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Supreme Court Nominees Should Disclose Views On Constitutional Issues, USA Today Opinion Piece States
One thing that "has been conspicuously absent" from the confirmation hearings for Supreme Court nominee Sonia Sotomayor is "substance," Jonathan Turley, the Shapiro Professor of Public Interest Law at George Washington University, writes in a USA Today opinion piece. According to Turley, "The vast majority of questions and answers remained on a shallow and predictable level where Sotomayor did little more than describe current doctrines and case law -- avoiding disclosures of her own views." He continues, "What is most striking is how Sotomayor"s statements were virtually identical to both her conservative and liberal predecessors," including her comments that Roe v. Wade and Planned Parenthood v. Casey are "the precedent of the court."Turley writes, "The content-light character in these hearings is largely the product of the "Ginsburg rule" -- named after Justice Ruth Bader Ginsburg, who refused to answer questions in her 1993 confirmation hearing about any case or matter upon which she might later vote." According to Turley, "Later nominees for both parties have relied on the Ginsburg rule to turn the hearings into prolonged photo-ops for senators, who largely ask wafer-thin questions to solicit largely scripted answers." The rule "allows nominees to get by with meaningless sound bites that promise to respect precedent, the Framers [of the Constitution] and collegiality in general," he adds. Furthermore, it "tells the public nothing about a nominee"s philosophy or purpose before giving her life tenure on the world"s most powerful court," Turley writes.According to Turley, there is a "simple solution to returning substance to the confirmation process: End the Ginsburg rule by insisting that nominees answer questions about their specific views on constitutional rights." Although "the current system works well for presidents, nominees and senators," it "does little for the public or the system of justice," he writes (Turley, USA Today, 7/16).
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Yale And University Of Malaya Join Forces To Battle HIV In Prisons
In the hope of stemming one of the biggest public health crises in Southeast Asia, Yale University is partnering with the University of Malaya to fight the spread of HIV among drug users in Malaysia who are completing prison terms and transitioning back into the community. The two universities recently signed a letter of intent expressing their continued commitment to this partnership, which is funded by a $4.1 million grant from the National Institutes of Health.
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Study Shows The Negative Side To Positive Self-Statements In Self-Help Books
In times of doubt and uncertainty, many Americans turn to self-help books in search of encouragement, guidance and self-affirmation. The positive self-statements suggested in these books, such as "I am a lovable person" or "I will succeed," are designed to lift a person"s low self-esteem and push them into positive action. According to a recent study in Psychological Science, a journal of the Association for Psychological Science, however, these statements can actually have the opposite effect.
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USC Researchers Uncover Mechanism That Allows Influenza Virus To Evade The BodyÂðs Immune Response

California (USC) have identified a critical molecular mechanism that allows the influenza virus to evade the bodyÂðs immune response system. The study will be published in the May 21 issue of the journal Cell Host & Microbe. ÂöWe have found a mechanism that the influenza virus uses to inhibit the bodyÂðs immune response that emphasizes the vital role of a specific protein in defending against viruses," says Jae Jung, Ph.D., professor and chair of the Department of Molecular Microbiology and Immunology at the Keck School of Medicine of USC, and the principal investigator of the study. ÂöAlong with our previous studies (Nature 2007 and PNAS 2008), this finding could provide researchers with the information needed to create a new drug to enhance immunity and block influenza virus infection and replication." Several specific intracellular receptors are responsible for detecting the virus and activating the bodyÂðs defensive mechanisms. When a virus" RNA enters the intracellular fluid, a receptor known as retinoic-acid-inducible gene I (RIG-I) detects it and triggers a response that limits virus replication and calls the bodyÂðs defenses into action. RIG-I acts as the sensor and security force against attacks, Jung explains. Then, a protein known as TRIM25 helps RIG-I transmit an alarm signal, which ultimately floods the cell and surrounding tissue with antiviral interferons. The influenza virus is highly infectious and poses a serious and sometimes deadly health risk because of its ability to mutate into new strains and spread quickly during seasonal epidemics, as seen in the recent outbreak of the H1N1 swine flu virus, Jung says. Researchers have long been working to understand how respiratory influenza is able to slip past the bodyÂðs innate immune responses. They have found that the influenza A virus has evolved by incorporating Non-structural protein 1 (NS1) into its genome to escape the RIG-I alarm system. This process is one reason why the virus kills an average of 36,000 people every year. In fact, the 1918 "Spanish flu" pandemic influenza virus, which killed over 40 million people worldwide, muted the RIG-I response and interferon activity much more efficiently than contemporary flu viruses, Jung notes. "Despite the conceptual linking of RIG-I with flu virus NS1, however, the precise mechanism has been unclear for a long period of time," he says. By studying the immune responses of animal models, researchers found that the influenza A virus NS1 attacks TRIM25, inhibiting its ability to assist RIG-I trigger the alarm system against the virus. Remarkably, a flu virus carrying an NS1 mutant defective for this activity loses its virulence in animal models, Jung says. "We now know that the influenza virus escapes recognition via the interaction of NS1 with TRIM25, which inhibits the bodyÂðs immune response," he says. ÂöUnderstanding this host-virus interaction is an essential step in developing safe and effective drugs to target the influenza virus.² This work was performed in collaboration with Adolfo Garcia-Sastre, Ph.D., at Mt. Sinai Medical School and the final doctorate experiments of Michaela Gack, Ph.D., who is the paperÂðs first author and currently a faculty member at Harvard Medical School. "Influenza A Virus NS1 Targets the Ubiquitin Ligase TRIM25 to Evade Recognition by the Host VIral RNA Sensor RIG-I." Michaela Ulrike Gack, Randy Allen Albrecht, Tomohiko Urano, Kyung-Soo Inn, I-Chueh Huang, Elena Carnero, Michael Farzan, Satoshi Inoue, Jae Ung Jung*, Adolfo Garica-Sastre*. Cell Host & Microbe. DOI: 10.1016/j.chom.2009.04.006. USC


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