慢性萎缩性胃炎胃粘膜血流量的研究

为探明慢性萎缩性胃炎者胃粘膜血供情况，应用激光多普勒血流仪测定２８例胃炎患者的胃粘膜血流量（ＧＭＢＦ），其中慢性萎缩性胃炎组１５例，非萎缩性胃炎组１３例。发现：（１）两组从十二指肠球部至胃底部，随着位置的升高，ＧＭＢＦ逐渐增加；（２）胃大弯侧高于小弯侧（前组胃窦部相反）；（３）前组各部位ＧＭＢＦ均低于后组（Ｐ＜０．０５，胃窦大弯侧Ｐ＜０．０１）。说明慢性萎缩性胃炎ＧＭＢＦ较非萎缩性胃炎明显降低，推测这是其发病及难以治愈的重要原因之一。     

表皮生长因子对胃粘膜保护作用的机理初探

报道表皮生长因子（ＥＧＦ）保护胃粘膜抵制损伤的作用。实验采用多普勒激光流量仪测定ＧＭＢＦ，将ＳＤ鼠随机分成两组（移出内源性ＥＧＦ组和未移出组）并应用不同剂量外源性ＥＧＦ，观察其对ＧＭＢＦ和胃损伤的影响。结果显示：移出组加重酒精诱发的胃损伤（Ｐ＜０．０５），对ＧＭＢＦ虽有所下降，但无统计学意义。在预先加用外源性ＥＧＦ织，胃粘膜损伤减轻，ＧＭＢＦ增加（二者Ｐ＜０．０５），而且ＧＭＢＦ增长与ＥＧＦ剂量（从３．２５μｇ～２５μｇ）呈正相关，相关系数ｒ＝０．６８，Ｐ＜０．００１；与损伤指数呈负相关，ｒ＝－０．７５，Ｐ＜０．００１。因此本文结论是ＥＧＦ对粘膜的保护可能是通过完整的ＧＭＢＦ所介导。     

冠心病患者尿纤维蛋白肽A检测初步报告

应用高效液相色谱法检测１０例稳定型心绞痛（ＳＡ组）、１２例不稳定型心绞痛（ＵＡ组）、１２例急性心肌梗塞（ＡＭＩ组）患者、４２例正常人（对照组）的尿纤维蛋白肽Ａ（ＦＰＡ）水平，结果分别为：２８．１±１３．３、３９．６±１１．８、８８．２±２８．９、２５．４±１０．３ｎｇ／ｍｇＣｒ．ＡＭＩ组明显高于其它各组（Ｐ＜０．０１）ＵＡ组高于ＳＡ组（Ｐ＜０．０５）、对照组（Ｐ＜０．０１）．ＳＡ组与对照组的尿ＦＰＡ无显著差异．表明冠心病患者体内存在高凝状态．提示，尿ＦＰＡ的定量对冠心病类型的鉴别有一定价值，认为通过动态观察尿ＦＰＡ变化有助于判断病情．     

胃肠激素在肝硬变胃粘膜病变发病机制中的作用

目的探讨胃肠激素（ＧＩＨ）在肝硬变胃粘膜病变发病机制中的意义．方法用ＲＩＡ法测定临床诊断为肝硬变伴胃粘膜病变（ＣＧＭＬ）１７例，肝硬变（ＬＣ）３２例，胃溃疡（ＧＵ）１０例，轻度浅表性胃炎（ＣＳＧ）２３例及正常对照者３６例的空腹血浆生长抑素（ＳＳ），血管活性肠肽（ＶＩＰ），胃动素（ＭＴＬ）及促胃液素（Ｇａｓ）的变化，并结合各疾病组的内镜特点，分析ＣＧＭＬ与某些ＧＩＨ的关系．结果血浆ＳＳ水平（ｎｇ／Ｌ）在ＣＧＭＬ及ＧＵ组分别为４１２±２１２及３７６±１４３，与正常对照组（６１２±１７０）、ＬＣ组（６６２±３０９），ＣＳＧ组（６４８±３９１）比较，Ｐ均＜００１；ＶＩＰ浓度（ｎｇ／Ｌ）则在ＣＧＭＬ组（６３４±３５８）、ＧＵ组（１１０９±４２４）、ＬＣ组（７７８±４２６）及ＣＳＧ组（６３４±３４７）均高于正常对照组（３２７±１４４），Ｐ均＜００１．ＣＧＭＬ，ＧＵ及ＣＳＧ具不同的内镜特点；ＣＧＭＬ的发病与食管静脉曲张（ＥＶ）关系密切，随ＥＶ程度的加重，发病率有增高的趋势．结论ＣＧＭＬ发病与门脉高压关系密切，激素代谢紊乱可能通过影响内脏血流及粘膜抗损害能力而参与其形成．     

脓毒败血症性肺损伤的实验研究

本实验利用盲肠结扎穿孔模型探讨脓毒败血症时肺功能及代谢改变。６３只家兔随机分为三组：（１）正常对照组；（２）实验组；（３）布洛芬处理组。实验中测定肺血液动力学指标、血气指标、花生四烯酸代谢产物（ＴＸＢ_２和６－Ｋｅｆｏ－ＰＧＦ_１α）、支气管肺泡灌洗中白蛋白含量［ＢＡＬＦａｌｂｕｍｉｎ］，及肺水肿参数等。结果显示ＰａＯ_２和ＰａＣＯ_２都是下降趋势，在盲肠结扎穿孔后８ｈ肺动脉压（２５．２±８．２ｍｍＨｇ）较对照组（１４．７±０．８）明显升高（Ｐ＜０．０５）。肺血流量（１９４±５７ｍｌ／ｍｉｎ）；较对照组（３１６±１７）明显降低（Ｐ＜０．０５）。手术后１２ｈＴＸＢ_２（１３６７±３６８ｐｇ／ｍｌ）和６－Ｋｅｔｏ－ＰＧＦ_１α（３４．０±２３）较术前（９２１±５５７；９．３±６．８）均有显著升高（Ｐ＜０．０５），而３０ｈ后仅６－Ｋｅｔｏ－ＰＧＦ_１α仍显著高于正常水平。布洛芬处理后仅显示出对１２ｈ点ＴＸＢ_２的抑制作用。实验组及处理组ＢＡＬＦａｌｂｕｍｉｎ均显著升高，提示肺通透性明显增加。上述功能改变可能与细菌、内毒素及代谢改变有关。     

苯那普利对高血压病患者胰岛素抵抗的影响

探讨苯那普利对高血压病（ＥＨ） 患者胰岛素抵抗的影响。测定３２ 例ＥＨ 患者用苯那普利治疗（１０～２０ ｍｇ／ 日,疗程４ 周） 前后及２０ 例正常对照组的空腹血糖（ＦＰＧ） 、空腹胰岛素（ＦＩＮＳ） ,以１／（ＦＰＧ×ＦＩＮＳ）作为胰岛素敏感性指标（ＩＳＩ） 。结果　１－ ＥＨ患者苯那普利治疗后血压较治疗前显著降低（ＳＢＰ：１７ ．８４ ±１ ．５７ ｋＰａ 比２２ ．６３ ±２ ．１３ ｋＰａ,Ｐ＜ ０ ．０１ ;ＤＢＰ：１０．５８ ±１．２１ ｋＰａ 比１４ ．３５ ±１ ．２６ ｋＰａ,Ｐ＜ ０．０１） ,总有效率８４ ．４ ％ 。２－ ＥＨ 组与对照组ＦＰＧ 无明显差异,而ＩＳＩ有显著差异（０ ．０１５ ±０ ．００７ 比０ ．０３１ ±０ ．０１３ ,Ｐ＜ ０ ．０１） ;ＥＨ组苯那普利治疗后ＩＳＩ较治疗前显著改善（０ ．０２３ ±０ ．０１１ 比０ ．０１５ ±０ ．００７ ,Ｐ＜ ０ ．０１） 。苯那普利在有效降压同时对ＥＨ 患者的胰岛素抵抗有明显改善作用     

经皮冠状动脉腔内成形术对不稳定型心绞痛患者心率变异的影响

应用长程心电图分析系统对１６例不稳定型心绞痛患者（ＵＡＰ组）入院后第２日、经皮冠状动脉腔内成形术（ＲＴＣＡ）后第１，３，３０日以及１４８例健康中、老年人（对照组）２４ｈ心电图进行心率变异（ＨＲＶ）分析。结果：ＵＡＰ组２４ｈ连续正常ＲＲ间期的标准差（ＳＤＮＮ）、２４ｈ内连续５ｍｉｎ节段平均正常ＲＲ间期的标准差（ＳＤＡＮＮｉ）、相邻ＲＲ间期差的均方根（ｒＭＳＳＤ），相邻两个正常心动周期差值大于５０ｍｓ个数占总搏数的百分比（ＰＮＮ５０）、低频功率（ＬＦ）及高频功率（ＨＦ）均明显低于对照组（分别为９２．７±１４．３ｍｓｖｓ１２８．９±１７．８ｍｓ、７８．８±１０．６ｍｓｖｓ１１８．６±１９．１ｍｓ、１９．３±７．７ｍｓｖｓ２９．８±１２．７ｍｓ、３．６±１．７％ｖｓ６．５±５．５％、３１７．２±１４８．３ｍｓ２ｖｓ４７６．５±２８７．３ｍｓ２，Ｐ均＜０．０５），而ＬＦ／ＨＦ高于对照组（３．５±１．３ｖｓ２．４±１．１，Ｐ＜０．０５）。ＰＴＣＡ术后３０天ＵＡＰ患者ＨＲＶ逐渐恢复正常。结果提示ＵＡＰ患者交感神经和迷走神经张力下降，而以后者更明显；ＰＴＣＡ后ＨＲＶ逐渐恢复，说明ＰＴＣＡ能改善ＵＡＰ患者的ＨＲＶ。     

心肌缺血大鼠的心率功率谱变化及其与心脏性猝死关系的研究

采用心率变异（ＨＲＶ）频域指标定量评价心肌缺血大鼠的心脏自主神经功能变化及其与心脏性猝死（ＳＣＤ）的关系。Ｈｏｌｔｅｒ监测仪记录假手术组（２０只）及心肌缺血后存活组（５４只）与ＳＣＤ组（３６只）大鼠的心电信号。结果显示存活组或ＳＣＤ组大鼠于心肌缺血初始１５ｍｉｎ内的低频（ＬＦ）及低频／高频比值（ＬＦ／ＨＦ）较假手术组明显升高〔ＬＦ（ｍｓ２／Ｈｚ）：１９８．８±４１．３或２２６．７±５６．４ｖｓ６５．４±１９．６，Ｐ均＜０．０１；ＬＦ／ＨＦ：４．０８±１．１或５．１２±１．４ｖｓ１．８７±０．７，Ｐ均＜０．０１〕，而且ＳＣＤ组大鼠的ＬＦ与ＬＦ／ＨＦ较存活组增高〔ＬＦ（ｍｓ２／Ｈｚ）：２２６．７±５６．４ｖｓ１９８．８±４１．３，Ｐ均＜０．０５；ＬＦ／ＨＦ：５．１２±１．４ｖｓ４．０８±１．１，Ｐ＜０．０５〕，各组间ＨＦ无明显变化；ＳＣＤ组大鼠于ＳＣＤ发生前１５ｍｉｎ内，心率功率谱动态变化表现为ＬＦ及ＬＦ／ＨＦ随死亡时间的濒临而呈进行性升高（Ｐ＜０．０１及０．０５）。表明大鼠心肌缺血后其交感神经活性明显亢进，ＨＲＶ降低与ＳＣＤ的发生密切相关。     

预激综合征患者多旁路的射频消融

１７４例预激综合征患者中１３例（７．５％）具有多旁路（２９条）。２９条旁路中２１条由基础电生理检查证实，８条在阻断其它旁路后显现。４例在双侧，９例在单侧消融。平均放电３２±１４次后将２７条（９３．１％）旁路阻断。多旁路与单旁路消融成功率相似（９３．１％ＶＳ９４．０％，Ｐ＞０．０５）；但放电次数多（３２±１４ＶＳ１４±１１，Ｐ＜０．０５），消融时程长（３．６±０．８ｈＶＳ２．１±０．９ｈ，Ｐ＜０．０１）；多旁路组复发率高（７．６％ＶＳ１．９％，Ｐ＜０．０１）．本研究证实射频消融是根治多旁路患者的有效方法。     

钙拮抗剂和β－受体阻滞剂的降压作用对胰岛素抵抗的影响

本文观察４５例轻、中度非肥胖高血压病患者口服异搏定、氨酰心安降压治疗２４周后对胰岛素抵抗的影响。结果：异搏定治疗后血浆葡萄糖浓度（ＰＧ）无变化；血浆胰岛素浓度（ＩＮＳ）下降（１３．９±３．６ｍＵ／Ｌ：１１．０±２．４ｍＵ／Ｌ，Ｐ＜０．０１）；胰岛素敏感性格数（ＩＳＩ）增加（－４．１０±０．３４：－３．９２±０．２７，Ｐ＜０．０１），表明其对胰岛素浓度有影响。氨酰心安治疗后ＰＧ升高（４．６０±０．４３ｍｍｏｌ／Ｌ：５．３８±０．４６ｍｍｏｌ／Ｌ，Ｐ＜０．００１）；ＩＮＳ下降（１４．７±４．８ｍＵ／Ｌ：１３．７±３．４ｍＵ／Ｌ，Ｐ＜０．０５）；ＩＳＩ减少（－４．１１±０．２９：１－４．２５±０．３０，Ｐ＜０．０５）．表明其加重了胰岛素抵抗。因此，对合并胰岛素抵抗的高血压病患者，应注意降压药物的选择。     

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.     

急性肺动脉栓塞心电图多指标关联时变模式研究

目的:研究急性肺动脉栓塞(APE)的临床心电图动态演化规律,阐明其多样性表现的机制。方法:收集42个APE病例的心电图系列,每一例按记录时间顺序对7个特征性指标(心率,SⅠ、QⅢ、TⅢ、TV1,、STV、RV1或r'V1波)采样。分析该7个特征指标的时变特征,并总结归纳出APE心电图的多指标关联时变模式。结果:该时变理论模式表明,典型APE患者心电图随病程的动态变化,以TV1波倒置达峰时间为界,可化分为3个阶段。发病至TV1波倒置达峰前为第一阶段,TV1波倒置逐渐加深,表现为下降线,其它各指标在该阶段即已迅速完成上升或下降的演变而进入快速回复期,其时变模式曲线呈"反S"型或"S"型;第二阶段即为TV1波倒置达峰阶段,其时间大概处于TVI波总演变时间的前1/3处;自TVI波倒置达峰后至回复发病前水平为第三阶段。结论:临床APE心电图表现之多样性,是不同阶段各指标的联合表现特征和形式多样性的反映。该时变模式曲线可应用于临床判断疾病阶段。     

115例布鲁菌病临床特点分析

目的 探索布鲁菌病(布病)患者临床特征及治疗转归情况,为临床诊治提供参考。方法 收集并分析115例成人布病患者的人口学和流行病学资料、临床表现、血液学指标及治疗与转归情况。结果 布病患者常常伴有发热、乏力、多汗、关节疼痛、肝脾肿大等临床症状,其HGB、红细胞压积(hematocrit,HCT)、嗜酸性粒细胞(eosinophil,EO)、红细胞分布宽度(red blood cell distribution width,RDW)和CRP异常率较高。而WBC、PLT、中性粒细胞计数、淋巴细胞计数、单核细胞计数、平均细胞体积、血小板分布宽度、ESR和降钙素原的异常率较低。治疗上大部分患者[53.04%(61/115)]接受利福平联合多西环素治疗,部分患者尤其是合并骨质侵犯患者常使用三联抗菌素治疗。其中47例并发骨关节痛患者,经规范足疗程治疗后皆好转或痊愈。结论 布病患者常伴有发热、乏力、多汗、关节疼痛、肝脾肿大等临床症状,其HGB、HCT、EO、RDW和CRP异常率较高,可作为布病的辅助诊断指标。布病临床表现多样,明确诊断后应尽早给予规范的抗菌治疗,抑制疾病进展,减少并发症发生。     

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。     

A comparison of methods of pathogen inactivation of FFP

Introduction Current methods for pathogen inactivation of plasma involve four major processes using solvent–detergent (SD), methylene blue (MB), amotosalen and riboflavin as additives. Three of these methods involve the use of visible or ultraviolet light. Methods A comparison of the four methods was made using publications in Medline, Pubmed, Embase and Biosis to obtain data on the logistics of use, the quality of the plasma proteins and the effectiveness of pathogen inactivation. Results Three of the methods, MB, amotosalen and riboflavin, are designed for use in a blood bank; the SD method is generally applied at a centralized manufacturing centre and involves large plasma pools. All methods result in a reduction in protein values with the per cent retention of FVIII activity in the range of 67–78% and fibrinogen of 65–84%. Protein S and alpha₂‐antiplasmin are lower following solvent–detergent treatment. Alterations in fibrinogen structure have been reported with methylene blue. Discussion Three of the methods are designed for small volume use in a blood bank. All four methods have some effect on the coagulant proteins; however, the final concentrations are within regulated limits. While there is variability in the effectiveness against pathogens, direct comparison is difficult because of the methodologies used. Nonetheless, all are effective in inactivating HIV and other lipid‐enveloped pathogens. Clinical studies on the effectiveness of these products are surprisingly sparse, and no randomized clinical trials have yet been performed with amotosalen or riboflavin plasmas.