安宫牛黄丸中小檗碱的HPLC法测定

本文报道用HPLC法测定黄连及含黄连中成药安宫牛黄丸中小檗碱型生物碱。实验结果表明选用硅胶柱为固定相,以醋酸乙酯—甲酸—乙醇(15:3:2)为流动相,能使样品中四种小檗碱型的生物碱获得最佳分离。用此法测得不同厂家生产的安宫牛黄丸中盐酸小檗碱的含量为0.331～0.456%,平均回收率为97.23%,变异系数为1.2%。     

Stochastic nanoroughness modulates neuron–astrocyte interactions and function via mechanosensing cation channels

Extracellular soluble signals are known to play a critical role in maintaining neuronal function and homeostasis in the CNS. However, the CNS is also composed of extracellular matrix macromolecules and glia support cells, and the contribution of the physical attributes of these components in maintenance and regulation of neuronal function is not well understood. Because these components possess well-defined topography, we theorize a role for topography in neuronal development and we demonstrate that survival and function of hippocampal neurons and differentiation of telencephalic neural stem cells is modulated by nanoroughness. At roughnesses corresponding to that of healthy astrocytes, hippocampal neurons dissociated and survived independent from astrocytes and showed superior functional traits (increased polarity and calcium flux). Furthermore, telencephalic neural stem cells differentiated into neurons even under exogenous signals that favor astrocytic differentiation. The decoupling of neurons from astrocytes seemed to be triggered by changes to astrocyte apical-surface topography in response to nanoroughness. Blocking signaling through mechanosensing cation channels using GsMTx4 negated the ability of neurons to sense the nanoroughness and promoted decoupling of neurons from astrocytes, thus providing direct evidence for the role of nanotopography in neuron–astrocyte interactions. We extrapolate the role of topography to neurodegenerative conditions and show that regions of amyloid plaque buildup in brain tissue of Alzheimer’s patients are accompanied by detrimental changes in tissue roughness. These findings suggest a role for astrocyte and ECM-induced topographical changes in neuronal pathologies and provide new insights for developing therapeutic targets and engineering of neural biomaterials.Cellular homeostasis in the brain tissue is believed to be regulated primarily by a complex spatiotemporal signaling environment involving soluble neurotrophic factors (1, 2). These factors, including neurotrophins such as brain-derived neurotrophic factor, the TGF-β family including bone morphogenetic proteins (BMPs), and the IL-6 superfamily including ciliary neurotrophic factor (CNTF), regulate survival, steer progenitor fate decision, and critically affect the development of the nervous system as well as the homeostasis of the adult CNS (3–6). However, developmental processes such as axon pathfinding, synapse formation, nervous system patterning, neuronal plasticity, and degeneration fail to be explained solely on the basis of soluble factors. There is increasing evidence that physical variables such as the stiffness of a cellular environment influence cell development (7–12). However, the cells of the brain tissue reside in a soft environment that is rich in polysaccharides (13, 14). In the context of neuronal development and neurophysiology, astrocytes have an established role in maintaining neuronal function. They form a vast network that provides the physical and biochemical matrix over which neurons thrive and function (15, 16). The plasticity found in the brain can be attributed in part to the morphological changes that occur in astrocyte processes that can not only alter the geometry of the neuronal environment but also induce dynamic changes in astrocyte–neuron interactions affecting neurotransmission, signal gradients, and the relationship between synapses (15). Interestingly, the changes to the physical aspects of a neuronal environment can originate from changes to morphology of support cells such as astrocytes and also changes to ECM structure and properties. Cells and ECM polysaccharides play an important role in growth, differentiation, and migration of neural precursors, as well as in repair and plasticity in the central nervous system (17, 18). However, in addition to a biological function, cells and macromolecules provide a physically defined environment (19, 20), and we postulate a significant role for topography in neural development. Studies to date have focused on the effects of microscale topography, deterministic roughness, and substrate chemistry on neurite outgrowth and neuronal function (7, 21–23). However, the influence of ECM-like nanotopography on neuronal development and fate is a realm that has not been investigated thus far. Therefore, in this work we specifically focus on the impact of stochastic nanoroughness as would be provided by neighboring cells and ECM molecules on neuronal cell interactions, function, and differentiation.     

论卫生船舶在登陆作战中的配置

在大规模登陆作战中需要大量的卫生船舶实施各种保障,因此必须对卫生船舶进行合理的配置,保证其既能有效地完成保障任务,又能避免重叠配置造成浪费．卫生船舶的配置应与指挥关系、保障任务战时分类相适应,具体配置时按医院船、卫生运输船、卫生救护艇的保障要求配置,并可根据保障任务的变化进行相应的调整．     

黄柏及中成药中小檗碱和巴马亭的高效液相色谱法测定

本文以正相高效液相色谱法,用窗口图解技术对色谱条件进行了优化。对黄柏及其中成药中的有效成分——小檗碱、巴马亭的提取、测定条件、标准曲线进行了研究。并对两种含黄柏的中成药样品进行了分析。其中小檗碱的回收率均在97%以上,巴马亭的回收率均在96%以上。     

Detection of colonic polyps on single-contrast barium enema study: emphasis on the elderly

A systems approach was employed to improve results of the single-contrast barium enema examination for detection of colonic polyps. Improvements were made in each of the following areas: radiographic-fluoroscopic equipment, fluoroscopic-television images, screen-film combinations, barium suspensions, examination techniques, imaging sequences, and quality controls. Radiologic-endoscopic correlation was undertaken for 137 colonic polyps seen endoscopically in 91 patients. The average age of the patients was 69 years. The sensitivity of the single-contrast examination for detection of all polyps was 80%. Polyps 5-9 mm in size were detected with 66% sensitivity, while 94% of polyps 10 mm or larger were detected. The results indicate that the sensitivity of a suitably performed single-contrast barium enema examination may approach that of the double-contrast study for the detection of colonic polyps, even in an elderly and infirm patient population.     

A Novel Therapeutic Strategy for Attenuating Neutrophil-Mediated Lung Injury In Vivo

OBJECTIVE: To evaluate the effect of inhalation of aerosolized opsonized dead Escherichia coli on inflammatory pulmonary neutrophil (PMN) apoptosis, lung injury, and survival in a PMN-mediated lung injury model in vivo. SUMMARY BACKGROUND DATA: Neutrophils that have transmigrated into an inflammatory focus display increased functional capacity and delayed apoptosis, resulting in an increased capacity to injure normal host tissue. The authors have previously shown that E. coli induces PMN apoptosis in vitro. METHODS: Lung injury mediated by PMNs was established by aortic occlusion and reperfusion. Adult male Sprague-Dawley rats were randomized into four groups: sham ischemia-reperfusion (I/R) treated with intratracheal inhalation of aerosolized normal saline, I/R treated with aerosolized normal saline intratracheally, I/R treated with aerosolized opsonized dead E. coli intratracheally, and I/R treated with aerosolized opsonized dead E. coli and the caspase inhibitor zVAD-FMK intratracheally 5 minutes before reperfusion. Both systemic and bronchoalveolar lavage PMNs were isolated and apoptosis was quantified at 0, 6, 12, 18, and 24 hours. Lung injury parameters including wet/dry lung weight ratio, histology, myeloperoxidase activity, and protein content were also assessed. In addition, a survival study was performed, both in a prophylactic and in a therapeutic setting. RESULTS: Administration of aerosolized dead E. coli before the reperfusion injury induced pulmonary PMN apoptosis and reversed the delayed apoptosis evident in the I/R plus normal saline group. There was also a significant improvement in lung injury parameters as well as in survival, both prophylactically as well as therapeutically. CONCLUSIONS: Directly modulating PMN cell death represents a novel mechanism for attenuating PMN-mediated lung injury and may ultimately benefit the outcome in patients with adult respiratory distress syndrome.     

肺源性心脏病急性发作期免疫功能的改变

目的:观察肺源性心脏病(简称肺心病)急性发作期患者免疫功能的变化。方法:选择南华大学附属第一医院2004-11/2006-01收治慢性肺心病急性发作期患者60例为肺心病组,于急性加重期入院第2天7:00,空腹抽取静脉血,采用流式细胞仪检测T细胞亚群CD3 、CD4 、CD8 及自然杀伤细胞活性,免疫浊度法检测体液免疫指标(IgG,IgM,IgA及补体C3)。以同期60例健康体检者为对照。结果:120例是否受试者均进入结果分析。①T细胞亚群:肺心病组CD3 ,CD4 水平低于对照组(0.52±0.06,0.62±0.04;0.32±0.06,0.41±0.06;P均<0.05),CD4 /CD8 高于对照组(1.96±0.26,1.84±0.78,P<0.05)。②免疫血清指标:肺心病组IgA、补体C3及自然杀伤细胞活性低于对照组[(1.26±0.74),(2.45±0.85)g/L;(6200±217),(9960±302)mg/L;0.34±0.08,0.57±0.07;P均<0.05]。结论:肺源性心脏病急性发作期患者的细胞免疫和体液免疫功能均受损,尤以细胞免疫功能受损更突出,且与病情呈平行关系。