Category Archives: Immunology

Dr. Cynthia Leifer honored with 2012 Pfizer Animal Health Award

LeiferDr. Cynthia Leifer, assistant professor of immunology at Cornell University’s College of Veterinary Medicine, has been selected to receive the Pfizer Animal Health Award for Veterinary Research Excellence. The award fosters innovative research by recognizing outstanding research and productivity from a faculty member early in his or her career. Nominees are selected for innovative research relevant to animal health that is likely to make national impact.

Leifer’s research sheds light on the currently cloudy causes of autoimmune disease by uncovering inner workings of the innate immune system. Afflicting one in five Americans, autoimmune diseases include a wide array of disorders from rheumatoid arthritis to the skin disease Lupus to irritable bowel syndrome.

“The immune system fights to protect us against invading microorganisms,” said Leifer. “But it must also recognize what to attack and keep its aggressive responses under control to prevent damaging our own bodies.”

When recognition and regulation fail, the immune system can attack the body and lead to autoimmune disorders. Leifer explores how immune cell receptors affect the way these cells recognize and respond to whatever they encounter, whether it’s a microbial invader or a piece of the self.

“Most innate immune receptors identify microbes by detecting unique structures found only on microbes,” said Leifer. “But some work by detecting structures present in both microbes and the self, such as DNA.”

Focusing her research on one such receptor, Toll-like receptor 9 (TLR9), Leifer recently discovered how TLR9 makes the kind of recognition mistakes that lead to autoimmune attacks, opening the door to new possible autoimmune disease therapies.

“Identifying immune-cell regulation systems may reveal therapeutic targets for managing TLR9 function, leading to new treatments for autoimmune diseases,” said Leifer.

Leifer will present her research at a special seminar to be held in September 2012. At a ceremony that follows she will receive an award of $1,000 and an engraved plaque.

“This is a great honor for Dr. Leifer at this stage of her career,” said Dr. Avery August, chair of the department of microbiology and immunology. “Her cutting-edge work on how the immune system senses pathogens is being recognized, and she will join a distinguished list of Cornell faculty who have received this award. We congratulate her on this great accomplishment.”

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College of Veterinary Medicine News
http://www.vet.cornell.edu/news/LeiferPfizer.cfm

 

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First discovery of cells expelling mitochondria uncovers newfound survival tactic

An ancient union between cell and organelle has shown the first sign of fracture, challenging common conceptions of a primordial partnership all multicellular organisms rely on to live. Cornell researchers have recorded the first direct evidence of cells expelling intact mitochondria, the cellular machinery responsible for energy production.

AAAmitochondria B

An illustrated mitochondrion

Malfunctioning mitochondria produce free-radicals that damage cells, contributing to aging, mitochondrial myopathies, and disorders ranging from schizophrenia, bipolar disorder, and dementia to Parkinson’s disease and multiple sclerosis. The newfound breakup behaviour, described in Mitochondrion 2011 Nov.11(6), may be an early cell-survival strategy to escape the toxic effects of damaged mitochondria.

“It is very surprising to see living cells actively jettisoning vital parts of themselves,” said Dr. Theodore Clark, immunologist at the College of Veterinary Medicine. “This is the first time full mitochondria have been found outside cells and it may account for 15 years’ worth of unexplained data showing mitochondrial DNA and protein in extracellular spaces. We think these cells’ behaviour reveals a newfound survival tactic deeply rooted in evolution.”

Today’s mitochondria evolved from freewheeling bacteria that settled down in other cells two billion years ago. In exchange for food and shelter, the bacteria helped cells break nutrients into energy. These helpful tenants became modern mitochondria: the power-plants inside all cells of nearly every animal, plant, fungus, and protozoan.

Yet domestic disputes over cellular housekeeping may spur divorce, according to findings from Clark’s lab showing mitochondria moving out.

Graduate student Yelena Bisharyan discovered this while studying an unrelated phenomenon: escape stunts of the fish parasite Ichthyophthirius multifiliis. Clark’s lab had observed these parasitic protozoa avoiding destruction by shaking off attacking antibodies and exiting their hosts and wanted to see how they escaped.

“Attacking antibodies bind to the parasite’s cell surface,” said Clark. “We suspected that when antibodies attach, the parasite can shed them by breaking off its surface proteins – sort of like a lizard shedding its tail.”

tetrehymena 2

Tetrahymena, a protozoan, sheds proteins and mitochondria in response to attacking antibodies

Applying antibodies to parasites in culture, Bisharyan observed the reactions of Ichtyophthirius and Tetrahymena, another ciliated protozoan used as a model system to study fundamental biological principles across species.

Using negative staining and electron microscopy techniques, Bisharyan recorded parasites sacrificing their surface proteins to rid themselves of attached antibodies. Yet her images also captured something completely unexpected: intact and fragmented mitochondria coming out of the parasite’s cells.

This surprising finding won Bisharyan an invitation to present at one of the 2011 Gordon Research Conferences, a prestigious international forum showcasing major discoveries across scientific fields.

“Mitochondria experts were very excited to see this,” said Clark. “Over the past 15 years several papers have reported mitochondrial DNA and proteins floating outside mammalian cells. No one knew how or why they got there. What we’ve found in protozoa may help explain similar processes in mammals.”

Mitochondria (m) are pushed to the surface and jettisoned from the cell

mitochondria shed

Mitochondria (red) discovered outside cells

Certain cellular stressors can trigger mitochondrial expulsion, according to Bisharyan’s study. In protozoa, for example, not only antibodies but also heat shock can induce this effect. These stressors elevate calcium levels within the cell, possibly damaging mitochondria and causing them to produce toxic free-radicals.

“Our hypothesis is that mitochondria become poisoned and these protozoa have found a way to rid themselves of the damaged powerplants before they can cause further harm,” said Clark. “We think their behaviour reveals an early adaption to cellular stress that other species may share.”

Mammals and fish parasites may bear little family resemblance these days, but a common ancestor may have equipped both with emergency mitochondria-removal systems. Understanding this process could illuminate new approaches to reducing mitochondria-induced damage in humans and other animals.

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Cornell University College of Veterinary Medicine news

http://vet.cornell.edu/news/Mitochondria.cfm

Icelandic horses travel to Cornell

Horses will help unlock immunological mysteries of allergies and herpes

For horses, Iceland is a safe haven from disease. Several pathogens never made it to the island, whose native horses evolved for almost 1,000 years in isolation. Without facing diseases common outside, such as equine herpesvirus type 1 (EHV-1) and insect-induced allergies (called sweet itch or summer eczema), Icelandic horses never had to develop immunity to them. But immunological ignorance comes at a price: When they leave the country, these internationally popular horses are unusually vulnerable.

Yet in a discrepancy that has long puzzled immunologists, expatriate Icelandic horses give birth to far hardier foals. Born outside Iceland, these foals are up to fifteen times less likely than their parents to develop allergies. In all breeds, foal and adult immune systems work very differently. Learning how and why could help prevent allergies earlier and enable better vaccines protecting foals from early-developing diseases like EHV-1.

Dr. Bettina Wagner, equine immunologist at the College of Veterinary Medicine, works with collaborators at Cornell and in Iceland to unravel the mystery of neonatal immune development with the help of Icelandic horses.

In February 2012, 15 pregnant mares traveled from their native Iceland to Cornell University, meticulously protected from exposure to several common pathogens. With the help of collaborators at the University of Iceland at the Institute for Experimental Pathology Keldur in Reykjavik, Dr. Wagner’s group receives regular samples from the mares’ first brood born in Iceland last Summer. Comparing foals in Iceland to their forthcoming U.S.-born siblings will reveal how separate factors (environmental and maternal) affect immune development.

Clinical collaborators at Cornell assisting with the project include Drs. Gillian Perkins and Dorothy Ainsworth. Dr. Klaus Osterrieder in Berlin, Germany will help in the study of EHV-1 while Dr. Mandi deMestre of the United Kingdom will collaborate on the immune regulations analysis. Cornell professor Dr. Hollis Erb will advise on the statistical analysis of the data.

“We want to know why foals born outside Iceland have better protection than those born in Iceland,” said Dr. Wagner. “It could be due to time of exposure, environment, or some combination of these, but the evidence points more to what the mother passes on.”

Dr. Wagner thinks that protective power may lie in a mare’s milk. Some mammals, including humans, start absorbing antibodies while in the uterus, but horses receive all immunities after birth. To absorb immune protection, newborn foals must quickly drink colostrum, which is packed with immune components.

Mares encountering new allergens may become hypersensitive to the antibodies their systems produce in response. But when they pass these antibodies on through milk, Dr. Wagner thinks that the foals’ budding immune systems may learn to use those same antibodies more constructively.

Dr. Wagner’s group investigates specific antibodies called immunoglobulin-E (IgE), which can go astray in allergic diseases, reacting to harmless stimuli and causing inflammation. Building our understanding of early immune development in horses and humans could help doctors treat allergies and early-striking diseases in both species.

“If we know how allergic diseases start early in life we can interfere before they develop,” said Dr. Wagner. “Horses are a valuable model for human allergies, for which regulatory mechanisms develop very early. It’s difficult to investigate human neonatal immunity, because most maternal immune transfer happens before birth. The horse system is more controllable, especially in Icelandic horses, and can reveal the separate effects of maternal transfer and environmental exposure.”

The study may improve protection from EHV-1, which often strikes before current vaccines designed for adult immune systems can protect foals.

“If we can learn how immune responses in foals differ from those in adults, we can use specific immune reactions that foals can mount early in life to develop better neonatal vaccines for earlier protection from a wide array of infectious diseases.”

This research is funded by the Harry M. Zweig Memorial Fund for Equine Research.

‘Scopes Magazine
February 2012

How unchecked alarms can spark autoimmune disease

November 29, 2011

A white blood cell engulfs an invading Bacillus anthracis

A neutrophil (yellow), the most abundant white blood cell type and the first line of defense against invading microbes, engulfs Bacillus anthracis (orange), the agent of anthrax. The bacteria break down, releasing DNA that triggers an immune response.

One in five Americans suffers from autoimmune disease, in which the immune system goes off-track and attacks the body’s own cells. Cornell researchers have identified a signaling mechanism in immune-system cells that may contribute to this mistake, opening the door for possible new therapies for autoimmune diseases such as lupus and arthritis.

Cynthia Leifer, assistant professor of microbiology and immunology in the College of Veterinary Medicine, and colleagues described the mechanism in the August issue of the European Journal of Immunology. The problem lies in what are called innate immune cells, the first responders to infection.

“Innate immune cells have internal watchdogs called TLR-9 receptors that set off alarms whenever they encounter invaders,” said Leifer. “They look for general classifying patterns [in DNA] to determine whether something is a virus, bacterium, protozoan, or part of self.”

However, some of these patterns exist both in invading organisms and the body’s own cells, so mistakes can arise.

Cynthia Leifer

Leifer

“We are mapping the critical regulatory mechanisms that keep these receptors from responding to self-DNA so that we can know if and how they predispose people to autoimmune disorders when they fail,” Leifer said.

Innate immune cells engulf things that look dangerous, tear them open, and release their components, including DNA. When TLR-9 receptors see DNA that identifies microbes, they send a signal to fire up more immune-system activity, including inflammation and the creation of antibodies. But before a receptor can work, enzymes in the cell must prepare it by chopping off part of the receptor molecule and leaving a part that can bind to microbe DNA.

From there, Leifer believes it’s a numbers game. If too many receptors are prepared, they may respond to the small amount of self-DNA that makes its way into immune cells, triggering an autoimmune response. So the immune cell has a regulatory mechanism, an enzyme pathway that cuts prepared receptors in a second place.

Working with cells in culture, Leifer identified this second chopping event, which cuts TLR-9 at a different site. This produces a molecule that binds to DNA, blocking it from reaching the prepared receptors, and does not send a signal.

“People without autoimmune diseases have the right balance of these two chopping events,” Leifer said. “Our studies suggest that people with a propensity for these diseases might have a defect in this pathway that allows more prepared receptors to signal for immune responses. This may be a potential target for therapies designed to help quiet those alarms.”

A second but interrelated problem Leifer has tackled involves how TLR-9 moves through an immune cell from the placewhere it is created to its working site. In earlier work she described the protein sequences in TLR-9 that act as address labels guiding where the receptor travels.

“We think they’re interrelated because if you don’t travel properly you don’t get chopped properly,” she said. “If TLR-9 ends up in the wrong place at the wrong time, it can sound a false alarm.

Leifer’s research is supported by the National Institutes of Health.

Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.

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Original Press Release:

Cornell University College of Veterinary Medicine news

http://www.vet.cornell.edu/news/leifer.cfm

 

Media Hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Nov11/LeiferDNA.html

Medical Xpress (PhysOrg)

http://medicalxpress.com/news/2011-11-unchecked-alarms-autoimmune-disease.html

MyScience

http://www.myscience.us/wire/how_unchecked_alarms_can_spark_autoimmune_disease-2011-cornell

Bionity

http://www.bionity.com/en/news/135431/how-unchecked-alarms-can-spark-autoimmune-disease.html

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http://www.rdmag.com/News/Feeds/2011/11/general-sciences-how-unchecked-alarms-can-spark-autoimmune-disease/

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http://www.ecnmag.com/News/Feeds/2011/11/blogs-the-cutting-edge-how-unchecked-alarms-can-spark-autoimmune-disease/

Futurity

http://www.futurity.org/top-stories/false-alarm-can-spark-autoimmune-disease/

How ‘promiscuous parasites’ hijack host immune cells

Sept. 19, 2011

By Carly Hodes

Toxoplasma gondii parasites can invade your bloodstream, break into your brain and prompt behavioral changes from recklessness to neuroticism. These highly contagious protozoa infect more than half the world’s population, and most people’s immune systems never purge the intruders.

Toxoplasma gondii

Toxoplasma gondii parasites, green, multiply inside an immune cell that lives in the brain.

Cornell researchers recently discovered how T. gondii evades our defenses by hacking immune cells, making it the first known parasite to control its host’s immune system. Immunologists from the College of Veterinary Medicine published the study Sept. 8 in PLoS-Pathogens, describing a forced partnership between parasite and host that challenges common conceptions of how pathogens interact with the body.

Eric Denkers

Dr. Eric Denkers

“Toxoplasma is an especially promiscuous parasite,” said Eric Denkers, professor of immunology. “It infects nearly all warm-blooded species, most nucleated cell types and much of the human population. Although it lives in vital brain and muscle tissues, it usually causes no obvious reaction. Infection can seriously harm people with weak immune systems, yet most hosts experience no overt symptoms because Toxoplasma has found a way to coerce cooperation.”

Famous for its manipulative powers, T. gondii has been shown to alter the brain chemistry of rodents so that they fearlessly pursue cats. Cats eat the rodents, delivering the parasites to their breeding ground in feline intestines. Similar manipulations have surfaced in human studies linking T. gondii infections to behavioral and personality shifts, schizophrenia and population variations, including cultural differences and skewed sex ratios. Denkers’ study maps T. gondii’s newfound ability to manipulate cells in the immune system at the molecular level.

Toxoplasma parasites

Toxoplasma parasites forming a walled cyst in a mouse brain, where they release chemicals that can affect behavior.

“We found that Toxoplasma quiets its host’s alarm system by blocking immune cells from producing certain cytokines, proteins that stimulate inflammation,” said Denkers. “Cytokines are double-edged swords: They summon the immune system’s reinforcements, but if too many accumulate they can damage the body they’re trying to defend. An unregulated immune response can kill you.”

When immune cells meet intruders, they release cytokines that summon more immune cells, which produce more cytokines, rapidly causing inflammation. T. gondii must allow cytokines to trigger enough of an immune response to keep its own numbers in check and ensure host survival. But too many cytokines cause an overwhelming immune response that could damage the host or eliminate the parasites.

cytokine production in uninfected immune cells

Green stain highlights cytokine production in uninfected immune cells. Cells infected with Toxoplasma parasites, orange, cannot make cytokines.

“Toxoplasma hijacks immune cells to enforce a mutually beneficial balance,” Denkers said. “Until recently we thought it walled itself away inside cells without interacting with its environment. It’s now clear that the parasite actively releases messages into cells that change cell behavior.”

To prove this, Barbara Butcher, a senior research associate working with Denkers, exposed immune cells in the lab to bacterial factors that typically stimulate the release of inflammatory cytokines.

“Cells infected with Toxoplasma produced no messages to trigger inflammation,” Denkers said. “Our colleagues at Stanford University found that Toxoplasma produces a specific protein called ROP16 to suppress inflammatory responses. Collaborating with parasitologists at Dartmouth Medical School, we found that Toxoplasma sends ROP16 to infiltrate communication channels in immune cells, causing them to lower cytokine production.

“We are excited to have found the first non-bacterial pathogen able to exert this kind of control,” said Denkers. “If Toxoplasma can do this, maybe other parasites can too. This is the first case where the whole process of immune system manipulation is close to being completely mapped out at the molecular level.”

That map may help steer future investigations into how pathogens interact with hosts, unveiling the inner workings of a spectrum of infectious diseases.

Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.

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Original Press Release:

Cornell University College of Veterinary Medicine news

http://www.vet.cornell.edu/news/toxoplasma.cfm

Media Hits:

Cornell Chronicle

http://www.vet.cornell.edu/news/toxoplasma.cfm

Answerclopedia

http://answerclopedia.com/promiscuous-parasites-hijack-host-immune-cells.html

Medical Xpress

http://medicalxpress.com/news/2011-09-promiscuous-parasites-hijack-host-immune.html

MyScience

http://www.myscience.cc/news/promiscuous_parasites_hijack_host_immune_cells-2011-cornell

Times of India

http://timesofindia.indiatimes.com/life-style/health-fitness/health/Promiscuous-parasites-make-you-reckless/articleshow/10079594.cms

NewKerala

http://www.newkerala.com/news/2011/worldnews-72626.html

LabSpaces

http://www.labspaces.net/113581/Researchers_discover_how__promiscuous_parasites__hijack_host_immune_cells

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http://www.topnews.in/health/promiscuous-parasites-can-make-you-reckless-213177

http://www.citybengaluru.com/promiscuous-parasites-can-make-you-reckless/

http://www.indiatalkies.com/2011/09/promiscuous-parasites-reckless.html

Amwayagent

http://www.amwayagent.com/researchers-discover-how-promiscuous-parasites-hijack-host-immune-cells.html

InfectionControlToday

http://www.infectioncontroltoday.com/news/2011/09/researchers-discover-how-promiscuous-parasites-hijack-host-immune-cells.aspx

ScienceDaily

http://www.sciencedaily.com/releases/2011/09/110921120056.htm

NewsWise

http://www.newswise.com/articles/researchers-discover-how-promiscuous-parasites-hijack-host-immune-cells

Science Codex

http://www.sciencecodex.com/researchers_discover_how_promiscuous_parasites_hijack_host_immune_cells

MedicalNewsToday

http://www.medicalnewstoday.com/releases/234798.php

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http://newsblaze.com/story/2011092108200300003.wi/topstory.html

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http://www.redorbit.com/news/science/1112386702/researchers-discover-how-promiscuous-parasites-hijack-host-immune-cells

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http://www.newyorkagconnection.com/story-state.php?Id=835&yr=2011

Biocompare

http://news.biocompare.com/News/NewsStory/394349/Researchers-Discover-How-promiscuous-Parasites-Hijack-Host-Immune-Cells.html

Science Newsline

http://www.sciencenewsline.com/biology/2011092117140007.html

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News Medical

http://www.news-medical.net/news/20110922/Cornell-researchers-identify-how-T-gondii-controls-hosts-immune-system.aspx

http://happinessbeyondthought.blogspot.com/2011/09/brain-parasite-in-most-of-us-prompts.html

Viral quality controls could halt herpes’ spread

Sept. 13, 2011

Herpesviruses are thrifty reproducers — they only send off their most infectious progeny to invade new cells. Two Cornell virologists recently have discovered how these viruses determine which progeny to release.

herpes simplex virion

Recently enveloped herpes simplex virion in the perinuclear space of an infected cell.

The College of Veterinary Medicine researchers report in the Aug. 23 (108:34) issue I of the Proceedings of the National Academy of Sciences on the mechanisms of this quality-control system, which helps streamline viral reproduction to optimize its spreading.

The virologists identified proteins in the nuclear membranes of infected cells that control which viral products exit. This map could be used to identify new targets for future drugs that would hamper viral reproduction by clogging inspection pathways to trap viruses in the cells they first infect.

“When a herpesvirus hijacks a cell, it turns the nucleus into a viral production factory,” said Joel Baines, the James Law Professor of Virology, who co-authored the study with postdoctoral research associate Kui Yang. “It makes protein shells called capsids, stuffs them with viral DNA and ships them out of the nuclear membrane to infect new cells. But errors in the assembly line leave some capsids empty, without DNA, and shipping these is a waste of resources.”

When capsids bud from the nuclear membrane, they take pieces of it with them, forming protective lipid envelopes that let them move to new cells. Empty capsids can’t reproduce, so the virus only allows capsids with DNA through. How the membrane could determine whether the capsid had DNA or not was a mystery until Yang and Baines mapped its method.

Joel Baines

Joel Baines

“We found clamplike proteins on the surface of herpesvirus capsids that hold them together and keep them from bursting when they’re stuffed full of DNA,” said Baines. “Those with DNA have far more of these than empty capsids. We also found a protein complex living in the host cell’s nuclear membrane that binds to these structural support proteins, selecting DNA-filled capsids to pull through the membrane. Thus the virus releases only its most infectious particles.”

This streamlining process has helped herpesvirus species spread prevalently and permanently across all animal species. Eight of the 25 known viruses in the herpes family regularly infect humans, posing a leading cause of human viral infection.

Once in a body, herpesvirus stays for life. It can flare up at any time, causing symptoms and diseases, ranging from infected sores to brain inflammation, birth defects and cancers of the nose, throat and lymphatic system. Though usually not fatal, herpes can prove dangerous to patients with weak immune systems, such as those with HIV/AIDS or infants who contract HIV/AIDS from their mothers.

Various species of Herpesvirus

Various species of Herpesvirus

There is no cure for herpes, but Baines’ map illustrates a viral reproduction system that can be subverted.

“Take away either component, the capsid’s clamplike proteins or the membrane’s inspector proteins, and nothing escapes the host cell,” said Baines. “This opens the door to developing drugs that could block the interactions between these protein complexes, covering the binding sites to clog the system so that no viral particles get through. This would significantly slow or even stop the virus’s spread between cells. Our lab is now working on even more detailed maps of these proteins’ exact interaction sites that will help drug developers pinpoint precise targets to thwart viral reproduction.”

The research was supported, in part, by the National Institutes of Health.

Carly Hodes ’10 is a communication specialist at the College of Veterinary Medicine.

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Original press release:

Cornell University College of Veterinary Medicine news
http://www.vet.cornell.edu/news/herpes.cfm

Media hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Sept11/HerpesMap.html

MyScience

http://www.myscience.cc/wire/discovery_could_lead_to_ways_to_halt_spread_of_herpesvirus-2011-cornell

Bionity

http://www.bionity.com/en/news/134351/study-uncovers-how-herpesvirus-spreads.html?WT.mc_id=ca0067

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http://medicalxpress.com/news/2011-09-discovery-ways-herpes.html

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Futurity

http://www.futurity.org/health-medicine/how-to-stop-herpes-from-going-viral/

Herpes Pain Relief

http://www.herpespainrelief.info/4349/cornell-chronicle-study-uncovers-how-herpesvirus-spreads/

Pregnancy paper picked by bio elite

A paper on pregnancy immunology from the lab of Dr. Doug Antczak has been selected by the Faculty of 1000, placing his work in a library of the top two percent of published articles in biology and medicine.

According to its website, the Faculty of 1000 (F1000) identifies and evaluates the most important articles in biology and medical research publications. Articles are selected by a peer-nominated global faculty composed of the world’s leading scientists and clinicians who rate chosen articles and explain their importance.

Antczak’s paper, “Functions of ectopically transplanted invasive horse trophoblast,” (Reproduction 2011 Mar. 9), was selected and evaluated by F1000 member Anthony Michael Carter.

“This paper advances understanding of how invasive trophoblast cells are able to establish endometrial cups in the mare,” wrote Carter in an evaluation describing Antczak’s discovery. Trophoblast cells, which form around embryos, can migrate to the uterus. In pregnant mares, these invading cells form ulcer-like structures in the uterus that produce equine gonadotropin. This hormone serves several functions in pregnancy including protecting the embryo from the mother’s immune system.
“Our work may have practical application in equine practice, for example in the development of new methods to prevent unwanted estrus in competition mares,” said Antczak. “It also has implications for biomedical use in the future, as a way to provide sustained delivery of biologically active molecules or drugs.”

The project’s lead scientist, Dr. Amanda de Mestre, was formerly a post-doctoral fellow in the Antczak lab, and is now a faculty member at the Royal Veterinary College in London. De Mestre’s training included two distinct experiences at Cornell. While still a veterinary student in her native Australia, she spent a summer conducting research in the Antczak lab as a participant in Cornell’s Leadership Program.

F1000’s database provides both a repository for peer-rated high-impact biology articles and a social media forum for serious science. Its community features enable discussions to be built around the selected publications. Additional faculty members may evaluate and rate the article, and subscribers can post comments. Antczak will be able to join the conversation, providing follow-up notes concerning his article and responding to ideas put forth by commenters and evaluators.
“As a post-publication peer review service, we embrace the idea that the impact of your article can deepen and spread in unforeseen ways with community interaction,” wrote Sarah Greene, Editor in Chief of the F1000, in a letter to Antczak announcing his inclusion. “Even your own reckoning of the article may advance toward further conclusions and result in new strategies and collaborations.”

This research is part of a continuing program in equine pregnancy immunology at the Baker Institute for Animal Health that has been supported for many years by the Zweig Memorial Fund, the Dorothy Russell Havemeyer Foundation, and the National Institutes of Health.

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Zweig News Capsule
No. 51, June 2011