凝血机制紊乱在SIRS发展中的作用

凝血机制紊乱在全身炎症反应综合症(SIRS)发展、恶化过程中起重要作用．对SIRS时凝血系统紊乱的形成机制、在SIRS发生发展过程中的作用及其对病情危重程度的预测价值作一综述．     

原发性肾小球疾病患者T淋巴细胞亚群变化的初探

本文应用磁性磷酸酶－抗碱性磷酸酶桥联酶标技术（APAAP），对27例原发性肾小球疾病患者外周血T淋巴细胞亚群进行观察。结果表明：本组病例表现为CD细胞升高，CD细胞减少，和CD／CD比值增加。提示原发性肾小球疾病可导致细胞免疫功能改变，T淋巴细胞亚群的变化，是肾组织损害的一个间接证据，可作为临床诊断一个有价值的参考指标。     

P波时限、P波离散度对特发性心房颤动的预测价值初探

Objective:To assess the sensitivity and the specifity of predicting idiopathic AF with P wave dura-tion and P wave dispersion. Methods: The maximum P wave duration and P wave dispersion in 36 patients with idio-pathic AF were measured and compared with those of sex-and age-matched healthy subjects. Results:The maxi-mum P wave duration and P wave dispersion were higher in patients with idiopathic Af than in control group. Themaximum P wave duration >110ms or P wave dispersion >40ms was used to differentiate patients from healthy     

特发性脊柱侧凸King型和型远端融合椎的选择

目的回顾采用椎弓根钩和螺钉CD技术治疗特发性脊柱侧凸King型和型患者,分析选择性缩短融合节段的治疗效果。方法2000年3月~2003年1月,治疗58例特发性脊柱侧凸单胸弯患者,男17例,女41例,年龄12~18岁,平均14岁。其中King型40例,King型18例。胸弯Cobb角平均64°(50~83°),柔韧性62%;腰弯Cobb角平均37°(16~48°),柔韧性105%。腰弯腰骶角平均为17°(10~22°)。所有患者C7重力垂线均不同程度地偏离骶骨中线。采用椎弓根钩和螺钉CD技术矫形治疗,以中立椎为基础选择远端融合椎,所有远端融合节段均未超过中立椎。术后随访摄站立前后位和侧位X线片,观察各项指标的变化。结果患者均获随访1年8个月~3年2个月,平均2.4年,均未出现明显的躯干侧方移位和双肩不平衡。术后Cobb角平均丢失3.1°(-1~5°);最后随访时,胸弯矫正率68%;除2例C7重力垂线偏离骶骨中线1~2cm外,其余均通过骶骨中线;腰弯腰骶角减少至平均8°(2~13°),矫正率为53%;48例远端融合椎为非稳定椎者术后成为稳定椎。与Harrington远端融合椎选择原则相比,患者远端融合椎平均节省1.4个节段(1~2个节段)。结论采用三维节段性器械内固定系统治疗特发性单胸弯时,以中立椎为基础选择远端融合椎,可获得较好的临床效果。     

Vascular endothelium and inflammatory process, in patients with combined Type 2 diabetes mellitus and coronary atherosclerosis: the effects of vitamin C.

AIMS: Type 2 diabetes mellitus (DM) and coronary artery disease (CAD) are both associated with endothelial dysfunction and elevated oxidative and inflammatory state. We examined the effect of vitamin C on endothelial function and levels of soluble vascular cell adhesion molecule (sVCAM-1), interleukin-6 (IL-6) and tumour necrosis factor (TNF-alpha), in DM patients with or without CAD and in non-diabetic subjects. METHODS: Thirty-seven patients with DM + CAD, 17 patients with DM without CAD and 21 non-diabetic subjects were divided into groups receiving vitamin C 2 g/day or no anti-oxidant for 4 weeks. Forearm blood flow was determined using venous occlusion gauge-strain plethysmography. Forearm vasodilatory response to reactive hyperemia was considered as index of endothelium-dependent dilation. RESULTS: Baseline levels of IL-6 and TNF-alpha were significantly higher in patients with DM + CAD compared with patients with DM (P < 0.01) or non-diabetic subjects (P < 0.01). IL-6 and TNF-alpha levels were also higher in DM compared with non-diabetic subjects (P < 0.05). sVCAM-1 levels were lower in non-diabetic controls compared with DM + CAD (P < 0.05) or DM (P < 0.05). Reactive hyperaemia was higher in non-diabetic controls compared with DM + CAD (P < 0.001) or DM (P < 0.001). Vitamin C significantly increased reactive hyperaemia only in the DM + CAD group, while it had no effect on serum levels of sVCAM-1, TNF-alpha and IL-6 in any of the groups. CONCLUSIONS: Type 2 diabetes mellitus is associated with impaired endothelial function and increased levels of TNF-alpha, IL-6 and sVCAM-1, especially in patients with DM and CAD. Vitamin C significantly increased forearm vasodilatory response to reactive hyperaemia only in patients with combined DM and CAD.     

Inflammation and the Aging Process: Devil or Angel

Inflammation is often viewed as a pathologic mechanism leading to tissue damage and interference with function, such as the process of chronic tissue scarring or fibrosis. However, it is important to note that inflammation is a crucial component of normal tissue repair as well as being fundamental to the body's defense against infection. Considering inflammation as a "causative agent in aging" belies the underlying mechanisms whereby the acute inflammatory response is necessary for survival, and efforts to reduce and control the inflammatory response leave the host susceptible to infectious agents and improper healing. Chronic inflammation inevitably has initiating mechanisms that include immune, autoimmune, and metabolic pathways, leading to the activation and presence of the host-protective response. It is more appropriate to target the underlying initiating conditions than the inflammatory process that ensues and treat the basic mechanisms of disease rather than interfere in a very important protective mechanism of the host.     

Comparison of the effect of intravenous ketoprofen, ketorolac and diclofenac on platelet function in volunteers

Background : Nonsteroidal anti–inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis which may result in impaired platelet function. Because NSAIDs have different abilities to inhibit cyclo–oxygenases we compared the effect of intravenous ketoprofen, ketorolac and diclofenac on platelet function in volunteers. Methods : Ten healthy male volunteers were given ketoprofen 1.4 mg kg^-1, ketorolac 0.4 mg kg^-1 and diclofenac 1.1 mg kg^-1 in saline i.v. on three different occasions, at more than one–week intervals, in a randomized double–blind crossover study. Platelet function was evaluated before (sample 0), 2 (sample 2) and 24 h (sample 3) after the beginning of the infusion. Results : Two of the volunteers had no secondary platelet aggregation in their aggregation curves before the experiment (sample 0, studied three times) and their results were excluded from the final analysis. Diclofenac inhibited adrenaline (0.9 μg–ml^-1) induced platelet aggregation less (median maximal aggregation 22.5%) than ketoprofen (18.3%) and ketorolac (15.7%) (P<0.05) in sample 2. In the ketorolac group in sample 3 an impairment of adrenaline (0.9 ng ml^-1) induced platelet aggregation was still seen (26.7%) (P<0.05) but not in the other groups. Diclofenac did not affect adenosine diphosphate (ADP) induced platelet aggregation. However, ketorolac caused an impairment in ADP (3 μM and 6 μM) induced platelet aggregation and ketoprofen in ADP (6 μM) induced platelet aggregation in sample 2. Bleeding time was prolonged (P<0.05) after ketoprofen and ketorolac (sample 2) but not after diclofenac. Platelet retention on glass beads was unaffected by the tested drugs. Conclusion : Ketoprofen, ketorolac and diclofenac caused a reversible platelet dysfunction. Diclofenac had the mildest effect, while platelet dysfunction was still seen 24 h after the beginning of ketorolac.     

Chromatic pattern-reversal electroretinograms (ChPERGs) are spared in multiple system atrophy compared with Parkinson’s disease

Abstract Idiopathic Parkinson’s disease (IPD) patients have abnormal visual evoked potentials (VEPs) and pattern electroretinograms (PERGs), attributed to dopaminergic transmission deficiency in visual pathway, probably the retina. VEP abnormalities are not reported in multiple system atrophy (MSA). The aim of this study was to investigate and compare chromatic (Ch) red-green (R-G) and blue-yellow (B-Y), and luminance yellow-black (Y-Bk) PERGs in patients with MSA and IPD. We investigated 6 MSA patients (mean age: 62±7.4 years) not undergoing any pharmacological treatment, as well as 12 early IPD patients (mean age: 60.1±8.3 years) and 12 age-matched normal observers. ChPERGs were recorded monocularly in response to full-field equiluminant R-G, B-Y and Y-Bk horizontal gratings. In MSA only responses to R-G stimuli showed minimal insignificant changes (slight but not significant amplitude reduction without any significant latency delay); no significant abnormality was detected for B-Y and luminance Y-Bk stimuli. By contrast, in IPD all responses were reduced in amplitude and delayed in latency, above all for B-Y stimuli. Present data indicate that both chromatic and achromatic PERGs are virtually unaffected in MSA, whereas in early IPD they are clearly impaired, suggesting different pathogenic retinal mechanisms and a useful simple tool for distinguishing MSA from IPD.