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Study Shows Januvia(TM) (sitagliptin) Offered Significant Blood Sugar-Lowering Efficacy In Combination With Insulin In Type 2 Diabetes
A new investigational study presented at the American Diabetes Association (ADA) 69th Annual Scientific Sessions showed that "Januvia" (sitagliptin), when added to ongoing insulin therapy with or without metformin, significantly improved blood sugar control.[i] Applications to use "Januvia" and "Janumet"* (sitagliptin/metformin) in combination with insulin have been accepted for review by the European Medicines Agency (EMEA) and by the U.S. Food and Drug Administration (FDA) and are currently under review.

Lobbyists Battle Over Biologic Drug Protections
"As Congress struggles with a massive health care overhaul, several lobbying powerhouses - including the pharmaceutical industry and the nation"s largest advocacy group for retirees - are locked in a contentious fight over the future of biotechnology drugs," USA Today reports in a front page package. "Both sides have spent heavily to sway lawmakers in the debate over how long to keep the expensive drugs exempt from generic competition." The pharmaceutical industry is fighting for 12 years of exclusivity, while President Barack Obama is "pushing for seven years of exclusivity as he looks to trim costs to help pay for his health care plan. ... The pharmaceutical industry counters that a longer period of exclusivity is needed to recover its investments in "biologic drugs," which are made from living organisms and used to treat cancer, multiple sclerosis and other serious diseases."
News of the day
Opinion Pieces Comment On Obama's Notre Dame Speech, Abortion Debate
Several newspapers recently published opinion pieces regarding President Obama"s commencement address at the University of Notre Dame. Summaries appear below.~ Cal Thomas, Washington Times: "Put aside the question of whether" Notre Dame should have invited President Obama to speak at its commencement ceremony on Sunday and "[f]ocus, instead, on [his] remarks and whether he is serious, or can be made so, about actually reducing the number of abortions in America," syndicated columnist Thomas writes in a Washington Times opinion piece. "Don"t put aside, however, the argument that there is only one reason to even want to reduce the number of abortions and that is that what is being killed, terminated, evacuated (choose your term) is, in fact, human life," Thomas adds. "In speaking of "original sin," the president hit upon why abortion has been so easily tolerated for so long," he writes, adding that Obama "spoke of "self-interest" and "crass materialism" but did so in the context of economics, not abortion." Thomas reports that Obama called for making adoption ""more available"" and providing ""care and support for women who do carry their children to term."" Thomas notes that Obama"s speech also included "an appeal for discussion and respect for people with different views," which was "a good beginning, but the ending is what counts, and the initial actions of this president when it comes to abortion and stem cell research have not been pro-life" (Thomas, Washington Times, 5/19).~ Tim Rutten, Los Angeles Times: After his commencement address at Notre Dame, "it"s now clear that the president is the rhetorical equivalent of a "money player,"" which is the "kind of competitor who steps up and delivers in the big games," Rutten writes in a Los Angeles Times opinion piece. Notre Dame"s invitation for Obama to speak at commencement and receive an honorary degree "bec[a]me an engine of controversy" because of protests from "reductionists," or conservative Catholics "who insist on bringing the broad sweep of Catholic social morality down to a single issue -- abortion," Rutten writes. However, Obama "negotiated the situation with remarkable ease," Rutten continues, adding that Obama was "speaking … to three audiences far from South Bend on Sunday." The first audience was the "crucial bloc of Catholic voters who seem to be looking for ways to remain in the Democratic Party," he writes. In addition, Obama was speaking to "those Catholic Democrats in public office ... who are under intense pressure from the reductionist bishops in their home dioceses" and to the U.S. Senate, which will likely ask Obama"s Supreme Court nominee about his or her views on abortion during confirmation hearings, Rutten continues. He concludes, "Even in Washington"s charged partisan atmosphere, it will be hard to ignore the president"s call for civility at Notre Dame" (Rutten, Los Angeles Times, 5/20).~ Clarence Page, Chicago Tribune: Obama "appropriately promoted" the "ability of adversaries to work together on mutual interests" in his commencement address, Page writes in a Tribune opinion piece. Page adds that the speech was "classic Obama the pragmatist: Look past ideology, try to ignore disagreements and work together on mutual interests." Obama said that "at some level, the views of the two camps are irreconcilable," Page writes, adding that it is "because Americans hold no values more dear than "life" and "choice."" Page adds that "[i]n the abortion debate, those values clash head-on." However, Obama"s "eloquent come-together oratory enabled him to leave the university like a hero, even though he glossed over the thorny specifics that drive wedges between people of goodwill when words are hammered into law," Page continues. "For now, by focusing on civility, the president apparently hopes to defuse the abortion powder keg long enough to address his higher priorities," Page writes, concluding, "The economy, national security and health care are going to be tough fight
Diagnostics

Reducing P38MAPK Levels Delays Aging Of Multiple Tissues In Lab Mice

In the new issue of the Developmental Cell journal, a team of scientists at Singapore"s Agency for Science, Technology and Research (A*STAR) and the University of North Carolina School of Medicine at Chapel Hill, report research findings about the molecular mechanisms behind the aging process, which has up till now been poorly understood, that offer the possibility that a novel, pharmacological approach could be developed to combat age-related disorders. In their research with lab rodents, the scientists found that the p38MAPK protein, already known for its role in inflammation, also promotes aging when it activates another protein p16, which has long been linked to aging. In addition, they found that reducing the levels of p38MAPK delayed the aging of multiple tissues. Through their experiments, the scientists found that partial inactivation of p38MAPK was sufficient to prevent age-induced cellular changes in multiple tissues, as well as improve the proliferation and regeneration of islet cells, without affecting the tumour suppressor function of p16 in mice. Dmitry Bulavin, M.D., Ph.D., research team leader and principal investigator in A*STAR"s Institute of Molecular and Cell Biology (IMCB), said, "We are excited by this new found role for p38MAPK in aging. Due to the previously established involvement of p38MAPK in inflammatory diseases, small molecule inhibitors of p38MAPK signalling have already entered clinical trials for the treatment of other medical conditions such as rheumatoid arthritis. Our latest discovery offers the possibility that a novel, pharmacological approach could be developed to combat age-related disorders." In the paper, the scientists described how they studied the role of p38MAPK in aging by using genetically modified mice. They found that several organs, including the pancreas, in the mice that had a reduced amount of p38MAPK protein exhibited a delayed degeneration as the mice grew older. These mice also displayed an improved growth and regeneration of pancreatic islet beta cells compared to the control group of mice with normal levels of p38MAPK. Beta cells make and release insulin. In Type 2 diabetes, these cells are unable to produce enough insulin to meet the body"s demand, partly due to a decrease in beta cell mass. In addition, the scientists also found that the forced activation of p38MAPK stunted the growth of insulin-producing islet beta cells and caused insulin resistance in mice, which is the basis of Type 2 diabetes. These results suggest that by controlling p38MAPK levels, scientists could potentially treat age-related degenerative conditions dependent on the p38MAPK signalling pathways. Such findings may prove important to the development of novel treatment approaches for Type 2 diabetes in the elderly. While investigating the effects of lowering p38MAPK levels to achieve a significant delay in aging in mice, the scientists had another consideration: insuring that the level of p16, a tumour suppressor, did not fall below the threshold that was required to protect the animals from developing tumours. Through their experiments, the scientists found that partial inactivation of p38MAPK was sufficient to prevent age-induced cellular changes in multiple tissues, as well as improve the proliferation and regeneration of islet cells, without affecting the tumour suppressor function of p16 in mice. The scientists went on to investigate the upstream mechanisms that regulated p38MAPK in old mice and that have not been widely studied to date. They found that high levels of the protein Wip1, a protein that has been known to be implicated in cancer, suppressed the activity of p38MAPK, and this led to islet proliferation, which in turn improved the pancreatic function in aging mice. Their results, therefore, identified Wip1 as an additional target to which anti-aging therapies could be directed. Neal Copeland, Ph.D., Executive Director of IMCB, said, "Dr. Bulavin"s team has achieved an important breakthrough in the study of ageing. These significant findings, together with other recent discoveries made by IMCB"s scientists, illustrate how IMCB has worked with its international collaborators to fully harness the knowledge and tools of modern medical science, to increase understanding of the causes behind common human diseases. The resulting knowledge will hopefully contribute to the development of effective treatment for clinical conditions." The research findings are described in the following article, "p38MAPK controls expression of multiple cell cycle inhibitors and islet proliferation with advancing age," published in the 21 July 2009 print issue of Developmental Cell. Authors: Esther Sook Miin Wong1,4, Xavier Le Guezennec1,4, Oleg N. Demidov1, Nicolette Theresa Marshall1, Siew Tein Wang2, Janakiraman Krishnamurthy3, Norman E. Sharpless3, N. Ray Dunn2 and Dmitry V. Bulavin1,* 1 Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore 2 Institute of Medical Biology, Agency for Science, Technology and Research, Singapore 3 Departments of Medicine and Genetics, The Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC, USA 4 These authors contributed equally to this work. * Corresponding author: Dr Dmitry Bulavin, dvbulavin@imcb.a-star.edu.sg Cathy Yarbrough Agency for Science, Technology and Research (A*STAR), Singapore


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