Role of omega 3 and omega 6 poly unsaturated fatty acids (PUFA) and vitamin D deficiency as risk determinants of metabolic syndrome in obesity: Worksite based case-control observational study

Background and aimsRisk factors for metabolic syndrome among obese population are not clear. The role of Eicosapentaenoic acid (EPA), Arachidonic acid (AA) Poly Unsaturated Fatty Acids (PUFA), their ratio and vitamin D deficiency as risk factors of metabolic syndrome (MS) was explored in obese worksite workers.MethodsThe 145 obese worksite workers were enrolled and MS was diagnosed using adult treatment panel III criteria. The levels of EPA, AA PUFA were estimated using liquid chromatography-Mass Spectrometer and vitamin D levels with ELISA method. The association of MS with the tertiles of EPA, AA PUFAs, their ratio and vitamin D was estimated by calculating odds ratio and 95% C.I., taking lowest tertiles as the reference group using logistic regression model adjusted for age and gender.Results105 out of 145 obese worksite workers; 72.4%, 95% C.I. (64.5%, 79.5%) had metabolic syndrome. The odd of MS was significantly lower in the group having highest tertiles of EPA 0.24 (0.09, 0.71) and was higher 2.0 (1.02, 3.89) in subjects with highest tertiles of AA: EPA ratio. The AA PUFA and vitamin D levels had no significant association with MS.ConclusionThe low levels of omega 3 PUFA (EPA) and elevated ratio of AA: EPA PUFA was significantly associated with MS in obese works site workers.     

Extracorporeal hydrophobic amino acid adsorbent therapy in rheumatoid arthritis

Summary We developed a new adsorbent utilizing hydrophobic amino acids in order to treat severe rheumatoid arthritis patients with extracorporeal adsorption therapy. In in vitro experiment, the new adsorbent selectively removed immune complexes and rheumatoid factors from RA plasma presumably due to hydrophobic adsorption. Six out of elevent patients markedly improved in clinical as well as laboratory parameters of disease activities, particularly in their extra-articular manifestations. We recommend preferential use of this treatment since it can spare the replacement protein solution and is expected to give similar efficacy to simple plasma exchange therapy.     

脑梗死患者颅内血管狭窄的危险因素分析

目的分析脑梗死患者颅内血管狭窄的危险因素。方法对186例脑梗死患者行经颅多普勒超声检查,检测血尿酸和血脂包括总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、甘油三酯。结果血管狭窄组患者总胆固醇(5.04±1.23 mmol/L)和低密度脂蛋白胆固醇水平(2.99±1.01 mmol/L)均显著高于无狭窄组患者(分别为4.60±1.12 mmol/L和2.59±0.69 mmol/L,P<0.05);Pearson相关分析表明,颅内血管峡窄与高血压史(r=0.206,P=0.005)、糖尿病史(r=0.238,P=0.001)、总胆固醇(r=0.181,P=0.016)、低密度脂蛋白胆固醇(r=0.227,P=0.003)及尿酸(r=0.132,P=0.016)相关;Logistic回归分析表明,高血压、糖尿病、低密度脂蛋白胆固醇、尿酸进入回归方程,它们对颅内血管狭窄的OR值分别为2.345、2.554、1.764和1.006(P<0.05)。结论除高血压和糖尿病外,尿酸和低密度脂蛋白胆固醇亦是脑梗死患者颅内血管狭窄形成的独立危险因素。     

Acid fibroblast growth factor reduces rat intestinal mucosal damage caused by ischemia-reperfusion insult

AIM: To detect the effects of acid fibroblast growth factor (aFGF) on apoptosis and proliferation of intestinal epithelial cells in differentiation or proliferation status to explore the protective mechanisms of aFGF. METHODS: Wistar rats were randomly divided into sham-operated control group (C, n= 6), intestinal ischemia group (I,n = 6), aFGF treatment group (A, n= 48) and intestinal ischemia-reperfusion group (R,n= 48). Apoptosis of intestinal mucosal cells was determined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) technique. Proliferating cell nuclear antigen (PCNA) protein expression and distribution were detected with immunohistochemical method. Plasma levels of D-lactate were determined with modified Brandts method. RESULTS: In A group, administration of exogenous aFGF could improve intestinal histological structure and decrease plasma D-lactate levels at 2-12 h after the reperfusion compared with R group. The apoptotic rates and PCNA protein expressions were not increased until 2 h after reperfusion and were maximal at 12 h. After reperfusion for 2-12 h, the apoptotic rates were gradually augmented along the length of jejunal crypt-villus units. Administration of aFGF could significantly reduce the apoptotic response at 2-12 h after reperfusion (P<0.05). Apoptosis rates in villus and crypt epithelial cells in A group at 12 h after reperfusion were (62.5±5.5)% and (73.2±18.6)% of those in R group, respectively. Treatment of aFGF could apparently induce protein expression of PCNA in intestinal mucosal cells of A group compared with R group during 2-12 h after reperfusion (P<0.05). There were approximately 1.3- and 1.5-times increments of PCNA expression levels in villus and crypt cells in A group at 12 h after reperfusion compared with R group, respectively. CONCLUSION: Intestinal I/R insult could lead to histological structure change and apoptotic rate increment. The protective effects of aFGF against ischemia/reperfusion in rat intestinal mucosa might be partially due to its ability to inhibit ischemia/reperfusion-induced apoptosis and to promote cell proliferation of crypt cells and villus epithelial cells.     

肝细胞生长因子对小鼠轻症急性胰腺炎影响的实验研究

及时、有效地控制轻症急性胰腺炎可防止其向重症急性胰腺炎演变，因而具有重要的临床价值。近年来，肝细胞生长因子(HGF)能否减轻啮齿动物的急性胰腺炎正日益受到关注：目的：观察外源性HGF能否减轻小鼠轻症急性胰腺炎，并探讨其作用机制。方法：以雨蛙肽腹腔注射诱发小鼠轻症急性胰腺炎，在制模前和制模中予各组小鼠皮下注射不同浓度的重组人HGF(rhHGF)，部分小鼠同时皮下注射抗rhHGF、单抗。根据血清淀粉酶、脂肪酶水平、胰腺组织学炎症评分和胰腺超微结构的变化评估炎症程度，并测定胰腺匀浆中花生四烯酸代谢产物血栓素(TX)B2和6-酮(keto)-前列腺素(PG)Fla的水平。结果：与单纯炎症组相比，给予4μg／kg或20μg／kg rhHGF小鼠的血清淀粉酶、脂肪酶水平和胰腺组织学炎症评分显著降低，胰腺匀浆中TXB2水平显著降低，6-keto-PGFla。水平显著增高，但4μg／kg与20μg／kg rhHGF。的疗效无显著差异。给予rhHGF。的同时给予抗rhHGF单抗，小鼠的上述各项参数与单纯炎症组无显著差异。结论：外源性HGF能减轻雨蛙肽诱导的小鼠轻症急性胰腺炎，其机制可能与对花生四烯酸代谢的影响有关。抗HGF。单抗能抵消HGF的生物学作用。     

重组腺相关病毒介导的细胞色素P450表氧化酶基因对TNF-α诱导人脐静脉内皮细胞炎症的影响

目的研究过度表达细胞色素P450表氧化酶基因引起内源性EETs产生增加是否能抑制由TNF—α诱导的内皮炎症。方法以携带三种不同表氧化酶基因的重组腺相关病毒rAAV- CYP2C11、rAAV—CYP2J2和rAAV—CYPF87V转染人脐静脉内皮细胞,然后再以TNF—α干预,来研究它们对内皮VCAM-1的表达及外周血单核细胞PBMC与内皮细胞粘附的影响。结果TNF-α诱导了 HUVEC中VCAM-1蛋白质的表达,rAAV—CYP2C11、rAAV—CYP2J2能明显抑制TNF-α的这一作用。 TNF-α诱导了PBMC与HUVEC的粘附(100±0．0％ vs 620．1±65．3％),rAAV-CYP2C11、rAAV- CYP2J2能明显抑制TNF-α的这一作用(分别为120．3±33．4％ vs 387．7±27．4％．131．0±28．7％ vs 535．0±69．7％)。结论CYP2C11和CYP2J2基因具有显著的保护内皮细胞、对抗炎症介质介导的内皮损伤的作用。     

Morphometric observations on the effects of ischemia in the isolated perfused rat heart.

The design of the experiment was to observe the changes which took place in the isolated perfused rat heart, that was made ischemic according to the technique of Neely et al. [16], using quantitative stereological techniques. The results showed that 24 min after myocardial failure there was a significant decrease in the fractional volume of myofibrils, mitochondria, T-system, and sarcoplasmic reticulum. The decrease in fractional volume of subcellular organelles can most probably be explained by myocardial cell swelling secondary to intercellular edema. There was also a decrease in the sarcoplasmic reticulum membrane area, and quantitative measurements indicated that this compartment was dilated. Observations on the intercalated disc indicated that there was a migration of acid phosphatase positive multivesicular bodies toward the disc interspace in ischemic hearts. This was found to be associated with the dissolution of gap junctions. Stereological measurements indicated that in ischemic hearts there was a 5-fold increase in the percentage of membrane area of the disc made up of open gap junctions, and that the number of vesicles from multivesicular bodies observed per μm³ of disc interspace was also proportionately higher. It is suggested that the multivesicular bodies represent elements of the lysosomal system and are responsible for the dissociation of the intercalated disc in ischemic hearts.     

胆汁反流、胃酸和幽门螺杆菌感染共同作用对胃黏膜损伤程度和分布的影响

背景:胆汁反流、胃酸和幽门螺杆菌（H.pylori）感染均是胃黏膜损伤的独立致病因素。然而,它们共同存在时有无协同致病作用尚不清楚。目的:探讨胆汁反流、胃酸和H.pylori感染共同作用对胃黏膜损伤程度和分布的影响。方法:37例胃镜检查疑有十二指肠胃反流者均经24h胃内胆汁监测证实,同时行胃内PH监测。胃体和胃窦黏膜有或无活动性炎症、萎缩、肠化和不典型增生分别记2分或1分。分别以胃体和胃窦黏膜的各项病理学改变为应变量,以胃内胆红素吸收值>0.14的时间百分比、pH<4的时间百分比和H.pylori感染状态指标为自变量进行多变量逐步Logistic回归分析。结果:37例患者胃内胆红素吸收值>0.14的时间百分比为34.49％±22.69％,pH<4的时问百分比为78.68％土 9.91％,H.pylori阳性率为29.73％。胆汁反流出现在以胃体和胃窦黏膜肠化以及胃体黏膜活动性炎症为应变量的Logistic回归模型中,H.pylori出现在以胃体黏膜活动性炎症为应变量的回归模型中。结论:胆汁反流是胃黏膜肠化的危险因素;胃内有胆汁反流存在时,H.pylori感染是导致胃体新膜炎症的重要病因。     

Significance of acid amyloglucosidase in sulphonylurea-induced insulin release

Summary The effect of exogenous acid amyloglucosidase on sulphonylurea-induced insulin release was investigated in mice and rats. 1. Pretreatment of mice with acid amyloglucosidase enhanced insulin release induced by the different sulphonylurea derivatives, carbutamide, tolbutamide, glibenclamide, and glibornuride. 2. A dose-response relationship between glibenclamide-induced insulin response and amyloglucosidase dosage covering a 64-fold concentration range was established in mice. 3. Pretreatment of the animals with other macromolecules of similar physiological or chemical properties to acid amyloglucosidase such as-amylase,-glucuronidase and albumin did not influence glibenlamide-induced insulin release. 4. The effect of acid amyloglucosidase pretreatment on insulin release induced by different agents known to affect the islet-cell adenylate cyclase-cyclic AMP system such as secretin, L-isopropylnoradrenaline (L-IPNA), arginine, glibenclamide and 3-isobutyl-1-methylxanthine (IBMX) was tested. It was observed that in animals pretreated with acid amyloglucosidase, insulin release was enhanced when stimulated by glibenclamide, a phosphodiesterase inhibitor, but it was similarly enhanced by arginine, a phosphodiesterase activator. Insulin release induced by secretin, L-IPNA, and IBMX was unaffected. 5. Acid amyloglucosidase pretreatment in rats enhanced plasma immunoreactive insulin levels following glibenclamide injection not only in the peripheral veins but also in the portal vein. 6. Mice fasted for 24 hrs displayed a markedly depressed insulin response to tolbutamide injection. Pretreatment of the fasted animals with acid amyloglucosidase could restore the tolbutamide-induced insulin release to the same level as that recorded in a group of freely fed mice. It is suggested that acid amyloglucosidase plays an important role in insulin secretion induced by sulphonylureas. Most evidence suggests that this effect is exerted within the B-cell although an additional effect on the liver cannot be ruled out.     

老年男性各年龄组骨密度与骨代谢生化指标的关系

目的　测定老年男性不同年龄组骨密度及血、尿中与骨吸收和骨形成有关的生化指标 ,观察其与年龄的关系 ,探讨以上生化指标对早期诊断原发性骨质疏松的临床意义。方法　采用双能量 X线骨密度测定仪测定前臂骨密度 ;采用全自动生化分析法测定血清碱性磷酸酶(ALP)、尿钙 (Ca)、肌酐 (Cr) ;采用放免法测定骨钙素 (BGP)、抗酒石酸酸性磷酸酶 (TRAP)、尿羟脯氨酸 (HOP)。将年龄 60～ 95岁的老年男性 97例分为 60～ 69岁、 70～ 79岁和 80岁以上三组并与 60岁以下男性进行比较。再将其分为骨质疏松组与非骨质疏松组 ,比较其测定值。结果　老年男性骨密度及骨形成与骨吸收指标呈现随着年龄增长而降低的趋势。其中 ,骨质疏松组较非骨质疏松组骨钙素 (BGP)、抗酒石酸酸性磷酸酶 (TRAP)、尿羟脯氨酸 (HOP) ,明显下降 (P<0 . 0 5)。结论　老年男性骨质疏松属于低转换型 ,骨转换指标随增龄而呈下降趋势