醒脑静注射液对高血压脑出血微创碎吸术后患者血细胞因子的影响

目的观察醒脑静注射液对高血压脑出血微创碎吸术后患者血中细胞因子水平及疗效的影响。方法将80例行微创碎吸术高血压脑出血患者随机分为两组,每组40例。对照组术后采用常规治疗,观察组加用醒脑静注射液治疗,同时选10名健康人血清作为健康对照组,连续监测血清中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)的动态变化。按脑卒中患者临床神经功能缺损程度评分标准进行临床疗效评定。结果两组患者的TNF-α及IL-6含量均高于健康对照组。观察组患者TNF-α及IL-6含量达峰时间早,对照组患者TNF-α及IL-6含量达峰时间较晚且水平较高。与对照组相比,观察组患者总体有效率高。结论高血压脑出血患者微创碎吸术后予醒脑静注射液治疗,可降低血清中TNF-α及IL-6水平,改善患者预后。     

丹红注射液对2型糖尿病肾病患者CRP、TNF-α水平的影响

目的观察丹红注射液对2型糖尿病肾病患者血清C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)的影响,探讨丹红注射液治疗2型糖尿病肾病的可能机制。方法采用常规西药加丹红注射液治疗30例2型糖尿病肾病患者为治疗组,取常规西药组30例作为对照组观察,于治疗前后检测患者血液中炎性因子CRP、TNF-α水平。结果丹红注射液治疗2型糖尿病肾病总有效率66.7%,而对照组总有效率为43.3%,两组比较差异有统计学意义(P<0.05);治疗前治疗组CRP、TNF-α水平与对照组比较差异无统计学意义(P>0.05);治疗后治疗组CRP、TNF-α显著降低,与对照组比较差异有统计学意义(P<0.05);治疗组治疗前和治疗后24h尿蛋白量下降与CRP、TNF-α水平呈正相关。结论丹红注射液结合西医治疗对2型糖尿病肾病有效,可能与丹红注射液能调节炎性因子的产生,抑制炎性反应有关。     

醒脑静与甘露醇联用对脑出血患者伴肺部感染的临床疗效及其对凝血功能的影响

目的:探究醒脑静与甘露醇联用对脑出血患者伴肺部感染的临床疗效及其对凝血功能的影响。方法:选取2017年2月—2018年12月期间收治的脑出血伴肺部感染患者78例资料,根据治疗方法不同将其分为对照组和观察组(每组39例);对照组患者给予甘露醇注射液与缬沙坦片常规治疗,观察组患者在对照组基础上加用醒脑静注射液治疗,比较两组患者治疗前与治疗28 d按国立卫生研究院卒中量表(NIHSS)评分的评分值、凝血功能指标即纤维蛋白原(FIB)、D-二聚体(D-Dimer)以及炎性因子即肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平测得值的变化情况。结果:两组患者治疗前的NIHSS评分值、FIB、D-Dimer、TNF-α和IL-6水平测得值经组间比较其差异均无统计学意义(P>0.05),治疗后的FIB水平测得值高于治疗前(P<0.05),NIHSS评分值、IL-6和TNF-α水平测得值均低于治疗前(P<0.05);观察组患者治疗后的FIB水平测得值高于对照组(P<0.05),NIHSS评分值、D-Dimer、TNF-α和IL-6水平测得值均低于对照组(P<0.05)。结论:采用醒脑静注射液与甘露醇注射液联用治疗脑出血伴肺部感染患者的临床疗效较为确切,有效改善了其凝血功能指标和炎性因子水平。     

急性肾功能衰竭患者炎性反应与心钠素的关系

目的 探讨急性肾功能衰竭患者慢性炎性反应与心钠素的关系.方法 测定75例急性肾功能衰竭患者慢性炎性指标血C-反应蛋白(CRP)、IL-6、TNF-α及心钠素,分析它们之间的关系.结果 有62.7%急性肾功能衰竭患者心钠素超过正常参考值,心钠素升高组血清CBP、IL-6显著高于心钠素降低组(均P<0.05);血心钠素与CRP(P<0.01)、IL-6及TNF-α呈正相关(P<0.05).结论 急性肾功能衰竭患者存在炎性反应,可能引起心钠素等代谢异常.     

己酮可可碱对脑梗死患者血清C反应蛋白,TNF-α,IL-6的影响

目的:探讨己酮可可碱对脑梗死患者血清C反应蛋白(CRP),肿瘤坏死因子-α(TNF-α),白介素-6(IL-6)的影响.方法:60例脑梗死患者随机分为己酮可可碱治疗组30例和对照组30例,治疗时间4周,观察治疗前后CRp,TNF-d,IL-6在各组之间的差异.结果:治疗前CRP、TNF-α、IL-6在两组之间差异无显著性,治疗后治疗组CRp、TNF-α、IL-6水平较对照组明显降低.结论:己酮可可碱可使脑梗死患者炎性反应显著减轻,有利于脑梗死患者的恢复.     

普伐他汀对急性冠状动脉综合征患者血清TNF-α和IL-6水平的影响

目的 探讨普伐他汀对急性冠状动脉综合征(ACS)患者血清肿瘤坏死因子α(TNF-α)及白细胞介素6(IL-6)水平变化的影响.方法 将ACS患者50例随机分为普伐他汀组25例和常规治疗组25例,分别于治疗前及治疗4周后行血清TNF-α及IL-6检测,均采用放射免疫分析方法.另选同期健康体检的20例作为对照组.结果 ACS组治疗前血清IL-6、TNF-α水平均明显高于对照组(均P<0.01).普伐他汀组治疗后血清IL-6、TNF-α水平均明显低于治疗前,但仍高于对照组(均P<0.05).常规治疗组患者治疗后血清IL-6、TNF-α降低不明显(P>0.05).结论 IL-6、TNF-α水平升高与ACS发病密切相关,普伐他汀可降低ACS患者血IL-6、TNF-α水平,具有减轻病变部位炎性反应和保护内皮细胞的作用.     

探索血必净注射液调节细胞因子在治疗新冠肺炎中的作用

目的探讨血必净注射液调节细胞因子、平衡机体免疫应答在治疗重症肺炎中的作用,以期为血必净注射液治疗新型冠状病毒引起的肺炎(NCP)提供一定的循证支持。方法汇总中国知网、万方、维普、Pubmed数据库中有关血必净注射液对急性肺损伤(ALI)/全身炎症反应动物模型的细胞因子产生影响的实验室研究文献以及临床重症肺炎患者加用血必净注射液干预治疗后对细胞因子和临床疗效产生影响的相关文献,并对文献进行分析。结果动物实验研究显示:血必净注射液干预可有效保护受损伤的肺组织,抑制血清促炎因子TNF-α、IL-1、IL-6、IL-8升高。对重症肺炎患者的临床研究显示:重症肺炎患者在常规治疗基础上加血必净注射液干预后,治疗有效率和相关临床指标均有显著改善;同时血清促炎因子TNF-α、IL-1、IL-6、IL-8比未加用血必净注射液的常规治疗组下降,抗炎因子IL-10比常规治疗组上升。结论血必净注射液可能通过抑制TNF-α、IL-1、IL-6、IL-8等细胞因子,有效调节机体因受病毒等侵扰形成的免疫应答,阻止炎症对脏器的进一步损害,从而发挥对重症肺炎的治疗作用,从免疫调节的角度上阐述了血必净注射液在NCP重症患者中的治疗作用。     

氯沙坦对原发性高血压患者血清TNF-α和IL-6水平的影响

目的 观察氯沙坦对原发性高血压患者血清细胞因子肿瘤坏死因子-α (TNF-α)和白细胞介素-6(IL-6)水平的影响.方法 70例原发性高血压患者随机分为对照组和治疗组,每组35例,对照组服用非洛地平缓释片,治疗组服用氯沙坦钾片,治疗8周,分别于治疗前后检测患者血清中细胞因子TNF-α和IL-6水平.结果 2组治疗前比较,血清TNF-α、IL-6水平差异无统计学意义(P＞0.05).2组治疗后比较,TNF-α和IL-6水平差异有统计学意义(P＜0.05).结论 氯沙坦能降低原发性高血压患者的血压,同时能够降低原发性高血压患者的炎性细胞因子、抑制炎性反应.     

慢性阻塞性肺疾病患者血细胞因子变化及N-乙酰半胱氨酸对其影响

目的检测慢性阻塞性肺疾病（COPD）患者血清细胞因子IL-6、IL-8,TNF-α,观察N-乙酰半胱氨酸对其影响。方法40例COPD急性发作期患者分为两组,治疗组：服用N-乙酰半胱氨酸（1次200mg,3次/d）,并给予抗炎、对症治疗;对照组：予抗炎、对症治疗;另设正常组。放射免疫法进行检测。结果COPD急性发作期患者血清细胞因子IL-6、IL-8,TNF-α水平升高,治疗后有所下降,但仍高于正常组。治疗组与对照组治疗前后比较差异无统计学意义。结论N-乙酰半胱氨酸短期治疗对COPD患者血清细胞因子IL-6、IL-8,TNF-α无明显影响。     

血必净对脓毒症患者的临床疗效及对相关细胞因子的影响

目的观察血必净注射液对脓毒症患者的临床疗效,以及其对患者血清细胞因子IL-6和TNF-α的影响。方法将78例脓毒症患者随机分为治疗组(39例)与对照组(39例),两组均使用常规基础治疗,治疗组加血必净注射液治疗。疗程结束后,主要评价患者接受治疗后28d病死率,以及APACHEⅡ评分;并在治疗前后采集两组患者静脉血,对患者血清细胞因子IL-6及TNF-α含量比较。结果治疗后治疗组28d病死率明显低于对照组,且脓毒症及严重脓毒症患者中均有明显降低趋势,但差异无统计学意义(P0.05)。而治疗后两组患者APACHEⅡ评分及细胞因子IL-6及TNF-α含量均明显下降,与治疗前比较差异均有统计学意义(P0.05或P0.01);且治疗组改善较对照组明显,两组差异有统计学意义(P0.05或P0.01)。结论单纯西医基础治疗及联合血必净治疗对脓毒症患者APACHEⅡ评分及细胞因子IL-6、TNF-α含量均有明显改善作用,联合血必净治疗作用优于单纯西药治疗。并可能通过改善以上指标对脓毒症患者28d病死率有一定的改善作用。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Trichinellosis in immigrants in Switzerland

We describe a case of trichinellosis diagnosed at the Division of Infectious Diseases, Hospital of Lugano, in January 2009. This case was associated with a cluster of cases and was traced to the consumption of contaminated meat after a wild boar hunt in Bosnia.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.