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1.
米非司酮作用于兔输卵管收缩活动与Ca^2+关系的研究   总被引:1,自引:0,他引:1  
通过“结合化学分离与原子吸收分光光度法”对Ca^2 含量测定和离体输卵管肌条收缩记录方法,研究米非司酮(Ru486)对增加假孕(4d)兔输卵管平滑肌收缩频率,而不改变其收缩张力和振幅时与Ca^2 之间的关系,结果提示:(1)Ru486对输卵管分泌液和组织内Ca^2 的含量分布无明显影响;(2)Ru486具有降低细胞外液高Ca^2 浓度促Ca^2 内流,而使收缩增强的效应,且能协同Ca^2 通道阻断剂(Verapamil)抑制细胞外Ca^2 内流,而致收缩减弱的效应。  相似文献   
2.

Background  

The pathogenesis of idiopathic Parkinson's disease (PD) remains elusive, although evidence has suggested that neuroinflammation characterized by activation of resident microglia in the brain may contribute significantly to neurodegeneration in PD. It has been demonstrated that aggregated α-synuclein potently activates microglia and causes neurotoxicity. However, the mechanisms by which aggregated α-synuclein activates microglia are not understood fully.  相似文献   
3.
There were 40 cases of Achromobacter xylosoxidans bacteremia during a 6-year period in a medical center in northern Taiwan. Males outnumbered females (72.5% vs 27.5%). Common underlying diseases and conditions in these 40 bacteremic patients were malignancies (57.5%), central venous catheter implants (55%), surgery (35%), neutropenia (30%) and use of steroids (25%). Recurrent bacteremia occurred in 4 patients (10%), all of whom had a central venous catheter implant which was considered the most probable source of infection. More than one-quarter (27.5%) of the cases were community acquired. The mortality rate due to A. xylosoxidans bacteremia was 47.5%. Risk factors significantly associated with mortality were nosocomial acquisition and polymicrobial bacteremia. Disk susceptibility testing showed that these isolates were resistant to aminoglycosides and most cephalosporins but were susceptible to piperacillin, imipenem, ceftazidime and trimethoprim-sulfamethoxazole.  相似文献   
4.
Burn survivors experience myriad associated symptoms such as pain, pruritus, fatigue, impaired motor strength, post-traumatic stress, depression, anxiety, and sleep disturbance. Many of these symptoms are common and remain chronic, despite current standard of care. One potential novel intervention to target these post burn symptoms is transcranial direct current stimulation (tDCS). tDCS is a non-invasive brain stimulation (NIBS) technique that modulates neural excitability of a specific target or neural network. The aim of this work is to review the neural circuits of the aforementioned clinical sequelae associated with burn injuries and to provide a scientific rationale for specific NIBS targets that can potentially treat these conditions. We ran a systematic review, following the PRISMA statement, of tDCS effects on burn symptoms. Only three studies matched our criteria. One was a feasibility study assessing cortical plasticity in chronic neuropathic pain following burn injury, one looked at the effects of tDCS to reduce pain anxiety during burn wound care, and one assessed the effects of tDCS to manage pain and pruritus in burn survivors. Current literature on NIBS in burn remains limited, only a few trials have been conducted. Based on our review and results in other populations suffering from similar symptoms as patients with burn injuries, three main areas were selected: the prefrontal region, the parietal area and the motor cortex. Based on the importance of the prefrontal cortex in the emotional component of pain and its implication in various psychosocial symptoms, targeting this region may represent the most promising target. Our review of the neural circuitry involved in post burn symptoms and suggested targeted areas for stimulation provide a spring board for future study initiatives.  相似文献   
5.
目的:探讨鼠类携带莱姆病螺旋体情况。方法:用BSK培养基分离病原、单克隆抗体鉴定。结果:从白腹巨鼠和褐家鼠体内分离出2株疏螺旋体,经用莱姆病螺旋体种属特异的单克隆抗体进行间接免疫荧光抗体试验,证实均为莱姆病螺旋体,命名为MD21和MD55。结论:首次从病原学证实鼠类为粤东地区莱姆病螺旋体的主要宿主动物。  相似文献   
6.
In this study, the failure mechanisms of Cu-Cu joints under thermal cycling were investigated. Two structures of dielectrics (PBO/underfill/PBO and SiO2) were employed to seal the joints. Stress gradients induced in the joints with the different dielectrics were simulated using a finite element method (FEM) and correlated with experimental observations. We found that interfacial voids were forced to move in the direction from high stress regions to low stress ones. The locations of migrated voids varied with the dielectric structures. Under thermal cycling, such voids were likely to move forward to the regions with a small stress change. They relocated and merged with their neighboring voids to lower the interfacial energy.  相似文献   
7.
Hemorrhage is recognized as a new independent predictor of adverse outcomes following acute myocardial infarction. However, the mechanisms of its effects are less understood. The aim of our study was to probe the downstream impact of hemorrhage towards chronic remodeling, including inflammation, vasodilator function and matrix alterations in an experimental model of hemorrhage. Myocardial hemorrhage was induced in the porcine heart by intracoronary injection of collagenase. Animals (N = 18) were subjected to coronary occlusion followed by reperfusion in three groups (six/group): 8 min ischemia with hemorrhage (+HEM), 45 min infarction with no hemorrhage (I ? HEM) and 45 min infarction with hemorrhage (I + HEM). MRI was performed up to 4 weeks after intervention. Cardiac function, edema (T2, T1), hemorrhage (T2*), vasodilator function (T2 BOLD), infarction and microvascular obstruction (MVO) and partition coefficient (pre‐ and post‐contrast T1) were computed. Hemorrhage was induced only in the +HEM and I + HEM groups on Day 1 (low T2* values). Infarct size was the greatest in the I + HEM group, while the +HEM group showed no observable infarct. MVO was seen only in the I + HEM group, with a 40% occurrence rate. Function was compromised and ventricular volume was enlarged only in the hemorrhage groups and not in the ischemia‐alone group. In the infarct zone, edema and matrix expansion were the greatest in the I + HEM group. In the remote myocardium, T2 elevation and matrix expansion associated with a transient vasodilator dysfunction were observed in the hemorrhage groups but not in the ischemia‐alone group. Our study demonstrates that the introduction of myocardial hemorrhage at reperfusion results in greater myocardial damage, upregulated inflammation, chronic adverse remodeling and remote myocardial alterations beyond the effects of the initial ischemic insult. A systematic understanding of the consequences of hemorrhage will potentially aid in the identification of novel therapeutics for high‐risk patients progressing towards heart failure.  相似文献   
8.
9.

Introduction

It has been proved that integrin αv activity is related to cell proliferation, differentiation, migration, and organ development. However, the biological functions of integrin αv in human dental pulp cells (hDPCs) cultured on silicate-based materials have not been explored. The aim of this study was to investigate the role of integrin αv in the proliferation and odontogenic differentiation of hDPCs cultured with the effect of calcium silicate (CS) cement and β-tricalcium phosphate (TCP) cement.

Methods

In this study, hDPCs were cultured on CS and TCP materials, and we evaluated fibronectin (FN) secretion and integrin αv expression during the cell attachment stage. After small interfering RNA transfection targeting integrin αv, the proliferation and odontogenesis differentiation behavior of hDPCs were analyzed.

Results

The results indicate that CS releases Si ion–increased FN secretion and adsorption, which promote cell attachment more effectively than TCP. The CS cement facilitates FN and αv subintegrin expression. However, the FN adsorption and integrin expression of TCP are similar to that observed in the control dish. Integrin αv small interfering RNA inhibited odontogenic differentiation of hDPCs with the decreased formation of mineralized nodules on CS. It also down-regulated the protein expression of multiple markers of odontogenesis and the expression of dentin sialophosphoprotein protein.

Conclusions

These results establish composition-dependent differences in integrin binding and its effectiveness as a mechanism regulating cellular responses to biomaterial surface.  相似文献   
10.
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