STUDIES OF NITRATE TRANSPORT BY MARINE PHYTOPLANKTON USING 36Cl-ClO3− AS A TRANSPORT ANALOGUE. I. PHYSIOLOGICAL FINDINGS1

Transport of a nitrate analogue, ³⁶Cl-ClO₃⁻, was examined in two diatoms, Skeletonema costatum (Greve.) Cleve and Nitzschia closterium (Ehrenb) W. Sm. A dinoflagellate, Gonyaulax polyedra did not transport ClO₃⁻. Transport of ³⁶Cl-ClO₃⁻ by diatoms appeared to be active and showed saturation kinetics. The data were fitted by Michaelis-Menten equation at all but the lowest chlorate concentrations (where plots of S vs. v showed a slight concave bend). Affinity of cells for nitrate was considerably higher than for chlorate. The K_i for nitrate inhibition of chlorate transport was calculated assuming competitive inhibition. Light had little or no effect on chlorate transport. Pulse-chase experiments demonstrated that (1) ClO₃⁻ (hence NO₃⁻) was stored in two intracellular compartments of equal size, (2) internal ClO₃⁻ was exchangeable with external ClO₃⁻ (rates of efflux and influx were measured), and (3) efflux of intracellular ClO₃⁻ showed transient states following a chase of ClO₃⁻ or NO₃⁻ which stabilized after 10–20 min. Transport of chlorate was a function of growth phase.     

假体隆胸患者手术前后生命质量和自尊的评估

目的:通过对接受假体法隆胸患者的手术前后的生命质量和自尊水平进行主观的评价,得到真实、可靠的手术效果评价结果,最终提高隆胸手术患者的满意度。方法:选取接受假体法隆胸术患者共60例,在手术之前、术后6个月使用SF-36生命质量量表和Rosenberg自尊量表进行生命质量状况和自尊状况的测量评估,并和常模进行比较。结果:接受假体法隆胸患者术前SF-36生命质量量表中社会功能(SF)和精神健康(MH)两项得分明显低于常模(P0.01);术后6个月量表中社会功能(SF)和精神健康(MH)两项水平有显著改善(P0.01);Rosenberg自尊量表显示患者术后6个月的自尊水平较术前有明显的改善(P0.001)。结论:假体法隆胸手术能使患者的生命质量得到一定程度的改善,隆胸手术对患者的自尊水平有积极的显著的影响。     

髋关节骨性关节炎患者生存质量现状及其影响因素分析

目的：探讨髋关节骨性关节炎患者生存质量现状及其影响因素。方法：选择60 例髋关节骨性关节炎患者作为观察组,60 例 健康者作为对照组。采用SF-36 生存质量评价量表,比较观察组与对照组SF-36 量表各维度评分;分析影响患者生存质量的因素。 结果：①观察组SF-36 量表各维度评分均显著低于健康对照组,差异均具有统计学意义（P＜0.05）;②经Pearson 单因素分析, SF-36 量表综合得分在性别、职业、病程、治疗前景、内科慢性疾病数、10m 步行速度及K-L 分级方面的差异均具有统计学意义 （P＜0.05~0.01）;③经多元Logistic 回归分析,病程（beta=0.772,S.E.=0.689,Wald=34.027,P＜0.05,OR=1.99）、治疗前景（beta=0.778,S. E.=0.542,Wald=55.638,P＜0.05,OR=1.88）、内科慢性疾病数（beta=0.929,S.E.=0.301,Wald=12.382,P＜0.05,OR=1.72）、10m 步行速 度（beta=0.661,S.E.=0.381,Wald=19.929,P＜0.05,OR=1.69）及K-L 分级（beta=0.992,S.E.=0.526,Wald=28.371,P＜0.05,OR=2.31）为影 响髋关节骨性关节炎患者生存质量的危险因素。结论：髋关节骨性关节炎患者生存质量明显差于健康者,病程、治疗前景、内科慢 性疾病数、10m步行速度及K-L分级是影响患者生存质量的危险因素。     

Hrr25: An emerging major player in selective autophagy regulation in Saccharomyces cerevisiae

As with the case of the mechanism of autophagosome formation, studies in yeast have taken a leading role in elucidating the molecular basis of target recognition during selective autophagy. Degradation targets are recognized by receptor proteins, which also bind to Atg8 homologs on growing phagophore membranes, leading to the loading of the targets into autophagosomes. However, it remains to be elucidated how these processes are regulated. In yeast, receptors also interact with the scaffold/adaptor protein Atg11, which subsequently recruits core Atg proteins onto receptor-target complexes to initiate autophagosome formation. Recently, we found that Hrr25, a homolog of CSNK1D/casein kinase 1δ, regulates 3 of 4 selective autophagy-related pathways in the budding yeast Saccharomyces cerevisiae by a uniform mechanism: phosphoregulation of the receptor-scaffold interaction.     

Oxidized LDL induces phosphorylation of non-muscle myosin IIA heavy chain in macrophages

Oxidized LDL (oxLDL) performs critical roles in atherosclerosis by inducing macrophage foam cell formation and promoting inflammation. There have been reports showing that oxLDL modulates macrophage cytoskeletal functions for oxLDL uptake and trapping, however, the precise mechanism has not been clearly elucidated. Our study examined the effect of oxLDL on non-muscle myosin heavy chain IIA (MHC-IIA) in macrophages. We demonstrated that oxLDL induces phosphorylation of MHC-IIA (Ser1917) in peritoneal macrophages from wild-type mice and THP-1, a human monocytic cell line, but not in macrophages deficient for CD36, a scavenger receptor for oxLDL. Protein kinase C (PKC) inhibitor-treated macrophages did not undergo the oxLDL-induced MHC-IIA phosphorylation. Our immunoprecipitation revealed that oxLDL increased physical association between PKC and MHC-IIA, supporting the role of PKC in this process. We conclude that oxLDL via CD36 induces PKC-mediated MHC-IIA (Ser1917) phosphorylation and this may affect oxLDL-induced functions of macrophages involved in atherosclerosis. [BMB Reports 2015; 48(1): 48-53]     

New insights into the role of connexins in pancreatic islet function and diabetes

Multi-cellular systems require complex signaling mechanisms for proper tissue function, to mediate signaling between cells in close proximity and at distances. This holds true for the islets of Langerhans, which are multicellular micro-organs located in the pancreas responsible for glycemic control, through secretion of insulin and other hormones. Coupling of electrical and metabolic signaling between islet β-cells is required for proper insulin secretion and effective glycemic control. β-cell specific coupling is established through gap junctions composed of connexin36, which results in coordinated insulin release across the islet. Islet connexins have been implicated in both Type-1 and Type-2 diabetes; however a clear link remains to be determined. The goal of this review is to discuss recent discoveries regarding the role of connexins in regulating insulin secretion, the regulation of connexins within the islet, and recent studies which support a role for connexins in diabetes. Further studies which investigate the regulation of connexins in the islet and their role in diabetes may lead to novel diabetes therapies which regulate islet function and β-cell survival through modulation of gap junction coupling.     

Cd36, a class B scavenger receptor, functions as a monomer to bind acetylated and oxidized low-density lipoproteins

Cd36 is a small-molecular-weight integral membrane protein expressed in a diverse, but select, range of cell types. It has an equally diverse range of ligands and physiological functions, which has implicated Cd36 in a number of diseases including insulin resistance, diabetes, and, most notably, atherosclerosis. The protein is reported to reside in detergent-resistant microdomains within the plasma membrane and to form homo- and hetero-intermolecular interactions. These data suggest that this class B scavenger receptor may gain functionality for ligand binding, and/or ligand internalization, by formation of protein complexes at the cell surface. Here, we have overexpressed Cd36 in insect cells, purified the recombinant protein to homogeneity, and analyzed its stability and solubility in a variety of nonionic and zwitterionic detergents. Octylglucoside conferred the greatest degree of stability, and by analytical ultracentrifugation we show that the protein is monomeric. A solid-phase ligand-binding assay demonstrated that the purified monomeric protein retains high affinity for acetylated and oxidized low-density lipoproteins. Therefore, no accessory proteins are required for interaction with ligand, and binding is a property of the monomeric fold of the protein. Thus, the highly purified and functional Cd36 should be suitable for crystallization in octylglucoside, and the in vitro ligand-binding assay represents a promising screen for identification of bioactive molecules targeting atherogenesis at the level of ligand binding.     

Mitochondrial ribosomal protein S36 delays cell cycle progression in association with p53 modification and p21(WAF1/CIP1) expression

Ribosomal biogenesis is correlated with cell cycle, cell proliferation, cell growth and tumorigenesis. Some oncogenes and tumor suppressors are involved in regulating the formation of mature ribosome and affecting the ribosomal biogenesis. In previous studies, the mitochondrial ribosomal protein L41 was reported to be involved in cell proliferation regulating through p21(WAF1/CIP1) and p53 pathway. In this report, we have identified a mitochondrial ribosomal protein S36 (mMRPS36), which is localized in the mitochondria, and demonstrated that overexpression of mMRPS36 in cells retards the cell proliferation and delays cell cycle progression. In addition, the mMRPS36 overexpression induces p21(WAF1/CIP1) expression, and regulates the expression and phosphorylation of p53. Our result also indicate that overexpression of mMRPS36 affects the mitochondrial function. These results suggest that mMRPS36 plays an important role in mitochondrial ribosomal biogenesis, which may cause nucleolar stress, thereby leading to cell cycle delay.