பிதாகரஸ் தேற்றம்

கணித தேர்விற்காக பிதாகரஸ் தேற்றத்தை மனப்பாடம் செய்து கொண்டிருந்தாள் அமிர்தா.
இதை... கேட்டபடியே உள்ள வந்து கொண்டிருந்த அமிர்தாவின் பாட்டனார் இரத்தினம், "என்னம்மா பிதாகரஸ் தேற்றத்தை மனப்பாடம் செய்கிறாயா?" என்றார்.
"ஆமாம் தாத்தா. ரொம்ப கடினமா இருக்கு, இதை எப்படித்தான் கண்டுபிடிச்சாங்களோ!" என்றாள்.

இரத்தினம் தாத்தா: "இந்த தேற்றம் கி.மு 500ல் பிதாகரஸ் என்ற கணித அறிஞர் தொகுத்தார், அதனால் "பிதாகரஸ் தேற்றம்" என்று பெயர் வந்தது. ஆனால் அதுக்கும் முந்தியே நம்ம தமிழ் அறிவியலாளர்கள் அதை பாட்டாவே சொல்லிருக்காங்க தெரியுமா"

அமிர்தா: "சும்மா பொய் சொல்லாதீங்க தாத்தா"

இரத்தினம் தாத்தா: "சொல்றேன் கேள்,
இன்றைக்கு நாம் அனைவரும் சொல்லிக்கொண்டிருக்கின்ற பிதாகரஸ் கோட்பாடு (Pythagoras Theorem) என்ற கணித முறையை, பிதாகரஸ் என்பவர் கண்டறிவதற்கு முன்னரே, போதையனார் என்னும் புலவர் தனது செய்யுளிலே சொல்லியிருக்கிறார்.

"ஓடும் நீளம் தனை ஒரேஎட்டுக்
கூறு ஆக்கி கூறிலே ஒன்றைத்
தள்ளி குன்றத்தில் பாதியாய்ச் சேர்த்தால்
வருவது கர்ணம் தானே"
- போதையனார்
விளக்கம்:

இவற்றின் பொருள் செங்கோண முக்கோணத்தின், நீளத்தில் (அடிப்பாகம்) 8 பங்கில் ஒன்றைக் கழித்துவிட்டு உயரத்தில் பாதியை எடுத்து கூட்டினால் வரும் நீள அளவே கர்ணம் என்பதாகும். இவ்வளவு எளிமையாக கர்ணத்தின் நீளம் காணும் வாய்ப்பட்டை விட்டுவிட்டு வர்க்கமூலம், பெருக்கல் என பிதார்கரஸ் தியரம் சொல்லிவருவதை நாம் பயன்படுத்துகிறோம் இன்று.

இக்கணித முறையைக் கொண்டுதான், அக்காலத்தில் குன்றுகளின் உயரம் மற்றும் உயரமான இடத்தை அடைய நாம் நடந்து செல்லவேண்டிய தூரம் போன்றவைகள் கணக்கிடப்பட்டுள்ளன.

போதையனார் கோட்பாட்டின் சிறப்பம்சம் என்னவென்றால், வர்க்கமூலம் அதாவது Square root இல்லாமலேயே, நம்மால் இந்த கணிதமுறையை பயன்படுத்த முடியும்.

தமிழன் ஒரு வேலை கற்றலையும் / கல்வியையும் பொதுவுடமையாக, உலகறியச் செய்து இருந்தால் .... அவர்கள் தரணி எங்கும் அறியப்பட்டு இருப்பார்கள்." என்றார்.

அமிர்தா: "தாத்தா இது ரொம்ப எளிதாக இருக்கு, இதை படிச்சாலே நான் எளிதாக தேர்வில் எழுதி முழு மதிப்பெண்ணும் வாங்கிடுவேன். ரொம்ப நன்றி தாத்தா" என்றாள்.

நாமும் நம்மிடையே உள்ள சிறப்புகளை, எடுத்துரைத்தால் இன்றைய மாணவர்களும் எளிதில் தேர்ச்சி பெறுவார்கள் என்பது திண்ணம்.

சிந்திப்பார்களா நம் ஆசிரியர்கள்!

C = [{a-(a/8)}+{b/2}]

-- 
K.Kunanathan
Assistant Commissioner of Local Government,
St.Antony's Road,
Trincomalee.

எம்பி3 பிளேயரை, ஹெட் செட் மாட்டி கேட்டு வருபவர் களுக்கு, மிக இளம் வயதிலேயே காது கேட் கும் திறன் படிப்படியாக குறையத் தொடங் குகிறது

வாக்மேன் மறைந்து எம்பி3 பிளேயர் வந்த போது, இசையை ரசிக்க, அனைவரும் அதற்கு மாறினர். மிகத் துல்லிதமான இசை, எவ்வளவு நேரம் வேண்டுமானாலும் தொடர்ந்து பிரச்னை இன்றி தரும் வசதி ஆகியவற்றினால், பலரும் இதன்பால் ஈர்க்கப்பட்டனர்.

ஆனால், இது வேறு சில பிரச்னைகளைத் தருவதாக, டெல் அவிவ் பல்கலைக் கழகம் நடத்திய ஆய்வில் தெரிய வந்துள்ளது. தொடர்ந்து எம்பி3 பிளேயரை, ஹெட் செட் மாட்டி கேட்டு வருபவர் களுக்கு, மிக இளம் வயதிலேயே காது கேட் கும் திறன் படிப்படியாக குறையத் தொடங் குகிறது என்று கண்டறிந்துள்ளனர்.

தற்போது நால்வரில் ஒருவருக்கு இது உறுதிப்படுத்தப்பட்டுள்ளது என்றும் இந்த ஆய்வினை மேற்கொண்ட விஞ்ஞானிகள் எச்சரித்துள்ளனர். எம்பி3 பிளேயர் மட்டு மின்றி, தற்போது பரவலாகப் பயன்படுத்தப்பட்டு வரும் ஐ-பாட் மியூசிக் பிளேயர் பயன் படுத்துபவர்களின் கதியும் இதே தான் என வும் கூறி உள்ளனர்.

இதனால், இன்னும் 10 அல்லது 20 ஆண்டுகள் கழித்து, ஒரு சந்ததியே செவிகளின் கேட்புத் திறன் குறைவாக உள்ளதாக அமைந்துவிடும் என்றும் எச்சரித்து உள்ளனர்.

அதிக சத்தத்தில் பாடல்களைக் கேட்பதனால், தொடர்ந்து தாங்க முடியாத அளவிற்கு ஒலி அலைகள் காதுகள் வழியாகமூளைக்குப் பயணமாகின்றன. இவை ஏற்படுத்தும் தீய விளைவுகளை, உடனடி யாக நாம் அறிய முடிவதில்லை. படிப் படியாக அவை நம் கேட்கும் திறனைக் குறைக்கின்றன.

தெரிய வரும்போது இதற்கான தீர்வு கிடைப்பதில்லை. வளரும் இந்த தீய பழக்கம் குறித்து பள்ளிகள் மற்றும் கல்லூரிகளில் மாணவர் களுக்கு அறிவித்தால் நல்லது.

Preventing cancer development inside the cell cycle

Researchers from the NYU Cancer Institute, an NCI-designated cancer center at NYU Langone Medical Center, have identified a cell cycle-regulated mechanism behind the transformation of normal cells into cancerous cells. The study shows the significant role that protein networks can play in a cell leading to the development of cancer. The study results, published in the October 21 issue of the journal Molecular Cell, suggest that inhibition of the CK1 enzyme may be a new therapeutic target for the treatment of cancer cells formed as a result of a malfunction in the cell’s mTOR signaling pathway.

In the study, NYU Cancer Institute researchers examined certain multi-protein complexes and protein regulators in cancer cells. Researchers identified a major role for the multi-protein complex called SCF^βTrCP . It assists in the removal from cancer cells the recently discovered protein DEPTOR, an inhibitor of the mTOR pathway. SCF (Skp1, Cullin1, F-box protein) ubiquitin ligase complexes are responsible for the removal of unnecessary proteins from a cell.

This degradation of proteins by the cell’s ubiquitin system controls cell growth and prevents malignant cell transformation. Researchers show that inhibiting the ability of SCF^βTrCP to degrade DEPTOR in cells can result in blocking the proliferation of cancer cells. In addition, researchers discovered that the activity of CK1 (Casein Kinase 1), a protein that regulates signaling pathways in most cells, is needed for SCF^βTrCP to successfully promote the degradation of DEPTOR.

“Low levels of DEPTOR and high levels of mTOR activity are found in many cancers, including cancers of the breast, prostate, and lung,” said senior study author Michele Pagano, MD, the May Ellen and Gerald Jay Ritter Professor of Oncology and Professor of Pathology at NYU Langone Medical Center and a Howard Hughes Medical Institute Investigator. “It is critical for researchers to better understand how the protein DEPTOR is regulated. Our study shows it would be advantageous to increase the levels of DEPTOR in many types of cancer cells to inhibit mTOR and prevent cell proliferation.”

The mTOR pathway (mammalian Target Of Rapamycin) regulates the growth, proliferation, and survival of a cell, and its proper regulation is essential to prevent the formation of cancer cells. DEPTOR interrupts the mTOR pathway by binding to mTOR protein complexes and blocking their enzymatic activities, restraining cell growth. This helps support the proliferation and survival of cancer cells.

Study experiments showed that a reduction of SCF^βTrCP and CK1 proteins in cells resulted in accumulation of DEPTOR. Also, DEPTOR was destroyed in cells only when SCF^βTrCP and CK1 were both present. Thus, inhibition of SCF^βTrCP or CK1 represents a novel and promising way to inhibit the mTOR pathway. A pharmacologic inhibitor of CK1 was tested by researchers and shown to successfully stabilize DEPTOR in cells, while other pharmacological agents had no effect.

“Our study findings demonstrate that DEPTOR is regulated by the protein complex in cells reentering the cell cycle, and deregulation of this event could contribute to the aberrant activation of the mTOR pathway in cancer,” said lead author Shanshan Duan, PhD, a post-doctoral fellow in the Department of Pathology at NYU School of Medicine in Dr. Pagano’s Laboratory. “This study suggests a novel approach to stop the deregulation of the mTOR pathway in cancer cells with promising small molecule inhibitors of CK1.This study is another step forward in the translation of laboratory findings into more effective approaches to cancer prevention and treatment.”

_____________

This study was done in collaboration with the NYU Cancer Institute, Howard Hughes Medical Institute, The Lautenberg Center for Immunology, and Hebrew University in Israel.

Delivery system for gene therapy may help treat arthritis

Researchers report that a DNA-covered submicroscopic bead used to deliver genes or drugs directly into cells to treat disease appears to have therapeutic value just by showing up.

Within a few hours of injecting empty-handed DNA nanoparticles, Georgia Health Sciences University researchers were surprised to see increased expression of an enzyme that calms the immune response.

Researchers report in the study featured on the cover of The Journal of Immunology that the enhanced expression of indoleamine 2,3 dioxygenase, or IDO, significantly reduced the hallmark limb joint swelling and inflammation of this debilitating autoimmune disease in an animal model of rheumatoid arthritis.

“It’s like pouring water on a fire,” said Dr. Andrew L. Mellor, Director of the GHSU’s Medical College of Georgia Immunotherapy Center and the study’s corresponding author. “The fire is burning down the house, which in this case is the tissue normally required for your joints to work smoothly,” Mellor said of the immune system’s inexplicable attack on bone-cushioning cartilage. “When IDO levels are high, there is more water to control the fire.”

Several delivery systems are used for gene therapy, which is used to treat conditions including cancer, HIV infection and Parkinson’s disease. The new findings suggest the DNA nanoparticle technique is also valuable for autoimmune diseases such as arthritis, type 1 diabetes and lupus. “We want to induce IDO because it protects healthy tissue from destruction by the immune system,” Mellor said.

The researchers were exploring IDO’s autoimmune treatment potential by inserting the human IDO gene into DNA nanoparticles. They hoped to enhance IDO expression in their arthritis model when Dr. Lei Huang, Assistant Research Scientist and the paper’s first author, serendipitously found that the DNA nanoparticle produced the desired result. Exactly how and why is still being pursued. Early evidence suggests that immune cells called phagocytes, white blood cells that gobble up undesirables like bacteria and dying cells, start making more IDO in response to the DNA nanoparticle’s arrival. “Phagocytes eat it and respond quickly to it, and the effect we measure is IDO,” Mellor said.

Dr. Tracy L. McGaha, a GHSU immunologist and co-author of the current study, recently discovered that similar cells also prevented the development of systemic lupus erythematosus in mice.

Follow-up studies include documenting all cells that respond by producing more IDO. GHSU researchers work with biopolymer experts at the Massachusetts Institute of Technology, the University of California, Berkeley and the Georgia Institute of Technology to identify the optimal polymer.

The polymer used in the study is not biodegradable, so the researchers need one that will eventually safely degrade in the body. Ideally, it would also target specific cells, such as those near inflamed joints, to minimise any potential ill effects.

“It’s like a bead, and you wrap the DNA around it,” Mellor said of the polymer. While the DNA does not have to carry anything to get the desired response, in this case, DNA itself is essential to make cells express IDO. To ensure that IDO expression was responsible for the improvements, they also performed experiments in mice given an IDO inhibitor in their drinking water and in mice genetically altered to not express IDO. “Without access to the IDO pathway, the therapy no longer works,” Mellor said.

Drs. Andrew Mellor and David Munn reported in 1998 in the journal Science that the fetus expresses IDO to help avoid rejection by the mother’s immune system. Subsequent studies have shown that tumours also use IDO for protection, and clinical trials are studying the tumour-fighting potential of an IDO inhibitor. On the flip side, there is evidence that increasing IDO expression can protect transplanted organs and counter autoimmune disease.

________

Mellor is the Bradley-Turner and Georgia Research Alliance Eminent Scholar in Molecular Immunogenetics at MCG. The research was funded by the Carlos and Marguerite Mason Trust and the National Institutes of Health, and a patent is pending on the findings.

Researchers make promising discovery in pursuit of effective lymphoma treatments

Scientists optimistic that targeting pathway’s cellular transcription process will lead to death of multiple myeloma cells

Researchers at NYU School of Medicine have identified a target for slowing the progression of multiple myeloma by using currently available drugs.

Published recently in Nature Cell Biology, the study reveals a pathway that, if deactivated, may help slow the development of the disease.

Lymphoma is a type of cancer that begins in immune system cells called lymphocytes.

“We have the ability to target this pathway with drugs that already exist,” said lead investigator Michele Pagano, MD, the May Ellen and Gerald Jay Ritter Professor of Oncology in the Department of Pathology and a member of the NYU Cancer Institute at NYU Langone Medical Center, and a Howard Hughes Medical Institute investigator. “Many other lymphomas are also controlled by this pathway, so while we’re optimistic that this discovery will provide a way to kill multiple myeloma cells, we’re also very hopeful that this can be applied to other lymphomas and that it will have a major impact on these aggressive cancers.”

Pagano and colleagues put together several new pieces of the puzzle surrounding the survival and spread of multiple myeloma cells and the Nuclear Factor kappa B (NF-кB) pathway. This complicated pathway induces transcription of genes that control inflammation, immunity, and certain developmental processes. It is also known to frequently be involved in disease.

In normally functioning cells, the NF-кB pathway turns off and on, triggered by the accumulation and then degradation, or breakdown, of a protein called p100. When the pathway is “on,” p100 is degraded, allowing for pathway-dependent gene transcription. Several hours after the pathway’s activation, p100 begins to accumulate in the cell’s nucleus, naturally blocking the pathway, so that the gene transcription signal is temporarily blocked and transcription is halted.

In lymphomas, including multiple myeloma, however, the NF-кB pathway remains active, providing a refuge for lymphoma cells to hide. In fact, within this active pathway, the lymphoma cells are able to evade apoptosis, or cell death, allowing them to proliferate in an uncontrolled way.

“Activating mutations in the NF-кB pathway does not generally represent the initial oncogenic event,” Dr. Pagano said. “But they are necessary for the survival and spread of the cancer.”

Dr. Pagano explained the steps involved with pathway’s activation and deactivation in more scientific detail: The process begins in the pathway’s off state, with the accumulation of p100. To clear the pathway and naturally turn it back on, a sequence of events has to happen. First, a kinase, which the team identified as GSK3, phosphorylates p100. The phosphorylation draws the attention of Fbxw7α, a subunit of a ubiquitin ligase, which binds to the portion of p100 that has been phosphorylated by GSK3. The addition of Fbxw7α to the p100 protein then causes ubiquitin to seek out p100. Ubiquitin attaches to the protein and modifies it in a way such that it is recognized by a protease whose job it is to recognize and degrade any protein that has been modified by ubiquitin conjugation. As a result, p100 is degraded in the nucleus of the cell and the pathway is cleared and activated, turning on the gene transcription signal.

These new findings lead the researchers to conclude that the intersection of GSK3, Fbxw7α and p100 may serve as a potential intervention point for the treatment of multiple myeloma. Researchers believe if they can find a way to target the elimination of p100 they may be able to inactivate the pathway, which would eliminate the tumor cells’ safe haven so that they would be susceptible to apoptosis. This would in turn promote the death of multiple myeloma cells.

According to Dr. Pagano, this strategy may not be too far from becoming a reality. There are already drugs being tested in clinical trials for Alzheimer’s Disease that work by inhibiting GSK3. With the current study, the research team from NYU School of Medicine has shown that, by blocking GSK3 from phosphorylating p100, it is possible to prevent the degradation of p100, which then blocks the NF-кB pathway, thereby halting gene transcription and blocking tumor cells’ safe zone. Alternatively, pharmaceutical research may find a way to target Fbxw7α, which would keep the pathway turned off in the same way.

“Cancers are persistent and tenacious,” Dr. Pagano said. “There are millions of pieces to the puzzle of how they work and we’ve discovered a few more pieces of that puzzle. It is very possible that we can find an inhibitor of Fbxw7α since there are already drugs being tested that inhibit very similar enzymes.”

Moreover, Dr. Pagano explained, it is likely that the effects observed in multiple myeloma may be generalized to other B-cell neoplasms, types of lymphomas, especially those in which the tumor cells hide out in the NF-кB pathway.

“These new findings strongly suggest that by targeting this enzyme, we will kill multiple myeloma cells and other B-cell lymphomas,” he said. “And that, from a researcher’s perspective, is a very exciting prospect.”

_________

The study was funded by the National Institutes of Health, the National Cancer Institute, the National Institute of General Medical Sciences, the Multiple Myeloma Research Foundation, the American Italian Cancer Foundation, and the Howard Hughes Medical Institute.

Courtesy NYU Langone Medical Center / New York University School of Medicine 

Different mechanisms of pain revealed

Researchers at the University of Leeds have found a previously unknown mechanism through which pain is signaled by nerve cells – a discovery that could explain the current failings in the drug development process for painkillers and which may offer opportunities for a new approach.

The team, led by Dr Nikita Gamper of the University’s Faculty of Biological Sciences, is investigating the difference between persistent pain, such as toothache, and pain that results from the increased sensitivity of nerves in injured or diseased tissue (for example when we touch inflamed skin), known as hyperalgesia.

In research published online this week, (w/c 14 May) in Proceedings of the National Academy of Sciences (PNAS), Dr Gamper’s team has discovered that these two types of pain are generated by the same nerves, but result from different underlying mechanisms.

The project, funded jointly by the Wellcome Trust and the Medical Research Council, investigated the painful effects of two substances that cause local inflammation: bradykinin and substance P. Both substances bind to specific receptors on nerve cells, generating signals to the central nervous system. Because the receptors are from the same family, it has always been presumed they stimulate the same signalling pathway.

However, the team found that each receptor produces different signals; the one associated with bradykinin causing both hyperalgesia and persistent pain, whereas the one associated with substance P only caused hyperalgesia.

“Dr Gamper says: “Pain originates from a series of electrical signals sent by nerve cells in to the central nervous system and ultimately the brain. Despite much progress, we still don’t know enough about the mechanisms by which these pain signals are generated. However, this research has shown that whilst the sensation of pain can be similar between various conditions, the underlying molecular mechanisms may in fact be very different.”

Existing painkillers are ‘non-specific’, designed to generally dull the reception of these signals in the central nervous system, and some stronger pain killers can provoke unwanted side effects such as disorientation, drowsiness or nausea. So while the search for new better drugs is pressing, the lack of progress in developing targeted analgesics has led to several pharmaceutical companies dropping this area of research altogether.

“What’s exciting about these findings is that substance P may actually suppress the activation of the pain sensing nerves themselves,” says Dr Gamper.

“It’s increasingly evident that current strategies for testing and validating new painkillers often do not take into account a possible difference in how pain signals are generated. For instance, drugs for persistent pain are often tested solely for their ability to reduce hyperalgesia, and as a result, some of the drugs that are effective in the lab, fail in subsequent clinical trials. These findings challenge current approaches in drug development research and may offer new strategies,” he says.

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Courtesy University of Leeds 

Cancer Research:Understanding Breast Cancer

Landscape of cancer genes and mutational processes in breast cancer

In a study published today in Nature, researchers describe nine new genes that drive the development of breast cancer. This takes the tally of all genes associated with breast cancer development to 40.

The team examined all the genes in the genomes of 100 cases of breast cancer. The mutated cancer-causing genes differed in different cancer samples, indicating that breast cancer is genetically diverse. Understanding the consequences of this diversity will be important in progressing towards more rational treatment.

Changes to DNA lie behind all cases of cancer. Cancer develops as a result of mutations – called somatic mutations – that are acquired during a person’s lifetime. Driver mutations occur in cancer genes and are a small subset of somatic mutations that drive cancer development.

“Breast cancer is the most common cancer in women,” explains Dr Patrick Tarpey, first author from the Wellcome Trust Sanger Institute. “To identify new cancer genes that lead to the development of breast cancer, we searched for driver mutations in over 21,000 genes and found evidence for nine new cancer genes involved in the development of this cancer.”

These genome analyses directly survey the landscape of driver mutations in breast cancer. The team found driver mutations in at least 40 cancer genes. Most individual cancers had different combinations of mutated cancer genes, demonstrating the substantial genetic diversity in breast cancer.

“In 28 cases we found only a single driver, but the maximum number of driver mutations in an individual cancer was six,” says Professor Mike Stratton, lead author and Director of the Wellcome Trust Sanger Institute. “We found that breast cancer can be caused by more than 70 different combinations of mutations.

“If we consider three breast cancers, each with four driver mutations, they might share none of those driver mutations – so each is a different genetic ‘animal’. They are different cancers driven by different genes. We need to classify them as carefully as we can. This study is a step towards that goal.”

“One of the most striking things about breast cancer is how it progresses differently in each patient and how each patient responds differently to therapy,” explains Professor Andy Futreal, until recently, Head of Cancer Genomics at the Wellcome Trust Sanger Institute and currently an Honorary Faculty Member at the Institute. “Our results can help us to understand these differences.”

Our genomes are scarred by decades of continual assault that leave mutations scattered though our DNA. This is the most comprehensive study thus far of mutations in breast cancers, discovering nine new mutated genes that cause breast cancer, and revealing the full diversity of the driving events that convert normal breast cells into breast cancers.

“The picture is certainly more complicated than we would have wanted, but as with many other things knowledge is our strongest weapon. These comprehensive insights reveal the faulty wiring of the cellular circuit board that causes cells to behave as cancers. Understanding our enemy at this level of detail will allow us to take more rational approaches to therapy, to understand why some cancers respond to drugs and others do not, and direct us to new vulnerabilities to be exploited in new treatments,” adds Professor Stratton.

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Publication Details

Stephens and Tarpey et al ‘The landscape of cancer genes and mutational processes in breast cancer’

This paper will be published electronically on Nature‘s website on 16 May DOI: 10.1038/nature11017

Funding

A full list of funding agencies can be found in the papers

Participating Centres

A full list of participating centres can be found in the papers.

Courtesy Wellcome Trust Sanger Institute 

Health experts narrow the hunt for Ebola virus

Wildlife Conservation Society (WCS) and partners recommend focusing on carcasses rather than live animals for samples

Response efforts to outbreaks of Ebola hemorrhagic fever in Africa can benefit from a standardized sampling strategy focusing on the carcasses of gorillas, chimpanzees and other species known to succumb to the virus, according to a consortium of wildlife health experts.

In a recently published study of 14 previous human Ebola outbreaks and the responses of wildlife teams collecting animal samples, the new study's authors conclude that most efforts to collect samples from live animals (i.e. rodents, bats, primates, birds) failed to isolate Ebola virus or antibodies. However, they found that collecting samples from animal carcasses during outbreaks was a more effective method for Ebola detection. The early detection of Ebola in animal populations near a human outbreak is crucial for learning more about this virus, which can strike human populations with a mortality rate of more than 80 per cent.

“You can’t test every single animal, so we used information from historical outbreaks to figure out how to help the field response team focus their effort,” according to Wildlife Conservation Society (WCS) wildlife epidemiologist Sarah Olson, the new report's lead author. “It turns out that carcass sampling yields a 50 percent chance of finding Ebola virus or antibodies compared to less than six percent when sampling free-ranging live animals.”

The scientific consortium that participated in the study, published in an online issue of Emerging Health Threats, are key partners in PREDICT, part of USAID’s Emerging Pandemic Threats Program that is improving global capacity to respond to emerging infectious diseases that originate in wildlife. PREDICT is led by the University of California at Davis, in partnership with Ecohealth Alliance, Global Viral Forecasting Initiative, the Smithsonian Institution, and the Wildlife Conservation Society.

 Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study.  Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study.  Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study.  Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study.  Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study.  Dr. Jonna Mazet, the Director of PREDICT and the One Health Institute at the University of California, Davis School of Veterinary Medicine, praised the Emerging Pandemic Threats program as a visionary investment by USAID to protect and improve global health. The program identifies novel pathogens in wildlife that could pose pandemic threats to humans on a global scale, pre-emptively. PREDICT is using science to improve our ability to detect lethal diseases like Ebola, which is demonstrated in this study. 

The study was designed to develop a set of animal sampling recommendations to maximize the effectiveness of Ebola outbreak response efforts with limited resources. Specifically, the study was prompted by a 2011 outbreak near Kampala, Uganda, in which a 12-year-old girl died from Ebola hemorrhagic fever. PREDICT wildlife veterinarians were sent to the victim’s village to screen wildlife as a potential source of the virus.

“This study digests over 30 years of accumulated knowledge so field teams can arrive informed and prepared,” adds WCS epidemiologist and senior author, Damien Joly.

The authors also point to some scientific “loose ends” that can be incorporated into future animal sampling efforts during Ebola outbreak response. For instance, despite some evidence of Ebola in dogs and pigs, the number of samples acquired from these animals is limited to just two outbreaks; the authors recommend increasing the number of samples collected from these groups in the future to better determine their role in Ebola outbreaks. The study also confirms that while fruit bats should be a focus of investigation as a potential reservoir for Ebola, field teams need to be prepared to sample hundreds of bats because virus prevalence across all bats sampled to date is very low, estimated at 3 percent.

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The co-authors of the study, titled, “Dead or alive: animal sampling during Ebola hemorrhagic fever outbreaks in humans,” include: Sarah Olson of the Wildlife Conservation Society and the University of Wisconsin; Patricia Reed, Ken Cameron, and Damien Joly of the Wildlife Conservation Society; Benard Ssebide of Gorilla Doctors, Kampala, Uganda; Jonna Mazet and Christine Johnson of the University of California at Davis; Stephen Morse of Columbia University; and William Karesh of EcoHealth Alliance.

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