Professor Suzanne Cory Awarded 2009 Pearl Meister Greengard Prize

Professor Suzanne Cory, the former director of the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, has been named the recipient of the 2009 Pearl Meister Greengard Prize.



Professor Cory will receive her prize, created to recognise the accomplishments of outstanding female scientists, at The Rockefeller University in the US on 5 November.



The prize was founded by Rockefeller Nobel laureate Paul Greengard and his wife Ursula von Rydingsvard in honor of Professor Greengard's mother, Pearl Meister Greengard, who died giving birth to him. It has been awarded annually since 2004.



Previous recipients of the prize include 2009 Nobel Prize winners Professor Elizabeth Blackburn and Professor Carol Greider for their work on the enzyme telomerase; and developmental biologist Professor Nicole Marthe Le Douarin, who is renowned for her studies of chimeras.



The 2009 Pearl Meister Greengard Prize was awarded to Professor Cory for her work in cancer and immunogenetics.



Professor Cory has had a career-long scientific partnership with her husband Professor Jerry Adams. In the 1970s, they pioneered recombinant DNA technology in Australia, in order to investigate how immunoglobulin genes encode the antibodies needed to fight infectious agents.



In the 1980s, Professors Cory and Adams switched their attention to the genetic errors that provoke lymphomas and leukaemias. They discovered that the chromosome translocation associated with Burkitt's lymphomas activates an oncogene known as myc, which promotes cell proliferation. With colleagues David Vaux and Andreas Strasser, they later made the surprising discovery that bcl-2, the oncogene activated by chromosome translocation in human follicular lymphoma, stops cells from dying. Their research remains focused on the pathways that control cell death.



Professor Cory said it was a great honour to receive the Pearl Meister Greengard Prize. "I am thrilled be awarded this prize and to be acknowledged alongside women such as Elizabeth Blackburn, Carol Greider and Nicole Le Douarin, for whom I have enormous professional and personal respect," Professor Cory said.



"So many women have made vital contributions to the advancement of scientific knowledge but too often in the past, as in other fields, they have been under-recognised. To have awards such as the Pearl Meister Greengard Prize to recognise their achievements is of enormous significance and provides great encouragement to women to take up a career in science."



Professor Cory was director of the Walter and Eliza Hall Institute for 13 years from 1996 and has recently returned to running a research laboratory in the institute's Molecular Genetics of Cancer Division.




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Growing Number Of UAW Members Oppose Plan That Would Shift Responsibility Of Retiree Health Care Costs To Union

Some United Auto Workers members are opposed to the creation of a voluntary employee beneficiary association for management of retiree health benefits, which could be established during contract negotiations between the union and Ford Motor, General Motors and Chrysler Group, USA Today reports. They are concerned that the VEBA one day could go bankrupt and leave current and future retirees uninsured or underinsured (Silke Carty, USA Today, 9/4). Ford and GM in August asked UAW to assume responsibility for the health care benefits of more than 1.5 million working and retired employees. Under the arrangement, the companies would transfer retiree health care obligations to an independent trust fund that the union would manage. Such a request was largely anticipated and would free the automakers from future retiree health obligations. The contract negotiations began in July (Kaiser Daily Health Policy Report, 8/29).

According to USA Today, the automakers want to fund a VEBA at 60% to 70% of projected health care costs. Past attempts at creating a VEBA failed because UAW wanted the automakers to fund the VEBA at 100% of costs. David Cole, chair of the Center for Automotive Research, said the Big Three must fund a VEBA below full costs to be financially prudent, adding that if they pay more than 70% of costs, they would fail to reduce labor costs adequately to increase competitiveness with rival Asian automakers.

However, some labor activists are campaigning against a VEBA funded at that level. USA Today reports that Future of the Union, a "dissident labor group," has been working to sway union members to oppose a VEBA agreement in light of failed VEBAs established by UAW with Caterpillar and Detroit Diesel, both of which ran out of funds.

Funding Levels in Question
All three automakers want to establish a VEBA, but the "clock is ticking" because the contracts for all three companies expire on Sept. 14, according to USA Today (USA Today, 9/4). The Detroit News reports that the discussion on a VEBA has come down to "two critical questions: How much the automakers should pay, and how they should pay for it."














People close to the negotiations have said UAW agrees that it only will make sense for the automakers to establish a VEBA if they can do so at a reduction of total health care liabilities, but union leaders and the companies do not agree on the amount. An executive of one company told the News that his company could afford 60% but that 70% would be "pushing it." Fitch Ratings, which sets credit ratings for Ford and GM, has estimated that a VEBA could cost GM between $30 billion and $35 billion, Ford between $14 billion and $17 billion, and Chrysler between $6 billion and $9 billion, depending on how much of a discount is authorized. Signing a deal could raise credit ratings for Ford and GM, the automakers have said.

Funding Mechanisms Considered
Should a VEBA be approved, the companies also must decide how to fund it. Analysts have said that although GM and Ford have cash on their balance sheets, they need that funding for restructuring plans. Therefore, they would seek to fund a significant portion of a VEBA with stock. Cole said that funding a VEBA with stock might be beneficial to UAW because the value of Ford and GM stock likely will increase after signing contracts including a VEBA. "That alone could significantly increase the value of the stock," Cole said, adding, "They could take advantage of that kick." If the companies' stock improves as analysts expect under a VEBA deal, UAW could sell the shares and diversify its investments, according to the News.

Another funding option would be to spread the payments out over time. The News reports that both options might be a hard sell to UAW members because spreading payments out over time or taking stock payment from companies with financial troubles is risky. "Those benefits are vulnerable right now, and (union leaders) know it," Cole said, adding, "They have to have sustainably profitable companies, or they have no future" (Hoffman, Detroit News, 9/4).

The New York Times reports that UAW is being advised on the deal by financial consultant Lazard, with which it has consulted on past health care negotiations. If the negotiations for a VEBA fall through, the companies are likely to ask for "significant concessions in other aspects of the contract, including wages, benefits and work rules," according to the Times (Bunkley/Maynard, New York Times, 9/4).

UAW Unlikely To Select Lead Negotiator
UAW likely will negotiate contracts individually with each automaker instead of selecting a lead negotiator, which is a "break from traditional tactics," the Washington Post reports. In the past, UAW has picked the company with the best financial situation as its lead contract negotiator in order to increase its chances of "extracting major concessions," but sources close to the negotiations have said union officials are working with all three companies separately, according to the Post. UAW still could pick a lead company at any time (Freeman, Washington Post, 9/4).

Experts say that if a leader is chosen, it likely will be GM because it is "healthier than Ford and the most intent on creating a VEBA fund," the New York Times reports. However, the leader also could be Ford because UAW President Ron Gettelfinger has a long-standing relationship with the company. Chrysler is the least likely option (New York Times, 9/4).

Strike Vote Takes Place
With the contract's expiration near, UAW has asked its members to authorize a strike, and voting ended on Friday, the AP/Chicago Tribune reports. The move is standard and does not indicate that a strike will occur. The tally has not been finalized yet, but it is typical for authorization to be approved by a wide margin (Krisher, AP/Chicago Tribune, 9/3). Company executives and analysts have said a strike is not expected to occur because it could severely hinder the automakers or even bankrupt one of them, according to the Post (Washington Post, 9/4).

Comments
Bradley Rubin of BNP Paribas said, "It will be a bloodbath if [a VEBA] doesn't happen," adding, "That's why it has to happen." Cole said, "The discount and how to fund it are the really tricky issues right now," adding, "(But) from what I've heard, they're coming together. I think it's going to happen" (Detroit News, 9/4). David Gregory, a professor of law at St. John's University, said, "It would be really remarkable if there was a strike. You'd need a complete collapse of negotiations," adding, "A strike this time around could be absolutely lethal for the company being struck" (New York Times, 9/4).

UAW Vice President Cal Rapson, who is on the GM negotiation team, on Saturday in Flint, Mich., told hundreds of UAW members that UAW is "determined not to put any more costs on retirees for their health care" (Aguilar, Detroit News, 9/2).


Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation. © 2005 Advisory Board Company and Kaiser Family Foundation. All rights reserved.


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Heart Attacks Are More Serious If They Occur At Certain Times Of The Day

People who have a heart attack are likely to be more seriously affected if
the attack happens in the morning, reveals research published ahead of
print in Heart journal.


Heart attacks that occur between 6am and noon are more likely to leave a
20% larger area of dead tissue (infarct) caused by the attack, which is
more serious for the person affected, than at any other time of the day.


It is well established that a person's 24 hour body clock influences
several cardiovascular physiological processes including the incidence of
heart attacks, which tend to happen more around the time when a person is
waking up from sleep, but what is less known is the extent of damage that
this leads to.


Researchers in Madrid, Spain set out to determine the impact of time of
day
of a heart attack on the size of the dead tissue (infarct) caused in
patients with an ST segment elevation myocardial infarction (STEMI) - a
type of heart attack caused by a prolonged period of blocked blood supply.


They analysed data on 811 patients with a STEMI heart attack admitted to
the coronary care unit of Hospital Clinico San Carlos in Madrid between
2003 and 2009. They calculated the size of infarct by looking at enzyme
release in patients.


The time of STEMI onset was divided into four 6-hour time periods in phase
with 24-hour body clock rhythms.


Patients with the largest infarct size were found to be those who had a
heart attack in the dark to light transition period of 6am to noon. These
patients were found to have around a 21% higher level of enzymes in this
period (which indicated a larger infarct size) than patients who had their
heart attack between 6pm and midnight.


The greatest number of patients (269) had their heart attack in the 6am to
noon period, followed by 240 patients who had their attack between noon
and
6pm, 161 during the 6pm to midnight period, and 141 between midnight and
6am.


They also found that patients with a STEMI that happened in the anterior
wall of the heart were left with a larger size of infarct than patients
whose heart attacks happened in other locations.


The authors conclude: "If confirmed, these results may have a significant
impact on the interpretation of clinical trials of cardioprotective
strategies in STEMI."


Source
HEART


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The Future Of The National Programme For IT, UK

A Department of Health review of the National Programme for IT has concluded that a centralised, national approach is no longer required, and that a more locally-led plural system of procurement should operate, whilst continuing with national applications already procured.


A new approach to implementation will take a modular approach, allowing NHS organisations to introduce smaller, more manageable change, in line with their business requirements and capacity. NHS services will be the customers of a more plural system of IT embodying the core assumption of 'connect all', rather than 'replace all' systems. This reflects the coalition government's commitment to ending top-down government and enabling localised decision-making.


The review of the National Programme for IT has also concluded that retaining a national infrastructure will deliver best value for taxpayers. Applications such as Choose and Book, Electronic Prescription Service and PACS have been delivered and are now integrated with the running of current health services. Now there is a level of maturity in these applications they no longer need to be managed as projects but as IT services under the control of the NHS. Consequently, in line with the broader NHS reforms, the National Programme for IT will no longer be run as a centralised national programme and decision making and responsibility will be localised.


Health Minister, Simon Burns, said:


"Improving IT is essential to delivering a patient-centred NHS. But the nationally imposed system is neither necessary nor appropriate to deliver this. We will allow hospitals to use and develop the IT they already have and add to their environment either by integrating systems purchased through the existing national contracts or elsewhere.


"This makes practical sense. It also makes financial sense. Moving IT systems closer to the frontline will release ВЈ700 million extra in savings. Every penny saved through productivity gains will be reinvested to improve patient care."


Director General for Informatics, Christine Connelly, said:


"It is clear that the National Programme for IT has delivered important changes for the NHS including an infrastructure which the NHS today depends on for providing safe and responsive health care. Now the NHS is changing, we need to change the way IT supports those changes, bringing decisions closer to the front line and ensuring that change is manageable and holds less risk for NHS organisations."


Source:

Department of Health, UK

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Cholesterol Regulator Plays Key Role In Development Of Liver Scarring, Cirrhosis

UCLA researchers have demonstrated that a key regulator of cholesterol and fat metabolism in the liver also plays an important role in the development of liver fibrosis the build-up of collagen scar tissue that can develop into cirrhosis. Cirrhosis, in turn, is a major cause of premature death and is incurable without a liver transplant.


Published in the March issue of the journal Gastroenterology, the study shows that liver X receptors (LXRs), master regulators of cholesterol, fat and inflammatory gene expression, also control the fibrosis-making cells of the liver, known as hepatic stellate cells.


In the face of chronic liver injury due to excess fat, chronic viral hepatitis or alcohol abuse, for example stellate cells become activated and launch an inflammatory and fibrotic cascade that eventually results in the build-up of collagen scar tissue in the liver.


LXRs, when stimulated, "turn on" several hundred genes that hold instructions to create proteins for carrying out bodily processes in cells, from transporting and excreting cholesterol to synthesizing fat in the liver. They have also been shown to suppress inflammatory processes in several contexts.


"Our work sets the stage for looking at new ways to modulate cholesterol and/or fat metabolism in order to have therapeutic potential for the treatment of fibrosing liver diseases," said lead author Dr. Simon Beaven, an assistant professor of digestive diseases at the David Geffen School of Medicine at UCLA.


The research was done in the laboratory of senior author Dr. Peter Tontonoz, a professor of pathology and laboratory medicine at the Geffen School of Medicine and a Howard Hughes Medical Institute investigator.


Beaven noted that the recent rise in obesity has resulted in a surge in the prevalence of a condition known as fatty liver, which can be a precursor to fibrosis and chronic liver disease. Simple fatty liver, also known as non-alcoholic fatty liver disease, or NAFLD, is one of the most common reasons patients consult a liver doctor in the United States. Cirrhosis due to fatty liver is skyrocketing and within a decade may become the most common indication for liver transplantation.


Beaven said the need to find better treatments for liver disease is crucial.


"A 'holy grail' for liver researchers is to develop anti-fibrotic treatments that target activated stellate cells in order to slow or prevent the development of cirrhosis," Beaven said. "Our study offers the first detailed look at how LXRs specifically impact the activation of hepatic stellate cells and the subsequent development of liver fibrosis in animal models."


UCLA researchers have found that LXRs normally play a role in helping to reduce the collagen-producing actions of stellate cells when the cells are "activated" by liver damage. For the study, UCLA scientists first tested how activated stellate cells taken from mice would react when a chemical that induces LXR activity was added to the cell culture.


In stellate cells from normal mice, LXRs suppressed the inflammatory and fibrosis-promoting program. But in those taken from mice genetically lacking LXRs, that same program of genes significantly increased because the inhibitory effect of LXRs was no longer present.


"We showed that LXRs dampen stellate cell activation by repressing inflammatory and collagen-producing genes," Beaven said.


To further gauge the strength of the response, scientists took the medium from the cultures of LXR-deficient cells and added it to stellate cells from normal mice. These cells then showed a markedly exaggerated inflammatory and collagen-producing response, suggesting that LXR-deficient stellate cells are secreting signals to promote fibrosis.


The researchers noted that these experiments demonstrate that LXRs control a fibrotic response in stellate cells that can have a wide influence on neighboring cells.


The scientists also found that after replicating chronic liver injury, mice without LXRs had dramatically more liver fibrosis than normal mice.


"The genetic loss of LXRs rendered the mice susceptible to developing fibrotic liver disease," Beaven said.


But LXRs are also known to have important functions in the immune system. The researchers then wanted to know whether the effects they were seeing in animals were due to changes in stellate cell activity specifically or whether immune cells derived from bone marrow accounted for most of the effect. After extensive testing, the researchers found no differences


in the level of liver fibrosis among normal mice and animals lacking LXRs, suggesting that the contribution from the immune system was negligible.


"This finding, along with the cell culture studies, suggests that LXRs' influence on fibrosis most likely resides in altering stellate cell function in the liver," Beaven said. "This is a critical finding and opens an entire new field of study for stellate cell biologists."


Additional studies will further identify which genes in stellate cells are activated by LXRs and help researchers better understand the role of cholesterol metabolism in the fibrotic response.


This study was funded primarily by grants from the National Institutes of Health and the Howard Hughes Medical Institute. Collaborators from the University of Southern California were funded by core grants from the NIH and the Southern California Research Center for ALPD and Cirrhosis.


Other study authors included senior investigator Dr. Peter Tontonoz of the Howard Hughes Medical Institute; Kevin Wroblewski and Cynthia Hong from Tontonoz's lab; Jiaohong Wang and Hide Tsukamoto of the Southern California Research Center for ALPD and Cirrhosis, USC's Keck School of Medicine and the Department of Veterans Affairs Greater Los Angeles Healthcare System; and Steven Bensinger of the department of pathology at the David Geffen School of Medicine at UCLA.


Source: University of California, Los Angeles (UCLA)

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Gov. Crist's Cover Florida, Two Other State Health Programs Delayed

Florida Gov. Charlie Crist's (R) Cover Florida program and two other proposed measures intended to expand health care coverage to more state residents have stalled, Florida Health News reports. State officials on Wednesday were expected to announce which of the nine health insurance companies, which submitted bids to offer basic low-cost health plans to residents, had been chosen as part of Crist's program. However, Florida Agency for Health Care Administration Secretary Holly Benson earlier this week said that the availability of the information on which companies were selected would be delayed until between Oct. 15 and Oct. 22. AHCA spokesperson Fernando Senra said "scheduling challenges" caused the delay. The goal is to close the contracts by "mid to late" November so that the plan can be implemented by Jan. 1, 2009, Benson said.

Meanwhile, a change in insurance law that would extend to 30 the age a young adult can remain on a parent's health coverage has been delayed over questions concerning who decides -- the employer offering the coverage or the parent of the young adult -- whether a young adult can remain on the policy, according to Florida Health News. On Monday, Blue Cross and Blue Shield of Florida announced that it will suspend optional coverage for dependents ages 25 to 40 until the provisions of the law have been clarified.

In addition, a 15-member board that would have provided oversight of the Florida Health Choices, a program that would offer a virtual health insurance marketplace for employees statewide, has yet to be formed. One member has been appointed by the state House speaker, Florida Health News reports. The House speaker, Crist and the state Senate president each would make four appointments, while the final three members would be representatives from AHCA, the state Office of Insurance Regulation and the state Department of Management Services (Jordan Sexton, Florida Health News, 10/1).


Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.

© 2008 Advisory Board Company and Kaiser Family Foundation.В  All rights reserved.


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Boosting The Efficacy Of Anticancer Vaccines

There are several challenges to be overcome if therapeutic anticancer vaccines, which are designed to boost the patient's anticancer immune response, are to be successfully developed. For example, the viruses used to deliver the tumor protein to the patient's immune system are themselves targeted by the patient's immune system, inducing neutralizing and suppressive responses.



However, a team of researchers, led by Michael Morse, at Duke University Medical Center, Durham, has developed a way to overcome these neutralizing and suppressive responses by using an alphavirus packaged in virus-like replicon particles. Repeated administration of such particles carrying the tumor protein CEA to patients with metastatic cancer expressing CEA induced clinically relevant immune responses targeted to CEA. As the presence of such immune responses was associated with longer overall patient survival, the authors hope their approach might be of therapeutic use in many cancer settings.



Title:
An alphavirus vector overcomes the presence of neutralizing antibodies and elevated numbers of Tregs to induce immune responses in humans with advanced cancer



Source:

Karen Honey


Journal of Clinical Investigation


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