锻炼心理学中动机理论：自我决定理论的新进展

目的:对锻炼心理学中的自我决定理论进行简要概述与分析。资料来源:检索中国期刊网、EBSCO和UMI资料库1997-01/2006-10有关自我决定理论的文献,检索词(限制为标题)为“self-determination theory,sport and exercise”,限定语言种类为英文。资料选择:对所获得的文献进行仔细研读,从中选择有关自我决定理论在锻炼心理学中实证研究的文章,排除重复研究类文章。资料提炼:在53篇文献中,删除7篇内容重复的文献;对46篇文献进行分类整理,其中30篇选为参考文献。资料综合:自我决定论是新近发展起来的一种认知动机理论,代表着当下动机理论研究的趋向。它把人类的动机看成是一个从外在调节到内在动机之间的动态的连续体,并依据自主的程度对动机的类型进行了详细的划分,同时从满足人们基本心理需要的角度对促进外在动机内化的条件进行了探讨。结论:自我决定理论还有许多待以完善的地方,关于自我决定理论的一些假设还有待于进一步的验证。     

氧化应激对糖尿病肾病时细胞、细胞外基质及血管通透性的影响机制

目的:糖尿病肾病及其引起的终末期肾病近年来在全球的发病情况逐年提高,该病预后差、治疗费用高,成为世界范围内严重危害人类健康的公共卫生问题。糖尿病肾病发病机制错综复杂,氧化应激被认为是重要的共同的机制之一。本文探讨氧化应激对糖尿病肾病的影响。资料来源:应用计算机检索MEDLINE,CBM,CNKI数据库及手工检索1997-01/2006-11期间的相关文献。包括临床研究(不限研究对象的年龄、性别、种族。)和基础研究,不限体内或体外研究。中文检索词包括“氧化应激”,“活性氧类”,“糖尿病肾病”和“发病机制”;英文检索词有“diabetic nephropathies”,“oxidative stress”,“reactive oxygen species”,“PKC”和“TGF-β”。资料选择:共收集到相关文献991篇,阅读全部文章的文题和大部分文章的摘要。选择文献所述内容与糖尿病肾病时氧化应激作用相关的文献。排除重复性研究和Meta分析类文章。资料提炼:共得到符合纳入条件的文献142篇,排除849篇。选择其中30篇进行分析,其中英文25篇,中文5篇,英文有1篇为手工检索的增刊。资料综合:糖尿病肾病的发病机制错综复杂,肾脏的结构和功能变化包括高滤过、肾脏和肾小球的肥大、细胞外基质的堆积、肾小球基底膜的增厚和肾小球滤过屏障功能的异常。这些变化是多因素共同作用的结果,在众多发病机制中,氧化应激被认为是共同机制之一。在正常情况下,活性氧的产生和抗活性氧水平二者处于平衡状态,当活性氧蓄积过多就会攻击机体,即氧化应激。氧化应激的产生主要是活性氧类产生过多和清除减少以及糖尿病肾病患者体内氧化应激水平增加导致的。氧化应激对糖尿病肾病的影响包括活性氧类可以增加细胞膜的通透性;使肾细胞内的谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶等抗氧化酶发生糖化或氧化,肾组织抗氧化能力降低,细胞内关键酶和转运蛋白Na-K-ATP酶失活等。结论:氧化应激作用可以增加细胞膜的通透性,使肾组织抗氧化能力降低,是糖尿病肾病的重要发病机制之一。     

Iron, ascorbate and copper status of Sowetan Blacks with calcific chronic pancreatitis

Vitamin C can be used to overcome oxidative stress and ease pain in chronic pancreatitis. But its use is deprecated in conditions of tissue iron overload, because its bioactive form, ascorbate, can accelerate free-radical reactions that are driven by transition metals. We measured iron, ascorbate and copper in Sowetan Blacks (RSA) with chronic pancreatitis, obtaining serum/plasma from 14 consecutive patients and 15 controls. Compared with data from corresponding groups in Manchester, African samples had less ascorbate (p < 0.0001), but more caeruloplasmin (p < 0.0001). African and British controls had comparable iron and iron-binding capacity. Plasma from African patients had less ascorbate than that from African controls (p < 0.005) and in six samples, ferritin exceeded 300 micrograms/l (677 pmol/l). Low- molecular-mass iron or copper, capable of participating in free radical reactions, was not detected. British patients, had similar caeruloplasmin levels to African patients but higher ascorbate levels. There is no evidence of iron overload in our African samples. Outwardly healthy controls from Soweto have elevated levels of caeruloplasmin, possibly to compensate for dietary deficiency of ascorbate. Persistent oxidative stress is a unifying feature of chronic pancreatitis, but its degree is higher in African than British patients. Supplements of vitamin C should be safe in Blacks of southern Africa.      

Failure of Dietary Protein and Phosphate Restriction to Retard the Rate of Progression of Chronic Renal Failure: A Prospective, Randomized, Controlled Trial

SUMMARY Ninety-five patients (63 male, 32 female), age 45±2 years(mean±SEM) with chronic renal failure of varied aetiologywere randomized to receive either a conventional low proteindiet (0.6 g/kg/day protein, 800 mg phosphate; n=33), a low phosphatediet (providing approximately 1000 mg phosphate plus an orallyadministered phosphate binder, minimum protein intake 0.8 g/kg/day;n=30) or to control (minimum protein intake 0.8 g/kg/day, nophosphate restriction; n=32). Patients were reviewed for a minimumof 6 months before randomization and were withdrawn from thestudy if plasma creatinine exceeded 900 µmol/1, plasmaphosphate was > 2.0 mmol/1 or at the onset of uraemic symptoms. Following randomization patients were studied for an averageof 19±3 months. Mean plasma creatinine rose from 398±33to 600±50 µmol/1. Dietary protein intake was estimatedat 0.69±0.02 g/kg/day in the low protein group, 1.02±0.05in the low phosphate and 1.14±0.05 in the controls, phosphateintake was 815±43, 1000± 47, and 1315±57mg/day, respectively. Urinary urea excretion and protein catabolicrates were significantly reduced (p<0.01) only in those onprotein restriction, at 213±9 mmol/24 hours and 0.71g/kg/day, respectively. Phosphate excretion was significantlylower (p<0.05) in both the low protein group (17.9±0.8mmol/24 hours) and the low phosphate group (18.6±1.0mmol/24 hours) compared to controls. Changes in body weight,muscle mass and serum transferrin, albumin and immunoglobulinswere comparable between the groups. Mean blood pressure followingrandomization was 150/89±3/1 (low protein), 148/87±3/1(low phosphate) and 146/87±3/1 (controls). Progression of renal failure was analysed by rate of fall ofcreatinine clearance (ml/min/ 1.73 m²/month), by rate of deteriorationderived from reciprocal plasma creatinine against time plots(1/mmol/year) and to assess individual patient's response totreatment by two phase linear regression (‘breakpoint’)analysis of reciprocal plasma creatinine/time plots. Progressionwas analysed only in patients seen for at least 3 months followingrandomization. The rate of fall of creatinine clearance was not significantlydifferent between the groups (ANOVA): 0.56±0.08 ml/min/1.73m2/month (low protein, n=28), 0.44±0.07 (low phosphate,n=23) and 0.69±0.11 (control, n=27). In 50 patients (18low protein, 16 low phosphate and 16 control) whose rate ofprogression could be calculated before and after randomization,there was a fall in rate of progression averaging 0.18 ml/min/1.73m2/month in those on low protein diet and those on low phosphatediet, but a rise of 0.08 in the controls. These differenceswere, however, not statistically significant. Similar resultswere obtained when the rates of deterioration were calculatedfrom plasma creatinine. Significant individual improvements(p<0.01) in rates of progression by ‘breakpoint’analysis occurred in 17 patients: six on low protein, sevenon low phosphate and in four controls. Sixty-one (72 per cent)of the patients examined by this method showed no significantchange in the rate of progression while seven patients had acceleratedprogression. There was no difference in the requirement formaintenance dialysis facilities between groups. No significant benefit of protein and phosphate restrictionwas therefore demonstrated.     

Loss of high-affinity thrombin receptors during platelet concentrate storage impairs the reactivity of platelets to thrombin

BACKGROUND: The storage of platelet concentrates (PCs) induces a reduction in the platelet surface expression of glycoprotein (GP) Ib alpha. The location of the platelets' high-affinity binding site for thrombin has been postulated as being located on GPIb alpha. This study attempts to determine whether loss or alteration of GPIb alpha during storage of PCs is related to impairment in the reactivity of platelets to thrombin. STUDY DESIGN AND METHODS: In this study, platelet surface expression of GPIb alpha was monitored by means of flow cytometry, throughout standard storage of PCs for up to 10 days. Two thrombin- induced platelet responses, the binding of radiolabeled fibrinogen and the platelet surface expression of P-selectin, were evaluated. Thrombin- binding assays were also performed to assess the number of thrombin receptors in platelets. RESULTS: The surface expression of the GPIb/IX complex declines during storage of PCs. The thrombin-induced maximal binding of fibrinogen in platelets stored for 3, 7, and 10 days was 77 +/? 7 percent, 60 +/? 20 percent, and 34 +/? 25 percent, respectively, of that found in fresh platelets. Moreover, the concentration of thrombin needed for 50 percent of platelets to express the CD62 antigen P-selectin at the surface increased from 0.05 U per mL in fresh platelets to 0.11, 0.56, and 1.2 U per mL in platelets stored for 3, 7, and 10 days, respectively. Thrombin-binding experiments demonstrated a significant reduction in the number of high-affinity binding sites throughout storage of PCs (55 +/? 21 sites/platelet in 10-day-stored platelets vs. 73 +/? 25 in fresh platelets). A significant correlation was also observed between the number of high-affinity thrombin-binding sites and surface expression of GPIb alpha. Selective blockage of the thrombin-binding site on GPIb alpha with monoclonal antibody LJ-Ib10 also inhibited the response of fresh platelets to thrombin, up to a level equivalent to that found in 3-day-stored platelets. CONCLUSION: The loss of the GPIb alpha-located high-affinity thrombin-binding site may impair the ability of platelets to become activated by thrombin as storage time increases.