国医大师张学文教授治疗原发性高血压病肝热血瘀证用药规律研究

目的 应用中医传承辅助系统软件,挖掘分析张学文教授治疗原发性高血压病肝热血瘀证的用药规律。方法 收集张学文教授近5年治疗原发性高血压病肝热血瘀证的病例,采用关联规则、系统熵聚类等数据挖掘方法,分析张学文教授治疗原发性高血压病肝热血瘀证的用药经验和用药规律。结果 对筛选出的116首典型处方进行统计分析,得出处方中药物的使用频次、药物之间的关联规则、药物核心组合和新处方。结论 张学文教授诊治原发性高血压病肝热血瘀证,以天麻钩藤饮和（或）脑清通汤为基础方加减,多用平肝熄风、活血化瘀药以治标,再加补肾、安神等药以扶正,标本兼治。     

妊娠中期猪羊水来源干细胞EGFP基因转化及体外分化

本研究旨在获得妊娠中期猪羊水来源千细胞,并通过用EGFP对干细胞进行标记,为以EGFP作为示踪标记对干细胞进行体内移植研究奠定基础.利用羊水来源干细胞培养技术体系,从胎龄60 d猪胎儿羊水中分离获得干细胞,通过脂质体介导转染将EGFP基因导入干细胞,诱导转基因干细胞向肌细胞和神经细胞分化,观察其分化特点.采用RT-PCR技术检测干细胞和分化细胞表面标志或相关基因.结果成功分离培养出妊娠中期猪羊水来源干细胞,并获得转EGFP基因干细胞.干细胞在表达EGFP的同时仍具有分化潜能.干细胞中Oct4、CD-90和Sox2表达阳性;体外诱导的干细胞能分化为肌细胞(表达myf-6和myoD)、星形胶质细胞(表达GFAP)、少突胶质细胞(表达GalC)和神经元细胞(表达NF、NSE和MAP2).研究表明,从妊娠中期猪胎儿羊水中分离干细胞具有可行性和有效性,转EGFP基因干细胞具有自我更新、增殖和分化潜能,可以用EGFP对羊水来源干细胞进行标记、追踪,为EGFP作为示踪标记对干细胞用于体内移植研究奠定了基础.     

ACQUIRED PORTAL COLLATERAL CIRCULATION IN THE DOG AND CAT

We describe patterns of acquired portal collateral circulation in dogs and in a cat using multidetector row computed tomography angiography. Large portosystemic shunts included left splenogonadal shunts in patients with portal hypertension. Small portal collaterals were termed varices; these collaterals had several patterns and were related either to portal vein or cranial vena cava obstruction. Varices were systematized on the basis of the venous drainage pathways and their anatomic location, namely left gastric vein varix, esophageal and paraesophageal varices, gastroesophageal and gastrophrenic varices, gallbladder and choledocal varices, omental varices, duodenal varices, colic varices, and abdominal wall varices. As reported in humans and in experimental dog models, esophageal and paraesophageal varices may result from portal hypertension that generates reversal of flow, which diverts venous blood in a cranial direction through the left gastric vein to the venous plexus of the esophagus. Blood enters the central venous system through the cranial vena cava. Obstructions of the cranial vena cava can lead to esophageal and paraesophageal varices formation as well. In this instance, they drain into the azygos vein, the caudal vena cava, or into the portal system, depending on the site of the obstruction. Gallbladder and choledocal varices, omental varices, duodenal varices, phrenico-abdominal varices, colic varices, abdominal wall varices drain into the caudal vena cava and result from portal hypertension. Imaging plays a pivotal role in determining the origin, course, and termination of these vessels, and the underlying causes of these collaterals as well. Knowledge about these collateral vessels is important before interventional procedures, endosurgery or conventional surgery are performed, so as to avoid uncontrollable bleeding if they are inadvertently disrupted.     

p38 MAPK specific inhibitor SB203580 down-regulates acute pulmonary thromboembolism-induced pulmonary artery hypertension and monocyte chemoattractant protein-1 in rats

AIM：To explore the hypothesis that initiation of pulmonary hypertension involves the up-regulation of monocyte chemoattractant protein-1 (MCP-1) in acute pulmonary thromboembolism (PTE), and to evaluate the role of p38 mitogen-activated protein kinase (MAPK) in this process. METHODS：One hundred and fifty male SD rats were randomly divided into five groups (n=30): normal control group, solvent control group, acute PTE group, acute PTE plus SB203580 (a p38 MAPK specific inhibitor) pretreatment group and acute PTE plus C1142 (a rodent chimeric monoclonal antibody neutralizing rat MCP-1) pretreatment group. Thirty rats in each group were further divided into 1, 4 and 8 h subgroups (n=10). A rat model of acute PTE was established by infusion of an autologous blood clot into the pulmonary artery through a polyethylene catheter. SB203580 or C1142, dissolved in 1% dimethyl sulfoxide (DMSO), was administered to the animals through caudal vein 1 h prior to the beginning of acute PTE modeling. Rats in normal control group and solvent control group were injected with normal saline and 1% DMSO, respectively. The mean pulmonary artery pressure (MPAP) and the mRNA and protein expression of MCP-1 were measured at each time point. RESULTS：Acute PTE elicited significant increase in MPAP, and up-regulated the expression of MCP-1. Pretreatment with SB203580 or C1142 significantly reduced MPAP, and down-regulated the expression of MCP-1. CONCLUSION：These findings suggest that MCP-1 is involved in the formation of acute PTE-induced pulmonary hypertension, and SB203580 down-regulates the expression of MCP-1 via p38 MAPK signaling pathway, thus attenuating pulmonary hypertension.     

肺动脉高压肉鸡肺小动脉中膜5-HT量及其与肺血管重构的关系

静脉注射纤维素粒子复制肉鸡肺动脉高压模型,观察肺小动脉中膜5-羟色胺(5-HT)表达和肺小动脉管壁病理形态学变化,探讨5-HT与肺血管重构的关系。80羽科宝肉鸡分为对照组(n=30)和试验组(n=50)。20日龄时,试验组每羽鸡静脉注射0.3 mL的纤维素悬液;对照组每羽鸡静脉注射等体积生理盐水。记录肺动脉高压综合征(PHS)发病率,并分别于21、28、35、42 d从各组随机抽样,测定右心室/全心室质量比(RV/TV)、红细胞压积(PCV)、血红蛋白(Hb)、肺小动脉管壁面积/管总面积(WA/TA)、平均中膜厚度(mMTPA)和肺厚壁末梢血管百分比(TWPV%);采用免疫组化方法标记5-HT,并用病理图像分析软件检测肺小动脉5-HT的量。结果表明:试验组肉鸡PHS发病率显著高于对照组(P<0.05);RV/TV值在35、42 d时显著升高(P<0.05);PCV在28、35 d时显著升高(P<0.05);Hb值在35 d时显著升高(P<0.05);血管mMTPA、WA/TA和TWPV%在35、42 d时均显著升高(P<0.05);肺小动脉5-HT含量升高,在各时间点均差异显著(P<0.05),且5-HT含量...     

Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross‐sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta‐caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta‐caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.     

ACVIM consensus statement guidelines for the diagnosis,classification, treatment,and monitoring of pulmonary hypertension in dogs

Pulmonary hypertension (PH), defined by increased pressure within the pulmonary vasculature, is a hemodynamic and pathophysiologic state present in a wide variety of cardiovascular, respiratory, and systemic diseases. The purpose of this consensus statement is to provide a multidisciplinary approach to guidelines for the diagnosis, classification, treatment, and monitoring of PH in dogs. Comprehensive evaluation including consideration of signalment, clinical signs, echocardiographic parameters, and results of other diagnostic tests supports the diagnosis of PH and allows identification of associated underlying conditions. Dogs with PH can be classified into the following 6 groups: group 1, pulmonary arterial hypertension; group 2, left heart disease; group 3, respiratory disease/hypoxia; group 4, pulmonary emboli/pulmonary thrombi/pulmonary thromboemboli; group 5, parasitic disease (Dirofilaria and Angiostrongylus); and group 6, disorders that are multifactorial or with unclear mechanisms. The approach to treatment of PH focuses on strategies to decrease the risk of progression, complications, or both, recommendations to target underlying diseases or factors contributing to PH, and PH-specific treatments. Dogs with PH should be monitored for improvement, static condition, or progression, and any identified underlying disorder should be addressed and monitored simultaneously.