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Neurobiological Technologies' Partner, Celtic Pharma, Announces Results Of XERECEPT(R) Phase 3 Clinical Program
Neurobiological Technologies, Inc. (Nasdaq: NTII) (NTI(R)) announced that Celtic Pharmaceutical Holdings L.P. (Celtic Pharma) has announced the results from its Phase 3 Clinical Program for XERECEPT(R) in patients with edema associated with brain tumors and from preclinical studies of XERECEPT in brain tumor models.
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Maternally Inherited Neurological Disorder In Golden Retriever Dogs Is Caused By A Mutation In Mitochondrial DNA
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Jaloma Pacifiers Recalled Due To Choking Hazard
The Connecticut Department of Consumer Protection is notifying consumers about a voluntary recall announced by the U.S. Consumer Product Safety Commission. The recalled Jaloma Pacifiers were sold in retail stores in New Jersey and New York from February 2008 through March 2009, for approximately $1.00. Although not sold in Connecticut stores, this recalled product may have been purchased while visiting the above noted states or may have been sent to Connecticut as a gift. The pacifiers were manufactured in Mexico and imported by Gromex Inc., of Passaic, New Jersey. Although no injuries and/or incidents have been reported, the potential for injury is high due to the pacifier mouth guard and the ventilation holes are too small and fail to meet federal safety standards, for this reason, the pacifier poses a choking hazard to young children.
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Role For CISD2 Gene In Human Disease And Lifespan Control

In the May 15th issue of G&D, Dr. Ting-Fen Tsai (The National Yang-Ming University, Taiwan) and colleagues present a new animal model of human Wolfram Syndrome, and effectively link CISD2 gene function, mitochondrial integrity and aging in mammals. Wolfram Syndrome (WFS) is a rare, inherited neurodegenerative disorder. It is clinically heterogeneous, but it is primarily characterized by juvenile-onset diabetes mellitus, optic atrophy and premature death. Two different categories of WFS (WFS1 and 2) are recognized, each with its own subset of variable symptoms, and resulting from mutations in the WFS1 and CISD2 genes, respectively. The CISD2 gene is located on the long arm of human chromosome number 4, which has been previously implicated in the regulation of human longevity through a comparative genome analysis of centenarian siblings. Dr. Tsai"s group sought to uncover the physiological function of CISD2. The researchers engineered CISD2-deficient knock-out mice and, by 8 weeks old, observed an obvious premature-aging phenotype. The prematurely-aging CISD2-mutant mice displayed decreased body weight, shortened lifespan, and lower subcutaneous fat deposition, as well as clinical symptoms of WFS2 patients, including early-onset degeneration of optic, muscular and nervous tissues, and glucose sensitivity. Further study revealed that the Cisd2 protein is localized to the mitochondria, where it is required for proper mitochondrial structure and function. This work establishes WFS2 as a mitochondrial-mediated disorder, whereby dysfunction in these cellular energy factories underlies muscle and neural cell degeneration, and accelerated ageing. Future work will examine the utility of this CISD2 mouse model to understand WFS2 pathogenesis, as well as explore the potential lifespan-extending effects of increased Cisd2 expression. Heather Cosel-Pieper Cold Spring Harbor Laboratory


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