The University of Michigan and the Lecturers? Employee Organization announced Wednesday that they have reached a tentative five-year contract that will be ratified one week before new right-to-work legislation takes effect. According to a story in the Detroit News, the previous deal between U-M and the union had been set to expire April 20.
Michigan union members protested right-to-work legislation before it was passed at Michigan's capitol. Since the bill's passing, many unions have reached new deals before the provisions take effect.
J. Scott Park | MLive Media Group
The Lecturers Employee Organization represents about 1,500 non-tenure track instructors on University of Michigan campuses in Ann Arbor, Flint, and Dearborn. The organization?s contract with the university contains language that allows lecturers to either join the union or pay a service fee.
Negotiations had been ongoing since November, and a joint statement from the two parties said the agreement was reached in good faith. The contract will be ratified by mail with a deadline of March 21.
Are you interested in foster care or foster adoption or respite/relief care? Are you wondering if one of these paths is right for your family and how to get started?
If so, join Tapestry on Sunday, March 10, from 2:00 to 4:00 pm, in Room West D for a brief information meeting for anyone interested in knowing more about foster care, adoption from foster care or respite/relief care.?This meeting is a great opportunity to simply get more information about foster care and foster adoption that can help you decide what path might be best for you and your family.
For those wanting to move forward, training classes will be offered at Irving Bible Church in April.?Check the?Tapestry Events page?for more details.
For questions or more information contact Amy Monroe at?tapestry@irvingbible.org.
How the body's energy molecule transmits 3 types of taste to the brainPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA Saying that the sense of taste is complicated is an understatement, that it is little understood, even more so. Exactly how cells transmit taste information to the brain for three out of the five primary taste types was pretty much a mystery, until now.
A team of investigators from nine institutions discovered how ATP the body's main fuel source is released as the neurotransmitter from sweet, bitter, and umami, or savory, taste bud cells. The CALHM1 channel protein, which spans a taste bud cell's outer membrane to allow ions and molecules in and out, releases ATP to make a neural taste connection. The other two taste types, sour and salt, use different mechanisms to send taste information to the brain.
Kevin Foskett, PhD, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, and colleagues from the Monell Chemical Senses Center, the Feinstein Institute for Medical Research, and others, describe in Nature how ATP release is key to this sensory information path. They found that the calcium homeostasis modulator 1 (CALHM1) protein, recently identified by the Foskett lab as a novel ion channel, is indispensable for taste via release of ATP.
"This is an example of a bona fide ATP ion channel with a clear physiological function," says Foskett. "Now we can connect the molecular dots of sweet and other tastes to the brain."
Taste buds have specialized cells that express G-protein coupled receptors (GPCRs) that bind to taste molecules and initiate a complex chain of molecular events, the final step of which Foskett and collaborators show is the opening of a pore in the cell membrane formed by CALHM1. ATP molecules leave the cell through this pore to alert nearby neurons to continue the signal to the taste centers of the brain. CALHM1 is expressed specifically in sweet, bitter, and umami taste bud cells.
Mice in which CALHM1 proteins are absent, developed by Feinstein's Philippe Marambaud, PhD, have severely impaired perceptions of sweet, bitter and umami compounds; whereas, their recognition of sour and salty tastes remains mostly normal. The CALHM1 deficiency affects taste perception without interfering with taste cell development or overall function.
Using the CALHM1 knockout mice, team members from Monell and Feinstein tested how their taste was affected. "The mice are very unusual," says Monell's Michael Tordoff, PhD. "Control mice, like humans, lick avidly for sucrose and other sweeteners, and avoid bitter compounds. However, the mice without CALHM1 treat sweeteners and bitter compounds as if they were water. They can't taste them at all."
From all lines of evidence, the team concluded that CALHM1 is an ATP-release channel required for sweet, bitter, and umami taste perception. In addition, they found that CALHM1 was also required for "nontraditional" Polycose, calcium, and aversive high-salt tastes, implying that the deficit displayed in the knockout animals might best be considered as a loss of all GPCR-mediated taste signals rather than simply sweet, bitter and umami taste.
Interestingly, CALHM1 was originally implicated in Alzheimer's disease, although the link is now less clear. In 2008, co-author Marambaud identified CALHM1 as a risk gene for Alzheimer's. They discovered that a CALHM1 genetic variant was more common among people with Alzheimer's and they went on to show that it leads to a partial loss of function. They also found that this novel ion channel is strongly expressed in the hippocampus, a brain region necessary for learning and memory. So far, there is no connection between taste perception and Alzheimer's risk, but Marambaud suspects that scientists will start testing this hypothesis.
###
Co-authors include Akiyuki Taruno, Valerie Vingtdeux, Makoto Ohmoto, Zhongming Ma, Gennady Dvoryanchikov, Ang Li, Leslie Adrien, Haitian Zhao, Sze Leung, Maria Abernethy, Jeremy Koppel, Peter Davies, Mortimer M. Civan, Nirupa Chaudhari, Ichiro Matsumoto, and Goran Hellekant.
This work was supported in part by the National Institutes of Health (GM56328, MH059937, NS072775, DC10393, EY13624, R03DC011143, P30 EY001583, P30DC011735).
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2011, Penn Medicine provided $854 million to benefit our community.
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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.
How the body's energy molecule transmits 3 types of taste to the brainPublic release date: 6-Mar-2013 [ | E-mail | Share ]
Contact: Karen Kreeger karen.kreeger@uphs.upenn.edu 215-349-5658 University of Pennsylvania School of Medicine
PHILADELPHIA Saying that the sense of taste is complicated is an understatement, that it is little understood, even more so. Exactly how cells transmit taste information to the brain for three out of the five primary taste types was pretty much a mystery, until now.
A team of investigators from nine institutions discovered how ATP the body's main fuel source is released as the neurotransmitter from sweet, bitter, and umami, or savory, taste bud cells. The CALHM1 channel protein, which spans a taste bud cell's outer membrane to allow ions and molecules in and out, releases ATP to make a neural taste connection. The other two taste types, sour and salt, use different mechanisms to send taste information to the brain.
Kevin Foskett, PhD, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, and colleagues from the Monell Chemical Senses Center, the Feinstein Institute for Medical Research, and others, describe in Nature how ATP release is key to this sensory information path. They found that the calcium homeostasis modulator 1 (CALHM1) protein, recently identified by the Foskett lab as a novel ion channel, is indispensable for taste via release of ATP.
"This is an example of a bona fide ATP ion channel with a clear physiological function," says Foskett. "Now we can connect the molecular dots of sweet and other tastes to the brain."
Taste buds have specialized cells that express G-protein coupled receptors (GPCRs) that bind to taste molecules and initiate a complex chain of molecular events, the final step of which Foskett and collaborators show is the opening of a pore in the cell membrane formed by CALHM1. ATP molecules leave the cell through this pore to alert nearby neurons to continue the signal to the taste centers of the brain. CALHM1 is expressed specifically in sweet, bitter, and umami taste bud cells.
Mice in which CALHM1 proteins are absent, developed by Feinstein's Philippe Marambaud, PhD, have severely impaired perceptions of sweet, bitter and umami compounds; whereas, their recognition of sour and salty tastes remains mostly normal. The CALHM1 deficiency affects taste perception without interfering with taste cell development or overall function.
Using the CALHM1 knockout mice, team members from Monell and Feinstein tested how their taste was affected. "The mice are very unusual," says Monell's Michael Tordoff, PhD. "Control mice, like humans, lick avidly for sucrose and other sweeteners, and avoid bitter compounds. However, the mice without CALHM1 treat sweeteners and bitter compounds as if they were water. They can't taste them at all."
From all lines of evidence, the team concluded that CALHM1 is an ATP-release channel required for sweet, bitter, and umami taste perception. In addition, they found that CALHM1 was also required for "nontraditional" Polycose, calcium, and aversive high-salt tastes, implying that the deficit displayed in the knockout animals might best be considered as a loss of all GPCR-mediated taste signals rather than simply sweet, bitter and umami taste.
Interestingly, CALHM1 was originally implicated in Alzheimer's disease, although the link is now less clear. In 2008, co-author Marambaud identified CALHM1 as a risk gene for Alzheimer's. They discovered that a CALHM1 genetic variant was more common among people with Alzheimer's and they went on to show that it leads to a partial loss of function. They also found that this novel ion channel is strongly expressed in the hippocampus, a brain region necessary for learning and memory. So far, there is no connection between taste perception and Alzheimer's risk, but Marambaud suspects that scientists will start testing this hypothesis.
###
Co-authors include Akiyuki Taruno, Valerie Vingtdeux, Makoto Ohmoto, Zhongming Ma, Gennady Dvoryanchikov, Ang Li, Leslie Adrien, Haitian Zhao, Sze Leung, Maria Abernethy, Jeremy Koppel, Peter Davies, Mortimer M. Civan, Nirupa Chaudhari, Ichiro Matsumoto, and Goran Hellekant.
This work was supported in part by the National Institutes of Health (GM56328, MH059937, NS072775, DC10393, EY13624, R03DC011143, P30 EY001583, P30DC011735).
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
The Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $479.3 million awarded in the 2011 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2011, Penn Medicine provided $854 million to benefit our community.
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?
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.
This undated image provided by Samsung on Saturday, Feb. 23, 2013 shows the Samsung GALAXY Note 8 with a stylus. Samsung Electronics is beefing up its tablet range with a competitor to Apple?s iPad Mini that sports a pen for writing on the screen. The Korean company announced on Sunday, Feb. 24, 2013 in Barcelona, Spain that the Galaxy Note 8.0 will have an 8-inch screen, putting it very close in size to the Apple?s tablet. (AP Photo/Samsung)
This undated image provided by Samsung on Saturday, Feb. 23, 2013 shows the Samsung GALAXY Note 8 with a stylus. Samsung Electronics is beefing up its tablet range with a competitor to Apple?s iPad Mini that sports a pen for writing on the screen. The Korean company announced on Sunday, Feb. 24, 2013 in Barcelona, Spain that the Galaxy Note 8.0 will have an 8-inch screen, putting it very close in size to the Apple?s tablet. (AP Photo/Samsung)
SAN FRANCISCO (AP) ? A federal judge on Friday slashed nearly half of the $1 billion damage award a jury ordered Samsung Electronics to pay Apple Inc. after a high-profile trial over the rights to the design and technology running some of the world's most popular smartphones and tablet computers.
U.S. District Court Judge Lucy Koh lowered the damages awarded to Apple Inc. by $450.5 million for 14 Samsung products including some products in its hot-selling Galaxy lineup, saying jurors had not properly followed her instruction in calculating some of the damages.
She also concluded that mistakes had been made in determining when Apple had first notified Samsung about the alleged violations of patents for its trend-setting iPhone and IPad.
Koh ordered a new trial to recalculate damages for those products.
"We are pleased that the court decided to strike $450,514,650 from the jury's award," Samsung spokeswoman Lauren Restuccia said. "Samsung intends to seek further review as to the remaining award."
Apple declined to comment on the Koh's ruling.
The ruling reduced Samsung Electronics' bill to just under $599 million. The judge said the tab will probably increase after the appeals of both companies are resolved.
Apple is seeking more damages and Samsung a complete dismissal of the case in the U.S. Court of Appeals for the Federal Circuit, the Washington, D.C.-based court that handles all patent appeals. The new trial to recalculate the damages could also increase the award.
Still, the ruling was the second significant setback in Koh's courtroom since the headline grabbing verdict was announced.
In December, Koh refused to order a sales ban on the products the jury found infringed Apple's patents. She said Apple failed to prove the purloined technology is what drove consumers to buy a Samsung product instead of an Apple iPhone or iPad. Samsung says that it is continues to sell only three of the two dozen products found to have infringed Apple's patents.
After a three-week trial closely followed in Silicon Valley, the jury decided that Samsung ripped off the trailblazing technology and sleek designs used by Apple to create its revolutionary iPhone and iPad. Jurors ordered Samsung to pay Apple $1.05 billion.
Apple filed another lawsuit last year accusing Samsung's newer line of products of continuing to use technology controlled by Apple. Koh has scheduled trial in that case for early next year. She has implored both companies on several occasions to settle their difference with little success.
Apple filed its patent infringement lawsuit in April 2011 and engaged legions of the country's highest-paid patent lawyers to demand $2.5 billion from its top smartphone competitor. Samsung Electronics Co. fired back with its own lawsuit seeking $399 million.
The jury found that several Samsung products illegally used such Apple creations as the "bounce-back" feature when a user scrolls to an end image, and the ability to zoom text with a tap of a finger.
Samsung has mounted an aggressive post-trial attack on the verdict, raising a number of legal issues that allege the South Korean company was treated unfairly in a federal courtroom a dozen miles from Apple's Cupertino headquarters. Samsung alleges that some of Apple's patents shouldn't have been awarded in the first place and that the jury made mistakes in calculating the damage award.
Samsung has emerged as one of Apple's biggest rivals and has overtaken it as the leading smartphone maker. Samsung's Galaxy line of phones run on Android, a mobile operating system that Google Inc. has given out for free to Samsung and other phone makers.
Apple and Samsung have filed similar lawsuits in eight other countries, including South Korea, Germany, Japan, Italy, the Netherlands, Britain, France and Australia.
Los Angeles Angels' Mark Trumbo, left to right, Mike Trout, Albert Pujols and Josh Hamilton pose for photographers during photo day before a spring training baseball workout Thursday, Feb. 21, 2013, in Tempe, Ariz. (AP Photo/Morry Gash)
Los Angeles Angels' Mark Trumbo, left to right, Mike Trout, Albert Pujols and Josh Hamilton pose for photographers during photo day before a spring training baseball workout Thursday, Feb. 21, 2013, in Tempe, Ariz. (AP Photo/Morry Gash)
A young fan wears a fish-shaped foam hat in honor of Los Angeles Angels center fielder Mike Trout during an exhibition spring training baseball game against the Seattle Mariners Monday, Feb. 25, 2013, in Peoria, Ariz. (AP Photo/Charlie Riedel)
Los Angeles Angels left fielder Mike Trout, left, and center fielder Peter Bourjos chase after a triple hit by Seattle Mariners' Dustin Ackley during an exhibition spring training baseball game, Monday, Feb. 25, 2013, in Peoria, Ariz. (AP Photo/Charlie Riedel)
TEMPE, Ariz. (AP) ? The Los Angeles Angels renewed the contract of AL Rookie of the Year Mike Trout for $510,000, prompting an angry response from the outfielder's agent.
Craig Landis said his client was disappointed with the decision announced Saturday. The salary is $20,000 above the major league minimum.
"During the process, on behalf of Mike, I asked only that the Angels compensate Mike fairly for his historic 2012 season, given his service time," Landis said in a statement. "In my opinion, this contract falls well short of a 'fair' contract and I have voiced this to the Angels throughout the process. Nonetheless, the renewal of Mike's contract will put an end (to) this discussion."
Trout has 1 year, 70 days of major league service and is likely to be eligible for arbitration after the 2014 season and for free agency after the 2017 World Series. Teams can renew the contracts of unsigned players on their 40-man rosters from March 2-11
"Mike, himself, does not wish to comment on this matter," Landis said. "As when he learned he would not be the team's primary center fielder for the upcoming season, Mike will put the disappointment behind him and focus on helping the Angels reach their goal of winning the 2013 World Series."
Speedy Peter Bourjos is set to be the Angels' primary center fielder, flanked by Trout in left and 2010 AL MVP Josh Hamilton in right.
Trout had a $482,500 salary last year, when he finished second to Detroit's Miguel Cabrera in AL MVP voting. Trout hit .326 with 30 homers and 83 RBIs, and led the majors with 129 runs and 49 steals.
He also earned a $10,000 bonus for winning Rookie of the Year.
Los Angeles also agreed to one-year deals with 21 players, including Bourjos and Mark Trumbo.
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Public release date: 6-Mar-2013
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