微电极阵列细胞传感器芯片技术的研究进展

综述了目前国际上基于微电极阵列技术的细胞传感器芯片的研究状况。介绍了微电极阵列的工艺设计、界面模型以及在细胞电生理研究中的应用,同时分析了细胞胞外记录技术在实现组织-细胞以及细胞间信号传导过程的实时动态检测的特点和目前存在的问题。在此基础上,介绍了单细胞以及细胞传感器网络芯片技术的发展。最后,提出微电极阵列细胞传感器研究的发展方向。     

Physicochemical Properties and Fiber-Drawing Ability of Tellurite Glasses in the TeO2-ZnO-Y2O3 Ternary System

Glasses in the TeO₂-ZnO-Y₂O₃ (TZY) ternary system are examined in the present work. The vitrification domain of the chosen oxide matrix is determined and differential scanning calorimetry as well as X-ray diffraction measurements are carried out. The material characterizations reveal that Y₂O₃ incorporation cannot exceed 5 mol.% without causing detrimental crystallization within the glass. Optical transmission and refractive index investigations are conducted on compositions yielding fully amorphous samples. Next, the fiber drawing ability of selected yttrium-containing zinc-tellurite glasses is assessed and fiber-attenuation measurements in the mid-infrared are presented. Finally, a multimode step-index fiber is fabricated by combining a TZY cladding glass with a La₂O₃-based tellurite core glass. It is believed that yttrium-containing glasses could prove useful in association with other high glass transition temperature (>300 °C) TeO₂-based materials for the design of robust optical fibers with precisely engineered refractive index profiles.     

Juvenile mild traumatic brain injury elicits distinct spatiotemporal astrocyte responses

Mild-traumatic brain injury (mTBI) represents ~80% of all emergency room visits and increases the probability of developing long-term cognitive disorders in children. To date, molecular and cellular mechanisms underlying post-mTBI cognitive dysfunction are unknown. Astrogliosis has been shown to significantly alter astrocytes' properties following brain injury, potentially leading to significant brain dysfunction. However, such alterations have never been investigated in the context of juvenile mTBI (jmTBI). A closed-head injury model was used to study jmTBI on postnatal-day 17 mice. Astrogliosis was evaluated using glial fibrillary acidic protein (GFAP), vimentin, and nestin immunolabeling in somatosensory cortex (SSC), dentate gyrus (DG), amygdala (AMY), and infralimbic area (ILA) of prefrontal cortex in both hemispheres from 1 to 30 days postinjury (dpi). In vivo T2-weighted-imaging (T2WI) and diffusion tensor imaging (DTI) were performed at 7 and 30 dpi to examine tissue level structural alterations. Increased GFAP-labeling was observed up to 30 dpi in the ipsilateral SSC, the initial site of the impact. However, vimentin and nestin expression was not perturbed by jmTBI. The morphology of GFAP positive cells was significantly altered in the SSC, DG, AMY, and ILA up to 7 dpi that some correlated with magnetic resonance imaging changes. T2WI and DTI values were significantly altered at 30 dpi within these brain regions most prominently in regions distant from the impact site. Our data show that jmTBI triggers changes in astrocytic phenotype with a distinct spatiotemporal pattern. We speculate that the presence and time course of astrogliosis may contribute to pathophysiological processes and long-term structural alterations following jmTBI.     

Vers de nouveaux phénotypes et de nouvelles nosographies : de l’obésité aux maladies du tissu adipeux

The definition of obesity is based on thresholds of body mass index associated with an increase in morbimortality. This approach is relevant at a population level but it reaches some limits as far as the individual is concerned. Advances in epidemiology, physiopathology and clinics of obesity should lead to new phenotypes and nosography of obesity included in a general framework of adipose tissue disorders     

茶多酚对硝酸羟胺染毒小鼠血常规和血清生化值的影响

目的　观察绿茶提取物茶多酚对硝酸羟胺染毒小鼠血常规、血清生化值的影响。方法　采用腹腔注射硝酸羟胺建立中毒模型。雄性ICR小鼠随机分为正常组、硝酸羟胺染毒组、茶多酚预防组、茶多酚治疗组 ,常规测量各组外周血细胞和生化指标。结果　经过统计学分析 ,茶多酚可明显促进硝酸羟胺中毒导致的小鼠血常规的WBC、RBC、HGB、PLT计数改变的恢复 ,部分血清生化值AST/ALT、ChE、ALB、LDH、UA、Fe病理性改变的恢复。结论　茶多酚灌胃给药对硝酸羟胺中毒引起的氧化损伤具有一定的保护作用     

The effect of pentoxifylline on the healing of intestinal anastomosis in rats with experimental obstructive jaundice

The aims of this study were (1) to investigate the effect of experimental obstructive jaundice on the healing of intestinal anastomosis, and (2) to investigate the effect of pentoxifylline on the healing of intestinal anastomosis in rats with obstructive jaundice. Obstructive jaundice was induced in rats by the ligation and division of the common bile duct. Four days after this operation, either pentoxifylline or isotonic saline solution was administered intraperitoneally to these jaundiced rats and controls, and then intestinal anastomosis was performed. The concentrations of serum tumor necrosis factor α (TNF-α) and serum triglyceride of jaundiced and nonjaundiced rats were measured, and the quality of healing was evaluated by measuring the bursting preasure and hydroxyproline content of the anastomoses on the fifth and tenth days of anastomotic healing. Obstructive jaundice resulted in an impaired wound healing of the intestinal anastomosis in the rats. The administration of pentoxifylline to the jaundiced rats resulted in better anastomotic wound healing. The beneficial effects of pentoxifylline on anastomotic healing in rats with obstructive jaundice was attributed to its inhibitor effect on the endotoxin-induced TNF-α release from macrophages and monocytes, and the stabilizing effect on the neutrophils. Received: March 29, 1999 / Accepted: March 24, 2000     

Epithelial cell adhesion molecule is a prognosis marker for intrahepatic cholangiocarcinoma

Background

Recently, we identified a gene signature of intrahepatic cholangiocarcinoma (ICC) stroma and demonstrated its clinical relevance for prognosis. The most upregulated genes included epithelial cell adhesion molecule (EpCAM), a biomarker of cancer stem cells (CSC). We hypothesized that CSC biomarkers could predict recurrence of resected ICC.

Methods

Both functional analysis of the stroma signature previously obtained and immunohistochemistry of 40 resected ICC were performed. The relationships between the expression of CSC markers and clinicopathologic factors including survival were assessed by univariate and multivariable analyzes.

Results

Gene expression profile of the stroma of ICC highlighted embryonic stem cells signature. Immunohistochemistry on tissue microarray showed at a protein level the increased expression of CSC biomarkers in the stroma of ICC compared with nontumor fibrous liver tissue. The overexpression of EpCAM in the stroma of ICC is an independent risk factor for overall (hazard ratio = 2.6; 95% confidence interval, 1.3–5.1; P = 0.005) and disease-free survival (hazard ratio = 2.2; 95% confidence interval, 1.2–4.2; P = 0.012). In addition, the overexpression of EpCAM in nontumor fibrous liver tissue is closely correlated with a worst disease-free survival (P = 0.035).

Conclusions

Our findings provide new arguments for a potential role of CSC on ICC progression supporting the idea that targeting CSC biomarkers might represent a promise personalized treatment.     

Genetic studies of neuropeptide Y and neuropeptide Y receptors Y1 and Y5 regions in morbid obesity

Summary Synthesis and release of neuropeptide Y (NPY) are both regulated by leptin binding to its hypothalamic receptor mediating some of the effects of leptin on food intake. Moreover, NPY administration is a powerful stimulant of feeding behaviour. Thus, we investigated the potential implication of NPY, NPY-Y1 and -Y5 subtype receptors [rNPY-Y1/-Y5] in the development of human obesity. Two complementary genetic approaches were used: 1) linkage analyses between obesity and polymorphic markers located nearby NPY and rNPY-Y1/-Y5 genes (respectively on chromosomes 7p15.1 and 4q[31.3–32]) in 93 French Caucasian morbidly obese families; 2) single strand conformation polymorphism (SSCP) scanning of the coding region of the NPY and rNPY-Y1 genes performed in 50 unrelated obese patients ascertained on the basis of a body mass index of 27 kg/m² or more and a family history of obesity. No evidence of linkage between morbid obesity or obesity-related quantitative traits and NPY and rNPY-Y1/Y5 regions was found in this population. Moreover, SSCP scanning revealed no mutation in the coding region of NPY and rNPY-Y1 genes among obese subjects. These results suggest that NPY and NPY-Y1/Y5 receptors are unlikely to be implicated in the development of human morbid obesity, at least in the French Caucasian population. [Diabetologia (1997) 40: 671–675] Received: 27 December 1996 and in revised form: 26 February 1997