西藏林芝地区性病疫情分析

目的了解当地性病流行状况和趋势。方法通过对当地性病疫情报告卡进行整理、统计,采用前后对比和比例成分分析的方法进行分析。结果林芝地区性病疫情逐年增长,发病率已高于全国和西藏自治区的平均水平,除HIV/AIDS外其它7种性病均有报告。结论林芝地区的性病疫情流行状况和趋势不容乐观,必须采取综合措施加以控制。     

助产士电话随访对产妇出院后产褥期心身健康的影响

目的探讨助产士电话访视对产褥期产妇生活质量的影响。方法入选2005年7月至2009年7月我院产科1108例经阴道分娩产妇,分为电话访视组（732例）及无电话访视组（376例）。产妇出院后4—14天由责任助产士通过电话访视对产妇进行产褥期健康教育,对如何预防产褥期感染、奶胀、乳头皲裂进行讲解,对产妇提出的疑问进行解答,让产妇学习产褥期护理的知识;产后8周对产妇产褥期感染、奶胀、乳头皲裂及产后心理进行评估。结果电话访视组产妇院后产褥期感染、奶胀、乳头皲裂及产后抑郁症的发生率分别为O％、4．0％、2．5％及2．9％;无电话随访组产妇院后产褥期感染、奶胀、乳头皲裂及产后抑郁症的发生率分别为0．7％、8．5％、5．1％及10．1％。两组比较,电话访视组产妇院后产褥期感染、奶胀、乳头皲裂及产后抑郁症的发生率明显降低,差异有统计学意义,P〈0．05。结论助产士电话随访能改善产妇院后产褥期心身健康,有助于产妇顺度过产褥期,预防疾病。     

Diagnosis and satisfaction scores in emergency department patients who return a mailed survey

Previous studies of patient satisfaction scores (PSS) have been of insufficient size to examine the influence of diagnosis on PSS. Our objective was to utilize a large database to determine if PSS for patients who return a widely used mailed proprietary survey differ with different diagnoses. We retrospectively analyzed a cohort at 11 hospital emergency departments of non-admitted patients who returned a mailed satisfaction survey. We grouped patients according to International Classification of Diseases, 9(th) Revision (ICD9) diagnoses and calculated mean scores for each diagnostic group. We rank-ordered by mean scores all ICD diagnoses having at least 50 survey responses. Scores were compared using analysis of variance. We analyzed 14,098 surveys. Among all diagnoses, 65 had at least 50 responses. The analysis of variance for the scores showed significant differences (p < 0.0001). Scores differ with respect to diagnosis. This could be used to choose interventions to improve scores of patients who return a mailed survey.     

Annexin A6 modifies muscular dystrophy by mediating sarcolemmal repair

Many monogenic disorders, including the muscular dystrophies, display phenotypic variability despite the same disease-causing mutation. To identify genetic modifiers of muscular dystrophy and its associated cardiomyopathy, we used quantitative trait locus mapping and whole genome sequencing in a mouse model. This approach uncovered a modifier locus on chromosome 11 associated with sarcolemmal membrane damage and heart mass. Whole genome and RNA sequencing identified Anxa6, encoding annexin A6, as a modifier gene. A synonymous variant in exon 11 creates a cryptic splice donor, resulting in a truncated annexin A6 protein called ANXA6N32. Live cell imaging showed that annexin A6 orchestrates a repair zone and cap at the site of membrane disruption. In contrast, ANXA6N32 dramatically disrupted the annexin A6-rich cap and the associated repair zone, permitting membrane leak. Anxa6 is a modifier of muscular dystrophy and membrane repair after injury.Dystrophin and its associated proteins stabilize the plasma membrane of muscle fibers (1). Mutations that disrupt dystrophin produce a fragile sarcolemma susceptible to contraction-induced damage and muscle fiber disruption (2). The dystrophin complex, which includes dystroglycan and the sarcoglycans, provides a mechanically strong link between the cytoskeleton and the extracellular matrix (3). Genetic loss of the sarcoglycan complex similarly weakens the sarcolemma, rendering it leaky and susceptible to damage (4). Dystroglycan adheres directly to the extracellular matrix in a manner dependent on its glycosylation status, underscoring the necessity of the membrane-matrix link for normal sarcolemmal function (5).Genetic modifiers can alter the outcome in muscular dystrophy (MD). The primary gene mutation in Duchenne and Becker muscular dystrophy (DMD/BMD) is the strongest determinant of outcome, but other genes also influence clinical manifestations. Mutations in γ-sarcoglycan (SGCG) cause Limb-Girdle mucular dystrophy 2C (LGMD2C), which is characterized by MD and cardiomyopathy similar to DMD. The SGCG mutation Δ521-T is associated with a variable age of ambulatory loss and severity of cardiopulmonary involvement (6). The γ-sarcoglycan (Sgcg) mouse model closely mimics the phenotype seen in humans with LGMD2C (7). The severity of disease is highly dependent on genetic background pointing to a role for genetic modifiers (8).The major cause of death in MD is cardiopulmonary failure. The major respiratory muscle, the diaphragm, is severely diseased in DMD and the LGMDs, a process well replicated in the mdx and Sgcg mouse models (7, 9). In DMD patients, accessory muscles become recruited to maintain breathing, and this includes the intercostal and abdominal muscles (10). In MD, cardiopulmonary involvement is highly variable. In brothers with dystrophin mutations, approximately half the sibships had significantly different courses of respiratory involvement (11).We used quantitative trait locus (QTL) mapping in the Sgcg mouse model of MD to identify modifiers. A region on chromosome 11 was found to significantly modify membrane damage in the abdominal muscles and also modify right ventricle mass, genetically linking traits relevant to cardiopulmonary function. Whole genome sequencing combined with RNA sequencing identified variation in Anxa6 that correlated with these traits. The severe DBA/2J allele creates a cryptic splice donor site that truncates the annexin A6 protein generating a carboxy-terminally truncated annexin A6, called ANXA6N32. The annexins are calcium-dependent membrane binding proteins involved in membrane repair (12). Live cell imaging demonstrated that annexin A6 was recruited rapidly to sites of sarcolemma disruption after laser induced damage, forming a tight cap over a vesicle-rich repair zone. ANXA6N32 disrupts the cap and repair zone, causing visible leak. Anxa6 modifies MD because annexin A6 orchestrates sarcolemmal repair.     

Identification and proteomic profiling of exosomes in human cerebrospinal fluid

Background  

Exosomes are released from multiple cell types, contain protein and RNA species, and have been exploited as a novel reservoir for disease biomarker discovery. They can transfer information between cells and may cause pathology, for example, a role for exosomes has been proposed in the pathophysiology of Alzheimer's disease. Although studied in several biofluids, exosomes have not been extensively studied in the cerebrospinal fluid (CSF) from humans. The objective of this study was to determine: 1) whether human CSF contains exosomes and 2) the variability in exosomal protein content across individuals.     

Effect of Zinc and Nitric Oxide on Monocyte Adhesion to Endothelial Cells under Shear Stress

This study describes the effect of zinc on monocyte adhesion to endothelial cells under different shear stress regimens, which may trigger atherogenesis. Human umbilical vein endothelial cells were exposed to steady shear stress (15 dynes/cm² or 1 dyne/cm²) or reversing shear stress (time average 1 dyne/cm²) for 24 h. In all shear stress regimes, zinc deficiency enhanced THP-1 cell adhesion, while heparinase III reduced monocyte adhesion following reversing shear stress exposure. Unlike other shear stress regimes, reversing shear stress alone enhanced monocyte adhesion, which may be associated with increased H₂O₂ and superoxide together with relatively low levels of nitric oxide (NO) production. L-N^G-Nitroarginine methyl ester (L-NAME) treatment increased monocyte adhesion under 15 dynes/cm² and under reversing shear stress. After reversing shear stress, monocyte adhesion dramatically increased with heparinase III treatment followed by a zinc scavenger. Static culture experiments supported the reduction of monocyte adhesion by zinc following endothelial cell cytokine activation. These results suggest that endothelial cell zinc levels are important for the inhibition of monocyte adhesion to endothelial cells, and may be one of the key factors in the early stages of atherogenesis.     

时域有限差分法研究长骨中的超声导波

目的基于时域有限差分(finite-difference time-domain,FDTD)法研究长骨弹性模量对超声导波传播特性的影响,为早期骨质疲劳的超声导波检测方法提供理论依据。方法对长骨进行理论建模,并对不同弹性模量下的长骨模型进行FDTD仿真;通过对仿真数据的分析,计算出不同模式导波的相速度、群速度、中心频率及能量等特性参数。结果长骨的弹性模量与超声导波的传播特性参数密切相关,各个导波模式的相速度、群速度、中心频率和能量均随弹性模量的减小而减小,其中L(0,5)模式的变化趋势最为显著。结论超声导波的传播特性参量能够反映出长骨弹性模量的变化,进而为长骨早期疲劳诊断提供了一种可能的方法。