芍甘海贝蒲术汤抗胃溃疡作用的实验研究

目的 :研究芍甘海贝蒲术汤对实验性胃溃疡的防治作用 ,并探讨其作用机制。方法 :观察预先应用中药对应激、乙醇及幽门结扎所诱发的胃粘膜损伤的影响 ;并观察连续应用中药 14d后醋酸性胃粘膜损伤的愈合情况 ;同时检测胃液量、总酸度、胃蛋白酶活性、胃壁结合粘液、胃粘膜超氧化物歧化酶 (SOD)、丙二醛 (MDA)及脑组织和胃粘膜的一氧化氮合酶 (NOS)的含量。结果 :芍甘海贝蒲术汤显著抑制应激、乙醇及幽门结扎性胃粘膜损伤 ,加速醋酸性胃溃疡的愈合 (P<0 .0 5 ,<0 .0 1) ;抑制胃液分泌和胃蛋白酶活性 ,显著增加胃粘膜组织 SOD、NOS含量 ,减低 MDA的生成 (P<0 .0 5 ,<0 .0 1)。结论 :芍甘海贝蒲术汤可能通过增强胃粘膜的细胞保护作用而产生抗胃溃疡的效应。     

植物油乳治疗胃溃疡的实验与临床研究

目的：对两种植物油乳──鸦胆子油乳（简称鸦乳）和豆油乳治疗胃溃疡的作用进行观察。方法：首先观察鸦乳对四种胃溃疡动物模型的疗效，进而探讨其对动物胃粘膜内源性PGE2、MDA、SOD活性和氧自由基相对含量的影响，然后通过开放性临床观察和随机双盲对照试验观察其临床疗效。结果：鸦乳对四种胃溃疡动物模型均有疗效（P＜0．01）；豆油乳对应激性胃溃疡动物模型亦有疗效，作用与鸦乳比较，差异无显著性（P＞0．05）；鸦乳增加动物及人体胃粘膜内源性PGE2（P＜0．01），降低动物胃粘膜SOD活性（P＜0．01），减低动物胃粘膜MDA和氧自由基相对含量（P＜0．01）。开放性临床观察及随机双盲对照临床观察均显示，鸦乳治疗胃溃疡的8周有效率＞91．62％，8周愈合率＞75％，疗效优于对照剂西咪替丁（国产）和石蜡油乳（P＜0.01），未发现不良反应。结论：鸦乳和豆油乳治疗胃溃疡的疗效是肯定的，其主要作用机理是增加胃粘膜内源性PGE2、减轻氧自由基对胃粘膜的损害。     

健脾理气颗粒对大鼠胃溃疡作用的研究

目的：研究健脾理气颗粒对大鼠胃溃疡及胃粘膜损伤的作用。方法：采用水浸应激致胃溃疡及口服乙醇致胃粘膜损伤法制模，再用健脾理气颗粒3个剂量组进行药效评价，并设对照组进行比较。结果：健脾理气颗粒3个剂量组对大鼠应激性胃溃疡的形成有明显的抑制作用（P＜0.05-0.01)，对口服乙醇致胃粘膜损伤也有保护作用，尤以10g/kg、20g/kg组为明显（P＜0.05-0.01)。结论：健脾理气颗粒具有明显地抑制大鼠胃溃疡及保护胃粘膜损伤作用。     

人参胃康片防治胃溃疡药理学研究

[目的]研究人参胃康片防治胃溃疡的药理作用。[方法]建立盐酸乙醇致大鼠胃黏膜损伤模型、冰乙酸诱发大鼠胃小弯溃疡模型、消炎痛致大鼠胃黏膜损伤模型、幽门结扎大鼠模型及小鼠冰乙酸致痛扭体模型，观察人参胃康片对各模型的药理作用。[结果]人参胃康片能防治盐酸乙醇致大鼠胃黏膜损伤、冰乙酸致大鼠胃小弯胃溃疡[但对该模型的髓过氧化物酶（MPO）和超氧化物歧化酶（SOD）无明显影响]及消炎痛所致大鼠胃黏膜损伤；对幽门结扎大鼠有抑制胃酸分泌的作用；能促进正常小鼠胃排空；对冰乙酸所致小鼠扭体有镇痛作用。[结论]人参胃康片有防治胃溃疡，保护胃黏膜，抑制胃酸分泌，促进胃肠蠕动及镇痛等药理作用，与临床主治相符，可供临床试验参考。     

胃康胶囊对消炎痛诱导大鼠胃粘膜损伤血液中相关细胞因子含量的影响

目的：观察胃康胶囊对消炎痛引起的大鼠急性胃粘膜损伤时血液中相关细胞因子[前列腺环素（PGI2）、血小板活化因子（PAG）、肿瘤坏死因子－α（TNF-α）、表皮生长因子（EGF）]含量的影响，探讨其在保护胃粘膜损伤过程中的分子机制。方法：Wistar大鼠30只灌胃给药1周后，用消炎痛复制成急性胃粘膜损伤模型，5h后处死大鼠进行以上血液相关细胞因子的检测。结果：胃康胶囊能降低急性胃粘膜损伤大鼠血液中PAF、TNF-α的含量，升高PGI2，EGF的含量，对抗胃酸分泌增加，结论：胃康胶囊对消炎痛引起的大鼠胃粘膜损伤有保护作用。对胃溃疡有预防作用。     

抗氧化剂对胃粘膜的保护作用

目的：研究抗氧化剂对大鼠和胃溃疡患者胃粘膜的保护作用。方法：大鼠用乙醇灌胃造模，给予抗氧化剂银杏制剂预防胃粘膜损伤，测定胃粘膜和血中的脂质过氧化物（LPO）含量。胃溃疡患者在根除幽门螺杆菌的同时服用硒卡拉胶囊治疗，测定治疗前后胃粘膜中的LPO含量，并与对照组进行比较。结果：银杏预防组大鼠胃粘膜和血中的LPO含量均明显低于乙醇模型组（P＜0.05和P＜0.01)。胃溃疡患者服用硒卡拉胶囊治疗后，胃粘膜中LPO含量的降低幅度明显大于对照组（P＜0.001)。结论：抗氧化剂银杏制剂和硒卡拉胶囊对大鼠和胃溃疡患者由氧自由基所致的胃粘膜损伤有保护作用。     

健脾益气中药对乙酸慢性胃溃疡大鼠热休克蛋白表达的影响

目的：研究健脾益气中药对大鼠乙酸慢性胃溃疡修复过程中热休克蛋白（ＨＳＰｓ）的影响,探索ＨＳＰｓ对胃溃疡的病理生理意义。方法：以ＳＡＢＣ免疫组织化学方法观察乙酸慢性胃溃疡大鼠模型溃疡周围胃粘膜的ＨＳＰ７０并进行图像分析,用Ｗｅｓｔｅｒｎ 斑点印迹法检测各组动物血清及胃粘膜匀浆ＨＳＰ２７,６０,７０ 的含量。结果：模型组和雷尼替丁组血清及胃粘膜ＨＳＰ２７,６０,７０ 表达较对照组增加（Ｐ＜ ０．０５,＜ ０．０１）,中药组进一步升高（Ｐ＜ ０．０５,＜ ０．０１）。结论：ＨＳＰ２７,６０,７０可能参与胃溃疡的病理生理过程,健脾益气中药通过ＨＳＰｓ的机制促进溃疡的愈合     

电针抗应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶的变化

观察应激性胃溃疡大鼠脑组织和胃粘膜中一氧化氮合酶（NOS）活性的变化．并对电外足三里穴和阳陵泉穴NOS的变化及与胃粘膜损伤的关系作了比较。结果发现,应激性胃溃疡大鼠脑组织和胃粘膜NOS均增高，尤其是胃粘膜NOS增高非常显著（P＜0.01）；电针足三里使脑和胃NOS回降，应激前先电针更为明显，使胃溃疡损伤指数显著下降（P＜0.01）；而电针阳陵泉．与应激组相比虽也下降，但无统计学意义。提示NOS参与了电针对应激所致胃粘膜损伤的保护．这种保护作用可能与中枢和肠神经系统对胃功能的双重调节有关，同时NOS的变化与电针胃经足三里穴位特异性有一定的联系。     

硫酸软骨素对鼠胃粘膜的保护作用研究

由冷冻－束缚应激、口服酸性乙醇及皮下注射利血平制备胃溃疡模型,观察硫酸软骨素（ＣＳ）对胃液分泌量、胃液酸度和胃蛋白酶活性的影响。结果：ＣＳ可抑制冷冻－束缚应激及利血平引起的胃粘膜损伤,认为ＣＳ对胃粘膜有良好的保护作用,可用于胃溃疡的治疗,且对大鼠胃液分泌量、胃液酸度和胃蛋白酶活性无明显影响。     

胃祺饮阻断胃癌前病变组织增殖作用的实验研究

目的：观察益气化瘀之胃祺饮阻断慢性萎缩性胃炎合并胃癌前病变（PLGC）的抗增殖作用。方法：甲基亚硝基胍溶液诱发Wistar大鼠癌前病变状态,用胃祺饮（中药组）与叶酸（对照组）预防和治疗,观察对胃粘膜萎缩和不典型增生的预防和治疗作用,以及对病变粘膜组织中增殖细胞核抗原（PCNA）、P21 H－ras基因蛋白、细胞凋亡水平的影响。结果：中药组能明显阻断化学致癌物对粘膜的炎性损伤,改善癌前病变组织粘膜萎缩和不典型增生程度,结果优于对照组（P＜0．05）。同时中药组合治疗后PCNA指数、P21 H－ras基因蛋白阳性指数分别为12．78％、10．34％,并能增强癌前病变组织细胞凋亡指数,疗效明显高于对照组（P＜0．05）。结论：益气化瘀为主的胃祺饮通过改善PLGC患者气虚血瘀的血瘀的病理基础,降低病变组织增殖水平,诱导细胞正常调邙,从而对胃癌前病变细胞的增殖和良好的阻断作用。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Angiographic diagnosis of the degree of serosal invasion of carcinoma of the colon

Angiography using Prostaglandin El^® was performed on 38 patients with carcinoma of the colon in order to diagnose the degree of serosal cancer invasion. The findings at angiography were classified into four groups:1) AG-S3, abnormal change (irregularity and/or encasement) up to marginal vessels; 2) AG-S2, abnormality up to vasa recta; 3) AG-S1, abnormality of penetrating branches of vasa recta within the wall of the colon; and 4) AG-S0, no distinct findings of abovementioned vessels. These angiographic findings were compared with both macroscopic and microscopic serosal cancer invasion. Angiographic diagnosis is in accord with the macroscopic findings in 84.2 percent of cases. Angiographic diagnosis is in accord with the microscopic findings in 32.4 percent of cases. Macroscopic findings confirm the angiographic diagnosis precisely but the conflict with microscopic findings should not be overlooked. This may be the result of inflammatory change, adhesion, and fibrosis around carcinoma of the colon.