子宫阔韧带内静脉的解剖学研究及其临床意义

子宫底和体上部的静脉汇集于子宫角处浅出,应称子宫上静脉。该静脉续为卵巢静脉。子宫上静脉1条者占30%,2条者占56.7%,3条者占13.3%。子宫上静脉与输卵管峡部中点相对处的口径是3.7±0.2mm,卵巢丛与子宫上静脉汇合后的口径为5.0±0.4mm。输卵管峡部中点与子宫上静脉的间距为6.3±0.6mm。在输卵管系膜中见有输卵管静脉汇入子宫上静脉。本文研究结果认为盆腔静脉淤血症的发生,与结扎手术中损伤子宫上静脉和输卵管静脉有关。     

心电信号预测冠心病的粗糙集方法

应用粗糙集理论对心电图波形所蕴涵的大量信息进行处理，目的是评价心电信号实测指标与冠心病的关系。通过对心电图导联I中采集的心电信号进行属性约简，降低决策表的冗余性，提取用于判别冠心病的重要属性和诊断规则。实例分析表明，粗糙集理论应用于心电信号分析，可得到清晰简明的诊断规则，有助于冠心病的临床诊断。     

实验性糖尿病对小鼠肝脏酶组织化学和超微结构的影响

实验用四氧嘧啶建造糖尿病动物模型，８周后取肝作组织学、酶组织化学和超微结构的观察，以探讨实验性糖尿病对肝组织结构和功能的影响。表明在糖尿病状态下，肝细胞的结构和功能均受到一定的损害。     

超声多普勒管壁搏动和血流信号的分离研究

本研究提出利用经验模式分解(EMD)算法分解混叠有管壁成分的超声多普勒血流信号来实现管壁搏动和血流信号的分离。该方法首先将混叠有管壁搏动的超声多普勒血流信号分解为少量有限的分量,即内模函数(IMFs),然后根据管壁搏动信号与血流信号的功率比变化曲线,用比值法自动确定并去除低频管壁博动成分。在仿真实验中用提出的方法处理模拟的多普勒信号,对于靠近管腔内壁的血流信号其在频域功率谱上的相对误差为50%,在时域幅度的相对误差为45%,与高通滤波器方法的相对误差95%相比,准确性得到提高。基于个人计算机用C语言编程实现提出的算法,对实际采集的人体颈动脉多普勒信号可实现实时分离处理。结果表明:基于经验模式分解的滤波方法能有效客观地滤除管壁搏动信号,更准确地保留低频血流信号成分。     

小胶质细胞极化介导炎症反应在脊髓损伤中的作用

背景:小胶质细胞极化参与脊髓损伤后的炎症反应,并在其中发挥关键作用。相关研究表明,有效诱导小胶质细胞从M1促炎表型向M2抗炎表型极化,可以减轻脊髓损伤后的炎症反应,促进组织的修复再生和神经功能的恢复。目的:文章对小胶质细胞的功能和极化、小胶质细胞极化对脊髓损伤的影响及其潜在调控策略以及脊髓损伤后炎症反应进行综述。方法:检索PubMed、Web of Science和中国知网数据库,英文检索词为“microglia,polarization,spinal cord injury,inflammation”,中文检索词为“小胶质细胞、极化、脊髓损伤、炎症”,按纳入和排除标准共纳入80篇文献进行总结。结果与结论:①由小胶质细胞介导的稳定而持续的炎症反应,对脊髓损伤的预后至关重要。②在生理条件下,小胶质细胞处于M0静止表型,但在脊髓损伤后,小胶质细胞活化,进而极化成M1促炎表型,导致神经组织修复能力降低和出现持续性神经炎症。③在脊髓损伤的炎症反应过程中,调控小胶质细胞向M2表型极化或至少向M2表型倾斜,有利于抑制氧化应激反应、调节突触重塑、促进轴突再生和血管生成,是一种有效的调控策略。④截止到目前的研究表明,间充质干细胞、外泌体、临床药物、天然产物、miRNAs和靶点分子可调控小胶质细胞在M1和M2表型之间的转换,这为脊髓损伤后神经组织的修复提供了一种新的思路,未来需进一步研究小胶质细胞在脊髓损伤过程中调控极化的详细机制。     

内痔粘膜及血管上皮细胞VEGF/FGF2的表达与内痔分期的相关性分析

目的 通过观察人体内痔不同分期粘膜及血管内皮细胞生长因子（VEGF）及碱性成纤维细胞生长因子（FGF2）的表达，探讨内痔的发生及发展机制。 方法 收集南方医院肛肠科门诊手术切除的Ⅰ、Ⅱ、Ⅲ期内痔标本134例（Ⅰ期42例，Ⅱ期45例，Ⅲ期47例），内痔周围正常肠壁组织40例作为对照，采用HE染色观察组织的病理学变化，采用免疫组织化学方法检测血管内皮细胞VEGF及FGF2的表达。 结果 正常组及Ⅰ期内痔黏膜层被覆上皮完整，未见扩张血管；Ⅱ期内痔黏膜层被覆上皮破坏，黏膜肌层破坏，黏膜层内见新生血管；Ⅲ期内痔黏膜层被覆上皮破坏，见血管管壁增厚迂曲，管腔扩张；与正常粘膜成纤维细胞相比VEGF在粘膜层成纤维细胞表达水平明显升高，并随分期增高而增高（F=883.961，P<0.01），FGF2也存在相同表达（F=656.013，P<0.01）；与正常组相比VEGF在血管内皮细胞表达水平明显升高，并随分期增高而增高（F=776.561，P<0.01），FGF2在血管内皮细胞的表达水平存在相同趋势（F=1066.458，P＜0.01）。 结论 VEGF及FGF2在内痔的形成过程中具有促进血管内皮细胞和粘膜下成纤维细胞增生的作用，同时可作为内痔发生发展的分子标志物。     

Connexin26 gene ( GJB2): prevalence of mutations in the Chinese population

The connexin26 gene ( GJB2) has been shown to be responsible for DFNB1 and DFNA3 (Autosomal Recessive Hereditary Nonsyndromic Deafness Locus 1 and Autosomal Dominant Hereditary Nonsyndromic Deafness Locus 3). Two hundred ten independently ascertained Chinese probands with nonsyndromic hearing loss (NSHL) were evaluated for mutations in GJB2, including 43 probands from families with more than one sib with NSHL, likely indicating dominant inheritance, and sporadic cases of NSHL, compatible with recessive inheritance. Of the 210 probands, 43 (20%) were homozygous or heterozygous for mutations in GJB2. Four different mutations were identified: 35delG, 109G-A, 235delC, and 299-300delAT. It was confirmed that GJB2 mutations are an important cause of hearing loss in this population. Of these four mutations, 235delC was the most prevalent at 93%; yet the 35delG mutation, which is the most common GJB2 mutation in Caucasian subjects (Europeans and Americans), was found in low frequency in the present study. It appears from our limited data and reports from other East Asians that 235delC is the most prevalent GJB2 mutation in these populations. GJB2 mutations are consistent with ethnic predilections.     

Cardiac natriuretic peptides and continuously monitored atrial pressures during chronic rapid pacing in pigs

Changes in atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide and brain natriuretic peptide (BNP) were evaluated in relation to continuously monitored atrial pressures in a pacing model of heart failure. Pigs were subjected to rapid atrial pacing (225 beats min-1) for 3 weeks with adjustments of pacing frequencies if the pigs showed overt signs of cardiac decompensation. Atrial pressures were monitored by a telemetry system with the animals unsedated and freely moving. Left atrial pressure responded stronger and more rapidly to the initiation of pacing and to alterations in the rate of pacing than right atrial pressure. Plasma natriuretic peptide levels were measured by radioimmunoassay and all increased during pacing with BNP exhibiting the largest relative increase (2.9-fold increase relative to sham pigs). Multiple regression analysis with dummy variables was used to evaluate the relative changes in natriuretic peptides and atrial pressures and the strongest correlation was found between BNP and left atrial pressure with R 2=0.81. Termination of pacing resulted in rapid normalization of ANP values in spite of persistent elevations in atrial pressures. This may reflect an increased metabolism or an attenuated secretory response of ANP to atrial stretch with established heart failure. In conclusion, 3 weeks of rapid pacing induced significant increases in atrial pressures and natriuretic peptide levels. All the natriuretic peptides correlated with atrial pressures with BNP appearing as a more sensitive marker of cardiac filling pressures than ANP and N-terminal proatrial natriuretic peptide.     

Pkd2 haploinsufficiency alters intracellular calcium regulation in vascular smooth muscle cells

Autosomal-dominant polycystic kidney disease is a multiorgan disease and its vascular manifestations are common and life-threatening. Despite this, little is known about their pathogenesis. Somatic mutations to the normal PKD allele in cystic epithelia and cyst development associated with the unstable Pkd2(WS25) allele suggest a two-hit model of cystogenesis. However, it is unclear if this model can account for the cardiovascular pathology or if haploinsufficiency alone is disease-associated. In the present study, we found a decreased polycystin-2 (PC2, protein encoded by Pkd2 gene) expression in Pkd2( +/-) vessels, roughly half the wild-type level, and an enhanced level of intracranial vascular abnormalities in Pkd2 (+/-) mice when induced to develop hypertension. Consistent with these observations, freshly dissociated Pkd2 (+/-) vascular smooth muscle cells have significantly altered intracellular Ca(2+) homeostasis. The resting [Ca(2+)](i) is 17.1% lower in Pkd2 (+/-) compared with wild-type cells (P=0.0003) and the total sarcoplasmic reticulum Ca(2+) store (emptied by caffeine plus thapsigargin) is decreased (P<0.0001). The store operated Ca(2+) (SOC) channel activity is also decreased in Pkd2 (+/-) cells (P=0.008). These results indicate that inactivation of just one Pkd2 allele is sufficient to significantly alter intracellular Ca(2+) homeostasis, and that PC2 is necessary to maintain normal SOC activity and the SR Ca(2+) store in VSMCs. Based on these findings, and the fact that [Ca(2+)](i) signaling is essential to the regulation of contraction, production and secretion of extracellular matrix, cellular proliferation and apoptosis, we propose that the abnormal intracellular Ca(2+) regulation associated with Pkd2 haploinsufficiency is directly related to the vascular phenotype.     

我国HIV-1 B''亚型毒株gag基因变异特征研究

目的研究我国人免疫缺陷病毒1型（HIV-1）B’亚型主要流行株在宿主免疫压力下的基因变异及抗原表位的变化特征，探讨选择压力、基因离散率和抗原表位变化之间的关系。方法从确诊的HIV-1感染者的全血样本中提取基因组DNA，经套式聚合酶链反应（PCR）扩增后，将扩增产物进行纯化和测序。然后将所得序列进行系统进化树和氨基酸变异分析，使用GCG软件包的Distance程序对P17和P24两个区段计算基因距离，用Diverge程序计算同义替换（1（s）和非同义替换（1（a）及二者之间的比值，并对我国人群中较常见的HLA型别限制的CTL表位的突变情况进行分析。结果HIV-1B’亚型毒株的P17区段的Ks／Ka值〈1，而P24区段的Ks／Ka值〉1；P24部分的基因离散率低于P17部分；P17区段抗原表位的保守率为34．94％，而P24区段抗原表位的保守率为67．38％；从基因离散率、所受的选择压力及抗原表位的突变率3个方面来看，HIV-1的P17区段均明显大于P24区段。结论HIV-1B’亚型毒株的P17区段的抗原表位变化较大，而P24区段的抗原表位相对较为保守。提示P24区段的CTL表位更适合于表位疫苗的研制。