G + C mol%

of strain JC230(T) was 54 1% Distinct morphol

G + C mol%

of strain JC230(T) was 54.1%. Distinct morphological, physiological and genotypic differences from the previously described taxa support the classification of strain JC230(T) as a representative of a new species in the genus Spirochaeta, for which the name Spirochaeta lutea sp. nov. is proposed. The type strain is JC230(T) (=KCTC 15387(T) = DSM 29074(T)). JIB-04 (C) 2014 Elsevier GmbH. All rights reserved.”
“TRAIL (TNF-related apoptosis-inducing ligand) is a promising anticancer agent that can be potentially used as an alternative or complementary therapy because of its specific antitumor activity. However, TRAIL can also stimulate the proliferation of cancer cells through the activation of NF-kappa B, but the exact mechanism is still poorly understood. In this study, we show that chronic exposure to subtoxic concentrations of TRAIL results in acquired resistance. This resistance is associated with the increase in miR-21, miR-30c, and miR-100 expression, which target tumorsuppressor genes fundamental in the response to TRAIL. Importantly, down-regulation of caspase-8 by miR-21 blocks receptor interacting JQEZ5 protein-1 cleavage and induces the activation of NF-kappa

B, which regulates these miRNAs. Thus, TRAIL activates a positive feedback loop that sustains the acquired resistance and causes an aggressive phenotype. Finally, we prove that combinatory treatment of NF-kappa B inhibitors and TRAIL is able to revert resistance and reduce tumor growth, with important consequences for the clinical practice.”
“Ishida K, Matsumoto T, Taguchi K, Kamata K, Kobayashi T. Mechanisms underlying altered extracellular nucleotide-induced contractions in mesenteric arteries from rats in later-stage type 2 diabetes: effect of ANG II type 1 receptor antagonism. Am J Physiol Heart Circ Physiol 301: H1850-H1861, 2011. First published August 19, 2011; doi:10.1152/ajpheart.00502.2011.-Little

is known about the vascular contractile responsiveness to, and signaling pathways for, Dinaciclib extracellular nucleotides in the chronic stage of type 2 diabetes or whether the ANG II type 1 receptor blocker losartan might alter such responses. We hypothesized that nucleotide-induced arterial contractions are augmented in diabetic Goto-Kakizaki (GK) rats and that treatment with losartan would normalize the contractions. Here, we investigated the vasoconstrictor effects of ATP/UTP in superior mesenteric arteries isolated from GK rats (37-42 wk old) that had or had not received 2 wk of losartan (25 mg.kg(-1).day(-1)). In arteries from GK rats (vs.

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