急性前壁心肌梗死并下壁导联ST段压低与冠状动脉病变的关系

目的：观察急性前壁心肌梗死下壁导联ＳＴ段压低与冠状动脉病变的关系。方法：对６６例急性前壁心肌梗死患者均常规行冠状动脉造影术,根据常规心电图下壁导联ＳＴ段压低＞１ｍｍ分为ＳＴ段压低组（４８例）与ＳＴ段正常组（１８例）,比较分析心电图与冠状动脉造影之间的关系。结果：急性前壁心肌梗死患者２７．３％有下壁导联ＳＴ段压低,ＳＴ段压低组中冠状动脉病变支数与正常组无显著性差异（Ｐ＞０．０５）,７３．２％为左前降支（ＬＡＤ）近端病变,显著高于ＳＴ段正常组（４５．８％）。ＳＴ段压低组５５．６％伴有心电图ＳＴＩ,ａＶＬ抬高,显著高于ＳＴ段正常组（４．２％）（Ｐ＜０．０１）。结论：急性前壁心肌梗死并下壁导联ＳＴ段压低与冠状动脉病变支数无关,而与ＬＡＤ近端病变有关,可能反映高侧壁心肌缺血时的心电图对应性改变。     

急性前壁心肌梗塞直接经皮冠状动脉腔内成形术成功后ST段持续抬高的临床意义

目的：评价前壁急性心肌梗塞（ＡＭＩ）直接经皮冠状动脉腔内成形术（ＰＴＣＡ）成功后心电图ＳＴ段持续抬高与左心室功能的关系。　　方法：直接ＰＴＣＡ前后１ 小时记录心电图,测量ＳＴ段抬高幅度,根据术后１小时心电图抬高的ＳＴ段下移的幅度将２９ 例ＡＭＩ患者分为２组。Ａ组（ｎ＝ ２０）：患者术后１ 小时抬高的ＳＴ段下移大于５０％ ;Ｂ组（ｎ＝ ９）：患者术后１小时抬高的ＳＴ段下移小于５０％ 。左心室功能测定用超声心动图评价。　　结果：左心室射血分数在急性期２ 组间无明显差异,在３ 个月时左心室射血分数Ａ组较Ｂ组明显增高,分别为０．６４±０．０５及０．４３±０．０８（Ｐ＜ ０．０１）,平均随访５±１个月,Ａ组无心功能不全发生,Ｂ组有３例患者出现心功能不全。　　结论：本研究表明,直接ＰＴＣＡ成功后１小时ＳＴ段持续抬高与术后左心室功能恢复不佳有密切关系,在治疗上应采用减轻心脏负荷措施,避免心功能不全的发生     

二甲基硫脲对心肌细胞抗过氧化氢损伤的实验研究

为探讨二甲基硫脲（ＤＭＴＵ）保护心肌细胞抗过氧化氢（Ｈ２Ｏ２）损伤。３２瓶培养乳鼠心肌细胞随机分４组，每组８瓶：（１）对照组；（２）Ｈ２Ｏ２（５ｍｍｏｌ）组；（３）ＤＭＴＵ（２０ｍｍｏｌ）组；（４）Ｈ２Ｏ２（５ｍｍｏｌ）＋ＤＭＴＵ（２０ｍｍｏｌ）组。在３７℃、５％ＣＯ２的ＭＥＭ培养４小时。结果发现：（１）与对照组比，Ｈ２Ｏ２组乳酸脱氢酶（ＬＤＨ，Ｕ／１００ｍｌ）释放多（２８２．３８±４７．２８比７７．２５±１８．２５，Ｐ＜０．０１）、ＴＢＡ反应物（ＴＢＡＲＳ，ｎｍｏｌ／ｍｇＰｒ．）产生多（２．２５±０．５３比０．７９±０．３６，Ｐ＜０．０１）；（２）与Ｈ２Ｏ２组比，Ｈ２Ｏ２＋ＤＭ－ＴＵ组ＬＤＨ释放少（９９．２５±４１．８８比２８２．３８±４７．２８，Ｐ＜０．０１）；ＴＢＡＲＳ产生少（０．５９±０．１８比２．２５±０．５３，Ｐ＜０．０１）；此外，我们还发现ＤＭＴＵ组超氧化物歧化酶（ＳＯＤ，μｇ／ｍｇＰｒ．）比对照组高（８．４９±３．６５比１．９２±１．４０，Ｐ＜０．０１）。ＤＭＴＵ能保护心肌细胞抗Ｈ２Ｏ２损伤，机制与灭活羟自由基（·ＯＨ）、保护ＳＯＤ活性有关     

前壁急性心肌梗死V_1和V_(3R)导联ST段变化与冠状动脉分布的关系

目的：探讨前壁急性心肌梗死病人Ｖ１和Ｖ３Ｒ导联ＳＴ段变化与冠状动脉分布的关系。方法：前壁急性心肌梗死病人３４例，入院时均采集标准１２导联及Ｖ３Ｒ导联心电图，入院１０天内进行冠状动脉造影，评价心电图变化与冠状动脉分布的关系。根据Ｖ１导联ＳＴ段抬高幅度将病人分为两组：Ａ组（ＳＴ段抬高≥１．５ｍｍ，１５例）和Ｂ组（ＳＴ段抬高＜１．５ｍｍ，１９例）。将起源于右冠状动脉的圆锥动脉分为两种类型：小圆锥支型和大圆锥支型。结果：Ｖ３Ｒ导联ＳＴ段抬高在Ａ组和Ｂ组分别为１４例（９３％）和６例（３２％，Ｐ＜０．００１），小圆锥支型者在Ａ组和Ｂ组分别为１２例（８０％）和３例（１５％，Ｐ＜０．００１），大圆锥支型者１３例，均来自Ｂ组。结论：前壁急性心肌梗死病人入院时Ｖ１导联ＳＴ段抬高与Ｖ３Ｒ导联ＳＴ段抬高密切相关，均为小圆锥支型者。前壁急性心肌梗死Ｖ１导联无ＳＴ段抬高，表明除左前降支的间隔支供血外，心室间隔还得到大圆锥支型的血液供应而受到保护。     

冠心病患者血清免疫球蛋白E水平的动态观察

采用酶联免疫吸附试验测定１３０例冠心病患者血清免疫球蛋白Ｅ（ＩｇＥ）含量。结果显示：急性心肌梗死（ＡＭＩ）组和不稳定心绞痛（ＵＳＡＰ）组显著高于稳定性心绞痛（ＳＡＰ）组和对照组（Ｐ＜０．００１）；ＡＭＩ组显著高于ＵＳＡＰ组和对照组（Ｐ＜０．０１）；而ＳＡＰ组与对照组无显著差异（Ｐ＞０．０５）。ＡＭＩ组发病后血清ＩｇＥ水平逐渐升高，至发病后第７天达高峰，以后逐渐下降，至２１天时降至初始水平。心肌梗死后无并发症组血清ＩｇＥ水平较有严重并发症组显著升高（Ｐ＜０．００１），但二者的动态波动规律一致。     

冠心病患者血浆降钙素基因相关肽水平的临床观察

选择符合ＷＨＯ诊断标准的急性心肌梗死（ＡＭＩ）２０例，心绞痛（ＡＰ）３０例，应用放射免疫分析法动态观察血浆降钙素基因相关肽（ＣＧＲＰ）含量变化，并与３０例正常人作对照。结果显示：对照组血浆ＣＧＲＰ含量为５１．３３±３７．１０ｎｇ／Ｌ，ＡＭＩ组发病第１天血浆ＣＧＲＰ含量为３５．７４±１０．４２ｎｇ／Ｌ，显著低于对照组（Ｐ＜０．０１），发病第３天开始升高（４４．０４±１２．４１ｎｇ／Ｌ），第７天趋于正常（５１．２４±１３．１０ｎｇ／Ｌ），与对照组比较无显著差异（Ｐ＞０．０５）。ＡＰ组在心绞痛发作期血浆ＣＧＲＰ含量为２３．１０±１７．１０ｎｇ／Ｌ，显著低于对照组（Ｐ＜０．００１），经治疗２ｗ症状缓解后复查血浆ＣＧＲＰ含量升高至３０．５５±２９．５８ｎｇ／Ｌ（Ｐ＜０．０５）。提示循环血中ＣＧＲＰ含量不足是ＡＭＩ、ＡＰ发病的重要因素之一。     

尿激酶溶栓治疗对急性心肌梗塞范围的影响

７６例发病≤６ｈ的急性心肌梗塞（ＡＭＩ）患者随机分为两组，根据常规心电图初始ＳＴ段的抬高预计和最后ＱＲＳ改变估计心肌梗塞范围（ＭＩＳ），观察尿激酶对ＭＩＳ的影响。结果表明：ＭＩＳ在对照组治疗前后差异无显著性意义（Ｐ＞０．０５）；在尿激酶组治疗前后差异有显著性意义（Ｐ＜０．０１）；两组ＭＩＳ变化百分比差异有显著性意义（Ｐ＜０．０１）。其中尿激酶组未通亚组治疗前后ＭＩＳ差异无显著性意义（Ｐ＞０．０５），再通亚组治疗前后ＭＩＳ差异有显著性意义（Ｐ＜０．０１）。在两组未通病例中ＭＩＳ变化百分比差异有显著性意义（Ｐ＜０．０５）。提示尿激酶溶栓治疗可显著减少ＭＩＳ。挽救缺血濒死的心肌，这一效果在冠状动脉（冠脉）再通的病例中尤为突出，对冠脉未通病例也有一定作用。     

冠心病患者可溶性肿瘤坏死因子受体的改变与临床意义

目的：观察冠心病患者可溶性肿瘤坏死因子受体（ＳＴＮＦＲ）的改变与临床意义。方法：ＳＴＮＦＲ采用酶联免疫双抗体夹心法测定。结果：血清ＳＴＮＦＲ（ｎｇ／ｍｌ）在急性心肌梗死患者（３．５５±２．０１，ｎ＝２９）和冠心病心肌缺血患者（１．９９±０．６２，ｎ＝２３）中均较正常对照有所升高（０．９３±０．２９，ｎ＝６１，Ｐ均＜０．０１），急性心肌梗死并发心力衰竭死亡时ＳＴＮＦＲ升高达正常值７．７倍（７．２３±１．６０，ｎ＝５），心肌缺血患者中心功能ＩＩ、ＩＶ级（２．５３±０．４６，ｎ＝７）较Ｉ、Ｉ级者（１．７３±０．５０，ｎ＝１６）升高明显（Ｐ＜０．０１）。结论：冠心病患者中ＳＴＮＦＲ水平与病情严重程度密切相关，并能预测急性心肌梗死患者预后。     

急性心肌梗死患者溶栓对心率变异性的影响

选取急性心肌梗死（ＡＭＩ）患者３１例，并设正常对照组。采用时域法和频域法研究ＡＭＩ溶栓治疗后心率变异性（ＨＲＶ）的改变。其结果显示:在ＡＭＩ再通组，其ＳＤＮＮ为１０８．１４±２８．４０ｍｓ，高于未通组的６２．６７±２６．１２ｍｓ（Ｐ＜０．０１）但低于对照组的１２８．４７±３５．６１ｍｓ（Ｐ＜０．０５）；其高频面积为２８４．８２±２７６．４５，大于未通组的（１３５．６８±１１７．８２ｂｐｍ２／Ｈｚ，Ｐ＜０．０５）但小于对照组的（６９４．３５±５４０．１１ｂｐｍ２／Ｈｚ，Ｐ＜０．０１）；其低频面积／高频面积为０．９３±０．７１，小于未通组的１．７４±１．０７（Ｐ＜０．０５），但大于对照组的０．５３±０．６１（Ｐ＜０．０１）；其低频面积虽大于未通组和小于对照组，但无统计学意义。本结果表明，ＡＭＩ后ＨＲＶ变小，其迷走神经活性下降，交感神经作用相对增强；溶栓再通后的ＨＲＶ增大，其迷走神经兴奋性增高，交感神经作用减弱。故成功的溶栓治疗对改善ＡＭＩ后自主神经系统功能失衡和减少由此引起的致命性心律失常等事件的发生有积极意义     

48小时动态心电图分析原发性高血压患者无症状心肌缺血与心率变异性的关系

目的：为探讨原发性高血压（ＥＨ）患者无症状性心肌缺血（Ｓｉｌｅｎｔ ｍｙｏｃａｒｄｉａｌ ｉｓｃｈｅｍｉａ,ＳＭＩ）与心率变异性的关系。方法：根据连续２天（即４８小时）动脉心电图（ＤＣＧ）分析,将（ＥＨ）患者２天ＳＴ段均无ＳＭＩ发作组３０例６０份ＤＣＧ资料与２天ＳＴ段均无ＳＭＩ发作组５５例１１０份ＤＣＧ资料进行对比分析;再将同一患者１天有ＳＭＩ发作另１天没有ＳＭＩ发作的２８例ＳＭＩ发作日与非ＳＭＩ发作日心电图进行对比分析。结果：ＳＭＩ发作组（Ｐ〈０．０１）、ＳＤＡＮＮ（Ｐ〈０．０１）、ＳＤＮＮｉ（Ｐ〈０．０５）以及ｒＭＳＳＤ（Ｐ〈０．０５）均低于无ＳＭＩ组。同一患者ＳＭＩ发作日ＳＤＮＮ（Ｐ〈０．０１）、ＳＤＡＮＮ（Ｐ〈０．０１）、ＳＤＮＮｉ（Ｐ〈０．０１）以及ｒＭＳＳＤ（〈０．０５）均低于非ＳＭＩ发作日。结论：     

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.     

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。     

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。     

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。     

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     

CagA-Hp抗体IgG与胃炎的组织学分析

研究幽门螺杆菌(Hp)感染与胃炎的关系。方法对204例慢性胃炎患者胃粘膜进行观察分析,并测定其中137例Hp阳性患者血清CagA-Hp抗体IgG水平,与组织学对照。结果慢性萎缩性胃炎伴肠上皮化生患者血清CagA抗体IgG明显高于对照组(P＜0.01);其他类型胃炎患者血清CagA抗体IgG水平无明显增高(P＞0.05)。结论CagA-Hp可能是导致慢性萎缩性胃炎伴肠上皮化生的因素之一,对这类患者应密切随访观察。     

慢阻肺急性加重期患者预后的影响因素分析

目的探讨慢性阻塞性肺病急性加重期(AECOPD)患者预后的相关危险因素。方法回顾性调查、收集58例AECOPD患者可能影响其预后的相关因素,并对其分别进行单因素分析。并进行Logistic多元逐步回归进行多因素分析,筛选影响AECOPD患者预后的独立危险因素。结果单因素分析后将结果 P0.1的因素纳入多因素Logistic回归,分析发现是否合并呼吸衰竭、气促程度、白细胞计数、APACHEⅡ、应用抗氧化剂、慢阻肺治疗依从性为影响AECOPD患者预后不佳的独立因素(P0.05)。结论根据AECOPD患者预后的独立危险因素,及早判断,选择合适的后续治疗方案,对提高其生存率及生存质量具有重要意义。