Post-stimulus depression of reflex changes in circular muscle activity in the guinea pig small intestine.

The extent and time course of depression of successive reflex responses recorded with intracellular microelectrodes from the circular smooth muscle of the guinea pig small intestine were determined. Two stimuli were used, distension and distortion of the mucosa by compression; these were applied either at the same or at different sites. Excitatory responses oral and inhibitory responses anal to the stimuli were recorded. Post-stimulus depression of both ascending excitatory and descending inhibitory reflexes occurred, but the extent of depression was slightly less for the descending inhibition. A conditioning distension lasting 9 s depressed the excitatory response to a test distension applied 2 s later at the same site by 90%. After 30 s the depression was 50% and test responses were normal if inter-stimulus intervals were increased to 2 min. Increasing the duration of the conditioning stimulus increased the depression. Post-stimulus depression was less for compression stimuli than for distension stimuli and prior mucosal compression had almost no effect on responses to subsequent distension. The post-stimulus depression was greater if conditioning and test stimuli were at the same rather than different sites. For different sites, conditioning stimuli at 15 mm from the recording site (near) depressed responses to stimuli at 30 mm (far) to a greater extent than far stimuli depressed responses to near stimuli. If the conditioning stimulus at 15 mm was maintained until after the far test stimulus was applied, depression of the test response did not occur. It is concluded that the major sites of post-stimulus depression are at the synapses between primary sensory neurons and the first interneurons of reflex pathways, and that post-stimulus depression also occurs at other places in the pathway, presumably at synapses between interneurons or between interneurons and motor neurons.     

Soluble Fcγ receptors in periodontal lesions

Soluble Fcγ-binding components were detected in gingival fluid from periodontal lesions by incubation with biotinylated human Fcγ fragments. FcγIII receptor was identified by incubation of gingival fluid with monoclonal antibody. Sodium dodecyl sulfate-polyacrylamide gel electophoresis and Western transfer showed that most of the Fcγ-binding components had minimal mobility in a 4–15% gradient gel under nonreducing conditions. Under reducing conditions, the main band of Fcγ-binding components in gingival fluid migrated corresponding to protein A of 49 kDa. The pattern of Fcγ-binding components was similar in serum and gingival fluid except for the observation in gingival fluid of Fcγ-binding components migrating like standard proteins of 19 to 20 kDa, a size that corresponds to the polypeptide part of FcγII receptor and FcγIII receptor.     

Rehabilitation of the patient with chronic back pain. A search for outcome predictors

This prospective study was initiated 3 years ago to evaluate the outcome and to identify predictors of success or failure in patients admitted to a rehabilitation program for chronic low-back pain. Multiple parameters were evaluated, including psychologic data (MMPI, personal interview, pain drawing, etc.), physical measurements (flexibility, strength and endurance), and demographic data concerning the patient's home and working environment. Information was available on each patient admitted to the program prior to his admission, at completion of the program, 6 weeks following completion of the program and 3 months following completion of the program. A telephone interview was carried out 2 1/2 years following the patient's discharge from the program. Linear regression analysis was used to identify the important independent variables with regard to the dependent variables of relief of back pain, return to work and increased activities at home. Demographic data were of no value as a predictor with the exception of age and returning to work. The patients over the age of 50 returned to work with much less frequency than those less than 50. Psychologic information from the MMPI and similar tests were of no value. The personal preadmission interview of a trained psychologist, however, was a good predictor of an individual's eventual return to work and overall improvement. Worker's Compensation and other litigation was a negative factor in a patient's prognosis. The treatment team's prognosis at the time of discharge from the program was the best overall predictor of a patient's chance of success or failure in the longterm.     

血脂代谢紊乱与冠状动脉病变严重程度的关系

目的:分析血脂代谢异常与冠状动脉狭窄程度的关系.方法:对366例因胸痛而就诊的患者行选择性冠状动脉造影,按冠状动脉狭窄程度分为正常对照组、单支病变组、双支病变组、多支病变组.同时观察患者血脂各成分,并对各组指标进行统计学分析.结果:总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C),在各组之间存在差异,尤其多支病变组与正常组之间差异显著(P＜0.01).TC、TG、LDL-C随冠状动脉病变加重而增加,HDL-C随冠状动脉病变加重而减少,LDL-C与冠状动脉狭窄程度呈正相关,HDL-C与冠状动脉狭窄程度呈负相关.结论:血脂代谢紊乱与冠状动脉狭窄的发生发展有内在的联系,对于预测有无冠状动脉病变及其进展有一定临床意义.     

中国男性原发不育的遗传高风险因子:Y染色体DAZ基因拷贝缺失

目的 探讨Y染色体无精症因子C区(azoospermia factor C，AZFe)无精症缺失基因(deleted-in-azoospermia，DAZ)家族基因拷贝缺失与中国男性原发不育之间的关系。方法 运用多重PCR与PCR-RFLP检测技术，对210例已生育男性、216例原发无精症与189例严重少精症患者Y染色体AzFc区域DAZ基因家族的基因拷贝数进行分析。结果 在所有已生育男性中未检出DAZ基因拷贝的完全或部分缺失，而在原发无精症与严重少精症患者中DAZ基因拷贝完全缺失率分别为8．8％和12．2％，DAZ1／DAZ2共缺失率分别为8．3％和5．3％。结论 在中国男性原发无精症与严重少精症患者中存在较高频率的DAZ基因拷贝缺失现象，提示Y染色体AZFc区域DAZ基因家族基因拷贝的完全与部分缺失是中国男性原发不育的遗传高风险因子。     

重症肌无力胸腺切除术后呼吸道管理与并发症的防治

目的 探讨重症肌无力胸腺切除术后呼吸道管理与并发症的防治.方法 32例ICU收治的重症肌无力胸腺切除术后的患者,根据危象预测积分,分为普通组(积分＜12分,n=21)和高危组 (积分＞12分,n=11),对两组患者术后呼吸机支持时间、拔管前后肌力恢复情况、自主呼吸情况、动脉血气分析情况以及两组患者术后体温、胸片和痰培养结果进行统计分析.结果 高危组患者术后呼吸支持时间(18 ～ 30 h,平均26 h)大于普通组患者(4 ～ 28 h,平均14 h),两组有显著性差异(P＜0.01),同时术后发热、胸片渗出影以及阳性痰培养结果的发生率也高于普通组.结论 术后给予高危患者严密的监测和充分的呼吸支持,有助于降低重症肌无力危象的发生率和死亡率,同时应充分重视气道护理和感染的防治.     

超声诊断异位妊娠249例临床分析

目的为了提高对异位妊娠的诊断技术。方法选择在我院经手术病理证实的异位妊娠249例住院患者行2DB超和CDFI的声像图特征进行分析。结果2D超声声像图特征在249例异位妊娠中内膜增厚223例，厚度为4—8mm／2；宫内假环状孕囊28例，大小为4．12mm；宫外探及孕囊178例，大小为8-48mm；盆腔混合性包块28例，大小为40．80mm：伴有黄体囊肿的123例，存活宫外孕3例，可显示原始心管搏动；CDFI声像图特征为宫外孕急性破裂的患者显示肿块及周围组织的彩色血流信号增多，动脉频谱血流速度增快，RI降低。结论超声检查对妇产科急诊有显著性作用，可直接指导临床明确诊断，选定治疗方案。     

Relationship among dosages of aminophylline, plasma levels of theophylline and variation of pulmonary arterial pressure]

The relationship among the dosages of aminophylline, plasma levels of theophylline and variations of mean pulmonary arterial pressure (mPAP) in 72 patients with COPD was investigated. The results showed that after a different loading dosage of aminophylline (6 mg/kg, 5 mg/kg and 4 mg/kg) was administered by intravenous injection, mPAP in the 6 mg/kg group was decreased more significantly (P less than 0.01) than that in the 4 mg/kg group. In the 6 mg/kg group, the decreased mPAP period sustained for 120 min, which was longer than that in the other 2 groups. The plasma levels of theophylline in the 6 mg/kg group of patients 30 to 120 min after loading dose injected were 115.54-79.04 mumol/L, which were higher than that in the others. Within the 120 min period of observation after the drug was administered no patients in any of these groups showed severe untoward effects. According to the results of this experiment, we suggest that the 6 mg/kg as a loading dose should be advised for the treatment of pulmonary hypertension in COPD. The optimum time to give the maintenance dosage should be set within 2 h after the loading dose. It is necessary to monitor the plasma levels of theophylline while aminophylline is administered, so that optimal therapeutic effects could be achieved without side effects.     

Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case.

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.     

Adenosine''s role in the genesis of bradyarrhythmias induced by acute myocardial hypoxia.

A close or even causal relation between myocardial adenosine and bradyarrhythmias during acute myocardial hypoxia was testified in guinea pig, rabbit and dog mainly by using specific competitive antagonist and synchronous quantitative analysis of 3 variables: intensity of myocardial hypoxia, degree of endogenous adenosine increment and severity of bradyarrhythmias. Results disclosed: A) striking resemblance of the bradyarrhythmias with hypoxic origin to those caused by exogenous adenosine, B) same locality of A-V conduction block induced by both myocardial hypoxia and exogenous adenosine, C) precise parallelism among the above-listed 3 variables with very high correlativity (r = 0.99, P < 0.01), D) frequent accompaniment of reversal of hypoxic bradyarrhythmias through resupply of 21% O2 with normalization of preexisted increase in myocardial adenosine, E) satisfactory blockade of hypoxic bradyarrhythmias by adenosine's specific antagonist--aminophylline and their augmentation by adenosine's uptake inhibitor--dipyridamole, F) close similarity of the characteristic curve representing relation among the above 3 variables to that among intensity of myocardial hypoxia, degree of endogenous adenosine increment and amount of coronary blood flow in which adenosine's role as a mediator has been well documented and G) reproducible persistence of bradyarrhythmias during myocardial hypoxia irrespective of preliminary vagotomy and atropinization, denoting independence of the occurrence of such dysarrhythmias upon vagal drive, suggestive of a mechanism other than vagotonia. We advocated that hypoxia-induced bradyarrhythmias was caused by increment in endogenous adenosine.