氢氧化钙应用于根管封药的临床研究

目的：观察氢氧化钙甘油糊剂用于根管封药的临床疗效。方法：选择244例慢性根尖周炎病例，随机分观察组（氢氧化钙甘油糊剂组）124例、 对照组（甲醛甲酚组）120例，观察封药一周后的临床疗效和细菌培养结果。结果：两组的临床效果有显著差异（P＜0．01）。Ca(OH2)组67．7％一次封药后即可行根管充填，FC组为40％，Ca(OH2)组治疗期间未产生疼痛，FC组则有8．3％产生疼痛，平均封药次数Ca(OH2)组1．38次，FC组1．76次，细菌培养结果与此呈正相关。结论：氢氧化钙甘油糊剂在杀灭微生物、减少治疗期间疼痛和 减低对根尖周组织和刺激性方面效果优良。     

Defects in regulation of apoptosis in caspase-2-deficient mice

During embryonic development, a large number of cells die naturally to shape the new organism. Members of the caspase family of proteases are essential intracellular death effectors. Herein, we generated caspase-2-deficient mice to evaluate the requirement for this enzyme in various paradigms of apoptosis. Excess numbers of germ cells were endowed in ovaries of mutant mice and the oocytes were found to be resistant to cell death following exposure to chemotherapeutic drugs. Apoptosis mediated by granzyme B and perforin was defective in caspase-2-deficient B lymphoblasts. In contrast, cell death of motor neurons during development was accelerated in caspase-2-deficient mice. In addition, caspase-2-deficient sympathetic neurons underwent apoptosis more effectively than wild-type neurons when deprived of NGF. Thus, caspase-2 acts both as a positive and negative cell death effector, depending upon cell lineage and stage of development.     

Comparison of biodegradable and newer generation durable polymer drug-eluting stents with short-term dual antiplatelet therapy: a systematic review and Bayesian network meta-analysis of randomized trials comprising of 43,875 patients

Journal of Thrombosis and Thrombolysis - Newer generation durable polymer drug-eluting stents (DP-DES) and biodegradable polymer DES (BP-DES) have similar efficacy with dual-antiplatelet therapy...     

Potential role of vascular endothelial growth factor,interleukin-8 and monocyte chemoattractant protein-1 in periodontal diseases

Host-mediated immunoinflammatory pathways activated by bacteria lead to destruction of the periodontal connective tissues and alveolar bone. The objective of this study was to elucidate the activation of the inflammatory processes in periodontal disease by quantitative assessment of cytokines and periodontopathogens. Gingival crevicular fluids (GCF) and subgingival plaque samples were collected from patients with chronic periodontitis and gingivitis and from periodontally healthy sites. Vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), and interleukin 8 (IL-8) in GCF were analyzed by enzyme-linked immunosorbent assay. Periodontopathogens, including Bacteroides forsythus, Campylobacter rectus, Porphyromonas gingivalis and Prevotella intermedia, were analyzed by immunofluorescence and dark-field microscopy. There was significantly more VEGF and IL-8 in chronic periodontitis and gingivitis sites than in periodontally healthy sites. There were significant positive correlations between the concentrations and total amounts of VEGF and IL-8 in chronic periodontitis and gingivitis sites, and between the levels of periodontopathogens and the total amounts of VEGF, MCP-1 and IL-8. These data indicate that inflammatory processes induced by periodontopathogens and the activation of certain cytokines (VEGF, MCP-1, IL-8) in periodontal diseases may be relevant to host-mediated destruction in chronic periodontitis.     

颈动脉粥样硬化及血流动力学变化与脑梗死的关系

目的应用双功能彩色多普勒超声观察脑梗死患者颈动脉粥样硬化斑块和颈动脉各部位的血流动力学变化及其相互关系。方法经头颅CT和(或)MRI检查确诊的58例脑梗死患者(脑梗死组)及45例健康体检者(对照组),采用多普勒超声检测颈动脉内膜中层厚度(IMT),并同时检测颈总动脉及颈内动脉血流动力学指标。结果脑梗死组颈总动脉、颈内动脉及颈总动脉分叉部IMT均明显高于对照组(P<0.01);脑梗死组颈动脉粥样斑块检出率显著高于对照组(P<0.01);脑梗死组颈总动脉收缩期峰值流速、舒张末期流速及最大剪切率明显低于对照组,搏动指数、阻力指数高于对照组,脑梗死组颈内动脉舒张末期流速及最大剪切率明显低于对照组,阻力指数高于对照组;颈总动脉最大剪切率与颈总动脉IMT及颈总动脉分叉部IMT呈负相关,颈内动脉最大剪切率与颈内动脉IMT呈负相关。结论颈动脉IMT、斑块的部位和性质及血流动力学变化与脑梗死的发生密切相关。     

Comparison of total hip and knee joint replacement in patients with rheumatoid arthritis and osteoarthritis: a nationwide,population-based study

INTRODUCTION

Patients with rheumatoid arthritis (RA) and osteoarthritis (OA) may require total hip replacement (THR) or total knee replacement (TKR). The present study aimed to compare the demographic characteristics and medical costs of RA and OA patients from Taiwan who underwent either THR or TKR.

METHODS

The medical records of patients who had undergone THR or TKR from 1 January 1996 to 31 December 2010 were obtained from the Taiwan National Health Insurance Research Database (NHIRD). In all, we found 49 and 146 RA patients who received THR and TKR, respectively, and 1,191 and 6,574 OA patients who received THR and TKR, respectively. The gender, age, Charlson comorbidity index (CCI), hospital grade, age at registration in the catastrophic illness dataset, and medical utilisation costs of the different groups were compared.

RESULTS

There were statistically significant differences in age, CCI score, drug costs and surgery costs between RA and OA patients. Joint replacement incidence was lower in RA patients than in OA patients, and among patients who underwent THR, total medical costs incurred were higher for RA patients than OA patients. RA patients who underwent THR incurred a significantly greater total medical utilisation cost in the outpatient department (3 months before surgery and 12 months after surgery) than OA patients who underwent THR.

CONCLUSION

Analysis of Taiwan NHIRD with regard to patients who had undergone either THR or TKR indicated that RA patients were younger than OA patients, and that significantly more medical resources were used for RA patients before, during and after hospitalisation for these procedures.     

Non-neuronal cholinergic machinery present in cardiomyocytes offsets hypertrophic signals

Recent work has provided compelling evidence that increased levels of acetylcholine (ACh) can be protective in heart failure, whereas reduced levels of ACh secretion can cause heart malfunction. Previous data show that cardiomyocytes themselves can actively secrete ACh, raising the question of whether this cardiomyocyte derived ACh may contribute to the protective effects of ACh in the heart. To address the functionality of this non-neuronal ACh machinery, we used cholinesterase inhibitors and a siRNA targeted to AChE (acetylcholinesterase) as a way to increase the availability of ACh secreted by cardiac cells. By using nitric oxide (NO) formation as a biological sensor for released ACh, we showed that cholinesterase inhibition increased NO levels in freshly isolated ventricular myocytes and that this effect was prevented by atropine, a muscarinic receptor antagonist, and by inhibition of ACh synthesis or vesicular storage. Functionally, cholinesterase inhibition prevented the hypertrophic effect as well as molecular changes and calcium transient alterations induced by adrenergic overstimulation in cardiomyocytes. Moreover, inhibition of ACh storage or atropine blunted the anti-hypertrophic action of cholinesterase inhibition. Altogether, our results show that cardiomyocytes possess functional cholinergic machinery that offsets deleterious effects of hyperadrenergic stimulation. In addition, we show that adrenergic stimulation upregulates expression levels of cholinergic components. We propose that this cardiomyocyte cholinergic signaling could amplify the protective effects of the parasympathetic nervous system in the heart and may counteract or partially neutralize hypertrophic adrenergic effects.     

Phosphorylation-regulated axonal dependent transport of syntaxin 1 is mediated by a Kinesin-1 adapter

Presynaptic nerve terminals are formed from preassembled vesicles that are delivered to the prospective synapse by kinesin-mediated axonal transport. However, precisely how the various cargoes are linked to the motor proteins remains unclear. Here, we report a transport complex linking syntaxin 1a (Stx) and Munc18, two proteins functioning in synaptic vesicle exocytosis at the presynaptic plasma membrane, to the motor protein Kinesin-1 via the kinesin adaptor FEZ1. Mutation of the FEZ1 ortholog UNC-76 in Caenorhabditis elegans causes defects in the axonal transport of Stx. We also show that binding of FEZ1 to Kinesin-1 and Munc18 is regulated by phosphorylation, with a conserved site (serine 58) being essential for binding. When expressed in C. elegans, wild-type but not phosphorylation-deficient FEZ1 (S58A) restored axonal transport of Stx. We conclude that FEZ1 operates as a kinesin adaptor for the transport of Stx, with cargo loading and unloading being regulated by protein kinases.