Nano-topography: Quicksand for cell cycle progression?

The 3-D spatial and mechanical features of nano-topography can create alternative environments, which influence cellular response. In this paper, murine fibroblast cells were grown on surfaces characterized by protruding nanotubes. Cells cultured on such nano-structured surface exhibit stronger cellular adhesion compared to control groups, but despite the fact that stronger adhesion is generally believed to promote cell cycle progression, the time cells spend in G1 phase is doubled. This apparent contradiction is solved by confocal microscopy analysis, which shows that the nano-topography inhibits actin stress fiber formation. In turn, this impairs RhoA activation, which is required to suppress the inhibition of cell cycle progression imposed by p21/p27. This finding suggests that the generation of stress fibers, required to impose the homeostatic intracellular tension, rather than cell adhesion/spreading is the limiting factor for cell cycle progression. Indeed, nano-topography could represent a unique tool to inhibit proliferation in adherent well-spread cells.     

5DF血球分析仪检测白细胞分类计数与瑞氏染色镜检结果对比研究

目的　探讨5DF血球分析仪白细胞分类计数与传统的瑞氏染色镜检计数结果之间的差异。方法　用5分类血球分析仪和瑞氏染色法同时对10 0份血样进行分类计数,并用统计学分析研究。结果　中性粒细胞、嗜酸、嗜碱性细胞和淋巴细胞分类计数两法无明显差异(P均>0 .0 5 ) ,但单核细胞分类计数仪器法比镜检法结果偏高(P <0 .0 0 1)。结论　对于一般血液常规检查可选用仪器法筛查,而血液系统疾病或某种原因引起的细胞结构改变应选用镜检法。     

PFKFB3基因在前列腺癌中的表达及其对前列腺癌细胞糖酵解及生长的影响

目的探讨6-磷酸果糖激酶-2/果糖双磷酸酶-2同工酶3（PFKFB3）基因在前列腺癌中的表达及其对前列腺癌细胞糖酵解及生长的影响。 方法收集我院病理科前列腺增生和前列腺癌蜡块组织,应用免疫组化技术检测PFKFB3的表达水平。通过荧光定量PCR和Western blot实验检测正常前列腺上皮细胞（RWPE-1）和四种前列腺癌细胞系（PC3、LNCaP、DU145、C4-2）中PFKFB3的表达。应用RNA干扰技术敲低PFKFB3表达,采用细胞糖酵解试剂盒、CCK-8和克隆形成实验检测PFKFB3对前列腺癌细胞的糖酵解和增殖活性的影响。 结果与前列腺增生组织相比,前列腺癌组织中的PFKFB3表达量明显增高[（59.7±0.25） vs （3.08±0.16）,P<0.05],且病理Gleason评分越高,PFKFB3表达量也越高。同样PFKFB3在不同前列腺癌细胞系中均明显高表达。抑制PFKFB3基因表达后,前列腺癌细胞的糖酵解和增殖能力显著降低。 结论PFKFB3基因在前列腺癌恶性进展中表达上调,促进肿瘤细胞的糖酵解和增殖,靶向PFKFB3可能为前列腺癌分子诊断和治疗提供潜在的应用价值。     

Connexin 43 upregulation in burns promotes burn conversion through spread of apoptotic death signals

BackgroundBurn wounds continue to worsen after initial injury in a process known as burn conversion, which lasts about 3–5 days. It causes burn wounds to enlarge and deepen, leading to greater morbidity. Apoptosis is one of the factors contributing to the conversion of the zone of stasis into the zone of coagulation. Suppression of apoptosis has been associated with reducing burn conversion. Connexin 43 (Cx43) gap junctions facilitate the spread of apoptotic signals from dying cells to healthy neighbouring cells in injured tissues through the bystander effect.ObjectivesThe study is to understand the role of Cx43 in burn conversion.MethodsIn our study, 15 burn tissue samples were arranged into three groups as early (beginning of burn conversion), intermediate (extensive burn conversion) and late (established burn conversion) burns.ResultsWe found a striking increase in the amount of Cx43 protein expressed in the dermal fibroblasts (identified with heat shock protein 47 (HSP47) staining) in the zone of stasis in early and intermediate burns. These dermal fibroblasts also express high levels of cleaved-Caspase 3 indicating on-going apoptosis.ConclusionsOur findings suggest that elevation of Cx43 may play an active role in burn conversion spreading apoptosis in the early and intermediate burn wound.     

蛙皮素及其同类物与肿瘤的关系

1971年Anastasi等从一种欧洲雨蛙的皮肤中分离出蛙皮素(BN),此后,又有学者在人及哺乳动物体内发现了蛙皮素的同类物:胃泌素释放肽(GRP)和神经调节肽B(NMB),并发现蛙皮素及其同类物可通过相应受体刺激多种肿瘤的生长。从此,人们对其进行了广泛的研究。现就近年来关于BN及其同类物与肿瘤生长关系的研究作一综述。     

急性冠脉综合征患者血浆中 NT-proBNP 和hs-CRP联合检测的应用价值

目的：检测急性冠脉综合征（ACS）患者血浆中氨基末端钠尿肽前体（NT-proBNP）和超敏CRP（hs-CRP）含量水平,以探讨其在ACS诊断及预后评估中的应用价值。方法将126例ACS患者作为观察组,58例健康体检者作为对照组;用放射免疫分析法和vitros ECi免疫发光法同时检测2组样本血浆中的hs-CRP和NT-proBNP含量水平,并采用t检验比较2组的x珋±s差异有无显著性,对NT-proBNP与hs-CRP水平关系运用Pearson相关性分析。结果ACS患者组血浆中的NT-proBNP和hs-CRP含量水平均显著高于对照组（P＜0．01）,对NT-proBNP与hs-CRP浓度水平关系运用Pearson相关性分析,结果表明二者呈显著正相关（P＜0．05）。结论联合检测血浆中的NT-proBNP和hs-CRP含量水平,对ACS的诊断和预后评估具有较重要的价值。     

Effects of prenatal chronic mild stress exposure on hippocampal cell proliferation,expression of GSK-3α, β and NR2B in adult offspring during fear extinction in rats

Stress during pregnancy has been implicated as a risk factor for the development of many mental disorders; however, the influence of prenatal stress on the fear or anxiety-related behaviors, especially the fear extinction in adult offspring has been little investigated. In order to investigate how prenatal stress affects fear extinction, which is regarded as a form of new learning that counteracts the expression of Pavlovian's conditioned fear, a rat model of prenatal chronic mild stress (PNS) was used to evaluate the effects of PNS on fear extinction in adult offspring. The expression of hippocampal glycogen synthase kinase-3s (GSK-3α, β), N-methyl-d-aspartic acid receptors (NMDARs)-2B and the hippocampal cell proliferation in dentate gyrus in the adult offspring during fear extinction were studied. Our results showed that PNS significantly reduced body weight of pups, indicating PNS might induce growth retardation in offspring. Moreover, PNS significantly enhanced the freezing behavior of offspring at the phase of extinction, suggesting PNS impaired the abilities of fear extinction learning. In addition, PNS significantly increased the levels of GSK-3α, β and NR2B, but reduced hippocampal cell proliferation during fear extinction. Taken together, our findings suggest that maternal stress during pregnancy can impair the fear extinction of adult offspring, probably by affecting the neural plasticity of brain.     

Glucocorticoid Induced Leucine Zipper inhibits apoptosis of cardiomyocytes by doxorubicin

Doxorubicin (Dox) is an indispensable chemotherapeutic agent for the treatment of various forms of neoplasia such as lung, breast, ovarian, and bladder cancers. Cardiotoxicity is a major concern for patients receiving Dox therapy. Previous work from our laboratory indicated that glucocorticoids (GCs) alleviate Dox-induced apoptosis in cardiomyocytes. Here we have found Glucocorticoid-Induced Leucine Zipper (GILZ) to be a mediator of GC-induced cytoprotection. GILZ was found to be induced in cardiomyocytes by GC treatment. Knocking down of GILZ using siRNA resulted in cancelation of GC-induced cytoprotection against apoptosis by Dox treatment. Overexpressing GILZ by transfection was able to protect cells from apoptosis induced by Dox as measured by caspase activation, Annexin V binding and morphologic changes. Western blot analyses indicate that GILZ overexpression prevented cytochrome c release from mitochondria and cleavage of caspase-3. When bcl-2 family proteins were examined, we found that GILZ overexpression causes induction of the pro-survival protein Bcl-xL. Since siRNA against Bcl-xL reverses GC induced cytoprotection, Bcl-xL induction represents an important event in GILZ-induced cytoprotection. Our data suggest that GILZ functions as a cytoprotective gene in cardiomyocytes.