碘杂环化合物IHC－72对心肌部分除极和触发活动的影响

用常规玻璃微电极技术，观察３，６－（二甲氨基）－二苯骈碘杂环依地酸盐（ＩＨＣ－７２）对豚鼠右０００室乳头肌细胞膜部分除极引发的慢反应动作电位（ＳＡＰ）、哇巴因引发的延迟后除极（ＤＡＤ）及触发活动（ＴＡ）的影响。２．５４μＭＩＨＣ－７２对ＳＡＰ各参数均无影响；２５．４，１０１．６μＭＩＨＣ－７２分别使动作电位幅值（ＡＰＡ）减少７．４％和１９．３％，０相最大上升速率（Ｖ＿（ｍａｘ））减少２．５％和３９．１％，复极１００％的动作电位时程（ＡＰＤ＿（１００））缩短７．１％和４１％。有效不应期（ＥＲＰ）相对延长４．９％和９ｌ．３％，静息膜电位（ＲＭＰ）不受影响。浓度为２５．４μＭＩＨＣ－７２对复极５０％的动作电位时程（ＡＰＤ＿（５０））无影响，而浓度为１０１．６μＭ时能使ＡＰＤ＿（５０）缩短４２．９％，且能抑制由哇巴因诱发的ＤＡＤ及ＴＡ。结果表明：ＩＨＣ－７２对慢钙内流有直接抑制作用；其抑制触发性心律失常的机理与钙拮抗有关。     

硒对大鼠心电图及心肌细胞动作电位的影响

目的　探讨硒对大鼠心电图及心肌细胞动作电位的影响。方法　对Ｗ ｉｓｔａｒ雄性大鼠腹腔内注射亚硒酸钠（２ｍ ｇ·ｋｇ－１·ｄ－１）,连续９ 周,应用心电图和细胞内玻璃微电极技术,观察正常大鼠和阿霉素致心肌损伤大鼠心电图及心肌细胞动作电位的变化。结果　硒组心电图较实验前及对照组无变化（ Ｐ ＞ ０．０５ ）,心肌细胞复极达峰值电位５０％ 所需时间（ＡＰＤ５０）延长（ Ｐ ＜ ０．０５ ）。ＡＤＭ 组和硒＋ ＡＤＭ 组心电图Ｑ－Ｔ 间期及心肌细胞ＡＰＤ５０、ＡＰＤ９０较对照组及试验前均延长（ Ｐ＜ ０．０１）。心率、静息电位（ＲＰ）、动作电位幅度（ＡＰＡ）及动作电位０ 相最大去极化速率（Ｖｍ ａｘ）无变化（ Ｐ ＞ ０．０５）。结论　硒能延长正常大鼠心肌细胞ＡＰＤ５０,不能逆转阿霉素心肌损伤大鼠ＡＰＤ５０、ＡＰＤ９０及Ｑ—Ｔ 间期延长。此结果对于心肌病的防治具有重要意义。     

锌对豚鼠心肌细胞跨膜电位及钙通道活动的影响

目的探讨锌对动作电位平台期的作用及锌与慢钙通道之间的关系。方法借助常规玻璃微电极技术和微机实时分析的方法,观察低钙、异搏定和锌对豚鼠心室乳头肌细胞电活动的作用。结果低钙、异搏定和锌对静息电位（ＲＰ）和动作电位峰值（ＡＰＡ）均无明显作用,但可使超射（ＯＳ）和最大去极化速率（Ｖｍａｘ）降低;并影响心肌细胞的复极化过程,使动作电位时程显著缩短,尤其是复极达峰值电位５０％和１０％的时程差（ＡＰＤ５０－１０）缩短更明显。结论实验结果表明,低钙、异搏定和锌均主要通过影响动作电位平台期而使动作电位时程缩短,动作电位时程的缩短与平台期的缩短是一致的,可见锌能阻断慢通道、降低钙离子内向电流,锌具有异搏定样慢通道阻滞剂的作用     

缺血对心室浦肯野纤维跨膜电位和起搏离子流的影响

采用细胞内微电极和双微电极电压箝制术，观察缺血对锦羊心室浦肯野纤维跨膜电位和起搏离子流（Ｉｆ）的影响。结果：模拟缺血溶液灌流３０ｍｉｎ，浦肯野纤维最大舒张电位（ＭＤＰ）、动作电位幅度（ＡＰＡ）明显减小；动作电位时程ＡＰＤ５０，ＡＰＤ９０明显缩短（Ｐ〈０．０１）；Ｉｆ幅度降低，激活曲线向超极化方向移位，最大激活时间瘃半最大激活时间延长（Ｐ〈０．０１）。上述结果表明：心肌缺血时，心室浦肯野细胞跨膜电位     

氟硒对豚鼠心室肌细胞动作电位的影响

应用灌流方法和细胞内微电极技术观察Ｆ－、Ｓｅ及Ｆ－加Ｓｅ对豚鼠心肌细胞电生理影响。结果用５．２６×１０－６ｍｏｌ／ＬＦ－灌流，随时间延长ＲＰ降低，ＡＰＤ５０、ＡＰＤ９０缩短，Ｖｍａｘ有下降趋势。用９．５０×１０－６ｍｏｌ／ＬＳｅ灌流，ＡＰＤ５０、ＡＰＤ９０明显延长。上述浓度的Ｆ－和Ｓｅ同时应用则灌流前后心肌电生理各参数无明显改变。此表明Ｆ－灌流可使心肌细胞膜电位降低，兴奋性降低，复极时间缩短，Ｓｅ可桔抗Ｆ－所致的此种心肌电生理异常。     

钙通道阻滞剂及L－精氨酸对肺动脉高压的影响

采用常压间竭低氧模型，观察了钙通道拮抗剂尼群地平（Ｎｉｔ）、硝苯吡啶（Ｎｉｆ）、内皮依赖性血管舒张因子（ＥＤＲＦ）合成前体Ｌ－精氨酸（Ｌ－Ａ）对大鼠慢性低氧性肺动脉高压的预防作用。结果提示：三者均能预防低氧性肺动脉高压形成和减轻低氧引起的右室肥大；Ｎｉｔ、Ｎｉｆ与Ｌ－Ａ比较无显著性差异（Ｐ＞０．０５）；Ｎｉｔ对低氧性肺动脉高压的降压作用较Ｎｉｆ稍好。     

严重烧伤早期心功能抑制的体液机制Ⅱ烧伤血浆毒性物质对离体豚鼠乳头肌电活动的影响

作者观察了严重早期烧伤及假伤（正常）血浆提取物（分别以ＢＰＴ及ＮＰＥ表示）对离体灌流正常豚鼠乳头肌细胞电活动的影响。结果发现：高、中、低３种浓度的ＢＰＴ，①均可使静息电位减小，其时程曲线略呈“Ｓ”形，其潜伏期有明显的浓度依赖性；②均可引起乳头肌节律不整的自发兴奋；③高浓度ＢＰＴ明显使动作电位幅度（ＡＰＡ）降低，中、低浓度的ＢＰＴ对ＡＰＡ及最大除极速度均无明显影响；④ＢＰＴ对复极化时程ＡＰＤ１０的影响不大，但使ＡＰＤ５０及ＡＰＤ９０显著延长，使动作电位波形在复极化初期出现明显的凹陷和平台期延长；⑤高浓度ＮＰＥ有相当于低浓度ＢＰＴ的生物效应。提示ＢＰＴ可能直接影响心肌细胞Ｋ＋、Ｃａ２＋的转运，对Ｎａ＋的离子转运影响较小     

降钙素基因相关肽拮抗垂体后叶素引起心肌缺血性电生理改变的观察

用浮置微电极技术观察垂体后叶素（Ｐｉｔ）对兔心肌细胞的异常电生理学效应及降钙素基因相关肽（ＣＧＲＰ）的保护作用。结果表明：静脉注射Ｐｉｔ后，心率减慢，心外膜电图ＳＴ段抬高，Ｔ波倒置，心室肌细胞跨膜动作电位（ＴＭＰ）的静息电位（ＲＰ）及动作电位振幅（ＡＰＡ）明显降低（Ｐ均＜０．０１）。复极化至３０％、５０％和９０％的动作电位时程（ＡＰＤ３０、ＡＰＤ５０、ＡＰＤ９０）亦明显缩短（Ｐ均＜０．０５）。静脉注射Ｐｉｔ同时注射ＣＧＲＰ，可见ＣＧＲＰ明显拮抗以上异常改变，从而起到保护心肌和稳定心肌的电生理作用。     

缺血对心室浦肯野纤维跨膜电位和起搏离子流的影响

采用细胞内微电极和双微电极电压箝制术，观察缺血对绵羊心室浦肯野纤维跨膜电位和起搏离子流（Ｉｆ）的影响。结果:模拟缺血溶液灌流３０ｍｉｎ，浦肯野纤维最大舒张电位（ＭＤＰ）、动作电位幅度（ＡＰＡ）明显减小；动作电位时程ＡＰＤ５０，ＡＰＤ９０明显缩短（Ｐ＜０．０１）；Ｉｆ幅度降低，激活曲线向超极化方向移位，最大激活时间及半最大激活时间延长（Ｐ＜０．０１）。上述结果表明:心肌缺血时，心室浦肯野细胞跨膜电位及正常起搏活动不是增强，而是减弱。提示缺血性室性心律失常不是由于正常心室自律活动异常增强引起。     

严重烧伤早期心功能抑制的体液机制Ⅱ烧伤血浆毒性物质对离体豚鼠乳头肌电活动的影响

作者观察了严重早期烧伤及假伤（正常）血浆提取物（分别以ＢＰＴ及ＮＰＥ表示）对离体灌流正常豚鼠乳头肌细胞电活动的影响。结果发现:高、中、低３种浓度的ＢＰＴ，①均可使静息电位减小，其时程曲线略呈“Ｓ”形，其潜伏期有明显的浓度依赖性；②均可引起乳头肌节律不整的自发兴奋；③高浓度ＢＰＴ明显使动作电位幅度（ＡＰＡ）降低，中、低浓度的ＢＰＴ对ＡＰＡ及最大除极速度均无明显影响；④ＢＰＴ对复极化时程ＡＰＤ１０的影响不大，但使ＡＰＤ５０及ＡＰＤ９０显著延长，使动作电位波形在复极化初期出现明显的凹陷和平台期延长；⑤高浓度ＮＰＥ有相当于低浓度ＢＰＴ的生物效应。提示ＢＰＴ可能直接影响心肌细胞Ｋ＋、Ｃａ２＋的转运，对Ｎａ＋的离子转运影响较小     

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.     

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。     

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。     

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.     

治疗高血压药物的经济学评价

重视高血压治疗中的经济学评价,对利用我国有限的卫生资源来遏制高血压对人民群众的危害有着重要的现实意义。药物经济学对于药物治疗的成本和治疗的结果给予同样的关注。因为治疗高血压的费用,不仅涉及药物价格,还包括患者的危险水平,降压疗效和对临床终点事件的影响,以及治疗的依从性和安全性。因此药物经济学更强调整体成本和价-效比。低危病人,若非药价低廉,治疗的价-效比不够理想。而在高危的患者,价-效比越小越经济而不是药费越便宜越好。