生物电阻抗法人体成分测量对慢性肾脏病非透析患者营养状态评估

目的：探讨生物电阻抗法人体成分测量在评价慢性肾脏病非透析患者营养状态中的作用。方法：选取门诊随访的原发病为肾小球肾炎的慢性肾脏病2～4期患者64例,排除糖尿病、大量蛋白尿、血尿、需要促红细胞生成素或免疫抑制剂治疗,以及近1月内有发热、消化道出血、使用类固醇激素者,采用人体生物电阻抗法人体成分测量、体重指数（BMI）和实验室检查等指标评价患者营养状态。结果：BMI显示11%的患者存在营养不良;实验室检查白蛋白均在正常范围内,球蛋白、前白蛋白与胆固醇均正常或高于正常,总蛋白、转铁蛋白、血红蛋白与三酰甘油低于正常的患者分别为2%,2%,17%,2%;生物电阻抗法检测显示52%的患者瘦体重低于正常,86%的患者干瘦体重低于正常,与其他指标相比差异有统计学意义（P〈0.01）。结论：生物电阻抗法人体成分测量可更早发现慢性肾脏病早中期患者营养不良,具有无创、安全、可重复性强的优点,值得临床推广应用。     

Nicotine Induces Mononuclear Leukocyte Adhesion and Expression of Adhesion Molecules,VCAM and ICAM,in Endothelial Cells In Vitro

The pathology of atherosclerotic cardiovascular disease (ASCVD) has been characterized as an inflammatory response to vessel injury. The initial steps of this response involve mononuclear leukocyte (MNL) attachment and infiltration into the vessel wall. Leukocyte adhesion is potentiated by expression of cellular adhesion molecules. Vascular cell adhesion molecule-1 (VCAM) and intracellular adhesion molecule-1 (ICAM) are markers of cellular activation and have the ability to attach leukocytes to the endothelium, which is an initial event in the inflammatory response in the vessel wall. Human umbilical vein endothelial cells (HUVEC) were plated in endothelial growth medium (EGM) on plastic coverslips and grown until cells were 75% confluent. Free base nicotine (FBN) was diluted in EGM to a concentration of 10^–8 M and added to experimental cells. At 3 hr, coverslips were removed and fixed. Immunohistochemical staining (IHCS) was performed using a monoclonal antibody to human ICAM and VCAM. Digital image analysis (DIA) was performed to quantify the expression of ICAM and VCAM. An intensity stain index (ISI) measuring area and intensity of stain/total cellular area was determined. Additional HUVEC grown in a similar manner were either exposed to 10^–8 M FBN in EGM or EGM control for 4 hr, then were exposed to MNL suspension for 10 min. Coverslips were removed, rinsed, and fixed. Hematoxylin and eosin staining was performed and cells examined under light microscopy. Leukocyte number per high power field (HPF) was counted and compared to controls. Data were analyzed using analysis of variants (ANOVA) and Students t-test. Differences were considered significant if p < 0.05. ICAM and VCAM expression was absent in control cells. Nicotine exposure at 3 hr induced expression of VCAM (ISI = 30.85 ± 0.77) and to a lesser extent ICAM (ISI = 16.6 ± 1.39) (p < 0.001). MNL adhesion was markedly increased in cells exposed to nicotine (79.4 ± 16.9/HPF) when compared to control cells (1.8 ± 0.91/HPF) exposed to MNL (p < 0.01). These data show nicotines ability to activate HUVEC as evidenced by induction of ICAM and VCAM expression in vitro. The biological effects of these adhesion molecules are demonstrated by a marked increase in MNL adhesion to HUVEC as demonstrated by leukocyte adhesion assay (LAA). MNL adhesion and subsequent migration into the intima, if occurring in vivo, may be a vital step in the pathogenesis of ASCVD associated with nicotine exposure.     

Expression of Adhesion Molecules and Cytokines on Saphenous Veins in Chronic Venous Insufficiency

The objective of this study was to assess the relationship of signaling molecules to monocyte/ macrophages as a precursor to venous valve and venous wall dysfunction in patients with varicose veins. One of the hallmarks of venous dysfunction is destruction of venous valves with subsequent reflux and elevation of distal venous pressure. We recently observed that monocytes/macrophages migrate into the venous walls and valves of patients with venous insufficiency. There, they may play a role in the pathogenesis of primary venous insufficiency. If so, an important element in their performance would be the interaction between the monocytes and the endothelium as a precursor of damage to venous valves and the venous wall. To explore this interaction, immunohistochemistry was carried out to detect adhesion molecules and cytokines in surgical specimens removed during surgical therapy. Twenty-four surgical specimens consisting of proximal saphenous vein and subterminal valve were obtained using minimally traumatic technique in 6 males and 18 females who ranged in age from 31 to 79 years. Reflux was confirmed preoperatively by duplex technique, and severity was classified by the CEAP classification of the American Venous Forum. Ten patient limbs were class 2, eight were class 3, four were class 4, and two were class 6. The venous specimens were labeled using monoclonal antibody against ICAM-1, E-selectin, IL-1alpha, and TNF-alpha. CD68 was used for detection of monocytes/macrophages. Our results indicate that not only luminal venous endothelium but also endothelium in the vasa vasora of refluxing saphenous veins is activated, as indicated by the up-regulation of ICAM-1. However, IL-1alpha and TNF-alpha were increased in only selected specimens and are mainly detected in the vein wall. The factors that serve as trigger mechanisms to activate cells in the pathogenesis of primary venous dysfunction remain to be explored.     

Soluble Adhesion Molecules in Coronary Surgery and Cardiopulmonary Bypass with Pump Prime Aprotinin

Objective : The purpose of the present study was to establish whether pump prime aprotinin could influence soluble adhesion molecules in patients undergoing elective coronary artery bypass surgery. Design : Thirty patients admitted for first-time elective coronary artery bypass surgery were randomized into control or aprotinin groups. Patients in the aprotinin group received 280 mg of aprotinin in the pump prime. Plasma levels of soluble adhesion molecules were analyzed perioperatively. Results : There were no significant changes in plasma sE-selectin after the operation in either group. Plasma sP-selectin increased significantly up to 20 h after reperfusion to the myocardium. Plasma sICAM-1 decreased in the early stage after cardiopulmonary bypass (CPB), then recovered at 4 h after reperfusion and a significant increase in sICAM-1 was observed 20 h later. There were no significant differences between the groups in postoperative changes in sP-selectin ( p = 0.21) and sICAM-1 ( p = 0.91). Conclusion : Pump prime aprotinin did not influence plasma levels of E-selectin, P-selectin and ICAM-1 in the present patients. The present results do not support the concept of an anti-inflammatory effect of pump prime aprotinin.     

CD15和CD15s在大肠癌中的表达及其与浸润转移的关系

目的:研究CD15和CD15s在大肠癌组织中表达状况及其与肿瘤发生、分化、转移及预后的关系.方法:应用催化信号放大法(CSA)检测90例大肠癌、51例转移淋巴结和30例远离癌组织的正常大肠粘膜CD15和CD15s的表达状况,并对其中53例患者进行随访.结果:CD15和CD15s阳性物质在远离癌组织的正常大肠粘膜中阳性表达率分别为93.3%和16.7%,而在大肠癌组织中阳性率分别为90.0%和94.4%,转移淋巴结标本中阳性率分别为68.7%和96.1%.结论:癌细胞膜Lewis糖抗原的唾液酸化及异常糖基的形成,可能与肿瘤转移行为有关.CD15s可以作为预测大肠癌侵袭、转移的肿瘤相关抗原,对评估患者预后较CD15具有更重要的临床意义.     

体外循环围术期细胞黏附分子CD11b/CD18,P选择素的表达及其意义

目的观察体外循环(CPB)心内直视手术围术期细胞黏附分子CD11b/CD18及可溶性P选择素(sP-selectin)的表达变化,探讨二者在CPB诱发的全身炎症反应(SIRS)中的作用。方法选择我院2008年1～8月在CPB下行风湿性心脏病瓣膜置换手术患者30例纳入研究,其中男18例,女12例;年龄29～55岁(45.3±8.1岁);分别于麻醉诱导后切开皮肤前(CPB前)、CPB后30min、1h、6h、12h和24h6个时点取桡动脉血,采用流式细胞技术检测外周血中性粒细胞CD11b/CD18分子的表达变化;酶联免疫吸附法测定血浆中内皮细胞sP-selectin的浓度。结果 30例患者外周血中性粒细胞CD11b/CD18于CPB后30min即开始升高,且在CPB后6h达峰值(581.44±215.26),与CPB前比较差异有统计学意义(P0.05);于CPB后12h开始下降,但仍高于CPB前水平,至CPB后24h时其表达低于CPB前水平,差异无统计学意义(P0.05);外周血sP-selectin的表达于CPB后30min明显升高并达峰值(51.44±10.06ng/ml),与CPB前比较差异有统计学意义(P0.05),自CPB后12h开始其活性表达下降,并低于CPB前水平,但差异无统计学意义(P0.05)。结论 CPB可促发外周血中性粒细胞CD11b/CD18及内皮细胞sP-selectin分子表达水平增高,在CPB导致的全身炎症反应中可能发挥重要作用。     

Serum Biomarkers of Iron Stores Are Associated with Increased Risk of All-Cause Mortality and Cardiovascular Events in Nondialysis CKD Patients,with or without Anemia

Open in a separate window     

Hyperlactatemia and Increasing Metabolic Acidosis in Hepatorenal Failure Treated by Hemofiltration

We report a case of increasing hyperlactatemia in the course of repeated treatment by machine hemofiltration (MHF) using a lactate-bujfered replacement solution. The hyperlactatemia was associated with a reduction in mean arterial pressure, and in the majority of treatments a metabolic acidosis developed. Hyperlactatemia due to exogenous lactate may not be as benign as previously discussed.     

Increasing incidence of injuries and fatalities inflicted by wild animals in Kashmir

Objective

To clarify the causes of the increased incidence of injuries inflicted by wild animals in Kashmir, and to suggest preventive measures.

Methods

A retrospective study reviewed records of these injuries. Data were collected from the hospital in Srinagar and from the Wildlife Protection Department of Kashmir.

Results

A total of 203 attacks (26 deaths and 177 near-fatal injuries) were recorded from January 2005 to October 2007, involving 145 (71.5%) male and 58 (28.5%) female victims. The attacking animal was a black bear in 104 (51.2%), a leopard in 18 (8.8%), a wolf in 7 (3.4%) and unidentified in 74 (36.4%) cases; 130 (64%) of these attacks occurred in southern Kashmir.

Conclusion

The steady increase in human population in areas close to jungle results in deforestation and destruction of wildlife habitat. The reduction in monkeys and deer (the staple food of leopards) causes these dangerous predators to search for food in the areas occupied by humans, who may then be attacked. Treatment of these cases requires a multidisciplinary approach, including an orthopaedic surgeon, plastic surgeon, microbiologist and psychiatrist, to achieve best cosmetic and functional results.     

Role of TNFα in Early Chemokine Production and Leukocyte Infiltration into Heart Allografts

The acute phase cytokines IL-1β, IL-6 and TNFα are produced early during inflammatory processes, including ischemia-reperfusion. The appearance and role of these cytokines in the early inflammation following reperfusion of grafts remain poorly defined. This study investigated the role of TNFα in the induction of early leukocyte infiltration into vascularized heart allografts. TNFα and IL-6 mRNA levels reached an initial peak 3 h posttransplant and a second peak at 9–12 h with equivalent levels in iso- and allografts. A single dose of anti-TNFα mAb given at reperfusion decreased neutrophil and macrophage chemoattractant levels and early neutrophil, macrophage and memory CD8 T-cell infiltration into allografts. Anti-TNFα mAb also extended graft survival from 8.6 ± 0.6 days to 14.1 ± 0.8 days. When assessed on day 7 posttransplant, the number of donor-reactive CD8 T cells producing IFN-γ in the spleen was reduced almost 70% in recipients treated with anti-TNFα mAb. Whereas anti-CD154 mAb prolonged survival to day 21, administration of anti-TNFα and anti-CD154 mAb delayed rejection to day 32 and resulted in long-term (>80 days) survival of 40% of the heart allografts. These data implicate TNFα as an important mediator of early inflammatory events in allografts that undermine graft survival.