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1.
2型糖尿病患者骨密度的测定   总被引:2,自引:2,他引:2  
INTRODUCTIONItisacceptedconclusionthattype1diabetescaninducedecreaseofbonemineraldensity犤1犦,butitisunderdiscussedwhethertype2diabetescaninducedecreaseofBMD.InordertoobservechangesofBMDintype2diabetespatients,weevaluateBMDoflumbarvertebraL2-4andproximalfemurintype2diabetespatientsbyusingdualenergyX-rayabsorptiometry(DEXA)andcomparedwithnormalcontrolwiththesamesex,age,weight.MATERIALSANDMETHODSMaterials63casesoftype2diabeteswerecamefrompatientsreceivedfrom…  相似文献   

2.
Boneisadynamictissue,thelevelofbonemassreflectsthebalanceofboneformationandresorption,whichinvolvesthecoor-dinateregulationofbone-formingcells(osteoblasts)andbone-resorbingcell(osteoclasts).Avarietyoflocalgrowthfactorsandcytokinesaswellassystemicpeptideandsteroidhormonesregulatethedifferentiationofimmatureprecursorcellsandtheactivityofmaturecellsinboththeosteoblasticandtheosteoclasticlineage,suchasbonemorphogeneticprotein-2(BMP-2)andosteoprotegenin(OPG)犤1犦.Inaddition,…  相似文献   

3.
Inthisstudy,wediscusstherelationbetweenthecourseoftype2diabetes(2DM)andbloodsugar,BMI,insulinresistance(INSresistance),andthesecretionfunctionofinsulin,andtheef-fectsofthesefactorstothelifequality.Wehopewecoulddosomegoodtothetherapyandrecoveryof2DM.1Subjectsandmethods1.1SubjectsThe233inpatientsandhealthexaminationobjectswerefrom38to83yearsold.Inthem146weremales,and87werefemales.AccordingtothediagnosisandclassificationstandardsofDMenactedbyWHOin1985…  相似文献   

4.
INTRODUCTIONIthasbeenprovedrecentlythatobesity,microalbuminuria(MAU)andlow-insulinresistanceareindependentriskfactorsandincreasethemortalityofcardiovasculardiseasesintype2diabeticpatients.Inordertostudytherelationshipbetweenmicroalbuminriaandearlylargerarterylesionsintype2diabeticpatients,weanalyzedthere-lationshipbetweenurinealbuminexcretoryrateandarterialhemo-dynamicchangeinlowerlimbs.MATERIALSANDMETHODSMaterials85casesoftype2diabeticpatientswerecollectedbetween1…  相似文献   

5.
Incidencerateofstrokeishighintype2diabetespatientswithgreatharmfulness.Weresearched202casestoinvestigatetherela-tivityofchangeofserumfatanduricacidchangeoftype2diabeticpatientsandstrokerelapse,whichdeliverscientificevidencetoearlyclinicalstrokepreventionoftype2diabetespatients.1Subjectandmethod1.1SubjectWeselectedrandomly202in-patientcasesinourhospitalfrom1993to1999,anddividedinto3groups:(1)Type2diabetesconcomitantstrokegroup:including60cases,34males,av…  相似文献   

6.
扩张型心肌病TNF,IL—1和SIL—2R的检测及其意义   总被引:3,自引:0,他引:3  
应用双抗体夹心法及小鼠胸腺细胞增殖法等分别检测了30例原发性扩张型心肌病(DCM)的血清肿瘤坏死因子(TNF)、白细胞介素(IL-1)及可溶性白细胞介素2受体(SIL-2R)的水平,结果发现DCM病人TNF、IL-1及SIL-2R均明显高于正常对照组(NC,P〈0.001,P〈0.01,P〈0.001),提示TNF,IL-1及SIL-2R可能在DCM的发病机理中有意义。  相似文献   

7.
654-2救治野芹中毒5例黑龙江省七台河市医院(154600)沙中泉,王志国,莫文涛佳木斯市汤原县中心医院(154700)南斗镇,王金凤用常规综合疗法抢救5例野毒芹中毒患儿.效果不佳,改用654-2治疗后,5例均获救。报道如下。1临床资料1.1发病情...  相似文献   

8.
Therelationshipbetweencerebro-vasculardiseases(CVD)andSRBDhasattractedpeople’sattentionmoreandmoreinthepastyears.WepresentinthispapertherelationshipofVBIandSRBDwhichhasnoteverbeenreportedbefore.1Subjectandmethod1.1SubjectFortyfivepatients,male32,female13,withanageof27~74yearsandanaveragedurationofillnessof2.1years(5daysto10years).1.2Criteriaofdiagnosis犤1犦(1)Transientvertigoattacksaccom-paniedbyotherVBIsymptomssuchasdiplopia,scintillation,visua…  相似文献   

9.
血管性痴呆患者血小板活化机制的研究   总被引:1,自引:0,他引:1  
Excessivelyaggregatingfunctionofplateletplayedtheimpor-tantroleinpathogenesisofacutecerebralinfarction(ACI).Inthecurrentstudy,restplatelet犤Ca2+犦,Ca2+,Mg2+-ATPaseactivityweremeasuredtoconfirmtheirrelationshipwithvasculardementiaandcorrelationbetween犤Ca2+犦withCa2+,Mg2+-ATPase.1Subjectandmethod1.1Subject32subjectswereincludedinvasculardementia(VD)group.Amongthesepatients,20weremale,12werefemaleaged61~78(meanage:66years).Diseasecourselas…  相似文献   

10.
1SubjectandMethods1.1SubjectFromSeptember1994toSeptember1999400pa-tientsofbreastcancerstagingfromstageItostageIIIaafterradicalormodifiedradicalmastectomyweredividedintotestandcontrolgroups.1.2Methods(1)Equipment:MultifunctionalmicrowavetreatingmachineforphysiotherapyofTianjinLY-IItypeused,withworkfre-quencyof2450MHzandcontinuousadjustablepowerbetween5~60W.S=1.29whenradiatinginthemuscletissue.(2)Allthepatientswereadministrated5-Fuof0.75…  相似文献   

11.
目的观察乌司他丁(UTI)对体外循环(CPB)心脏手术患者血栓素(TXA2)和前列环素(PGI2)的影响。方法将60例CPB择期心脏手术患者随机分为实验组和对照组,分别采用UTI1.2万U/kg稀释于10ml生理盐水中和等量生理盐水中,一次性加入CPB预充液中,分别于麻醉诱导后(L)、主动脉开放30min(T2)、术毕(T3)及术后6h(T4)4个时点,抽取桡动脉血用放射免疫法测定TXB2/6-keto—PGF1a浓度。结果CPB后两组患者T2、T3、T4血浆TXB2、TKG6-keto—PGF1a浓度均较T1浓度增加(P〈0.05),但实验组增加幅度低于对照组(P〈0.05),且术后6hTXB2、6-keto—PGF1a浓度己降到或低于术前水平(P〈0.05)。结论血浆TXA2和PGI2比值升高,可能是CPB后肺损伤的机制之一。乌司他丁对CPB后肺损伤的保,护作用可能与改善花生四烯酸代谢紊乱,抑制TXA2/PGI2比值升高有关。  相似文献   

12.
目的 探讨次声作用后脑皮层组织血栓素A2 (TXA2 )、前列环素 (PGI2 )代谢改变及及代谢性谷氨酸受体拮抗剂MCPG的作用。方法  40只SD大鼠随机分为正常对照、次声作用 1次、7次、14次及代谢性谷氨酸受体拮抗剂MCPG治疗 5组。采用第四军医大学研制的次声压力仓。用 8Hz、12 0dB的次声按规定次数 ,每次作用 2h。采用蛋白定量和放免法行脑TXA2 、PGI2 稳定代谢产物血栓素B2 (TXB2 )及 6 酮 PGF1α( 6 酮 )含量测定。结果  7次与 14次组 ,TXB2 含量有显著意义升高 (P <0 .0 1) ,6 酮含量明显降低 (P <0 .0 1)。TXA2 /PGI2 值呈递增趋势 ;治疗组 ,TXB2 及 6 酮含量与TXA2 /PGI2 值恢复致正常水平。结论 次声可以通过引起脑TXA2 、PGI2 代谢改变造成脑损害 ,是次声导致脑损害的关键因素之一。MCPG可能通过影响脑TXA2 、PGI2 代谢改变而起脑保护作用。  相似文献   

13.
目的:探讨急性颈髓损伤患者全血血小板活化因子(PAF)、血浆血栓素B2(TXB2)、6-酮-前列腺素F1a(6-keto-PGF1a)含量的动态变化及其临床意义。方法:分别采用定量生物分析法、放射免疫分析法检测了35例急性外伤性颈髓损伤患者全血PAF、血浆TXB2和6-keto-PGF1a的含量变化。结果:伤情越重、预后越差的患者,血液中PAF、TXB2含量和TXB2/6-keto-PGF1a(T/K)值在伤后早期升高越明显;8例颈髓损伤早期死于颈髓水肿、呼吸衰竭的患者,伤后当日全血PAF含量和T/K值分别为对照组的15.34倍和6.39倍。结论:伤后全血PAF、血浆TXB2和6-keto-PGF1a含量的动态变化反映脊髓损伤的严重程度及脊髓神经功能恢复状态。脂质炎性介质——PAF、TXB2和6-keto-PGF1a可能与急性颈髓水肿的病理生理过程有关。  相似文献   

14.
The behavior of two vasoactive prostanoids was studied in experimental acute pancreatitis (AP) in rats. The stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2), 6-keto-PGF1 alpha and TXB2, respectively, were measured during the course of experimental AP. Blood samples were taken at 3, 6, and 8 h after the induction of AP. In AP both plasma 6-keto-PGF1 alpha plasma TXB2 and serum TXB2 increased up to 6 h simultaneously (6-keto-PGF1 alpha from 271.1 +/- 77.2 pg/ml (mean +/- SD) to 459.4 +/- 192.6 pg/ml, plasma TXB2 from 752 +/- 350 pg/ml to 3640 +/- 2160 pg/ml and serum TXB2 from 22.3 +/- 14.8 micrograms/ml to 140.8 +/- 52.8 micrograms/ml). After 6 h 6-keto-PGF1 alpha remained elevated, whereas serum TXB2 dropped significantly. We suggest that in AP the balance of PGI2 and TXA2 is initially maintained, but later on an imbalance appears to favor vasodilatory PGI2. These agents may contribute to the regulation of the blood flow in the pancreas and thus play a role in the pathophysiology of AP.  相似文献   

15.
Increased renal thromboxane production in murine lupus nephritis.   总被引:6,自引:2,他引:6       下载免费PDF全文
To determine whether the amount of cyclooxygenase metabolites correlates with the development of lupus nephritis, intrarenal eicosanoid production was measured in autoimmune mice. Disease progression was related to the renal biosynthesis of prostaglandin (PGE2), prostacyclin (6 keto PGF1 alpha), and thromboxane (TXB2) using the MRL-lpr and NZB X NZW F1 hybrid mouse strains with predictably progressive forms of renal disease that mimic the human illness. Mice were evaluated for renal disease by measuring urinary protein excretion and renal immunopathological conditions and these features were related to renal eicosanoid production. These studies show that: (a) intrarenal synthesis of TXB2 increased incrementally in MRL-lpr and NZB X NZW F1 hybrid mice as renal function deteriorated and renal pathologic events progressed; (b) there were no consistent increases in the levels of two other cyclooxygenase metabolites, PGE2 or 6 keto PGF1 alpha; (c) increased TXB2 production occurred in the renal medulla, cortex, and within enriched preparations of cortical glomeruli; (d) when renal disease was prevented by pharmacologic doses of PGE2, intrarenal TXB2 did not increase; (e) administration of a dose of ibuprofen (9 mg/kg), a cyclooxygenase inhibitor capable of reducing 90% of platelet TXB2 without affecting intrarenal levels, did not retard the progression of renal damage. Taken together, these data indicate that the intrarenal level of TXB2 rises in relation to the severity of murine lupus nephritis. Furthermore, because of the potential deleterious effects of TXA2, enhanced production of this eicosanoid may be an important mediator of renal injury.  相似文献   

16.
We examined the effects of NTG on human saphenous and umbilical vein PGI2 and TXA2 generation. Vascular rings from both types of vessels generated TXA2 in addition to PGI2. The treatment of vascular rings with NTG in concentrations of 5 to 1000 ng/ml and subsequent incubation with AA caused a significant increase in PGI2 in the supernatants, as identified by bioassay (platelet aggregation inhibition) and by measurement of 6-keto-PGF1 alpha (stable hydrolysis product of PGI2). The maximum increase in PGI2 was observed with therapeutic concentrations of NTG, i.e., 5 to 10 ng/ml. The levels of vessel wall-generated TXB2 (stable metabolite of TXA2) were not affected by NTG treatment. A prior incubation of vascular rings with indomethacin abolished the increase in PGI2 after NTG treatment. In contrast, incubation of vascular rings with OKY 1581 (selective TXA2 inhibitor) resulted in a significant additional increase in PGI2 release but no change in TXB2 levels after NTG treatment. These studies indicate important effects of NTG on vascular PGI2 generation but not on TXA2 generation.  相似文献   

17.
目的本文旨在探讨ET-1、NO、TXA2和PGI2在缺氧时对心肌血流量的调节作用。方法大鼠随机分为平原组和急性缺氧组,用99mTc标记蟾蜍红细胞测定心肌血流量,用Gess法测量NO-、用放免法分别测量ET-1、TXA2、PGI2的含量。结果急性缺氧导致左、右心室心肌血流量、心肌NO2-、ET-1、血浆TXB2含量、TXB2/6-keto-PGF1ɑ比值明显增高(P0.05),左、右心室心肌血管阻力、ET-1/NO2-比值明显下降(P0.05),血浆6-keto-PGF1ɑ无明显变化。结论急性缺氧时,左、右心室心肌血流量增加,ET-1/NO、TXA2/PGI2参与了急性缺氧时心肌血流量的调节,以NO的扩血管作用为主。  相似文献   

18.
背景颅脑损伤诱发的花生四烯酸代谢瀑布过程中产生的前列腺素类和氧自由基的增加是其重要的一方面,消炎痛能强烈抑制环氧化酶活性,减少前列腺素类合成,并可能减少氧自由基的增加,从而可能具有减轻脑损伤作用.目的观察脑损伤后早期前列腺素的变化及消炎痛对其的干预作用,探讨其作用机制.设计以实验动物为研究对象,随机对照实验研究.单位一所大学医院的神经外科和一所大学医院的脑外科.材料实验于2000-03/09在东南大学医学院神经外科实验室完成.将36只杂种猫,随机分为正常对照组,脑损伤组和消炎痛干预组3组,每组12只.干预脑创伤按分级机械脑损伤实验动物模型制作,取中度脑损伤水平进行研究.伤后6 h测定脑静脉血中前列腺环素(PGI2)和血栓素(TXA2)的最终分解产物6-酮-前列腺素F1a(6-keto-PGF1α)和血栓烷素B2(TXB2)、脑组织总超氧化物歧化酶(SOD)及脑含水量.主要观察指标6-keto-PGF1α,TXB2,SOD含量和脑含水量测定.结果猫脑损伤后早期脑静脉中6-keto-PGF1α和TXB2均明显增加[由(0.057±0.010)g/L增至(0.264±0.126)g/L,由(0.060±0.012)g/L增至(0.134±0.048)g/L,6-keto-PGF1α增幅大于TXB2,TXB2/6-keto-PGF1α比值下降(由1.052±0.145降为0.545±0.184),脑含水量增加[由(77.39±0.36)%增至(78.06±0.41%)],同时脑组织总SOD明显降低[由(94.869±5.418)μkat/g降至(54.368±3.417)μkat/g](P<0.01);消炎痛干预组与脑损伤组比较,6-keto-PGF1α和TXB2明显降低,与正常对照组接近,而总SOD则有增加[(54.368±3.417)μkat/g增至(81.433±7.268)μkat/g](P<0.01),脑含水量略降低,但无统计学意义(P>0.1).结论猫脑损伤后早期PGI2和TXA2增加,并伴随自由基产生,由此加重脑损害.消炎痛通过调节脑损伤后PGT2/TXA2失衡,减少自由基产生,有助于减轻脑创伤后继发性脑损害.  相似文献   

19.
本研究观察了原发性血小板增多症(primary thrombocytosis,PT)患者临床血栓发生率及其与血小板功能变化的关系,探讨阿患者预防性应用血栓素A2抑制剂对其血小板活性的影响及其对血栓的预防和治疗的临床效果。以流式细胞术测定血小板表面的CD62P、PAC-1水平;ELISA方法测定血浆血栓素A2(TXA2)代谢产物TXB2和前列环素(PGI2)代谢产物6-K—PGF1α水平;观察和比较各组血小板功能的变化及其与血栓形成的关系。结果表明:奥扎格雷钠干预治疗前合并血栓组TXB2、CD62P、TXB2/6-keto—PGF1α比值均比未合并血栓组高,统计学差异具有显著性(P〈0.01);奥扎格雷钠干预治疗后2组各项血小板功能指标除6-keto—PGF1α外,均较治疗前有明显降低(P〈0.01),且合并血栓组在奥扎格雷钠治疗后除CD62P仍较朱合并血栓组高(p〈0.05)以外,其余指标均与未合并血栓组无显著性差异(P〉0.05)。结论:PT合并血栓者血小板多项功能指标均较未合并血栓者异常升高,血小板功能活化也是PT患者血栓发生的高危因素。奥扎格雷钠均可使2组患者血小板活化指标明显降低,体内TXA2的生成减少和TXA2/PGI2的比值改善.奥扎格雷钠不但具有治疗血栓作用,而且还有较好的预防血栓效果。  相似文献   

20.
Increase in thromboxane A2 (TXA2) generation has been proposed as a mechanism of dynamic vaso-occlusion and in vivo platelet thrombus formation. We have examined the effects of CGS-13080, an imidazole derivative, on rabbit and human TXA2-prostacyclin (PGI2) "balance." In rabbits given CGS-13080, serum levels of TXB2 (stable metabolite of TXA2) were inhibited 81% at 2 hours and 56% at 24 hours (both P less than or equal to 0.01). Collagen-induced platelet aggregation was inhibited at 2 hours after CGS-13080 administration. In contrast, serum levels of 6-keto-PGF1 alpha (stable hydrolysis product of PGI2) increased 587% compared with control values at 2 hours (P less than or equal to 0.01). Platelet and white blood cell counts were not significantly altered. In human blood incubated in vitro with CGS-13080, serum TXB2 was completely inhibited, whereas PGI2 generation was stimulated (both P less than or equal to 0.001). In other experiments, we demonstrated uptake of platelet-generated cyclic endoperoxides by leukocytes and generation of PGI2 in the presence of CGS-13080 but not indomethacin. Thus, CGS-13080 inhibits TXA2 and stimulates PGI2 production in rabbit and human blood. Increase in PGI2 generation with TXA2 inhibition may be of potential benefit in conditions characterized by platelet hyperactivity.  相似文献   

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