Category Archives: Cornell Chronicle

Stories that have been published in the Cornell Chronicle, the news service for the entire university.

Researchers discover what cancer cells need to travel

Feb. 21, 2012

By Carly Hodes

cancer cell

An invasive cancer cell moves with its leading edge.

Cancer cells must prepare for travel before invading new tissues, but new Cornell research has found a possible way to stop these cells from ever hitting the road.

Researchers have identified two key proteins that are needed to get cells moving and have uncovered a new pathway that treatments could block to immobilize mutant cells and keep cancer from spreading, says Richard Cerione, Goldwin Smith Professor of Pharmacology and Chemical Biology at Cornell’s College of Veterinary Medicine.

The study, co-authored by graduate student Lindsey Boroughs, Jared L. Johnson, Ph.D. ‘11, and Marc Antonyak, senior research associate, is published in the Journal of Biological Chemistry (286:37094-37107)

Most adult cells stay stationary, but the ability for some to move helps embryos develop, wounds heal and immune responses mobilize. When migrating cells go astray they can cause developmental disorders, ranging from cardiovascular disease to mental retardation. Metastasis (the spread of cancer from one part of the body to another) also relies on cell migration. How exactly cancer cells migrate
and invade tissues continues to be a mystery. However, Cerione’s lab uncovered a potentially important clue when it noticed that cancer cells gearing up to move would collect a protein called tissue transglutaminase (tTG) into clusters near the cell membrane.

meta“TTG is turning up in many aspects of human cancer research and seems to be contributing to the process that turns cells cancerous,” said Cerione. “Lindsey and Marc discovered that cells must gather tTG into a specific place in their membrane before they can move. But tTG is usually inactive, and we’ve been trying to understand how a cell gets this protein to the exact right place so that it can be activated to stimulate cell migration.”

Observing breast-cancer cells in culture, Cerione’s lab found a missing link in our understanding of cell migration: Cancerous cells become hyperactive invasion vehicles by using tTG together with other proteins like wheels, poking them through the surface to form a “leading edge” that pulls the cell forward. But to get the wheels to the leading edge, it turns out they need another protein to roll them there – a “chaperone” protein called heat-shock-protein-70 (Hsp70).

“We’ve known for years that Hsp70 acts as a chaperone to other proteins, ensuring that they assume the right structure and behave properly when a cell is under stress,” said Cerione. “Heat shock proteins have also been implicated in cancer, although scientists have been trying to understand their exact role in cancer. Our research has uncovered a previously unknown role for these chaperones – helping tTG get to the leading edge. TTG must be in this location for cancer to spread.”

migrating cervical cancer cell

A migrating cervical cancer cell stained for tissue transglutaminase (green). Cells must gather this protein at their leading edge in order to move.

When cells become stressed, Hsp70 influences the behavior of their “client” proteins, ensuring they keep the right shape. Cells need chaperones like Hsp70 to ensure that various proteins work correctly and don’t warp, but these same chaperones can help cancer cells spread by helping move tTG to the membrane surface. Using inhibitors that block the function of chaperones, Cerione and his team paralyzed Hsp70s and stopped breast cancer cells in culture from gathering tTG into a leading edge, effectively immobilizing them.

Exactly how Hsp70 gets tTG going remains unknown, but Cerione believes other proteins are involved.

“If we can better understand how Hsp70 influences tTG, we can figure out ways to modulate that interaction to immobilize cancer cells and keep them from becoming invasive,” said Cerione. “We suspect Hsp70 is using a third kind of protein to move tTG, and that’s what we’re trying to figure out now. Finding the next link in this chain of events could have important consequences for preventing cancer migration and metastasis.”

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/Migration.cfm

Media Hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Feb12/CancerMovers.html

Ithaca Journal

http://www.theithacajournal.com/article/20120222/LIFE/202220336/Cornell-scientists-find-cancer-cells-need-travel?odyssey=mod|newswell|text|Life|s

PhysOrg

http://www.physorg.com/news/2012-02-cancer-cells.html

ECNMag

http://www.ecnmag.com/News/Feeds/2012/02/blogs-the-cutting-edge-researchers-discover-what-cancer-cells-need-to-tra/

Zeit News

http://www.zeitnews.org/biotechnology/researchers-discover-what-cancer-cells-need-to-travel.html

My Science

http://www.myscience.cc/news/2012/what_cancer_cells_need_to_travel-2012-cornell

Reddit

http://www.reddit.com/r/science/comments/q0swt/cancer_cells_must_prepare_for_travel_before/

Laboratory Equipment

http://www.laboratoryequipment.com/news-Proteins-Key-to-Stopping-Cancer-from-Spreading-022312.aspx

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.

—–

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

R&D Mag

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

ECN

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/

Study shows drinking ‘raw’ milk puts farmworkers, babies, and others at higher disease risk

Nov. 8, 2011

By Carly Hodes

Will a fresh glass of “raw” milk nourish or poison you? Pasteurization almost always provides protection from contamination. Unpasteurized “raw” milk, on the other hand, provides a potential breeding ground for disease-causing bacteria such as E. coli, Listeria, Campylobacter and Salmonella, all of which have caused outbreaks spread by raw milk in the past year, said Ynte Schukken, professor of epidemiology and herd health at Cornell’s College of Veterinary Medicine.

researcher Ynte Schukken with dairy cows

Dr. Ynte Schukken, professor of epidemiology and herd health, with livestock.

He has co-authored a paper in the August issue of the Journal of Food Production quantifying the risk of contracting Listeria monocytogenes from raw milk. In collaboration with the U.S. Department of Agriculture’s Agriculture Research Service and the New York State Department of Agriculture and Markets, the four-year project of graduate student Alejandra Latorre produced a comprehensive map showing which populations were most at risk when buying from various sources.

“Listeria is one of the most virulent and deadly foodborne pathogens,” said Schukken. “Our study demonstrates the relative risk various populations face when ingesting raw milk, including farmworkers, pregnant women, young babies and the elderly. Compared to intermediate-aged adults, these last three groups were particularly susceptible.”

The researchers analyzed risk across various purchasing methods including buying from a farm’s on-site store, directly from its bulk tank or from a third-party retailer. “Raw milk from retailers proved most dangerous by far. But when it comes to milk, the safest purchasing decision you can make is to buy it pasteurized,” Schukken said.

Despite its dangers, 28 states permit the sale of raw milk. Enthusiasts claim health benefits from nutritious compounds supposedly destroyed by pasteurization.

“These claims are not backed by scientific evidence, and several studies have shown them to be myths,” said Schukken. “Pasteurization helped revolutionize health, effectively ending diseases such as tuberculosis and Q fever. Bypassing this safety measure could have serious consequences for public health, dramatically increasing bacterial infection and outbreaks.”

Other tips to minimize risk, says Schukken: “Make sure the farm is a legal raw milk farm participating in a testing program. Only buy what you can finish in a week, keep it cold in your fridge, and use it quickly.”

—–

Media Hits:

Cornell Chronicle

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

Medical Xpress (PhysOrg)

http://medicalxpress.com/news/2011-11-raw-poses-groups.html

MyScience

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

Minnesota Ag Connection

http://www.minnesotaagconnection.com/story-national.php?Id=2396&yr=2011

UPI

http://www.upi.com/Health_News/2011/11/19/Raw-milk-puts-babies-farm-workers-at-risk/UPI-75531321743525/?spt=hs&or=hn

Western Farm Press

http://westernfarmpress.com/management/running-risks-raw-milk-food-safety-blunder

Real Raw Milk Facts

http://www.realrawmilkfacts.com/raw-milk-news/story/cornell-drinking-raw-milk-puts-farmworkers-babies-and-others-at-higher-dise/

Public Opinion Online

http://www.publicopiniononline.com/living/ci_19445503

Bites

http://bites.ksu.edu/news/151355/11/11/09/us-running-risks-raw-milk-food-safety-blunder

Southwest Farm Press

http://southwestfarmpress.com/livestock/running-risks-raw-milk-food-safety-blunder

Oct. 26, 2011

By Carly Hodes

maned wolf

The maned wolf, native to southeast South America, a near-threatened species, is one of the kinds of animals that students in the new Cornell-Smithsonian joint graduate program may address as they learn to become wildlife conservation scientists.

At a time when extinction threatens nearly one-quarter of all known vertebrate species, Cornell and the Smithsonian Conservation Biology Institute (SCBI) have teamed up to offer a new shared doctoral program that will train the next generation of wildlife conservation scientists.

The Cornell-Smithsonian Joint Graduate Training Program (JGTP) began accepting applications this month to train students who will leverage basic research at Cornell with conservation initiatives pioneered by one of the nation’s pre-eminent wildlife research institutes. Using the facilities, resources and expertise at both institutions, students will learn to become independent investigators equipped to study and preserve some of the rarest species on the planet.

“We are in the midst of Earth’s sixth mass extinction, and this crisis is manmade,” said Alex Travis, director of the Cornell Center for Wildlife Conservation, who helped organize the program. “Although we must continue to take every effort to preserve natural ecosystems, numbers of more and more species have dropped so low that they require focused conservation efforts. We want to train top students in a setting in which they will be able to apply basic scientific approaches and cutting-edge techniques to the preservation of biodiversity. The knowledge these collaborations generate will then help solve real conservation problems around the world.”

Students in the five-year program benefit from the dual mentorship of a Cornell faculty member and an SCBI staff scientist. Collaborative research projects will utilize resources in Ithaca and SCBI campuses (in Front Royal, Va., and Washington, D.C.), allowing students the opportunity to work with advanced biomedical facilities at Cornell and endangered species populations such as cheetahs, clouded leopards, cranes and oryx at SCBI.

Jen Nagashima

Jennifer Nagashima, the first student admitted in the Cornell-Smithsonian Joint Graduate Training Program during last year's pilot phase, studies canine reproduction.

Jennifer Nagashima, the first JGTP student admitted during last year’s pilot phase, for example, works on canine reproduction. She studies aspects of female reproduction at SCBI, where she works on in-vitro egg maturation and fertility synchronization. In the Travis lab, she is learning new technologies to preserve genetic resources of male animals using spermatogonial stem cells. She’s also synthesizing both lines of training in studies on assisted reproduction techniques such as in-vitro fertilization and embryo transfer. She has rounded out her studies by delving into how hormones control the canine reproductive cycle with Ned Place, a reproductive endocrinologist at Cornell.

“These topics are highly complementary, and Jennifer’s study benefits tremendously from her work in these three labs,” said Travis. “Bringing these skills together could help manage captive populations of endangered canids such as the African wild hog and South America’s maned wolf. Interestingly, these same approaches could help dog breeders filter diseases out of domestic populations while also helping humans. There are over 400 human diseases having similarity to diseases in dogs. Identifying genetic causes of disease can then benefit everyone.”

Carly Hodes is a writer 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/doctoralprogram.cfm

 

Media hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Oct11/SmithsonianVet.html

US Ag Net

http://www.usagnet.com/state_headlines/state_story.php?tble=NY2011&ID=994

News from Planet Earth

http://www.newsfromplanetearth.com/60749/cornell-smithsonian-to-train-new-generation-of-wildlife-scientists/

High Beam Research

http://www.highbeam.com/doc/1G1-270907727.html

Media Newswire

http://media-newswire.com/release_1161547.html

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

TopNews.in

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

NewsBlaze

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

RedOrbit

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

New York Ag

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

Sify News

http://www.sify.com/news/promiscuous-parasites-can-make-you-reckless-news-international-ljwpuqjjiei.html

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.

—–

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

MedicalXPress (PhysOrg)

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

Electronic Component News

http://www.ecnmag.com/News/Feeds/2011/09/blogs-the-cutting-edge-discovery-could-lead-ways-to-prevent-herpes-spread/

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/

Simple physics predicts how guts grow

Growing embryos face a tight squeeze when it’s time to pack internal organs. A new study published in Nature Aug. 4 shows how simple mechanical forces between neighboring types of tissue help organs take shape and grow.

gut

The looped shape of an intact gut tube with its anchoring dorsal mesentery. Separation of the dorsal mesentery causes the gut tube to untangle and form a straight tube, as seen in the surrounding tube.

The work is among the first to uncover how an embryo develops from groups of cells into distinctly shaped organs. Though the research largely focuses on the mid-gut in chicken embryos, the findings are relevant to other vertebrates and the formation of other organs, including the heart. Such insights into how organs form could aid efforts to diagnose and prevent birth defects and diseases.

The research reveals how a vertebrate digestive system — a tube up to five times longer than the frame housing it — fits inside the body by packing itself into an organized bundle of intestinal coils. This formation, the researchers report, hinges on the growth of the dorsal mesentery, a bridge of artery-packed tissue anchoring the gut tube.

Natasza Kurpios

Dr. Natasza Kurpios

“Until now the dorsal mesentery seemed to offer only structural support; no one talked about its possible functions,” said developmental biologist Natasza Kurpios, assistant professor of molecular medicine at Cornell’s College of Veterinary Medicine and a first author with Thierry Savin and Amy Shyer of Harvard, where Kurpios conducted the study before she came to Cornell in 2009. “In adults, it’s a thin piece of tissue suspending the intestines and guiding arteries to them. But in embryos, we found that its properties aid construction by pulling back the gut and forcing it to loop.”

Using tiny surgical scissors Kurpios separated the looping gut tube from the dorsal mesentery.

“The gut instantaneously un-looped into a straight tube and the mesentery contracted like a relaxed rubber band,” said Kurpios. “Clearly the mesentery was under tension and the gut-mesentery connection had exerted tension on both that affected each other’s shape. We measured the organs’ growth rates throughout development and found that the gut tube grows far faster than the mesentery: nearly four-fold in chickens. The gut wants to grow, the slower mesentery holds it back, so the gut loops.”

At Harvard, Savin built a simple physical model using a latex sheet (to act as the mesentery) stitched to a rubber tube (to act as the intestine) to mimic the mechanical forces that create the gut looping. Experimenting with different physical properties in the two materials, Savin and colleagues developed a formula predicting the looping patterns based on the thickness and elasticity of the latex and the radius of the rubber tube.

Kurpios and her colleagues then applied the model to animals, finding that in chickens, quail, zebra finches and mice the model predicted the patterns and properties correctly. “We’ve found a simple physical explanation for what had seemed like a complex biological mystery,” Kurpios said.

By uncovering the basic mechanisms for how organs form, researchers may now begin to understand such developmental deformations as intestinal malrotation — which may cause knotting of tissue that blocks circulation — a birth defect in one in 500 newborns that can lead to death.

With the help of a newly funded grant from the March of Dimes, Kurpios says her Cornell lab is completing new research that identifies a hierarchy of specific genes responsible for gut development. “People have not understood how you can go from groups of cells to the actual shape of organs,” she said. “We are now uncovering that link.”

Dr. Natasza Kurpios

Dr. Natasza Kurpios

Other co-authors include Clifford Tabin and L. Mahadevan, both at Harvard. The research was funded by the National Science Foundation, National Institutes of Health and the MacArthur Foundation.

Carly Hodes is a writer at Cornell’s College of Veterinary Medicine.

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Original press release:

Cornell University College of Veterinary Medicine news

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

Media hits:

Cornell Chronicle

http://www.news.cornell.edu/stories/Aug11/GutForm.html

R&D Mag

http://www.rdmag.com/News/Feeds/2011/08/general-sciences-study-ids-mechanism-for-how-gut-forms-and-grows/

My Science

http://www.myscience.us/news/simple_physics_predicts_how_the_gut_forms-2011-cornell

Redorbit

http://www.redorbit.com/news/health/2093116/groundbreaking_research_reveals_clues_to_the_formation_of_hearts_intestines/

EurekAlert

http://www.eurekalert.org/pub_releases/2011-08/cu-grr080911.php

Newswise

http://www.newswise.com/articles/view/579309/?sc=rssn

Futurity

http://www.futurity.org/health-medicine/how-gut-grows-is-simple-physics/