Structural Mechanism for Viscosity of Semiflexible Polymer Melts in Shear Flow

The viscosities of semiflexible polymers with different chain stiffnesses in shear flow are studied via nonequilibrium molecular dynamics techniques. The simulation reproduces the experimentally observed results, giving a complete picture of viscosity as chain stiffness increases. Analysis of flow-induced changes in chain conformation and local structure indicates two distinct mechanisms behind a variety of viscosity curves. For polymers of small stiffnesses, it is related to flow-induced changes in chain conformation and, for those of large stiffnesses, to flow-induced instabilities of nematic structures. The four-region flow curve is confirmed for polymers of contour length close to persistence length and understood by combining the two structural mechanisms. Thus, these findings clarify the microscopic structures indicated by the macroscopic viscosity

Iron-Catalyzed, Microwave-Promoted, One-Pot Synthesis of 9-Substituted Xanthenes by a Cascade Benzylation−Cyclization Process

An efficient iron-catalyzed, microwave-promoted cascade benzylation−cyclization of phenols is reported. Benzyl acetates, benzyl bromides, and benzyl carbonates are suitable benzylating reagents. The reactions proceed to afford both 9-aryl and 9-alkyl xanthene derivatives in good to high yields using FeCl3 as the catalyst under MW irradiation conditions

DataSheet1_Kidney transcriptome and cystic kidney disease genes in zebrafish.docx

Introduction: Polycystic kidney disease (PKD) is a condition where fluid filled cysts form on the kidney which leads to overall renal failure. Zebrafish has been recently adapted to study polycystic kidney disease, because of its powerful embryology and genetics. However, there are concerns on the conservation of this lower vertebrate in modeling polycystic kidney disease.Methods: Here, we aim to assess the molecular conservation of zebrafish by searching homologues polycystic kidney disease genes and carrying transcriptome studies in this animal.Results and Discussion: We found that out of 82 human cystic kidney disease genes, 81 have corresponding zebrafish homologs. While 75 of the genes have a single homologue, only 6 of these genes have two homologs. Comparison of the expression level of the transcripts enabled us to identify one homolog over the other homolog with >70% predominance, which would be prioritized for future experimental studies. Prompted by sexual dimorphism in human and rodent kidneys, we studied transcriptome between different sexes and noted significant differences in male vs. female zebrafish, indicating that sex dimorphism also occurs in zebrafish. Comparison between zebrafish and mouse identified 10% shared genes and 38% shared signaling pathways. String analysis revealed a cluster of genes differentially expressed in male vs. female zebrafish kidneys. In summary, this report demonstrated remarkable molecular conservation, supporting zebrafish as a useful animal model for cystic kidney disease.</p

Clinical characteristics, risk factors, and prognostic analyses of coronary small vessel disease: a retrospective cohort study of 986 patients

Coronary small vessel disease (CSVD) is often associated with significant percutaneous coronary intervention (PCI) related complications, complex lesions, complex PCI, and poor long-term prognosis. We designed this retrospective study to clarify the characteristics, risk factors, and prognostic analyses of CSVD in Chinese populations A total of 986 patients who underwent coronary angiography and stent implantation at the First Affiliated Hospital of Zhejiang University School of Medicine were evaluated. Patients were grouped into CSVD or non-small vessel disease (non-CSVD) according to stent diameter. Clinical data, coronary angiography, and long-term follow-up were recorded. Multivariate logistic regression, the Kaplan–Meier method, Log-rank Test, and Cox regression model were used for statistical analysis. Alcohol consumption (OR = 0.420, 95% CI: 0.299–0.588, P P P P P P P = 0.008), stroke (1.9% vs. 0.3%, P = 0.007), target lesion revascularization (5.8% vs. 2.9%, P = 0.029), target vessel revascularization (6.8% vs. 3.4%, P = 0.016), and non-target vessel revascularization (7.8% vs. 4.0%, P = 0.012) were all substantially higher in CSVD patients. Troponin I level (OR = 1.008, 95% CI: 1.004–1.012, P P P  Compared to non-CSVD, CSVD was associated with more complex lesions, had worse revascularization efficacy, and a poorer prognosis.</p

Effect of rapamycin on cardiomyocyte cross-sectional area in HF.

<p>Representative left ventricular myocardial sections and grouped data for cardiomyocyte area in SHAM operated (1±0.04, n = 5), placebo treated HF (1.40±0.05, n = 5) and 8 mg/kg/day PO rapamycin treated HF mice (1.21±0.05, n = 6). Data are mean ± SEM. †: <i>P</i><0.05 vs SHAM, ‡: <i>P</i><0.05 vs. placebo treated HF mice.</p

Effect of rapamycin on myocardial mTOR signaling in normal mice.

<p>Western blots and grouped data are shown for S6K1 and Thr389 phosphorylated S6K1 (A), or S6 and Ser235/236 phosphorylated S6 (B) in rapamycin (8 mg/kg/day PO, n = 4) versus placebo treated normal mice (n = 4). Rapamycin treatment showed a strong trend towards decreasing total S6K1 expression, whereas Thr389 phosphorylated S6K1 and total and Ser235/236 phosphorylated S6 were all significantly decreased. Data are mean ± SEM. †: <i>P</i><0.05 vs. placebo.</p

Effect of rapamycin and/or losartan in TAC mice with heart failure (TAC-HF).

<p>BW: body weight; EF: ejection fraction; HW: heart weight; LV: left ventricular; LVEDD: Left ventricular end diastolic dimension; LVSP: LV systolic pressure. †: <i>P</i><0.05 vs TAC-HF + placebo and ‡: <i>P</i><0.05 vs TAC-HF + Rapamycin.</p

Effect of rapamycin on myocardial fibrosis in HF.

<p>Representative examples of picrosirius red stained left ventricular sections (A) and grouped data for interstitial fibrosis score (B) and relative collagen type I (C) and III (D) transcript levels in SHAM operated, placebo treated HF and 8 mg/kg/day PO rapamycin treated HF mice. Interstitial fibrosis scores were significantly higher in HF (n = 13) and HF + rapamycin mice (n = 11) when compared to SHAM (n = 8). For collagen type I and III transcripts, expression levels were significantly higher in HF (n = 5) and HF + rapamycin mice (n = 4) when compared to SHAM (n = 4). Data are mean ± SEM. †: <i>P</i><0.05 vs SHAM.</p

Effect of rapamycin on autophagy in HF.

<p>Representative Western blots and grouped data for LC3B-II expression (bottom band) in myocardium from SHAM operated (n = 6), placebo treated HF (n = 6) and 8 mg/kg/day PO rapamycin treated HF mice (n = 6). Std: A standard LV homogenate sample for reliable comparison across gels. Data are mean ± SEM. †: <i>P</i><0.05 vs SHAM, ‡: <i>P</i><0.05 vs. placebo treated HF mice.</p

Effect of rapamycin on myocardial mTOR signaling in HF.

<p>Representative Western blots and grouped data for total or Thr389 phosphorylated S6K1 (A) and total or Ser235/236 phosphorylated S6 (B) in SHAM operated (n = 6), placebo treated HF (n = 6) and 8 mg/kg/day PO rapamycin treated HF mice (n = 6). Std: A standard LV homogenate sample for reliable comparison across gels. Data are mean ± SEM. †: <i>P</i><0.05 vs SHAM, ‡: <i>P</i><0.05 vs. placebo treated HF mice.</p