Targeted overexpression of inducible 6-phosphofructo-2-kinase in adipose tissue increases fat deposition but protects against diet-induced insulin resistance and inflammatory responses

Increasing evidence demonstrates the dissociation of fat deposition, the inflammatory response, and insulin resistance in the development of obesity-related metabolic diseases. As a regulatory enzyme of glycolysis, inducible 6-phosphofructo-2-kinase (iPFK2, encoded by PFKFB3) protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance independently of adiposity. Using aP2-PFKFB3 transgenic (Tg) mice, we explored the ability of targeted adipocyte PFKFB3/iPFK2 overexpression to modulate diet-induced inflammatory responses and insulin resistance arising from fat deposition in both adipose and liver tissues. Compared with wild-type littermates (controls) on a high fat diet (HFD), Tg mice exhibited increased adiposity, decreased adipose inflammatory response, and improved insulin sensitivity. In a parallel pattern, HFD-fed Tg mice showed increased hepatic steatosis, decreased liver inflammatory response, and improved liver insulin sensitivity compared with controls. In both adipose and liver tissues, increased fat deposition was associated with lipid profile alterations characterized by an increase in palmitoleate. Additionally, plasma lipid profiles also displayed an increase in palmitoleate in HFD-Tg mice compared with controls. In cultured 3T3-L1 adipocytes, overexpression of PFKFB3/iPFK2 recapitulated metabolic and inflammatory changes observed in adipose tissue of Tg mice. Upon treatment with conditioned medium from iPFK2-overexpressing adipocytes, mouse primary hepatocytes displayed metabolic and inflammatory responses that were similar to those observed in livers of Tg mice. Together, these data demonstrate a unique role for PFKFB3/iPFK2 in adipocytes with regard to diet-induced inflammatory responses in both adipose and liver tissues.     

小鼠血管内膜增生模型的建立

该文主要介绍一种可以在小鼠中有效地诱导血管内膜增生的方法。该方法使用硅胶管嵌套小鼠股动脉,造成股动脉血管内膜增生。病理切片观察表明,实验组小鼠股动脉与假手术组相比出现了内膜层和中膜层不规则增厚,管腔狭窄,细胞排列紊乱,内膜炎症细胞浸润等。免疫组织化学染色显示内膜增生部分是由于血管平滑肌细胞（VsMCs）增生和基质积聚所致。该模型的建立对动脉粥样硬化病理机制研究和治疗药物的研发具有重要意义。     

有丝分裂细胞死亡

细胞死亡有坏死、凋亡、裂亡、自体吞噬等多种方式。细胞裂亡指细胞经过一次有丝分裂后才开始死亡的现象。本文综述了对于细胞裂亡这种新型细胞死亡方式的初步认识。     

The alternative pathway in cucumber seedlings under low temperature stress was enhanced by salicylic acid

The alternative pathway is a cyanide-resistant and non-phosphorylatory electron transport pathway in mitochondria of higher plants. Alternative oxidase (AOX) is the terminal oxidase of this pathway. Our present study investigated the effect of exogenous salicylic acid (SA) on alternative pathway in cucumber (Cucumis sativus L.) seedlings under low temperature stress. Results showed that during the process of low temperature stress, the alternative pathway capacity was enhanced as AOX expression increased in SA pretreated seedlings. Compared with seedlings without SA pretreatment, slower decrease of relative water content and lower levels of electrolyte leakage, H₂O₂ and malonyldialdehyde content were detected in SA pretreated seedlings. These results indicated that SA could alleviate the injury caused by low temperature on cucumber seedlings. Since the special protective functions of alternative pathway and AOX in plants, we suggested that the alternative pathway was related to SA-mediated plant resistance to environmental stresses such as low temperature.     

两种治疗方案对脑出血病人康复的影响

脑卒中是急性的脑部血液循环障碍造成的局部脑损害,又叫中风或脑血管意外,是现代中老年人健康的重要威胁,脑出血是其中的一种情况。采用由引导放松干预治疗的方法对脑出血患者进行护理干预,通过监测患者的血压、呼吸以及心率变化来判定干预效果,同时通过CT扫描来判定康复效果。干预结果表明：引导放松这种护理干预能够通过有效的稳定患者的收缩压和舒张压促进患者的康复。研究表明引导放松干预治疗对脑卒中病人的治疗具有一定的推广应用价值。     

Assessment of antifungal effects of a novel compound from <Emphasis Type="Italic">Burkholderia cepacia</Emphasis> against <Emphasis Type="Italic">Fusarium solani</Emphasis> by fluorescent staining

A novel compound CF66I produced by Burkholeria cepacia was investigated for its antifungal effects against Fusarium solani by three different fluorescent dyes. Dual staining with propidium iodide (PI) and fluorescein diacetate (FDA) demonstrated high doses of CF66I (120.0 μg ml⁻¹) killed the fungi by acting primarily on the cell membrane. However, at fungistatic concentration (20.0 μg ml⁻¹) of this compound, microscopic observations revealed swelling hyphae with abnormal chitin deposition, as determined by Calcofluor white (CFW) staining, which was indicative of the alterations in cell wall structure. In addition, inhibition of intracellular esterases activity was observed. These results led us to conclude that low doses of CF66I probably inhibited the fungal growth by interfering with the cell metabolic pathways.     

Angiostatin production in cultivation of recombinant Pichia pastoris fed with mixed carbon sources

A recombinant strain of Pichia pastoris with a phenotype of Mut^S was used to produce angiostatin. Due to the low methanol consumption rate of this strain, both methanol and glycerol feedings, that produced oscillation in dissolved O₂ concentration, were used during the expression phase to improve cell growth and angiostatin expression. However, enhanced cell growth led to nitrogen limitation that suppressed further production of angiostatin, but addition of ammonia allowed angiostatin concentration to reach 108 mg l^–1 after an expression period of 96 h. The ratio of consumed glycerol to methanol of 1.5:1 (w/w) in the expression phase suggested that methanol played an important role in the metabolism of carbon sources.     

半导体矿物介导非光合微生物利用光电子新途径

自然界中微生物按其能量代谢途径主要分为两种:光能营养微生物和化能营养微生物.化能营养微生物作为非光能营养微生物长期被排除在以日光为能量来源的能量利用途径之外.本文介绍了一种新的微生物能量利用途径,即非光能营养微生物通过半导体矿物光催化作用来利用太阳能进行生长.实验室模拟体系中,金属氧化物、金属硫化物等天然半导体矿物在模拟日光激发下产生的光电子促进了化能自养与异养微生物的生长.研究结果表明微生物的生长与光子能量和光子数量密切相关,同时不同波长光辐照下的微生物生长情况与矿物的光吸收谱相吻合.这一能量利用途径的光能-生物能转化效率为0.13‰-1.90‰.在含有天然半导体矿物与天然微生物的红壤体系中,进一步发现半导体矿物光催化能够明显改变环境微生物的种群结构.已有的研究揭示了一种新发现并极有可能长期在地球上存在的微生物能量利用途径,即通过自然界中半导体矿物日光催化作用产生的光电子能够促进非光能营养微生物的生长代谢活动.     

冬虫夏草寄主蒲氏钩蝠蛾的生物学

蒲氏钩蝠蛾Thitarodes pui是冬虫夏草Ophiocordyceps sinensis的寄主昆虫种类之一,分布在西藏色季拉山海拔4100～4650 m的高寒灌丛草甸和高寒草甸.采用野外调查和人工饲养相结合的方法,对蒲氏钩蝠蛾的生物学进行了研究.结果表明,蒲氏钩蝠蛾的世代发育需要3～4年历时约1095～1460 ...     

Cytoglobin Exhibits Anti-Fibrosis Activity on Liver In Vivo and In Vitro

Cytoglobin, generated using genetic engineering method, is a kind of recombinant human stellate cell activation-associated protein. We speculate that it could influence the development of hepatic fibrosis like Sellate cell activation-associated protein which was discovered by Kawada et al. Therefore, we investigated its anti-fibrosis effect on liver both in vivo and in vitro. During our research, we found that cytoglobin showed obvious effect compared with the control group on Thioacetamide-induced liver fibrosis in SD rats, including significantly decrease in aspartate aminotransferase, Hyaluronic acid, laminin and collagen I(Col I) levels in serum and hydroxyproline in livers, which are the important indices reflecting the degree of hepatic fibrosis. Meanwhile, the viability of rat hepatic stellate cell line T6 (HSC-T6) cells was inhibited by cytoglobin and the apoptosis induced by cytoglobin in HSC-T6 cells was detected by Annexin V/PI double staining. Activation of the caspase cascade including caspase-3 for the intrinsic pathways was demonstrated. The results also showed that the expression of Bcl-2 protein decreased whereas that of Bax protein increased, leading to an increase of the Bax/Bcl-2 ratio. Our results demonstrated that cytoglobin exhibited anti-fibrosis activity on livers in vivo and in vitro, involving apoptosis induction.