2,704 research outputs found
The Message From The U. S. A.
https://digitalcommons.library.umaine.edu/mmb-vp/4892/thumbnail.jp
Finding the Center of Mass of a Soft Spring
This article shows how to use calculus to find the center of mass position of
a soft cylindrical helical spring that is suspended vertically. The spring is
non-uniformly stretched by the action of gravity. A general expression for the
vertical position of the center of mass is obtained.Comment: LaTeX, 7 pages, 2 figures. Minor changes to agree with published
versio
PMH25 Medicaid population budget impact analysis of buprenorphine/naloxone film and tablet formulation
The long arm of childhood socioeconomic deprivation on mid‐ to later‐life cognitive trajectories:A cross‐cohort analysis
Polyphyly of non-bioluminescent Vibrio fischeri sharing a lux-locus deletion
available in PMC 2013 May 16This study reports the first description and molecular characterization of naturally occurring, non-bioluminescent strains of Vibrio fischeri. These ‘dark’V. fischeri strains remained non-bioluminescent even after treatment with both autoinducer and aldehyde, substrate additions that typically maximize light production in dim strains of luminous bacteria. Surprisingly, the entire lux locus (eight genes) was absent in over 97% of these dark V. fischeri strains. Although these strains were all collected from a Massachusetts (USA) estuary in 2007, phylogenetic reconstructions allowed us to reject the hypothesis that these newly described non-bioluminescent strains exhibit monophyly within the V. fischeri clade. These dark strains exhibited a competitive disadvantage against native bioluminescent strains when colonizing the light organ of the model V. fischeri host, the Hawaiian bobtail squid Euprymna scolopes. Significantly, we believe that the data collected in this study may suggest the first observation of a functional, parallel locus-deletion event among independent lineages of a non-pathogenic bacterial species.National Institutes of Health (U.S.) (NIH Molecular Biosciences (5T32GM007215-35))National Institutes of Health (U.S.) (NIH Microbes in Health and Disease, training grant (2T32AI055397-07))Gordon and Betty Moore FoundationBroad Institute of MIT and Harvard (SPARC programme)National Science Foundation (U.S.) (NSF IOS 0841507)National Institutes of Health (U.S.) (NIH R01 RR12294)National Science Foundation (U.S.) (NSF Microbial Systems in the Biosphere programme)Woods Hole Center for Oceans & Human Healt
Acute Overactive Endocannabinoid Signaling Induces Glucose Intolerance, Hepatic Steatosis, and Novel Cannabinoid Receptor 1 Responsive Genes
Endocannabinoids regulate energy balance and lipid metabolism by stimulating the cannabinoid receptor type 1 (CB1). Genetic deletion and pharmacological antagonism have shown that CB1 signaling is necessary for the development of obesity and related metabolic disturbances. However, the sufficiency of endogenously produced endocannabinoids to cause hepatic lipid accumulation and insulin resistance, independent of food intake, has not been demonstrated. Here, we show that a single administration of isopropyl dodecylfluorophosphonate (IDFP), perhaps the most potent pharmacological inhibitor of endocannabinoid degradation, increases hepatic triglycerides (TG) and induces insulin resistance in mice. These effects involve increased CB1 signaling, as they are mitigated by pre-administration of a CB1 antagonist (AM251) and in CB1 knockout mice. Despite the strong physiological effects of CB1 on hepatic lipid and glucose metabolism, little is known about the downstream targets responsible for these effects. To elucidate transcriptional targets of CB1 signaling, we performed microarrays on hepatic RNA isolated from DMSO (control), IDFP and AM251/IDFP-treated mice. The gene for the secreted glycoprotein lipocalin 2 (lcn2), which has been implicated in obesity and insulin resistance, was among those most responsive to alterations in CB1 signaling. The expression pattern of IDFP mice segregated from DMSO mice in hierarchal cluster analysis and AM251 pre-administration reduced (>50%) the majority (303 of 533) of the IDFP induced alterations. Pathway analysis revealed that IDFP altered expression of genes involved in lipid, fatty acid and steroid metabolism, the acute phase response, and amino acid metabolism in a CB1-dependent manner. PCR confirmed array results of key target genes in multiple independent experiments. Overall, we show that acute IDFP treatment induces hepatic TG accumulation and insulin resistance, at least in part through the CB1 receptor, and identify novel cannabinoid responsive genes
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