参归煎剂对双侧NBM损伤痴呆大鼠海马Ach含量及ChAT活性的 …

目的 探讨参归煎剂改善实验性痴呆动物模型学习记忆障碍的作用机制。方法 向大鼠基底前脑Ｍｅｙｎｅｒｔ基底核（ＮＢＭ）注入鹅蕈氨酸（Ｉｂ）,造成中枢胆碱能系统障碍性的阿尔茨海默病（ＡＤ）动物模型,通过放射免疫分析方法,观察参归煎剂对该模型大鼠海马内乙酰胆碱（Ａｃｈ）含量和胆碱乙酰转移酶（ＣｈＡＴ）活性的影响。结果 给药组大鼠海马及ＣｈＡＴ活性均明显高于模型组,结论 参归煎剂对ＡＤ模型大鼠学习记忆功能障     

大脑皮质及海马乙酰胆碱酯酶纤维分布及其与痴呆关系的研究

目的探讨脑内胆碱能性神经纤维与痴呆发病机理之间的关系。方法采用尸检脑组织标本，经乙酰胆碱酯酶（ＡＣｈＥ）酶组织化学染色及图像分析技术测定ＡＣｈＥ纤维密度，观察ＡＣｈＥ阳性纤维在非痴呆老年人、Ａｌｚｈｅｉｍｅｒ型老年性痴呆（ＳＤＡＴ）及多发梗塞性痴呆（ＭＩＤ）患者大脑皮质和海马内的不同分布及密度改变。结果（１）脑内ＡＣｈＥ纤维的分布以海马内最丰富，其次为额叶和颞叶，顶叶及枕叶内较稀疏；（２）ＳＤＡＴ和ＭＩＤ患者海马和额叶ＡＣｈＥ纤维密度均比非痴呆老年人明显降低，尤以海马部位明显（Ｐ＜０．００１），ＳＤＡＴ患者减少最显著；（３）额叶、颞叶和海马内ＡＣｈＥ纤维密度与生前长谷川痴呆量表（ＨＤＳ）得分有显著正相关性。结论中枢胆碱能神经功能障碍与痴呆程度密切相关，但可能不是ＳＤＡＴ的特异性发病因素。     

脑缺血及血管性疾呆形成过程中一氧化氮机制的实验研究

目的 探讨一氧化氮（ＮＯ）参与血管性疾呆（ＶＤ）形成的作用机制。方法 采用改良的YＰｕｌｓｉｎｅｌｌｉ４－血管阻断（４－ＶＯ）方法建立ＳＤ大鼠争性全脑缺血和ＶＤ 模型，同时采用硝酸还原酶法（ＮＯ２－／ＮＯ３＾－）测定脑缺血至疾呆形成过程中不同时点，以及分别经一氧化氮合酶抑制剂Ｎ＾Ｇ位硝基左型精氨酸（Ｌ－ＮＮＡ）和底物左型精氨酸（Ｌ－Ａｒｇ）干预后海马区ＮＯ水平，并采用迷宫试验对各组进行行为学定量测定     

β—淀粉样肽致大鼠Alzheimer病模型的研究

目的　建立β－淀粉样肽（β－ＡＰ）致大鼠Ａｌｚｈｅｉｍ ｅｒ病（ＡＤ）模型。并对大鼠海马内单胺类神经递质变化进行研究。方法　分别在两组大鼠海马内注射β－ＡＰ和生理盐水，然后用三等分迷宫测定大鼠的学习、记忆功能。迷宫实验结束后迅速处死大鼠，取出海马测定其中单胺类递质代谢产物的含量。结果　海马内注射β－ＡＰ的大鼠的学习、记忆功能出现明显障碍，其海马内的３－甲基－４－羟基苯乙二醇（ＭＨＰＧ）和５－羟吲哚乙酸（５－ＨＩＡＡ）水平明显下降，高香草酸（ＨＶＡ）水平无显著改变。结论　β－ＡＰ致大鼠ＡＤ模型是一种新的成功的ＡＤ动物模型。     

维生素E抑制痴呆模型大鼠海马结构淀粉样前体蛋白表达的实验研究

目的观察ＶＥ对ＡＤ大鼠海马β－ＡＰＰ表达的影响。方法使用三氯化铝诱导建立ＡＤ模型大鼠。用ＶＥ（１０ｍｇ／ｄ／只）对ＡＤ模型大鼠进行灌胃治疗３月。采用行为测试,光镜免疫细胞化学ＡＢＣ法,观测大鼠海马结构淀粉样前体蛋白反应阳性神经元的数目和β－淀粉样前体蛋白表达的变化。结果ＶＥ组大鼠受电击次数和潜伏期较对照组明显减少和延长（Ｐ＜０．０５）;ＶＥ组大鼠海马结构齿状回和ＣＡ１区淀粉样蛋白反应阳性神经元的数目较对照组均有明显减少（Ｐ＜０．０５）,β－淀粉样前体蛋白呈弱阳性表达。结论ＶＥ可以改善ＡＤ模型大鼠的学习记忆,降低海马结构β－淀粉样前体蛋白过度表达。     

药物诱发大鼠痴呆模型的初步研究

目的　建立一种模拟痴呆动物模型的制备方法。方法　按二水平三因素 Ｌ１６ （２１５ ）正交试验设计分组,应用 Ａ 因素（东莨菪碱）、 Ｂ 因素（氯胺酮）、 Ｃ 因素（ Ｄ半乳糖）皮下注射制备动物模型。利用 Ｍ Ｇ２ 迷宫检测大鼠学习记忆功能。通过组织病理学观察大鼠海马 Ｃ Ａ １ 区锥体细胞的数量和形态及神经元纤维缠结和老年斑等。结果　氯胺酮和 Ｄ 半乳糖分别可致大鼠记忆功能明显下降（ Ｐ ＜ ００５）和海马 Ｃ Ａ １ 区锥体细胞减少,并可见嗜神经细胞现象和胶质细胞小结。结论　大鼠注射氯胺酮或 Ｄ半乳糖可作为模拟痴呆模型的方法之一。     

湖北省土家族β地中海贫血IVS—II—654（C→T）和CD41—42（—TTCT）…

报道采用血红蛋白理化性质筛查实验，检出湖北土家族β地中海贫血２个家系，继用ＰＣＲ／ＡＳＯ探针斑点杂交技术，确诊先证１为ＩＶＳ－Ⅱ－６５４（Ｃ→Ｔ）／ＩＶＳ－Ⅱ－６５４（Ｃ→Ｔ）纯合子，其父母分别为ＩＶＳ－Ⅱ－６５４（Ｃ→Ｔ）／Ａ杂合子。先证ｚ为ＣＤ４１－４２（－ＴＴＣＴ）／ＩＶＳ－Ⅱ－６５４（Ｃ→Ｔ）双重杂合子，其父为ＣＤ４１－４２（－ＴＴＣＴ）／Ａ杂合子，其母为ＩＶＳ－Ⅱ－６５４（Ｃ→Ｔ）／Ａ杂     

脑心通胶囊对血管性痴呆大鼠行为学及海马组织的作用

目的观察脑心通胶囊对血管性痴呆（VD）模型大鼠行为学及海马组织形态学的作用。方法采用大脑中动脉闭塞法（MCAO）制作VD动物模型；跳台试验测定大鼠学习记忆成绩取脑组织作冰冻切片，HE染色，观察大鼠海马形态学改变。结果跳台实验中，与假手术组比较，模型组大鼠存在着明显的学习记忆障碍；与模型组比较。中药组、西药组大鼠学习记忆能力得到改善，且两组相比无统计学意义。光镜观察显示，假手术组大鼠海马CA1区锥体细胞排列紧密整齐，无明显神经元脱失；模型组大鼠海马CA1区锥体细胞排列稀疏、紊乱，神经元脱失明显，可见胶质细胞增生，中、西药治疗组可明显减轻大鼠CA1区海马神经元脱失现象，使锥体细胞形态较正常，排列较整齐，接近假手术组。结论脑心通胶囊对血管性痴呆模型大鼠有治疗作用．     

记忆增强肽对小鼠糖尿病海马神经元的形态学和胆碱乙酰转移？…

目的 研究糖尿病注鼠及用记忆增强肽（ＭＥＰ）保护的糖尿病小鼠组织形态学的改变，并比较小鼠海马内胆碱乙酰转移酶（ＣｈＴＡ）神经元的表达。ＭＥＰ是血管加压素（ＡＶＰ）４～８的５肽衍生物，是一种促进神经元内源性神经生长血子（ＮＧＦ）转录的多肽。方法用链脲佐菌素（ＳＴＺ）晟小鼠糖尿病模型，并皮下流射ＭＥＰ对糖尿病小鼠进行保护。４周后，小鼠灌注固定，取海马ＣＡＩ区组织进行光镜和电镜观察，并行冰切片，做ＣｈＡ     

大鼠蛛网膜下腔出血后急性脑血管痉挛血及脑组织一氧化氮和内皮素含量的动态观察

目的 探讨一氧化氮（ＮＯ）、内皮素（ＥＴ）在蛛网膜下腔出血（ＳＡＨ）后急性脑出血痉挛（ＣＶＳ）中的作用。方法 对ＳＡＨ模型组和假手术组大脑检测术后２４ｈ内局部脑血流量（ｒＢＣＦ）、血浆及脑组织ＮＯ、ＥＴ含量的动态改变,并测量基底动脉（ＢＡ）管径,３ｄ后行海马组织病理检查。结果 ＳＡＨ后２４ｈ内ｒＣＢＦ迅速而持续降低,ＢＡ痉挛;３ｄ后海马ＣＡ１区神经元明显受损,血清ＮＯ明显减少,脑组织ＮＯ显著增多,     

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.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.