Players divided regarding Dolphins' Martin

Miami Dolphins coach Joe Philbin talks to the media during a news conference after practice at the Dolphins training center in Davie, Fla., Wednesday, Nov. 6, 2013. NFL officials launched an investigation to try and determine who knew what and when about the troubled relationship between offensive lineman Richie Incognito and Jonathan Martin. (AP Photo/J Pat Carter)

Miami Dolphins coach Joe Philbin talks to the media during a news conference after practice at the Dolphins training center in Davie, Fla., Wednesday, Nov. 6, 2013. NFL officials launched an investigation to try and determine who knew what and when about the troubled relationship between offensive lineman Richie Incognito and Jonathan Martin. (AP Photo/J Pat Carter)

Miami Dolphins general manager Jeff Ireland, left, stands with head trainer Kevin O'Neill, right, during the NFL football team's practice Wednesday, Nov. 6, 2013, in Davie, Fla. (AP Photo/Lynne Sladky)

DAVIE, Fla. (AP) — In a culture that fosters conflict, Jonathan Martin sought to avoid it.

Upset by treatment he considered abusive, the Miami Dolphins tackle let the situation fester for months before leaving the team last week. Martin's agent then complained to the Dolphins, who suspended guard Richie Incognito.

The NFL is investigating whether Incognito harassed or bullied Martin, and whether their teammates and the organization mishandled the matter.

Some say Martin, a Stanford graduate who went about his business quietly, handled the situation well. But pro football is a macho world, and some players believe Martin should have responded more firmly.

"Is Incognito wrong? Absolutely. He's 100 percent wrong," New York Giants safety Antrel Rolle said. "No individual should have to go through that, especially in their workplace.

"But at the same time, Jonathan Martin is a 6-4, 320-pound man. I mean, at some point and time you need to stand your ground as an individual. Am I saying go attack, go fight him? No. I think we all understand we can stand our ground without anything being physical."

Dolphins players have robustly defended Incognito, long considered among the NFL's dirtiest players. He's now a notorious national villain, but teammates praise his leadership and loyalty.

They've been less passionate in their support of Martin, saying he and Incognito behaved like best friends.

"They did a lot of stuff together," tackle Tyson Clabo said. "So if he had a problem with the way he was treating him, he had a funny way of showing it."

Martin is with his family in California to undergo counseling for emotional issues.

A senior partner in a New York law firm was appointed by NFL Commissioner Roger Goodell to investigate possible misconduct and prepare a report. DeMaurice Smith, executive director of the NFL Players Association, said Thursday that he continues to be in touch with those involved.

"The NFLPA has taken steps to ensure that every one of our affected members is represented," Smith said in a statement. "It is our duty as a union to learn the full facts, protect the interests of players involved and hold management accountable to the highest standards of fairness and transparency."

The alleged bullying saga engulfing the Dolphins has shed a light on how damaging perceptions can be in the violent world of the NFL.

A Pittsburgh native, Martin is the son of Harvard graduates and his great grandfather also graduated from the school in 1924. At Stanford he protected Andrew Luck's blind side, and also majored in the classics.

Taken in the second round of the 2012 draft, Martin has what it takes physically to be an NFL player — size, skill, athleticism, intelligence. He won praise from the Dolphins for his diligent study of game and practice video.

But while has been a starter since the first game of his rookie season, Martin developed a reputation in the NFL for lacking toughness. That impression might have been reinforced by the way he handled his issues with Incognito, current and former teammates acknowledge.

"A lot of people might look at Jonathan Martin and think that he's soft because he stepped away from the game, and say, 'Why don't you just fight him?'" said Seattle Seahawks receiver Doug Baldwin, who played with Martin at Stanford. "Well, if you look at it with common sense and being logical, what options did Jonathan Martin have?

"He could fight Richie Incognito. He could go and tell on the players, which we know in the football locker room doesn't go over too well. Or he could remove himself from the situation and let the proper channels take care of itself. And I think he made the intelligent, smart choice without putting himself or Richie Incognito's physical abilities in danger."

Houston Texans Antonio Smith, who has accused Incognito of dirty play since they went against each other in college, said Martin should have responded more forcefully. Smith drew a three-game suspension this year for taking Incognito's helmet and hitting him during an exhibition game.

"I don't think that in my opinion a grown man should get bullied," Smith said. "And I think that if you're realistically getting bullied, there's only one way my mom taught me and my dad taught me how to get rid of bullies. They used to always say, 'You hit a bully in the mouth. It will stop him from bullying, no matter what you hit him with.'"

Incognito's harassment of Martin included text messages that were racist and threatening, two people familiar with the situation have told The Associated Press. Incognito is white, while Martin is biracial.

Two other people familiar with the situation have said Martin talked of quitting football earlier in his pro career before leaving the Dolphins. One person said Martin considered giving up the sport because of the way he was being treated by other offensive linemen on the team. The person added that Martin now wants to continue his football career.

The Dolphins (4-4) play for the first time since the scandal broke Monday night at Tampa Bay (0-8). At least 75 reporters and cameramen tracking the case were in the locker room after Thursday's practice, but receiver Brian Hartline said the scrutiny won't prevent the team from playing well.

"It almost heightens your awareness," he said. "You know it's going to take away from your focus, so it does the exact opposite. You overcompensate to make sure you stay aware of the game."

___

AP Sports Writers Tim Booth in Seattle, Tom Canavan in East Rutherford, N.J., and Kristie Rieken in Houston contributed to this report.

___

AP NFL website: www.pro32.ap.org and http://twitter.com/AP_NFL

___

Follow Steven Wine on Twitter: http://twitter.com/Steve_Wine

Associated PressSource: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2013-11-07-Dolphins%20Turmoil/id-1db19734992a47d5bc21cfd48b7db198
Category: calvin johnson   Benedict Cumberbatch   adam levine   Liam Payne   North West  

1 worm, 2 mouths

PUBLIC RELEASE DATE:

7-Nov-2013

[


| E-mail

]


Share

Contact: Erik Ragsdale
erik.ragsdale@tuebingen.mpg.de
49-070-716-01496
Max-Planck-Gesellschaft

A devious evolutionary path between genetics and environment

Depending on the environment in which the worm grows, the larva of the roundworm Pristionchus pacificus develops into either a wide-mouthed predator or a narrow-mouthed bacteria eater. A team of researchers at the Max Planck Institute for Evolutionary Biology in Tbingen, Germany, headed by Ralf J. Sommer have now discovered a developmental biological switch that determines the worm's mouth form. According to this, the scientists are now able to explain how organisms adapt to different surrounding conditions.

When it comes to survival, flexibility is a trump card. This principle also applies to the microscopic roundworm Pristionchus pacificus, which is being researched by scientists at the Max Planck Institute for Developmental Biology in a study headed by Ralf Sommer. Depending on the environment in which Pristionchus grows, it develops either a short wide mouth or a long narrow one. The wide-mouthed variant, which has a single, characteristic tooth, is suitable for carrying out predatory attacks. The narrow version, in contrast, is mainly used for grazing on bacterial food sources. The developmental path taken by a Pristionchus larva is not decided by its genes but by the environment. When the animals were starved or when too many worms crowded the Petri dish, the researchers observed the increased development of the wide-mouthed variant.

Erik Ragsdale, Manuela Mller, Christian Rdelsperger and Ralf Sommer have now discovered a crucial interface between the worm's environment and its developmental genes. The Tbingen-based scientists found a gene which functions like a switch and selects the suitable variant from the two possible mouth forms.

The discovery of this gene was the crowning success of a genetic experiment, to which roundworms are particularly suited due to their short generation time. Ragsdale and Mller discovered mutated worm lines which only produce worms with narrow mouths, irrespective of the environmental conditions, and in which the same gene, eud-1, is inactivated. "We were able to show that a gene that we found in a genetic experiment under laboratory conditions controls an ecologically significant characteristic," comments Max Planck Director Sommer, explaining the special significance of this discovery.

eud-1 is the gene for a sulfatase. Sulfatases are enzymes that chemically alter other proteins or molecules. The scientists in Tbingen do not yet know precisely which molecules are the targets of this special sulfatase. They presume, however, that eud-1 influences the characteristics of hormonal messenger substances. This would fit with their observation that eud-1 is mainly active in the worm's neurons where important messenger substances are produced.

Armed with the information about the eud-1 mutants, Ragsdale and his colleagues crosschecked their findings and introduced additional copies of the eud-1 gene into Pristionchus worms using genetic engineering tricks. Almost all of these transgenic worms developed the wide mouth form with the characteristic tooth.

eud-1 thus works like a train dispatcher at a large railway station who decides which platform a high-speed train can pull into based on the current traffic situation. During a critical phase in the worm's development, it follows the one-way track to a "wide mouth" or "narrow mouth".

The capacity of many organisms to tailor their development to the changing demands of the environment is known as "phenotypic plasticity". The discovery of the des eud-1 gene is important because the molecular-genetic mechanisms that facilitate this plasticity in the animals have been largely unknown up to now.

"Phenotypic plasticity is often referred to as an explanation for evolutionary adaptations to different environmental conditions. We provide an example of a genetic mechanism that enables such evolutionary bifurcations," says Sommer.

Exactly how the environment and genes interact is a controversial topic among evolutionary biologists in certain respects. It is clear that the environment selects between genetically different variants this is Darwin's natural selection. However, researchers like American biologist Mary-Jane West-Eberhard claim that the environment can also directly influence the emergence of new phylogenetic characteristics.

In the case of a "plastic" characteristic like the shape of the mouth aperture, external circumstances determine whether it presents in one form or another. West-Eberhard and other scientists suspect that a characteristic determined by the environment in this way can then become permanently defined at genetic level. Speciation or the division of species could even arise in this manner. However, this is little more than a controversial theory, for which hardly anything by way of experimental proof could be provided to date.

With the discovery of the switch gene eud-1, the Max Planck scientists in Tbingen have identified a genetic mechanism that fits well with this hypothesis. Hence, complex evolutionary models with plasticity and environmental influences as driving forces may perhaps be more than controversial musings.

###

Original publication

Erik J. Ragsdale, Manuela R. Mller, Christian Rdelsperger, Ralf J. Sommer

A Genetic Switch Coupled to Micro- and Macroevolution of a Developmental Plasticity Acts Through a Sulfatase
Cell, 7 November 2013

---

[


| E-mail


Share

]

 

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

PUBLIC RELEASE DATE:

7-Nov-2013

[


| E-mail

]


Share

Contact: Erik Ragsdale
erik.ragsdale@tuebingen.mpg.de
49-070-716-01496
Max-Planck-Gesellschaft

A devious evolutionary path between genetics and environment

Depending on the environment in which the worm grows, the larva of the roundworm Pristionchus pacificus develops into either a wide-mouthed predator or a narrow-mouthed bacteria eater. A team of researchers at the Max Planck Institute for Evolutionary Biology in Tbingen, Germany, headed by Ralf J. Sommer have now discovered a developmental biological switch that determines the worm's mouth form. According to this, the scientists are now able to explain how organisms adapt to different surrounding conditions.

When it comes to survival, flexibility is a trump card. This principle also applies to the microscopic roundworm Pristionchus pacificus, which is being researched by scientists at the Max Planck Institute for Developmental Biology in a study headed by Ralf Sommer. Depending on the environment in which Pristionchus grows, it develops either a short wide mouth or a long narrow one. The wide-mouthed variant, which has a single, characteristic tooth, is suitable for carrying out predatory attacks. The narrow version, in contrast, is mainly used for grazing on bacterial food sources. The developmental path taken by a Pristionchus larva is not decided by its genes but by the environment. When the animals were starved or when too many worms crowded the Petri dish, the researchers observed the increased development of the wide-mouthed variant.

Erik Ragsdale, Manuela Mller, Christian Rdelsperger and Ralf Sommer have now discovered a crucial interface between the worm's environment and its developmental genes. The Tbingen-based scientists found a gene which functions like a switch and selects the suitable variant from the two possible mouth forms.

The discovery of this gene was the crowning success of a genetic experiment, to which roundworms are particularly suited due to their short generation time. Ragsdale and Mller discovered mutated worm lines which only produce worms with narrow mouths, irrespective of the environmental conditions, and in which the same gene, eud-1, is inactivated. "We were able to show that a gene that we found in a genetic experiment under laboratory conditions controls an ecologically significant characteristic," comments Max Planck Director Sommer, explaining the special significance of this discovery.

eud-1 is the gene for a sulfatase. Sulfatases are enzymes that chemically alter other proteins or molecules. The scientists in Tbingen do not yet know precisely which molecules are the targets of this special sulfatase. They presume, however, that eud-1 influences the characteristics of hormonal messenger substances. This would fit with their observation that eud-1 is mainly active in the worm's neurons where important messenger substances are produced.

Armed with the information about the eud-1 mutants, Ragsdale and his colleagues crosschecked their findings and introduced additional copies of the eud-1 gene into Pristionchus worms using genetic engineering tricks. Almost all of these transgenic worms developed the wide mouth form with the characteristic tooth.

eud-1 thus works like a train dispatcher at a large railway station who decides which platform a high-speed train can pull into based on the current traffic situation. During a critical phase in the worm's development, it follows the one-way track to a "wide mouth" or "narrow mouth".

The capacity of many organisms to tailor their development to the changing demands of the environment is known as "phenotypic plasticity". The discovery of the des eud-1 gene is important because the molecular-genetic mechanisms that facilitate this plasticity in the animals have been largely unknown up to now.

"Phenotypic plasticity is often referred to as an explanation for evolutionary adaptations to different environmental conditions. We provide an example of a genetic mechanism that enables such evolutionary bifurcations," says Sommer.

Exactly how the environment and genes interact is a controversial topic among evolutionary biologists in certain respects. It is clear that the environment selects between genetically different variants this is Darwin's natural selection. However, researchers like American biologist Mary-Jane West-Eberhard claim that the environment can also directly influence the emergence of new phylogenetic characteristics.

In the case of a "plastic" characteristic like the shape of the mouth aperture, external circumstances determine whether it presents in one form or another. West-Eberhard and other scientists suspect that a characteristic determined by the environment in this way can then become permanently defined at genetic level. Speciation or the division of species could even arise in this manner. However, this is little more than a controversial theory, for which hardly anything by way of experimental proof could be provided to date.

With the discovery of the switch gene eud-1, the Max Planck scientists in Tbingen have identified a genetic mechanism that fits well with this hypothesis. Hence, complex evolutionary models with plasticity and environmental influences as driving forces may perhaps be more than controversial musings.

###

Original publication

Erik J. Ragsdale, Manuela R. Mller, Christian Rdelsperger, Ralf J. Sommer

A Genetic Switch Coupled to Micro- and Macroevolution of a Developmental Plasticity Acts Through a Sulfatase
Cell, 7 November 2013

---

[


| E-mail


Share

]

 

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-11/m-owt110713.php
Category: Real Madrid   Harry Styles  

Thousands flee before big typhoon hits Philippines

MANILA, Philippines (AP) — Thousands of people evacuated villages in the central Philippines on Thursday before one of the year's strongest typhoons strikes the region, including a province devastated by an earthquake last month.

Typhoon Haiyan intensified and accelerated as it moved closer to the country with sustained winds of 225 kilometers (140 miles) per hour and ferocious gusts of 260 kph (162 mph). It could further strengthen and pick up speed as it moves over the Pacific Ocean before slamming into the eastern province of Samar early Friday, government forecaster Buddy Javier said.

As of 9 p.m., the eye of the typhoon was 338 kilometers (211 miles) southeast of Eastern Samar province's Guiuan township. The storm was moving at 39 kph (24 mph), up from its earlier speed of 33 kph (20 mph).

The storm was not expected to directly hit Manila further north. The lowest alert in a four-level typhoon warning system was issued in the flood-prone capital area, meaning it could experience winds of up to 60 kph (37 mph) and rain.

The U.S. Navy's Joint Typhoon Warning Center in Hawaii said it was the strongest tropical cyclone in the world this year. Cyclone Phailin, which hit eastern India on Oct. 12, packed sustained winds of up to 222 kph (138 mph) and stronger gusts.

President Benigno Aquino III warned people to leave high-risk areas, including 100 coastal communities where forecasters said the storm surge could reach up to 7 meters (23 feet). He urged seafarers to stay in port.

Aquino also assured the public of war-like preparations: three C-130 air force cargo planes and 32 military helicopters and planes on standby, along with 20 navy ships.

"No typhoon can bring Filipinos to their knees if we'll be united," he said in a televised address.

Governors and mayors supervised the evacuation of landslide- and flood-prone communities in several provinces where the typhoon is expected to pass, said Eduardo del Rosario, head of the government's main disaster-response agency. School classes and plane flights were canceled in many areas.

Aquino ordered officials to aim for zero casualties, a goal often not met in an archipelago lashed by about 20 tropical storms each year, most of them deadly and destructive. Haiyan is the 24th such storm to hit the Philippines this year.

Edgardo Chatto, governor of Bohol island province in the central Philippines, where an earthquake in October killed more than 200 people, said soldiers, police and rescue units were helping displaced residents, including thousands staying in small tents, move to shelters. Bohol is not forecast to receive a direct hit but is expected to be battered by strong winds and rain, government forecaster Jori Loiz said.

"My worst fear is that the eye of this typhoon will hit us. I hope we will be spared," Chatto told The Associated Press by telephone.

Gov. Roger Mercado of landslide-prone Southern Leyte province said more than 6,000 residents had been evacuated to shelters, government and emergency personnel had been put on alert, and relief goods have been packed for distribution.

"All we are doing now is we are praying, praying hard," he told ABS-CBN News Channel.

Mayor Emiliana Villacarillo of Eastern Samar's Dolores township said residents of her town did not want to be evacuated because the weather was fine on Thursday but "we forced them and hauled them to evacuation centers."

Haiyan is forecast to barrel through the country's central region Friday and Saturday before blowing toward the South China Sea over the weekend, heading toward Vietnam.

___

Associated Press writers Oliver Teves and Teresa Cerojano contributed to this report.

• Natural Phenomena
• Nature & Environment
• Philippines

Source: http://news.yahoo.com/thousands-flee-big-typhoon-hits-philippines-114623838.html
Similar Articles: Halloween pictures   daylight savings time   Jordan Linn Graham   What Is Labor Day   neil armstrong  

Apple fixes Gmail bug in latest Mail update for Mavericks (update: and MacBook Pro issues too)

Mavericks may have brought a number of notable improvements to OS X, but Gmail integration was certainly not one of them. Users of Google's email service might've encountered an unpleasant surprise when they upgraded their operating systems to Apple's latest, as the changes to Apple Mail appeared to be incompatible with how Gmail worked. For background, Gmail apparently has a rather unorthodox method of using IMAP, so you needed to set up a roundabout method that prevents Mail from downloading every single message from Gmail twice (Basically, you had to tweak your Gmail settings so that "All Mail" is hidden from email programs).

Mavericks, however, broke that workaround, so users of both Gmail and Apple Mail ended up suffering from bloated inboxes. There were other issues too, like the inability to organize mailboxes and unread message numbers that are totally off. Thankfully, however, Apple has just released an update that fixes all that. The release states that it "fixes an issue that prevents deleting, moving, and archiving messages for users with custom Gmail settings" and "addresses an issue that may cause unread counts to be inaccurate." So for those who've bitten the Mavericks bug and want a Mail app that plays nicer with Google's email, you should definitely hit that update button right about now.

Update: Also, remember that keyboard and trackpad glitch on the 13" MacBook Pro? Well, Apple's apparently fixed that in an update as well. Get to downloading, everyone!

Source: http://www.engadget.com/2013/11/07/apple-fixes-gmail-bug-in-mail-mavericks/?ncid=rss_truncated
Similar Articles: National Cat Day   GTA 5 review   apple stock   djokovic   Lady Gaga Vma  

UT Southwestern researchers identify how body clock affects inflammation

PUBLIC RELEASE DATE:

7-Nov-2013

[


| E-mail

]


Share

Contact: Deborah Wormser
deborah.wormser@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center

DALLAS Nov. 7, 2013 UT Southwestern Medical Center researchers report that disrupting the light-dark cycle of mice increased their susceptibility to inflammatory disease, indicating that the production of a key immune cell is controlled by the body's circadian clock.

The study published in the Nov. 8 edition of Science identifies a previously hidden pathway by which the body's circadian clock controls the numbers of key inflammatory cells called interleukin-17-producing CD4+ T helper cells (T_H17). The work could lead to new ways to rev up the body's immune response to infection or dampen that response in the case of autoimmune diseases in which the body attacks its own tissues, said senior author Dr. Lora Hooper, Professor of Immunology and Microbiology and a Howard Hughes Medical Institute (HHMI) Investigator.

Co-authors include Neuroscience Chair and HHMI Investigator Dr. Joseph Takahashi, whose discovery of the mouse and human clock genes led to a description of a conserved circadian clock mechanism in animals. The lead author is Xiaofei Yu, an Immunology student in the UT Southwestern Graduate School of Biomedical Sciences.

"Virtually all life forms on Earth undergo physiological and behavioral changes on a 24-hour daily, or circadian, cycle in accordance with the changes in natural light. Human beings are no exception. Many of our physiological processes, such as eating and sleeping, vary dramatically between day and night. Such processes are controlled by a group of proteins, collectively termed the 'circadian clock,' which function together in individual cells, capturing light cues from the visual and nervous systems and using these cues to regulate gene expression," explained Dr. Hooper, who holds appointments in the Center for the Genetics of Host Defense and the Cancer Immunobiology Center.

Although the circadian clock is known to regulate metabolism and sleep-wake cycles, little was known about whether the circadian clock also regulates the immune system, the body's defense against infectious viruses and bacteria, she said.

Using a mouse model, the researchers identified a gene called Nfil3, which guides the development of the T_H17 cells that patrol mucosal surfaces like the intestinal lining and protect against bacterial and fungal infections.

"However, if their numbers are not controlled properly, T_H17 cells can produce too much friendly fire and lead to inflammatory diseases such as inflammatory bowel disease (IBD), which afflicts about 600,000 Americans each year," Dr. Hooper said.

"We found that Nfil3 regulates T_H17 development by controlling the cellular supply of a protein in T cells called Rorγt that directs the cells to develop into T_H17 cells. In mice, the amount of Rorγt in T cells changes during the day-night cycle and is higher at noon than at midnight. This fluctuation causes more T_H17 cells to develop at noon when the mice are sleeping," she said.

Mice are nocturnal, meaning their sleep-wake times are the opposite of those in humans.

"When we disrupted the normal day-night light cycles of mice, essentially giving them jet lag, we found that too many T_H17 cells developed and accumulated in the intestines. As a result, these mice were more prone to develop an IBD-like disease, due to friendly fire from the overabundance of those inflammatory T_H17 cells," she said, adding that it took more than a single day's disruption to change the T_H17 concentrations.

Dr. Hooper stressed that it is too soon to tell if the same thing is happening in people, but the possibility is worth studying.

The researchers point out that modern life often involves chronic circadian disruptions, such as night-shift work or jet lag, that other research studies have linked to human inflammatory disease.

"Our findings suggest that the pathologic consequences of circadian disruption may be due in part to direct interactions between the circadian clock and the pathways that regulate proinflammatory immune cell development," the researchers conclude.

###

Others UT Southwestern researchers involved include Dr. Carla Green, Professor of Neuroscience, and Jeremy Stubblefield, a Neuroscience student in the UT Southwestern Graduate School of Biomedical Sciences. Funding was provided by the National Institutes of Health, the Burroughs Wellcome Foundation, and the Howard Hughes Medical Institute.

About UT Southwestern Medical Center

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including five who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 90,000 hospitalized patients and oversee more than 1.9 million outpatient visits a year.

This news release is available on our home page at utsouthwestern.edu/home/news/index.html

To automatically receive news releases from UT Southwestern via email, subscribe at utsouthwestern.edu/receivenews

---

[


| E-mail


Share

]

 

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

PUBLIC RELEASE DATE:

7-Nov-2013

[


| E-mail

]


Share

Contact: Deborah Wormser
deborah.wormser@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center

DALLAS Nov. 7, 2013 UT Southwestern Medical Center researchers report that disrupting the light-dark cycle of mice increased their susceptibility to inflammatory disease, indicating that the production of a key immune cell is controlled by the body's circadian clock.

The study published in the Nov. 8 edition of Science identifies a previously hidden pathway by which the body's circadian clock controls the numbers of key inflammatory cells called interleukin-17-producing CD4+ T helper cells (T_H17). The work could lead to new ways to rev up the body's immune response to infection or dampen that response in the case of autoimmune diseases in which the body attacks its own tissues, said senior author Dr. Lora Hooper, Professor of Immunology and Microbiology and a Howard Hughes Medical Institute (HHMI) Investigator.

Co-authors include Neuroscience Chair and HHMI Investigator Dr. Joseph Takahashi, whose discovery of the mouse and human clock genes led to a description of a conserved circadian clock mechanism in animals. The lead author is Xiaofei Yu, an Immunology student in the UT Southwestern Graduate School of Biomedical Sciences.

"Virtually all life forms on Earth undergo physiological and behavioral changes on a 24-hour daily, or circadian, cycle in accordance with the changes in natural light. Human beings are no exception. Many of our physiological processes, such as eating and sleeping, vary dramatically between day and night. Such processes are controlled by a group of proteins, collectively termed the 'circadian clock,' which function together in individual cells, capturing light cues from the visual and nervous systems and using these cues to regulate gene expression," explained Dr. Hooper, who holds appointments in the Center for the Genetics of Host Defense and the Cancer Immunobiology Center.

Although the circadian clock is known to regulate metabolism and sleep-wake cycles, little was known about whether the circadian clock also regulates the immune system, the body's defense against infectious viruses and bacteria, she said.

Using a mouse model, the researchers identified a gene called Nfil3, which guides the development of the T_H17 cells that patrol mucosal surfaces like the intestinal lining and protect against bacterial and fungal infections.

"However, if their numbers are not controlled properly, T_H17 cells can produce too much friendly fire and lead to inflammatory diseases such as inflammatory bowel disease (IBD), which afflicts about 600,000 Americans each year," Dr. Hooper said.

"We found that Nfil3 regulates T_H17 development by controlling the cellular supply of a protein in T cells called Rorγt that directs the cells to develop into T_H17 cells. In mice, the amount of Rorγt in T cells changes during the day-night cycle and is higher at noon than at midnight. This fluctuation causes more T_H17 cells to develop at noon when the mice are sleeping," she said.

Mice are nocturnal, meaning their sleep-wake times are the opposite of those in humans.

"When we disrupted the normal day-night light cycles of mice, essentially giving them jet lag, we found that too many T_H17 cells developed and accumulated in the intestines. As a result, these mice were more prone to develop an IBD-like disease, due to friendly fire from the overabundance of those inflammatory T_H17 cells," she said, adding that it took more than a single day's disruption to change the T_H17 concentrations.

Dr. Hooper stressed that it is too soon to tell if the same thing is happening in people, but the possibility is worth studying.

The researchers point out that modern life often involves chronic circadian disruptions, such as night-shift work or jet lag, that other research studies have linked to human inflammatory disease.

"Our findings suggest that the pathologic consequences of circadian disruption may be due in part to direct interactions between the circadian clock and the pathways that regulate proinflammatory immune cell development," the researchers conclude.

###

Others UT Southwestern researchers involved include Dr. Carla Green, Professor of Neuroscience, and Jeremy Stubblefield, a Neuroscience student in the UT Southwestern Graduate School of Biomedical Sciences. Funding was provided by the National Institutes of Health, the Burroughs Wellcome Foundation, and the Howard Hughes Medical Institute.

About UT Southwestern Medical Center

UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution's faculty includes many distinguished members, including five who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 90,000 hospitalized patients and oversee more than 1.9 million outpatient visits a year.

This news release is available on our home page at utsouthwestern.edu/home/news/index.html

To automatically receive news releases from UT Southwestern via email, subscribe at utsouthwestern.edu/receivenews

---

[


| E-mail


Share

]

 

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-11/usmc-usr110713.php
Related Topics: Halloween pictures   Rebel Wilson   NBA 2K14   green bay packers   Dustin Keller  

Virginia Is for Losers

Why did Ken Cuccinelli lose? Depends on who you ask.

Photo by Jonathan Ernst/Reuters

The argument among Republicans over why they lost the governor’s race in Virginia feels like the debate over "who lost China" in the 1950s. Did Republican candidate Ken Cuccinelli lose because he was too conservative? Or, did he lose because the Republican establishment didn't support him? This isn’t just a matter of scapegoating. Every losing campaign has its fights and finger pointing (and the authors of Double Down would like to thank you for that), but sometimes it just stops there. There was no greater meaning to take away from the postgame tussle after Hillary Clinton's primary loss in 2008. This blame game is important, however, because it is really a fight about the Republican Party’s strategy for the future.

In the first round, the existing participants in the Republican internal party debate have pretty much played to type. Karl Rove, who is pushing the party to nominate "electable" candidates, writes that Cuccinelli's loss shows that GOP candidates need to unite the party’s factions instead of alienate them. The New York Times suggests Cuccinelli’s loss has reanimated the push to end the highly partisan nominating conventions that lead to people like the former Virginia attorney general being picked in the first place. Exit polls show that 50 percent of Virginia voters found Cuccinelli too extreme. Activist conservatives, on the other hand, blame the Republican Governors Association and the Republican National Committee for not putting enough money into the race. The Tea Party crowd claims the establishment sold the Tea Party out again, just as it did during the government shutdown when moderate GOP senators didn't have the guts to stand and fight over Obamacare. 

Same whine, new bottles, right? No. There is one important contributing factor to the loss that both sides agree on. Rove argued in his Virginia election post-mortem that the government shutdown contributed to Cuccinelli's defeat. Cuccinelli campaign strategist Chris LaCivita agrees: The government shutdown distracted from talking about the failure of Obamacare’s launch. “There was definitely a national mood that was moving, that is moving, that is continuing to move against the White House and the Affordable Care Act. And I can’t help but ask myself, what would have been the result had he had five weeks of this discussion instead of just two and a half?”

LaCivita would like to have October back, and spend the whole month beating Obamacare like a drum. Instead, more than half of the month was spent on the shutdown and the parlor game of whether the Republican Party would drive the country over the debt limit brink. The Cuccinelli camp can’t know for sure whether this strategy would have changed the election’s outcome. They didn’t do a poll in the last few weeks of the race and have no data to support their view. But the numbers don’t matter among Republicans who believe highlighting Obamacare’s failures is a campaign winner—the only question left to settle is the tactical wisdom or stupidity of the government shutdown.  

The debate over Obamacare and the shutdown was about tactics, where those who were not willing to do absolutely everything were seen as less committed to the cause. In this effort, Cuccinelli and his Republican brethren were on the same side. Cuccinelli and Sens. Mike Lee and Ted Cruz, two of the main authors of the effort to defund Obamacare, are fellow travelers. They believe that the health care law is so bad that all necessary measures should be taken to undermine it. Cuccinelli regularly boasted on the stump that he had been the first attorney general to lodge a suit against the Affordable Care Act. He had done everything in his power to undo the law. As senators, Cruz and Lee did their part too—pushing for a government shutdown, despite what the polls and many of their fellow Republicans told them. 

Such a forward-leaning, conservative stance was not just the right thing to do, argue its adherents, it was also the politically smart thing to do. It shows your most ardent supporters that you really mean what you say. Do controversial things in support of what you believe, and voters will flock to you. The opposite argument, offered by members of the "establishment," is that sometimes while everyone might agree on the goal, different tactics are required to get there, even if it means getting there in the long run. Many of these more pragmatic voices were in the Senate cloakroom, arguing that a government shutdown would hurt the Republican brand and distract from the better sport of watching Obamacare collapse under its own weight. 

That strikes the rising right as timid and weak. In the aftermath of the shutdown, when the GOP’s approval rating crashed, Tea Party supporters argued that while they may not have achieved their ultimate goal of stopping Obamacare, they highlighted the deficiencies in the program. They believed their antics had thrilled the public and those same voters would reward them for their principled stand. The Washington insiders might not have liked it, but the voters did.

But after Cuccinelli’s closer-than-expected election loss, that’s not how his camp sees it anymore. By blaming its woes on the shutdown distraction, the Cuccinelli campaign sounds an awful lot like establishment Republicans before the shutdown. Now, in the clear light of defeat, this band of conservatives seems to appreciate that sometimes there are costs to doomed acts of principle. To wonder about those costs in advance of the kamikaze strategy is not a sign that you are weak, unprincipled, or a RINO—it simply keeps you from having to blame the strategy when the election is over and it's too late.

Source: http://www.slate.com/articles/news_and_politics/politics/2013/11/ken_cuccinelli_s_failed_virginia_campaign_the_blame_game_and_the_future.html
Similar Articles: Giraffe Riddle Answer   Theresa Vail   USA VS Mexico   roger federer   Blurred Lines Lyrics  

Splintered Republicans Must Take Their Medicine

There is a path to sanity for the national Republican Party to be gleaned from the mixed election results on Tuesday night — not just sanity, actually, but victory.

The problem is that professional Republicans of all stripes will have to swallow some medicine — and as we know, everybody always thinks the other guy should take the medicine while he should get the candy.

Source: http://www.realclearpolitics.com/2013/11/07/splintered_republicans_must_take_their_medicine_319475.html
Similar Articles: World Series 2013   drew brees   world war z   lamar odom   Solheim Cup 2013