细针穿刺抽脓配合中药内服治疗阑尾周围脓肿

阑尾周围脓肿是临床常见病，部分病人用非手术抗炎治疗难以奏效，常需手术引流。临床常见手术引流病人痛苦大，并发症多。１９９１年以来，我们对２１例经非手术治疗效果不佳的病例，采用细针穿刺抽脓配合中药阑尾清化汤内服治疗，取得满意效果，现报告如下。一般资料２１...

FA-100型电脑化尿液分析仪对诊断泌尿系感染的探讨

我们对219例临床初步诊断泌尿系感染的患者进行了中段尿培养,用FA-100型电脑化尿液快速分析仪进行亚硝酸盐测定,及尿常规三种方法对照。报告如下:一、标本来源门诊初步诊断泌尿系感染的患者,常规消毒。

Aquaporins:Their role in cholestatic liver disease

This review focuses on current knowledge on hepato-cyte aquaporins(AQPs)and their significance in bile formation and cholestasis.Canalicular bile secretion results from a combined interaction of several solute transporters and AQP water channels that facilitate water flow in response to the osmotic gradients created. During choleresis,hepatocytes rapidly increase their canalicular membrane water permeability by modulating the abundance of AQP8.The question was raised as to whether the opposite process,i.e.a decreased canalicular AQP8 expression would contribute to the development of cholestasis.Studies in several experimental models of cholestasis,such as extrahepatic obstructive cholestasis,estrogen-induced cholestasis, and sepsis-induced cholestasis demonstrated that the protein expression of hepatocyte AQP8 was impaired. In addition,biophysical studies in canalicular plasma membranes revealed decreased water permeability associated with AQP8 protein downregulation.The combined alteration in hepatocyte solute transporters and AQP8 would hamper the efficient coupling of osmotic gradients and canalicular water flow.Thus cholestasis may result from a mutual occurrence of impaired solute transport and decreased water permeability.

Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

AIM： To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility. METHODS： Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide （LPS）. Male Wistar rats were randomly assigned to one of three treatment groups： magnolol prior to LPS injection （LPS/Mag group）; vehicle prior to LPS injection （LPS/Veh group）; vehicle prior to injection of saline （Control/Veh）. Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-α （TNF-α）, interleukin-10 （IL-10）, monocyte chemoattractant protein-1 （MCP-1） and inducible nitric oxide synthase （iNOS） mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-κB （NF-κB） activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde （MDA） concentration and superoxide dismutase （SOD） activity in the intestine 2 h after LPS iniection.RESULTS： Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPS- treated animals. TNF-α, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally,magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-κB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum. CONCLUSION： Magnolol prevents sepsis-induced suppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.

Effects of ketamine on proinflammatory cytokines and nuclear factor kappaB in polymicrobial sepsis rats

AIM： To explore the effects of ketamine on hemodynamics, plasma proinflammatory cytokine （TNF-α and IL-6） levels and nuclear factor kappa B （NF-κB） activation during polymicrobial sepsis. METHODS： Male Sprague-Dawlay rats were subjected to cecal ligation and puncture （CLP） or sham operation. The rats were randomly assigned into four equal groups： sham CLP group, CLP group, ketamine （KT）Ⅰ group and KTⅡgroup. Thirty minutes before CLP, ketamine （5 mg/kg per hour and 10 mglkg per hour, respectively） was infused continuously through the left femoral vein cannula in KT Ⅰ group or KTⅡgroup. Sham CLP group and CLP group received 0.9% saline only （5 mL/kg per hour）. The right femoral artery was cannulated to monitor mean arterial pressure （MAP） and heart rates （HR）,and draw blood samples. The proinflammatory cytokine （TNF-α and IL-6） levels of plasma were measured using enzyme-linked immunosorbent assays （ELISA）. The hepatic NF-κB activation was determined by Western blot and HPIAS 2000 image analysis system. Twenty hours after CLP, the rats were killed by right femoral artery phlebotomization. RESULTS： CLP produced progressive hypotension, and a first increase followed by a decrease in HR. The hypotension was prevented, and the HR was slightly steady in ketamine treated rats. TNF-α levels of plasma reached a peak value at 2 h after CLP. Ketamine （KT Ⅰ group or KTⅡgroup） caused a significant decrease compared with CLP group at 2, 5 and 9 h time points after CLP （14.3 ± 1.9 vs 4.3 ± 0.9, 9.7 ± 1.4 vs 4.3 ± 0.9; 9.3 ± 1.5 vs 4.3 ± 0.9, 8.7 ± 1.4 vs 4.3 ±0.9; 6.0 ± 1.5 vs 5.0 ± 1.7, 5.3 ± 0.8 vs 5.0 ± 1.7; P 〈 0.01, respectively）. The IL-6 levels of plasma firstly ascended and then descended in CLP group, and reached a peak value at 9 h after CLP. Ketamine （KT I group or KTH group） caused a significant decrease compared with CLP group at 5, 9 or 20 h after CLP （135.0 ± 52.6 vs 60.0 ± 16.3, 112.5 ± 52.6 vs 60.0 ± 16.3; 410.0 ± 68.7 vs 62.5 ± 12.5, 250.0 ± 28.0 vs 62.5 ± 12.5; 320.0 ± 25.9 vs 52.5 ± 10.1, 215.0 ± 44.6 vs 52.5 ± 10.1; P 〈 0.05, respectively）. The IL-6 levels of plasma in KTⅡgroup were lower than those of KT Ⅰ group at 9 h after CLP （250.0 ± 28.0 vs 410.0 ± 68.7; P 〈 0.05）. In addition, CLP increased hepatic NF-κB expression compared with sham CLP. Ketamine suppressed NF-κB activation in a dose-dependent manner at 4 h after CLP （237.7 ± 3.5 vs 246.9 ± 3.1; P 〈 0.05）. CONCLUSION： Ketamine stabilizes the hemodynamics, attenuates the proinflammatory cytokine responses, and inhibits hepatic NF-κB activation. These findings suggest that ketamine has protective effects against polymicrobial sepsis in rats.

Up-regulation interleukin-6 and interleukin-8 by activated protein C in lipopolysaccharide-treated human umbilical vein endothelial cells

Objective: To investigate the effect of activated protein C (APC) on inflammatory responses in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS). Methods: The second passage of collagenase digested HUVEC was divided into the following groups: serum free medium control group (SFM control), phosphate buffer solution control group (PBS control), LPS group with final concentration of 1 μg/ml (LPS group), APC group with final concentration of 7 μg/ml, Pre-APC group (APC pretreatment for 30 min prior to LPS challenge), and Post-APC group (APC administration 30 min after LPS challenge). Supernatant was harvested at 0, 4, 8, 12 and 24 h after LPS challenge. Interleukin-6 (IL-6) and Interleukin-8 (IL-8) levels were analyzed with ELISA. Cells were harvested at 24 h after LPS challenge, and total RNA was extracted. Mes-senger RNA levels for IL-6 and IL-8 were semi-quantitatively determined by RT-PCR. Results: Compared with control group, IL-6 and IL-8 levels steadily increased 4 to 24 h after LPS stimulation. APC treatment could increase LPS-induced IL-6 and IL-8 production. The mRNA levels of IL-6 and IL-8 exhibited a similar change. Conclusion: APC can further increase the level of IL-6 and IL-8 induced by LPS. The effect of these elevated cytokines is still under investigation.

Churg-Strauss syndrome complicated by colon erosion, acalculous cholecystitis and liver abscesses

We report on a case of Churg-Strauss syndrome (CSS)with colon erosion, cholecystitis and liver abscesses. A 21-year-old woman with a history of bronchial asthma for 3 years was admitted with a complaint of abdominal pain. Laboratory findings included remarkable leukocytosis and eosinophilia, and a colonoscopy revealed erosion from the rectum to the ileocecal region. In addition, a colonic biopsy specimen showed necrotizing vasculitis and marked eosinophilic infiltration. On the basis of the clinical features and histopathological findings, she was diagnosed with CSS and subsequently treated with oral prednisolone,after which the eosinophilia and abdominal pain disappeared. However, on the 15th d in hospital she developed cholecystitis and liver abscesses. She was therefore treated with antibiotics and as a result went into clinical remission.

Tie2 mRNA in peripheral blood： a new marker to assess damage of endothelial cells in a rat model of sepsis

Objective： To evaluate the endothelial cell damage by detecting the circulating Tie2 mRNA level in a rat model of sepsis. Methods： The model of sepsis was established by cecal ligation and puncture （CLP） in 90 rats which were divided into 6 groups： normal, sham, CLP-3 h, CLP-6 h, CLP- 12 h and CLP-24 h. Serum biochemical markers were detected by automatic biochemical analyzer. Serum IL-6 was measured with enzyme linked immunosorbent assay. The vascular permeability of liver, kidney, lung and heart was detected with Evans blue. Circulating endothelial cells （CEC） were separated using density gradient separation and counted. Total RNA of whole blood were extracted and the mRNA levels of two endothelial specific genes, Tie2 and vascular endothelial growth factor receptor 2 （VEGFR2）, were measured by quantitative real-time PCR. Results： The level of serum biochemical indexes increased after CLP. The amount of serum IL-6 in CLP-6 h, 12 h,and 24 h group was increased 6.5-fold （P〈 0.05）, 8.4-fold （P〈 0.01 ）, and 13.3-fold （P〈0.001 ） compared with normal group （ 170.68 pg/mli42.46 pg/ml） respectively （F= 14.319, P〈0.001）. Significantly increased organ vasopermeability of liver, kidney, lung and heart was observed after CLP respectively. The number of CEC peaked （11.83±1.94） 3 hours after CLP compared with normal control （5.33±1.21, P〈0.05）, and then decreased gradually （F=54.183, P〈0.001）. The mRNA level of Tie2 in CLP-3 h group （3.47±1.47） was also markedly higher than that in other groups （F=10.640, P〈0.001 ）. Conclusion： Using quantitative real-time PCR to measure the level of Tie2 mRNA in peripheral blood is a simple and relatively sensitive method to evaluate the damage of endothelial cells.