The outer membrane (OM) of Gram-negative bacteria is asymmetrical with its outer layer mainly populated with polyanionic lipopolysaccharide (LPS). Much empirical evidence shows how OM permeability can be altered electrostatically: if Mg(2+) or divalent cations are required for the integrity of the OM, antimicrobial peptides (AMPs) or ethylene-diaminetetraacetic acid (EDTA) can permeabilize it. Using a coarse-grained model of the outer LPS layer, in which the layer is viewed as forming discrete binding sites for opposite charges, we study how the LPS layer can be modified electrostatically. In particular, we capture systematically ion-pairing and lateral-charge correlations on the LPS layer. Our results offer a clear picture of (competitive) ion binding onto the LPS layer and its impact on the lateral packing of LPS molecules, similarly to what has been seen in experiments: divalent cations such as Mg(2+) not only neutralize the LPS layer but also make its planar charge distribution heterogeneous, thus tightening the LPS layer; on the other hand, polycationic AMPs or polyanionic EDTA can displace Mg(2+) ions from the LPS layer and counteract the favorable effect of Mg(2+). Our result will be useful for clarifying to what extent OM permeability can be modified electrostatically.
Background: Controversy still exists in the indication and timing of surgical treatment of pulmonary hamartoma (PH). The objective of this study is to summarize the experience and the outcome of the surgical treatment for pulmonary hamartomas, and to assess the effectiveness and necessity of surgical therapy administered in patients with pulmonary hamatoma as well as clinical and pathological features and long-term follow-up results.
Laying performance is an important economic trait in hens, and this physiological process is largely influenced by the liver function. The livers of hens at 20- and 30-week-old stages were investigated using the next generation sequencing to identify the differences of microRNA expression profiles. Compared with the 20-week-old hens, 67 down- and 13 up-regulated microRNAs were verified to be significant differentially expressed (false discovery rate, FDR ≤ 0.05) (SDE) in the 30-week-old. We also identified 13 down- and 6 up-regulated novel differentially expressed (DE) microRNAs. miR-22-3p and miR-146b-5p, which exhibit critical roles in mammalian lipid metabolism, showed the most abundant expression and the highest fold-change, respectively. A total of 648 potential target genes of the SDE microRNAs were identified through an integrated analysis of microRNAs and the DE genes obtained in previous RNA-sequencing, including FADS1, FADS2, ELOVL6 and ACSL5, which are critical lipid metabolism-related regulators. Bioinformatic analyses revealed that target genes were mainly enriched in lipid-related metabolism processes. This work provides the first study of the expression patterns of hepatic microRNAs between 20- and 30-week old hens. The findings may serve as a fundamental resource for understanding the detailed functions of microRNAs in the molecular regulatory systems of lipid metabolism.
Intraluminal stenting can prevent the formation of caustic esophageal stricture. The location of the cicatricial esophagus dictates whether to perform concomitant esophagectomy during esophageal reconstruction. Platysma myocutaneous flap repair is an excellent method for the treatment of severe cervical esophageal or anastomotic stricture.
The G protein ␣-subunit Gs␣ is required for hormone-stimulated cAMP generation. In pancreatic  cells, Gs␣ mediates the signaling of glucagon-like peptide 1 and other incretin hormones, which are implicated as important regulators of  cell survival and insulin release. Studies have suggested that G s␣/cAMP mediates these actions by stimulating insulin receptor substrate 2 (IRS2) expression. Mice with  cell-specific Gs␣ deficiency (GsKO) were generated by mating G s␣-floxed mice to rat insulin II promoter-cre recombinase mice. GsKO mice had poor survival and postnatal growth with low serum insulin-like growth factor 1 levels. GsKO mice also developed severe hyperglycemia and glucose intolerance with severe hypoinsulinemia and reduced islet insulin content and glucose-stimulated insulin release. GsKO mice had markedly reduced average islet size and  cell mass, which was partially explained by reduced  cell size. In addition, GsKO mice had significantly reduced  cell proliferation and increased  cell apoptosis and markedly reduced expression of the cell cycle protein cyclin D2. The effects on  cell mass and proliferation, but not apoptosis, were present from birth. Unexpectedly expression of Irs2 and the downstream gene Pdx1 were unaffected. These results show that G s␣/cAMP pathways are critical regulators of  cell function and proliferation that can work through IRS2-independent mechanisms.
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