the form of a web of nerve cells this is much easier.

"These connections are only possible at the nanoscale, that is to say the scale at which the material is only a few atoms thick. In combination with the iCub robot, it can be investigated how the experiences of the robot are recorded in such materials and how the robot is controlled by nano-neural circuitry. The bottleneck of the existing technical systems is often the energy consumption and the size. The limits of Moore's Law, the proposition that the number of transistors in a circuit doubles every two years through technological advances, are reached. In this area we are therefore also on the verge of many new applications."

Video: http://www.youtube.com/watch?v=ZcTwO2dpX8A

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Human brain tumor cells erased in mice

Sep. 23, 2013 — Working with mice, Johns Hopkins researchers have discovered that weeks of treatment with a repurposed FDA-approved drug halted the growth of -- and ultimately left no detectable trace of -- brain tumor cells taken from adult human patients.

The scientists targeted a mutation in the IDH1 gene first identified in human brain tumors called gliomas by a team of Johns Hopkins cancer researchers in 2008. This mutation was found in 70 to 80 percent of lower-grade and progressive forms of the brain cancer. The change occurs within a single spot along a string of thousands of genetic coding letters, and is disruptive enough to keep the seemingly innocuous protein from playing its role in converting glucose into energy. Instead, the mutation hijacks the protein to make a new molecule not normally found in the cell, which is apparently a linchpin in the process of forming and maintaining cancer cells.

Encouraged by the new findings, described online Sept. 16 in the open-access journal Oncotarget, the Johns Hopkins researchers say they want to work quickly to design a clinical trial to bring what they learned in mice to humans with gliomas. Despite the growing understanding of IDH1 mutant gliomas, the development of effective therapies has proven challenging, they say.

"Usually in the lab, we're happy to see a drug slow down tumor growth," says Alexandra Borodovsky, a graduate student in the Cellular and Molecular Medicine Program at the Johns Hopkins University School of Medicine who performed the experiments. "We never expect tumors to regress, but that is exactly what happened here."

"This therapy has worked amazingly well in these mice," says study leader Gregory J. Riggins, M.D., Ph.D., a professor of neurosurgery and oncology at the Johns Hopkins University School of Medicine. "We have spoken with neurosurgeons here, and as soon as possible, we want to start discussing the parameters of a clinical trial to see if this will work in our patients as a follow-up to surgery."

The researchers caution that many treatments have cured cancers in mice, and then failed in humans.

The IDH1 gene, whose name stands for isocitrate dehydrogenase 1, produces an enzyme that regulates cell metabolism. Mutations, or changes in the DNA code, force the IDH1 gene to increase production of a flawed version of the enzyme. The flawed enzyme produces large amounts of an entirely new molecule, called 2-hydroxyglutarate. This molecule is believed to cause groups of atoms called methyl groups to latch onto the DNA strand.

Although methylation is a normal cellular process, when too many methyl groups glom onto the DNA, Riggins says, this can interfere with normal cell biology and eventually contribute to cancer formation and growth.

Borodovsky, Riggins and their colleagues -- including Timothy A. Chan, M.D., Ph.D., of Memorial Sloan-Kettering Cancer Center in New York -- thought that a drug that could strip those methyl groups might be able to reverse the cancer process in those cancers with IDH1 mutations. They chose 5-azacytidine, which is approved to treat a pre-leukemia condition called myelodysplastic syndrome and is being tested on lung and other cancers at Johns Hopkins and elsewhere.

Riggins notes that one of the difficulties in developing treatments for IDH1 mutant brain cancers is finding a model in which to study them. Cell lines containing the IDH1 mutation are difficult to grow in the laboratory, for example. Borodovsky worked with Johns Hopkins neurosurgeons to obtain tumor cells from glioma patients likely to have IDH1 mutations and injected them under the skins of mice. She did this for months, before finally getting the tumor cells to grow.

Once the tumors grew, the researchers injected the mice with 5-azacytidine for 14 weeks and saw a dramatic reduction in growth and what appeared to be complete regression. Then they withdrew therapy. Seven weeks later, the tumors had not regrown. The researchers, however, said they do expect the tumors to regrow at some point, and are still monitoring the mice.

The type of tumor targeted by the researchers eventually progresses to a subtype of glioblastoma multiform -- the deadliest form of brain cancer -- known as progressive or secondary glioblastoma. They arise as a lower-grade glioma and are initially treated with surgery alone, but eventually they progress to the more lethal form of tumor. Survival is longer than with glioblastoma, but it is found in younger patients, those under the age of 50. While both types of tumor look the same at the end, they look very different at the molecular level, Riggins says, leading researchers to believe they may have a better chance at targeting the progressive tumors, which are more likely to have the IDH1 mutation.

Chan's team at Sloan-Kettering simultaneously published a paper in Oncotarget, along with Borodovsky and Riggins, which describes similar results in a different animal model using a similar drug. This is further evidence that the strategy is a sound one, Riggins says.

Other Johns Hopkins researchers involved in the Borodovsky paper include Charles G. Eberhart, M.D., Ph.D.; Jon D. Weingart, M.D.; Gary L. Gallia, M.D., Ph.D.; and Stephen B. Baylin, M.D.

The work was supported by the Conrad N. Hilton Foundation, the Virginia and D.K. Ludwig Fund for Cancer Research, Margaret H. Riggins, and the Irving J. Sherman Research Professorship in Neurosurgery. Funding also came from grants from the National Institutes of Health's National Cancer Institute (P30 CA006973) and the National Center for Research Resources (UL1 RR025005 and 1S10RR026824-01).

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Disease-specific human embryonic stem cell lines placed on NIH registry

Sep. 24, 2013 — Scientists from King's College London have announced that 16 human embryonic stem (hES) cell lines have been approved by the US National Institutes of Health (NIH) and placed on their Stem Cell Registry, making them freely available for federally-funded research in the USA. The stem cell lines, which carry genes for a variety of hereditary disorders such as Huntington's disease, spinal muscular dystrophy and cystic fibrosis, are considered to be ideal research tools for designing models to understand disease progression, and ultimately in helping scientists develop new treatments for patients.

King's is now one of the five biggest providers of disease-specific human embryonic stem cells lines on the NIH Registry, and the largest from the UK. The development is a significant milestone for King's and keeps the university at the forefront of global research into regenerative medicine.

Embryonic stem cell lines are grown from frozen embryos donated by patients undergoing preimplantation genetic diagnosis (PGD) in conjunction with IVF treatment. Unlike 'adult' stem cells, embryonic stem cells can differentiate into any type of cell within the body and are considered to be more useful for stem cell-based therapies. Disease-specific stem cell lines are created from embryos found to be affected with genetic disorders and therefore not suitable for implantation, but offer huge potential for research into disease development.

King's has already developed eight clinical-grade and more than 30 research-grade stem cell lines, which were approved by the UK Stem Cell Steering Committee to be deposited with the UK Stem Cell Bank (UKSCB) and distributed worldwide.

The sixteen lines of stem cells on the NIH Registry carry genes for various hereditary disorders including Duchenne Muscular Dystrophy, Huntington's disease, cystic fibrosis, and rarer conditions such as Von Hippel-Lindau Syndrome, Wiskott-Aldrich syndrome, spinal muscular atrophy, myotonic dystrophy and neurofibromatosis.

'Major contribution to global stem cell research'

Professor Peter Braude, Emeritus Professor of Obstetrics and Gynaecology, King's College London; and former director of the Stem Cell Programme and the Pre-Implantation Genetic Diagnosis Programme, Guy's and St Thomas' NHS Foundation Trust, said: 'We are delighted that the NIH has found our lines useful and their procurement and consents in line with the strict guidelines that they have set. This achievement is the culmination of over ten years of painstaking research and consistent belief in the scientific usefulness of these very special cells to improve our understanding of genetic disease processes.

'This is a huge milestone for King's, and will allow us to make a major contribution to global stem cell research by having these stem cell lines available to scientists in the USA.

'These research-grade stem cell lines are essential not only to address basic questions in development and disease, but to test and implement technical improvements in culture conditions that might affect hES cell viability and pluripotency.'

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Adjust the cells of the USC scientists ID protein anticancer therapy, human trafficking and potential.

Molecular microbiologist South California University （ USC Norris Comprehensive Cancer Center home ） but could lead to treatment for cancer and other disease treatment within a cell complex control mechanisms have been found. Have significance over the years on basic understanding of cell biology, their findings appear in the journal nature cell biology.

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Could E. Coli Vaccine for Cows Cut Human Infections?

TUESDAY, Sept. 17 (HealthDay News) -- Vaccinating cattle against E. coli bacteria could cut the number of human infections by 85 percent, far higher than previous estimates, British scientists say.

The researchers reviewed the way that E. coli is transmitted from cattle to humans, noting that the risk of infection is particularly significant during the brief periods when cattle are "super-shedding" extremely large amounts of the bacteria in their feces.

"As far as we can assess, the major risk to humans is from those animals that are shedding the bug heavily," said Stuart Reid, senior study author and a principal at the Royal Veterinary College at the University of London. "If the vaccine has an impact on these animals at that time, the risk to humans is disproportionately reduced."

Previous research has predicted that vaccination of cattle could reduce E. coli risk by 50 percent, but those studies did not take into account the effect of vaccination on "super-shedding," the researchers said.

The new study of Scottish cattle appeared in the Sept. 16-20 issue of the journal Proceedings of the National Academy of Sciences.

E. coli infection causes severe gastrointestinal illness in humans, in some cases leading to death. It is spread by consuming contaminated food or water, most often ground beef.

Nearly 1,100 confirmed cases of E. coli infection occurred in the United States in 2012, according to the U.S. Centers for Disease Control and Prevention. They led to 275 hospitalizations and two deaths. The CDC said that for every reported case of E. coli, there are probably 26 more that go undiagnosed.

Vaccines against E. coli have been approved for cattle in the United States and Canada, but farmers have not shown much interest in using them, the study authors said.

Farmers aren't vaccinating cattle against E. coli because cattle don't get sick from the bacteria, said Mike Doyle, a distinguished professor of food microbiology and director of the Center for Food Safety at the University of Georgia.

"The farmer doesn't get any bang for the buck from a production perspective," Doyle said. "The vaccine doesn't help the animal grow more healthy."

Government intervention likely would be required for widespread vaccination to occur. "Unless all farmers were required to vaccinate by the government, it wouldn't be cost effective or cost competitive for them to do that," Doyle said.

Such intervention should be seriously considered, said lead study author Dr. Louise Matthews, a senior research fellow in the Institute of Biodiversity, Animal Health and Comparative Medicine at the University of Glasgow.

"Treating cattle in order to reduce the number of human cases [of E. Coli] certainly makes sense from a human health perspective, and, while more work is needed to calculate the cost of a vaccination program, the public health justification must be taken seriously," Matthews said.

The researchers started their work first by identifying the genetic marker associated with E. coli super-shedding in cattle. They then studied the relationship between cattle predisposed to super-shed E. coli and human outbreaks of the illness, concluding that the types of E. coli linked to super-shedding cause the vast majority of cases.

The researchers now are working to develop even more effective vaccines that would further reduce the risk of E. coli outbreaks.

Doyle warned against generalizing the Scottish results to the United States, however, noting that farming methods are very different between the two. For example, Scottish beef is mostly grass fed.

"You can't automatically extrapolate what they find over there to what we have here," he said. "There's probably more research that would need to be done to see how useful or relevant this information is to American farmers."

Dr. Georges Benjamin, executive director of the American Public Health Association, said the results are intriguing. He said, however, that he's concerned that a vaccine might reduce emphasis on the common-sense food-safety methods that now provide effective protection against foodborne illness.

"I do want to emphasize [that] it does not replace careful monitoring of animal health and surveillance of the food-safety process as animals move through the pipeline to become our food," Benjamin said. "It also doesn't replace good food safety. You're still going to have to wash your hands. You're still going to have to make sure your food is prepared properly."

More information

For more about foodborne pathogens, visit the U.S. Centers for Disease Control and Prevention.

Copyright c 2013?HealthDay. All rights reserved.

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Human activity affects vertical structure of atmospheric temperature

Sep. 17, 2013 — Human influences have directly impacted the latitude/altitude pattern of atmospheric temperature. That is the conclusion of a new report by scientists from Lawrence Livermore National Laboratory and six other scientific institutions. The research compares multiple satellite records of atmospheric temperature change with results from a large, multi-model archive of simulations.

"Human activity has very different effects on the temperature of the upper and lower atmosphere, and a very different fingerprint from purely natural influences," said Benjamin Santer, the lead researcher in the paper appearing in the Sept.16 online edition of the Proceedings of the National Academy of Sciences. "Our results provide clear evidence for a discernible human influence on the thermal structure of the atmosphere."

Observational satellite data and the computer model-predicted response to human influence have a common latitude/altitude pattern of atmospheric temperature change. The key features of this pattern are global-scale tropospheric warming and stratospheric cooling over the 34-year satellite temperature record. (The troposphere is the lowest portion of Earth's atmosphere. The stratosphere lies above the troposphere.)

"Current climate models are highly unlikely to produce this distinctive signal pattern by internal variability alone, or in response to naturally forced changes in solar output and volcanic aerosol loadings," Santer said.

Natural internal fluctuations in climate are generated by complex interactions of the coupled atmosphere-ocean system, such as the well-known El Nino/Southern Oscillation. External influences include human-caused changes in well-mixed greenhouse gases, stratospheric ozone and other radiative forcing agents, as well as purely natural fluctuations in solar irradiance and volcanic aerosols. Each of these external influences has a unique "fingerprint" in the detailed latitude/altitude pattern of atmospheric temperature change.

Fingerprint information has proved particularly useful in separating human, solar and volcanic influences on climate.

"The pattern of temperature change that has been observed vertically in the atmosphere, from ground level to the stratosphere, fits with what is expected from human-caused increases in greenhouse gases. The observed pattern conflicts with what would be expected from an alternative explanation, such as fluctuations in the sun's output," Santer said.

Another LLNL co-author of the paper, Celine Bonfils, noted that major volcanic eruptions also can profoundly disturb the vertical structure of atmospheric temperature. "During the recovery from such eruptions, tropospheric warming and stratospheric cooling also occur" Bonfils said. "But in contrast to volcanic influences, human-caused atmospheric temperature changes affect all latitudes and last longer. This suggests that the recent changes in temperature are not simply a recovery from past volcanic events."

Other Livermore scientists include Jeff Painter, Peter Gleckler, Charles Doutriaux and Karl Taylor. The research team included scientists from Remote Sensing Systems (Carl Mears and Frank Wentz), the Massachusetts Institute of Technology (Susan Solomon), the University of Adelaide, Australia (Tom Wigley), the NASA/Goddard Institute of Space Studies (Gavin Schmidt), the Canadian Centre for Climate Modelling and Analysis (Nathan Gillett) and the Nansen Environmental and Remote Sensing Center, Norway (Peter Thorne).

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Study establishes human model of influenza pathogenesis

Sep. 13, 2013 — A National Institutes of Health (NIH) clinical study of healthy adult volunteers who consented to be infected with the 2009 H1N1 influenza virus under carefully controlled conditions has provided researchers with concrete information about the minimum dose of virus needed to produce mild-to-moderate illness. The study also gives a clearer picture of how much time elapses between a known time of infection, the start of viral shedding (a signal of contagiousness), the development of an immune response, and the onset and duration of influenza symptoms. The data obtained from this study provide a basis for more rapid, cost-effective clinical trials to evaluate new influenza drugs or to determine the efficacy of candidate vaccines for both seasonal and pandemic influenza.

In the study, 46 volunteers were divided into five groups and exposed to influenza virus in escalating doses. The virus, synthesized in the lab under Good Manufacturing Practice conditions, was genetically identical to the virus that caused 2009 H1N1 pandemic influenza. The volunteers all gave informed consent and subsequently were admitted to an isolation unit at the NIH Clinical Center in Bethesda, Md., for a minimum of eight days following virus exposure. The volunteers' health was closely monitored throughout their stay in the clinic and for two months afterward. The researchers sought to determine the minimum dose of virus needed to produce both shedding of live virus in nasal secretions and mild or moderate flu symptoms in 60 percent or more of dosed volunteers. When the scientists administered an influenza virus dose of 107 TCID50 (a measure of the amount of virus required to produce cell death in 50 percent of cultured cells inoculated with virus) to 13 volunteers, 9 (or 69 percent) shed virus and developed symptoms. Lower dosages did not generate responses that met this threshold, thereby establishing the minimum dose of influenza virus needed to produce mild-to-moderate illness.

Researchers from NIH's National Institute of Allergy and Infectious Diseases (NIAID) presented the preliminary study results at the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) meeting in Denver in September 2013.

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GSK extends its $2.6 billion offer for Human Genome

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AppId is over the quota

LONDON (Reuters) - GlaxoSmithKline has extended its $2.6 billion offer to buy long-time partner Human Genome Sciences until the end of June as it battles the U.S. biotech company's reluctant management.

The price remains unchanged at $13 a share under the longer tender, which will now expire at 5 p.m. EDT (2100 GMT) New York time on June 29, Britain's biggest drugmaker said on Friday.

The initial tender period ran out at midnight on June 7, by when GSK had secured less than 1 percent of Human Genome shares, which are trading at a premium to its offer.

People familiar with the situation had previously told Reuters that GSK was set to extend its tender offer - a direct appeal to Human Genome shareholders over the heads of management - as it begins a process to replace the entire Human Genome board with its own nominees.

The British company has already started reaching out to executives in the drug industry as well as finance and governance experts who could be nominated as independent directors of the 12-member board.

Sources said on May 30 that GSK intended to seek approval from Human Genome shareholders to replace the board under a "consent solicitation" process, which could come in the next few weeks. No details on the process were given on Friday.

Human Genome once again rejected GSK's bid as inadequate. It has launched an auction process, inviting GSK to participate, while at the same time adopting a "poison pill" shareholder rights plan in a bid to thwart the hostile takeover attempt.

The U.S. firm has had contacts with other companies and said on Friday that the process "continues to be active and fully underway". But no counterbidder to GSK has emerged and bankers say GSK has an advantage over rivals because of its partnerships around key drugs.

The two companies together sell Benlysta, a new drug for the autoimmune condition lupus, and they also collaborate on two other experimental drugs for diabetes and heart disease that could become significant sellers. GSK and Human Genome share rights to Benlysta, while GSK owns the majority of the commercial upside to the other products.

Buying Human Genome would give GSK full rights to these partnered drugs, underscoring the appetite among big drugmakers for biotech products to refill their medicine chests.

But GSK may have more work to do in persuading investors that its $13-per-share bid is good enough and shares in Human Genome traded 2 percent higher at $13.50 by 1430 GMT.

That indicates investors still expect a higher price, although the stock has fallen back from a high of more than $15 hit in April, soon after the unsolicited offer was made public.

(Editing by Kate Kelland and Hans-Juergen Peters)