大剂量氢化考的松在青霉素治疗钩端螺旋体病中的作用(附130例临床观察)

治疗钩端螺旋体病(钩体病)青霉素为首选药,但在治疗过程中易致赫氏反应(JHR)。我们于1980～1982年对130例钩体病人试用氢化考的松(氢考)和青霉素同时给予,以减少JHR发生率。现将结果报告于下。     

氢化考的松预防钩体病赫氏反应的效果观察

我们于1983~1984年用氢化考的松(下称氡考),有效地控制了钩端螺旋体病(简称钩体病)在青毒素(PNC)治疗过程中赫氏反应(JHR)的发生.现报告如下:临床资料1、病例选择:(1)有钩体病疫区接触史;(2)1年内未接受过钩体菌苗接种;(3)有典型临床症状、体征;     

钩端螺旋体病和急性肾功能衰竭——临床经验和文献复习

英国每年大约有50例钩端螺旋体病(以下简称钩体病)发生,其中10％发生急性肾功能衰竭,病死率约为5％,多死于伴发黄疸的肾功能衰竭。6例均系男性,年龄23～49岁,起病后2～10天内大多因发热、头痛、背痛、腹痛、呕吐、腹泻、肌痛、关节痛、躯干皮肤散在出血点、随后发生黄疸和少尿而入院。患者血尿素氮240～600mg％;血小板值低;常规凝血试验结果大多正常。6例中2例钩端螺旋体(以下简称钩体)补体结合试验结果阳性(效     

闽西钩端螺旋体病疫区血清流行病学的初步调查

<正> 1975年以来,闽西上杭县太拔乡钩端螺旋体病(钩体病)呈散发流行状态。1975～1991 年共发生钩体病43例,但发病者多为病势凶险的肺大出血型病人。病死率高,为9.30％(4/43)。为探讨其流行规律,作者于 1991年 8月在太拔乡开展了钩体病人群血清流行病学调查。现将结果报告如下。 一、材料与方法 对该乡临床医生报告的钩体病例均按文献进行核实诊断,确定为钩体病例者按统     

钩端螺旋体病脑动脉炎的发病机理与防治探讨(附87例临床分析)

本文报告钩端螺旋体(钩体)病脑动脉炎87例临床资料,认为本病的发生可能与钩体或钩体L型直接损伤脑血管密切相关。甲硝哒唑疗效优于青霉素,且可减少钩体病神经系统后发症。     

两种方案治疗钩端螺旋体病疗效比较

1982～1983年,我院收治钩端螺旋体病(下简称钩体病)采用大剂量和小剂量青霉素两种治疗方案,其治疗结果如下。一般资料:两年共收治临床及实验室检查典型钩体病者269例,其中男性200例,女性69例。年龄8～62岁,主要为青壮年。治疗分组:269例随机分为两组(见表1),每组均     

酶免疫斑点试验作钩体病血清学诊断的研究

本文用优选的最适条件对619份钩体病人血清和520份对照血清进行IgM-EIDT和MAT检测比较,发现早期病人血清IgM-EIDT阳性率显著高于MAT(P<0.001),恢复期血清则无差异。IgM-EIDT的诊断敏感性为95.53％,特异性为96.73％,两种方法对194份钩体病人双向血清的滴度检测呈显著正相关(r=0.7670)。对部分钩体病人血清用IgG-EIDT检测,其阳性率与MAT相似。因此,IgM-EIDT和IgG-EIDT结合使用,既可作钩体病的早期诊断,也可作追溯诊断和血清流行病学调查。     

螺旋体传染病

钩端螺旋体病的X线表现及分析——赖鸣晓(江西吉安县人民医院343100)；《井冈山医专学报》，2003，11(1)：45[目的：讨论钩体病病情和胸部X线改变之间的关系。方法：从15例钩体病胸片中对比观察钩体病治疗前后胸片改变。结果：钩体病皆可有胸部X线异常表现。     

万载县1985年钩端螺旋体病流行病学分析

<正> 江西省万载县1985年共发生钩端螺旋体病(简称钩体病)767例,发病率为190.38/10万,死亡6例,病死率为0.78％。现将其流行病学分析如下。 一、流行特征 1.地区分布:全县除高村、官元山2个乡未发生病例外,其余17个乡镇均有病例发生。丘陵发病高于     

钩端螺旋体病中枢神经系统后发症的血清学调查

<正> 钩端螺旋体病(简称钩体病),我省近几年来每年都有不同程度的流行发生,由于钩体病带菌动物多,菌型复杂,临床表现多样化,尤其是轻型钩体病人和隐性感染者,由于误诊和漏诊,未能及时得到正确治疗。据文献报道,上述因素是引起钩体病中枢神经系统后发症的重要原因之一。现将我们自1991年9月～1992年1月收检的29份临床上诊断为钩体病中枢神经系     

Jarisch-Herxheimer reaction among syphilis patients in Rio de Janeiro, Brazil

The Jarisch-Herxheimer reaction (JHR) is a syndrome observed after antimicrobial treatment of some infectious diseases. The syndrome has clinical characteristics of an inflammatory reaction to antibiotic treatment. A prospective study of patients with a clinical and laboratory diagnosis of syphilis was conducted at a sexually transmitted diseases clinic in Rio de Janeiro, Brazil. Patients were treated with benzathine penicillin and observed for the JHR. A total of 115 patients were included in this study. Fifty-one patients (44%) had secondary syphilis; 37 (32%), primary; 26 (23%), latent; and one (1%), tertiary syphilis. Ten patients (9%) developed the JHR. All JHRs occurred in patients with secondary and latent syphilis. No patients experienced an allergic reaction to penicillin. The JHR occurred less frequently than in previous studies. It is important that health-care professionals recognize the clinical characteristics of the JHR so that it is not misinterpreted as an allergic reaction to penicillin.     

Biomarkers of hypothalamic-pituitary-adrenal axis activity in mice lacking 11β-HSD1 and H6PDH

Glucocorticoid concentrations are a balance between production under the negative feedback control and diurnal rhythm of the hypothalamic-pituitary-adrenal (HPA) axis and peripheral metabolism, for example by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which catalyses the reduction of inactive cortisone (11-dehydrocorticosterone (11-DHC) in mice) to cortisol (corticosterone in mice). Reductase activity is conferred upon 11β-HSD1 by hexose-6-phosphate dehydrogenase (H6PDH). 11β-HSD1 is implicated in the development of obesity, and selective 11β-HSD1 inhibitors are currently under development. We sought to address the concern regarding potential up-regulation of the HPA axis associated with inhibition of 11β-HSD1. We assessed biomarkers for allele combinations of 11β-HSD1 and H6PDH derived from double heterozygous mouse crosses. H6PDH knock out (KO) adrenals were 69% larger than WT while 11β-HSD1 KO and double KO (DKO) adrenals were ～30% larger than WT - indicative of increased HPA axis drive in KO animals. ACTH-stimulated circulating corticosterone concentrations were 2.2-fold higher in H6PDH KO animals and ～1.5-fold higher in 11β-HSD1 KO and DKO animals compared with WT, proportional to the observed adrenal hypertrophy. KO of H6PDH resulted in a substantial increase in urinary DHC metabolites in males (65%) and females (61%). KO of 11β-HSD1 alone or in combination with H6PDH led to significant increases (36 and 42% respectively) in urinary DHC metabolites in females only. Intermediate 11β-HSD1/H6PDH heterozygotes maintained a normal HPA axis. Urinary steroid metabolite profile by gas chromatography/mass spectrometry as a biomarker assay may be beneficial in assaying HPA axis status clinically in cases of congenital and acquired 11β-HSD1/H6PDH deficiency.     

DNA diagnosis of pyruvate dehydrogenase deficiency in female patients with congenital lactic acidaemia

Summary The diagnosis of pyruvate dehydrogenase (PDH) E1α deficiency, which is an X-linked inborn error of metabolism, is usually established by the measurement of PDH complex activity in cultured cells. However, heterozygous female patients with PDH E1α deficiency may be misdiagnosed when the normal X chromosome is predominantly expressed in the cultured cells. Therefore, in female patients with convincing clinical presentations of PDH E1α deficiency and the normal enzyme activity, the X-inactivation pattern should be analysed and the PDH E1α gene screened for mutations. For this screening, we applied the method of single-strand conformational polymorphism (SSCP) and DNA sequencing and examined 11 female patients with congenital lactic acidaemia whose PDH complex activity was normal in cultured cells. In 2 of the 11 female patients, we found distinct pathogenic missense mutations in the PDH E1α gene (G89S and G291R). Both affected patients showed a similar clinical presentation and had been diagnosed as West syndrome. In 3 of the 11 patients, we found a polymorphic base-pair substitution in exon 9 of the PDH E1α gene which resulted in a changed amino acid residue (M282L). We conclude that PCR-SSCP analysis of the PDH E1α gene, followed by DNA sequencing, is a useful method to screen for mutations of the PDH E1α gene in female patients with congenital lactic acidaemia who have normal enzyme activities in available samples, normal ratio of lactate to pyruvate, and predominantly raised lactate concentration in cerebrospinal fluid.     

Pyruvate dehydrogenase activity is stimulated by growth hormone (GH) in human mononuclear cells: a new tool to measure GH responsiveness in man.

Human peripheral mononuclear cells (PMC) were used to examine the effects of hGH and insulin on the activity of the pyruvate dehydrogenase (PDH) complex. Incubation of PMC with 10(-7) mol/L hGH or insulin increased basal PDH activity. Hormonal effects were maximal (50-60% above control values) at 15 min. Later on, activation progressively decreased and was no longer detectable at 30 min. Total PDH activity was unaffected by hormonal treatment. PMC were subfractionated into lymphocytes and monocytes to assess the sensitivity of each cell types to the hormones. hGH significantly increased basal PDH activity in lymphocytes and monocytes (38% and 70% above control values, respectively), whereas insulin increased basal PDH activity only in monocytes (151% above control value). PMC from healthy subjects aged 1-45 yr were incubated for 15 min with 10(-7) mol/L hGH or insulin before PDH measurement. An increase of enzyme activity higher than 20% was observed in 26 patients out of 29 with hGH, and in 15 out of 18 with insulin. In conclusion, hGH is able to stimulate PDH activity of human mononuclear cells. This hormonal effect allows rapid evaluation of the cellular responsiveness of hGH in various pathophysiologic situations.     

Direct regulation of glucose and not insulin on hepatic hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1

Abnormal hepatic gluconeogenesis contributes significantly to both fasting and non-fasting hyperglycemia of patients with type 2 diabetes. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates the key hepatic gluconeogenic enzymes including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) through the amplification of glucocorticoid receptor (GR) - mediated tissue glucocorticoid action, and is crucially dependent on hexose-6-phosphate dehydrogenase (H6PDH) - generating NADPH system. Here, we observed that compared with fasting state, H6PDH and 11β-HSD1 expression in livers were all increased under non-fasting state in both normal and diabetic rats, and the non-fasting diabetic group was the highest among the four experimental groups. Moreover, incubation of primary hepatocytes with increasing glucose caused dose-dependent increases in H6PDH, 11β-HSD1, GR, PEPCK and G6Pase expression. Also, glucose-6-phosphate (G6P) had a positive regulation on H6PDH and 11β-HSD1 in hepatocytes. In addition, primary hepatocytes treated with different doses of insulin in high glucose induced alteration of H6PDH and 11β-HSD1 while in low glucose there was no significant effect. These findings suggest that glucose instead of insulin directly regulates H6PDH and 11β-HSD1 and suppression of the two enzymes could be considered as an effective target for the treatment of type 2 diabetes.     

Hexose-6-phosphate dehydrogenase confers oxo-reductase activity upon 11 beta-hydroxysteroid dehydrogenase type 1

Two isozymes of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) interconvert active cortisol and inactive cortisone. 11 beta-HSD2 (renal) acts only as a dehydrogenase, converting cortisol to cortisone. 11 beta-HSD1 (liver) is a bi-directional enzyme in cell homogenates, whereas in intact cells it typically displays oxo-reductase activity, generating cortisol from cortisone. We recently established that cortisone reductase deficiency is a digenic disease requiring mutations in both the gene encoding 11 beta-HSD1 and in the gene for a novel enzyme located within the lumen of the endoplasmic reticulum (ER), hexose-6-phosphate dehydrogenase (H6PDH). This latter enzyme generates NADPH, the co-factor required for oxo-reductase activity. Therefore, we hypothesized that H6PDH expression may be an important determinant of 11 beta-HSD1 oxo-reductase activity. Transient transfection of chinese hamster ovary (CHO) cells with 11 beta-HSD1 resulted in the appearance of both oxo-reductase and dehydrogenase activities in intact cells. Co-transfection of 11 beta-HSD1 with H6PDH increased oxo-reductase activity whilst virtually eliminating dehydrogenase activity. In contrast, H6PDH had no effect on reaction direction of 11 beta-HSD2, nor did the cytosolic enzyme, glucose-6-phosphate dehydrogenase (G6PD) affect 11 beta-HSD1 oxo-reductase activity. Conversely in HEK 293 cells stably transfected with 11 beta-HSD1 cDNA, transfection of an H6PDH siRNA reduced 11 beta-HSD1 oxo-reductase activity whilst simultaneously increasing 11 beta-HSD1 dehydrogenase activity. In human omental preadipocytes obtained from 15 females of variable body mass index (BMI), H6PDH mRNA levels positively correlated with 11 beta-HSD1 oxo-reductase activity, independent of 11 beta-HSD1 mRNA levels. H6PDH expression increased 5.3-fold across adipocyte differentiation (P < 0.05) and was associated with a switch from 11 beta-HSD1 dehydrogenase to oxo-reductase activity. In conclusion, H6PDH is a crucial determinant of 11 beta-HSD1 oxo-reductase activity in intact cells. Through its interaction with 11 beta-HSD1, H6PDH may represent a novel target in the pathogenesis and treatment of obesity.     

鲁斯可皂苷元通过抑制p38MAPK途径及心肌细胞焦亡改善小鼠阿霉素心肌病

目的 观察和探索鲁斯可皂苷元(Rus)对小鼠阿霉素(DOX)心肌病的影响及可能机制,旨在为临床上DOX心脏毒性的预防和治疗提供参考依据.方法 通过单次腹腔注射DOX(15mg/kg)的方式构建急性DOX心肌病小鼠模型,采用随机数表法将32只雄性C57BL/6小鼠(8～10周)随机分为空白对照组(Sham组)、Rus组、...     

Paraduodenal hernia: a treatable cause of upper gastrointestinal tract symptoms

Paraduodenal hernia (PDH) is an unusual condition that is caused by congenital intestinal malrotation. Noncatastrophic presenting symptoms and their responses to surgery have not been well-characterized. Barium upper gastrointestinal (UGI) series and small bowel follow-up x-rays, performed from December 1995 to September 1996, were sequentially reviewed by one radiologist (J.M.) to identify patients with small bowel series compatible with a PDH. Case histories were reviewed for symptomatic presentation, associated evaluation, and treatment. Based on the 294 UGIs and small bowel follow-throughs performed during this 10-month period, 6 cases were suspected to have a PDH. A right PDH was confirmed in the three patients who underwent surgical exploration (prevalence 1%). Preoperative patient symptoms included nausea, bilious vomiting, and right upper quadrant pain. Repair of the hernia defect resulted in complete resolution of chronic symptoms. Preoperative upper endoscopy, performed in three patients, was not helpful in identifying the disorder. Preoperative computerized tomography obtained in two patients was diagnostic for a right PDH. One symptomatic patient with vomiting and gastric stasis did not have surgery because of a terminal illness. The remaining two patients had no symptoms attributable to PDH. Patients with PDH frequently have chronic UGI symptoms. An upper endoscopy cannot be used to exclude this entity. After surgery, UGI symptoms from PDH are likely to resolve.     

Doxazosin, an alpha-1 antagonist, prevents further progression of the advanced atherosclerotic lesion in hypercholesterolemic hamsters

The aim of this study was to examine the effect of doxazosin (DOX) on the further progression and regression of the advanced atherosclerotic lesion in the hypercholesterolemic hamster. Thirty-six, male F(1)B Golden Syrian hamsters, 10 weeks of age, were divided into 3 groups of 12 and fed a nonpurified hypercholesterolemic diet (HCD) containing 10% coconut oil and 0.1% cholesterol (wt/wt) for 9 months (HCD 9). One group of hamsters was euthanized at 9 months and their aortas were collected, fixed, and stored until analysis. The remaining hamsters were either maintained on the HCD for an additional 6 months (HCD 15) or fed the HCD plus 20 mg/kg/d DOX for the 6 months. At the end of the study (15 months), the DOX-treated hamsters had significantly lower plasma total cholesterol (TC) (-68%), low-density lipoprotein-cholesterol (LDL-C) (-73%), and triglycerides (TG) (-74%) compared with the HCD 15. The lumenal narrowing and intimal thickening atherosclerotic lesions were significantly less in the DOX-treated hamsters compared with the HCD 15 (-66% and -70%, respectively). These data suggest that DOX treatment prevents further progression of the advanced atherosclerotic lesion possibly by lowering plasma TC, LDL-C, and TG in hypercholesterolemic hamsters.