367 research outputs found

    Myostatin dysfunction is associated with reduction in overload induced hypertrophy of soleus muscle in mice

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    Acknowledgements This project was also supported by Marie Curie International Reintegration Grant 249156 (A. Lionikas) and the grants VP1-3.1-SMM-01-V-02-003 (A. Kilikevicius) and MIP-067/2012 (T. Venckunas) from the Research Council of Lithuania as well as the grant from the Ministry of Higher Education of Saudi Arabia (Y. Alhind). We wish also to thank Mrs Indre Libnickiene for her excellent technical assistance provided during the project.Peer reviewedPostprin

    Obesity resistant mechanisms in the Lean polygenic mouse model as indicated by liver transcriptome and expression of selected genes in skeletal muscle

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    <p>Abstract</p> <p>Background</p> <p>Divergently selected Lean and Fat mouse lines represent unique models for a polygenic form of resistance and susceptibility to obesity development. Previous research on these lines focused mainly on obesity-susceptible factors in the Fat line. This study aimed to examine the molecular basis of obesity-resistant mechanisms in the Lean line by analyzing various fat depots and organs, the liver transcriptome of selected metabolic pathways, plasma and lipid homeostasis and expression of selected skeletal muscle genes.</p> <p>Results</p> <p>Expression profiling using our custom Steroltalk v2 microarray demonstrated that Lean mice exhibit a higher hepatic expression of cholesterol biosynthesis genes compared to the Fat line, although this was not reflected in elevation of total plasma or liver cholesterol. However, FPLC analysis showed that protective HDL cholesterol was elevated in Lean mice. A significant difference between the strains was also found in bile acid metabolism. Lean mice had a higher expression of <it>Cyp8b1</it>, a regulatory enzyme of bile acid synthesis, and the <it>Abcb11 </it>bile acid transporter gene responsible for export of acids to the bile. Additionally, a higher content of blood circulating bile acids was observed in Lean mice. Elevated HDL and upregulation of some bile acids synthesis and transport genes suggests enhanced reverse cholesterol transport in the Lean line - the flux of cholesterol out of the body is higher which is compensated by upregulation of endogenous cholesterol biosynthesis. Increased skeletal muscle <it>Il6 </it>and <it>Dio2 </it>mRNA levels as well as increased activity of muscle succinic acid dehydrogenase (SDH) in the Lean mice demonstrates for the first time that changes in muscle energy metabolism play important role in the Lean line phenotype determination and corroborate our previous findings of increased physical activity and thermogenesis in this line. Finally, differential expression of <it>Abcb11 </it>and <it>Dio2 </it>identifies novel strong positional candidate genes as they map within the quantitative trait loci (QTL) regions detected previously in crosses between the Lean and Fat mice.</p> <p>Conclusion</p> <p>We identified novel candidate molecular targets and metabolic changes which can at least in part explain resistance to obesity development in the Lean line. The major difference between the Lean and Fat mice was in increased liver cholesterol biosynthesis gene mRNA expression, bile acid metabolism and changes in selected muscle genes' expression in the Lean line. The liver <it>Abcb11 </it>and muscle <it>Dio2 </it>were identified as novel positional candidate genes to explain part of the phenotypic difference between the Lean and Fat lines.</p

    Measurement of Branching Fractions and Rate Asymmetries in the Rare Decays B -> K(*) l+ l-

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    In a sample of 471 million BB events collected with the BABAR detector at the PEP-II e+e- collider we study the rare decays B -> K(*) l+ l-, where l+ l- is either e+e- or mu+mu-. We report results on partial branching fractions and isospin asymmetries in seven bins of di-lepton mass-squared. We further present CP and lepton-flavor asymmetries for di-lepton masses below and above the J/psi resonance. We find no evidence for CP or lepton-flavor violation. The partial branching fractions and isospin asymmetries are consistent with the Standard Model predictions and with results from other experiments.Comment: 16 pages, 14 figures, accepted by Phys. Rev.

    Observation of time-reversal violation in the B0 meson system

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    The individually named authors work collectively as The BABAR Collaboration. Copyright @ 2012 American Physical Society.Although CP violation in the B meson system has been well established by the B factories, there has been no direct observation of time-reversal violation. The decays of entangled neutral B mesons into definite flavor states (B0 or BÂŻÂŻÂŻ0), and J/ψK0L or ccÂŻK0S final states (referred to as B+ or B−), allow comparisons between the probabilities of four pairs of T-conjugated transitions, for example, BÂŻÂŻÂŻ0→B− and B−→BÂŻÂŻÂŻ0, as a function of the time difference between the two B decays. Using 468×106 BBÂŻÂŻÂŻ pairs produced in ΄(4S) decays collected by the BABAR detector at SLAC, we measure T-violating parameters in the time evolution of neutral B mesons, yielding ΔS+T=−1.37±0.14(stat)±0.06(syst) and ΔS−T=1.17±0.18(stat)±0.11(syst). These nonzero results represent the first direct observation of T violation through the exchange of initial and final states in transitions that can only be connected by a T-symmetry transformation.DOE and NSF (USA), NSERC (Canada), CEA and CNRS-IN2P3 (France), BMBF and DFG(Germany), INFN (Italy), FOM (The Netherlands), NFR (Norway), MES (Russia), MINECO (Spain), STFC (United Kingdom). Individuals have received support from the Marie Curie EIF (European Union), the A. P. Sloan Foundation (USA) and the Binational Science Foundation (USA-Israel)

    Editorial: Advancing our commitment to antiracist scholarship

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    Social work prides itself as a profession committed to improving the lives of people who are vulnerable, oppressed, and living in poverty. Achieving this mission requires candid conversations about racism as a social justice and public health issue and the role of social work in dismantling white supremacy and promoting racial justice. At its core, research on social work practice and policy should focus on examining how racism and inequality undermine the health, well-being, and social mobility of diverse and marginalized populations. We write this statement as a call to social work researchers to prioritize pursuits that will surface and motivate action to address the causes and consequences of racism. We also call on researchers to renew their commitment to scholarship that alleviates the suffering in Black, Indigenous, and other communities of color
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