超声乳化联合房角分离术治疗原发性闭角型青光眼

目的探讨白内障超声乳化联合房角分离术治疗原发性闭角型青光眼的疗效。方法对合并老年性白内障的原发性闭角型青光眼患者31例47只眼,行白内障超声乳化人工晶体植入联合房角分离术,观察手术前后的视力、眼压、房角、UBM及视野的变化,随访3～15个月。结果其中40只眼术后视力均有不同程度提高;平均眼压由术前的(29.67±4.15)mmHg降至术后的(10.81±3.27)mmHg,中央前方深度术前:2.48±0.36,术后:3.51±0.33,视野无缩小。结论白内障超声乳化联合房角分离术是替代传统小梁切除术后二次行白内障手术治疗原发性闭角型青光眼合并老年性白内障的有效方法。     

后房型人工晶体二期植入治疗无晶体眼

目的评价用不同方法进行后房型人工晶体二期植入治疗各种原因的无晶体眼的疗效。方法各种原因导致的无晶体眼患者61例共67只眼,其中先天性白内障摘除术后8例13只眼,外伤性白内障摘除术后35例35只眼,并发性白内障9例10眼,老年性白内障9例9眼。根据患眼情况分别行囊袋内植入、睫状沟植入及睫状沟缝线固定术。结果67只眼均成功植入人工晶体,术后随访1～24个月,术后裸眼视力0.41±0.28,与术前最佳矫正视力(0.40±0.25)比较,差异无显著性(P>0.05)。结论后房型人工晶体二期植入能有效地治疗各种原因的无晶体眼。     

地氟病区及非氟区老年性白内障晶体微量元素分析（摘要）

对地氟病区(饮水含氟量1．4～12.0mg／L)老年性白内障晶体34个和非氟区(氟含量0．36～0．41mg／L)晶体22个，用原子吸收／火焰发射分光光度计测定氟和其它5种微量元素(锌、镁、铜、铁、锰)。结果表明．地氟病区晶体氟含量(0．7646±0．3759ppm)显高于非氟区(03645±0.2807，P<0.01)，     

皮肤病患者血清水溶性脂质过氧化物测定

水溶性荧光物质是一些脂类过氧化物降解产物和血清蛋白结合物,它们可以作为体内过氧化物指标。作者用荧光法对40例健康对照者及50例皮肤病患者进行了血清WSFS相对含量的测定,结果报告如下: 1 对象及实验方法 1.1 一般资料:本组病例均为门诊患者随机抽样。诊断明确,皮疹典型。其中银屑病20     

表麻下白内障超声乳化吸除折叠式人工晶体植入术的临床观察

目的 探讨表面麻醉下白内障超声乳化吸除折叠式人工晶体植入术的临床疗效。方法 对68例(71眼)老年性白内障患者,采用表面麻醉下做3.2mm阶梯状透明角膜切口,行超声乳化白内障吸除术,同时植入折叠式人工晶状体。结果 术后1天、1周、1个月和3个月视力≥0.4者分别为74.7％、83.1％、90.1％和93.0％。术后1周、1个月和3个月角膜平均散光度为(1.12±0.90)D,(1.10±0.85)D和(0.98±0.79)D,术后1周、1个月和3个月角膜平均散光度与术前比较,无显著性差异(P>0.05)。结论 表面麻醉下超声乳化手术给患者造成的痛苦小,手术顺利,术后恢复快,视力提高理想,不会对角膜上皮造成损伤。     

透明角膜小切口白内障超声乳化术后角膜散光的变化

目的评价角膜地形图引导的透明角膜小切口超声乳化白内障吸除折叠式人工晶体植入术后角膜散光的变化。方法将119例(130只眼)白内障患者分为A、B、C三组,A组为对照组,B组为循规性散光组,C组为逆规性散光组;A、B两组行上方透明角膜切口,C组行颞侧透明角膜切口,行超声乳化白内障吸除折叠式人工晶体植入,比较术后角膜散光的变化情况。结果A、B、C三组术后90d平均手术性角膜散光度分别为(0.64±0.65)D、(0.75±0.58)D和(0.69±0.55)D,两两比较无显著性差异(P>0.05);平均角膜散光度A组较术前增加0.07D,B、C两组较术前减少0.34、0.37D,与A组比较有显著性差异(P<0.05)。结论以透明小切口行超声乳化白内障吸出折叠式人工晶体植入术,术后角膜散光度小,角膜地形图可准确反映角膜曲率变化,对指导术前角膜切口位置的选择及评价白内障术后角膜散光的变化具有重要的临床意义。     

表麻下白内障超声乳化吸除折叠式人工晶体植入术的临床观察

目的探讨表面麻醉下白内障超声乳化吸除折叠式人工晶体植入术的临床疗效.方法对68例(71眼)老年性白内障患者 采用表面麻醉下做3.2mm阶梯状透明角膜切口 行超声乳化白内障吸除术 同时植入折叠式人工晶状体.结果术后1天、1周、1个月和3个月视力≥0.4者分别为74.7%、83.1%、90.1%和9 3.0%.术后1周、1个月和3个月角膜平均散光度为(1.12±0.90)D (1.10±0.85)D和(0.98±0.79)D 术后1周、1个月和3个月角膜平均散光度与术前比较 无显著生差异(P＞0.05).结论表面麻醉下超声乳化手术给患者造成的痛苦小 手术顺利 术后恢复快 视力提高理想 不会对角膜上皮造成损伤.     

糖尿病视网膜病变与果糖胺的关系

目的:观察和分析91例糖尿病患者的眼底荧光血管造影(FFA)的图像特点和果糖胺(FTM)的检测结果,探讨糖尿病视网膜病变(DR)与果糖胺的发病关系。方法:对91例2型糖尿病患者按常规操作行眼底血管荧光造影和彩色照片对照,并按检查结果分为正常眼底组、单纯型DR组、增殖型DR组,3组均采用比色法测定果糖胺的量。结果:果糖胺均值,正常眼底组为(373.02±118.48)μm o l/L;单纯型DR组为(425.32±138.91)μm o l/L;增殖型DR组为(538.09±249.23)μm o l/L。结论:本组增殖型DR组及单纯型DR组的果糖胺均值较正常眼底组明显升高,经统计学处理差异有显著性,提示果糖胺均值上升与DR进展呈正向关系。     

川芎嗪对增殖性肾炎病人血浆内皮素和脂质过氧化物的影响

目的 :观察川芎嗪对增殖性肾炎病人血浆内皮素 (ET)和脂质过氧化物 (LPO)的影响。方法 :将 5 8例病人分为川芎嗪组 (31例 )和对照组 (2 7例 )。对照组给予泼尼松、福辛普利、双嘧达莫、环磷酰胺等治疗 ,川芎嗪组在上述治疗基础上加用川芎嗪注射液。于治疗 4wk后测定血浆内ET ,2 4h尿蛋白定量、一氧化氮 (NO)、过氧化物岐化酶 (SOD )和LPO水平变化。结果 :治疗后治疗组尿蛋白、血脂降低 ,肾功能好转 ,ET含量由 (63± 8)ng·L- 1下降为 (5 7± 8)ng·L- 1(P <0 .0 1) ;LPO含量由 (3.8± 0 .7) μmol·L- 1下降为 (1.3± 0 .8) μmol·L- 1(P<0 .0 1)。结论 :川芎嗪可通过抑制血浆ET的产生、抗脂质过氧化作用 ,对增殖性肾炎病人的肾功能有一定保护作用。     

晶体溶解性青光眼

<正> 机体对自身分解变性的晶体蛋白,可以发生不同程度的过敏反应。这种过敏反应有三种形式:晶体过敏性眼内炎,晶体过敏性色素膜炎继发青光眼和晶体溶解性青光眼。前二者常因外伤或手术后破碎残留的皮质引起,后者乃因过熟期白内障引起吞噬细胞反应及伴之而来的急性青光眼。我院于1982年见到一例。鉴于本病易与膨胀期老年性白内障引起的青光眼、闭角性青光眼合并老年性白内障相混淆,故介绍于后。病例报告刘××,男,56岁,工人。住院号:98484。四年前左眼患老年性白内障住院,因同时患有肺结核     

不同年龄白内障患者晶状体特异性表达基因检测及分析

目的研究晶状体上皮细胞特异表达的基因LEP503在不同年龄白内障患者以及正常人晶状体中表达情况,探讨白内障的发生机制。方法收集白内障患者晶状体前囊膜50例(白内障低龄组和高龄组)、无白内障发生的晶状体前囊膜50例(正常对照低龄组和高龄组)。通过RT-PCR和Western-Blotting技术检测各组LEP503基因和蛋白表达情况,凝胶成像分析系统比较各组之间LEP503表达的差异。利用SPSS13.0软件包,t检验和线性回归进行统计学分析。结果RT-PCR和凝胶成像分析结果显示:白内障组LEP503基因表达明显比正常对照组高(P<0.01);其中白内障高龄组LEP503基因表达明显比低龄组高(P<0.01);Western-Blotting结果显示:白内障患者LEP503蛋白表达量明显比正常人高,且年龄越大LEP503蛋白表达越强。结论①LEP503基因在白内障患者中有表达且比正常人高;②白内障患者LEP503基因的表达量与患者年龄之间呈线性关系;③LEP503基因与晶状体上皮细胞增殖没有直接关系;④LEP503基因可能参与了老年人白内障和青年人白内障不同发病机制过程。     

老年性白内障双眼同时人工晶状体植入术临床研究

目的：探讨老年性白内障双眼同时进行白内障囊外出及人工晶状体植入术的手术效果。方法：36例老年性白内障同时进行白内障囊外出及人工晶状体植入术,术后观察矫正视力,眼内炎症和眼压,与同期老年性白内障单眼手术的眼进行对照。结果：同时手术的双眼与单眼同样手术的眼之间,不论是术后视力,眼压还是眼内炎症差异无显性,结论：老年性白内障双眼同时行囊外出及人工晶状体植入术在临床可积极采用。     

Effect of calpain on hereditary cataractous rat, ICR/f.

The crystallins in the lenses of ICR/f mutation rat, a known hereditary cataract model, were analyzed during cataractogenesis. Opacification of the mutant lenses was found to be accompanied by changes in crystallin structure and composition, including several deletions of the N-terminals of beta-crystallins and low molecular weight alpha- crystallins. Because similar deletions were observed when the soluble fraction of normal lens protein was incubated with calpain, we considered that calpain could be related to the deletions in mutant lenses. Although measurement of the content of calpain protein by the ELISA method revealed no significant difference between mutant and normal lenses, it was found that the concentrations of Ca2+ and K+ were different between the two lenses and that calpain activity was dependent on both ion concentrations. Endogenous m-calpain in the soluble fraction from normal lenses was activated by addition of 1 mm calcium chloride in the presence of 50 mm KCl (the same concentration as in mutant lenses), and insoluble protein was found in the fraction 1 d after calpain activation. On the other hand, the presence of 120 mm KCl (the concentration in normal lenses) inhibited calpain activity and prevented this insolubilization. These results suggest that calpain in mutant lenses is involved in the proteolysis of crystallins and the progression of cataract formation.     

Studies on protein and taurine in normal, senile and diabetic cataractous human lenses

An attempt has been made to explore the possible role of Taurine in cataractogenesis. Normal lenses were obtained from eye bank donors and cataractous lenses from patients who had undergone surgery for cataract extraction. Lenses were weighed and homogenised. Extraction, isolation and estimation of protein and taurine were carried out. It has been found that the lens wet weight increased progressively with the stage of maturation of cataract, i.e., from mature to hypermature which was significant and also with increase in age. Diabetic cataract group also showed an increase similar to that of senile cataract. Taurine and total protein decreases with different stages of maturation of cataract but not with age. It may be suggested that in the process of development of human senile cataract, there is (a) alteration in the structural integrity and permeability of lens membrane to protein and amino acids including taurine, (b) changes in the lens function including possible inhibition of proteins and amino acids (taurine) synthesis and transport across the cell membrane.     

Effect of magnesium deficiency on intracellular ATP levels in human lens epithelial cells

Cataractous lenses have an altered distribution of the intracellular ionic environment, and the lens ionic imbalance with increased levels of calcium (Ca2+) and sodium (Na+), coupled with decreased levels of magnesium (Mg2+) and potassium (K+), is related to cataract development in human senile cataracts. We previously found that the decrease of ATP in lenses caused lens ionic imbalance, and probably decrease in ATPase function. In this study, we investigated the effect of Mg2+ deficiency on cataract progression using human lens epithelial (HLE) cells. Expression levels of inducible nitric oxide synthase (iNOS) mRNA in HLE cells were significantly greater in Mg2+-deficient medium (Mg2+ 0.021 mM) than in normal Mg2+ medium (Mg2+ 0.77 mM). The NO release from the HLE cells cultured with Mg2+-deficient medium also increased. On the other hand, the ATP levels in HLE cells 24 h after incubation with Mg2+-deficient medium were lower than that with normal Mg2+ medium. The Ca2+- and Na+/K+-ATPase activities in HLE cells until 24 h incubation with normal Mg2+ or Mg2+-deficient medium did not change. Both diethyldithiocarbamate 10 microM and aminoguanidine 250 microM attenuated the increase of NO release, and caused an increase in ATP levels in HLE cells 24 h after incubation with Mg2+-deficient medium. These results suggest that Mg2+ deficiency enhances NO production via iNOS in the lens. It is possible that the excessive production of NO cause the decrease of ATP levels. These results show that Mg2+ deficiency in the lens may cause an acceleration of the progression of lens opacification.     

Transport of trace elements in lenses of normal and hereditary cataract UPL rats

The multitracer technique was applied to the determination of the uptake of trace elements in the lenses of normal and hereditary cataract UPL rats to investigate the transport mechanisms of trace elements during cataract development. Be, Na, Sc, V, Cr, Mn, Fe, Co, Zn, As, Se, Rb, Sr, Y, Zr, Tc, Ru and Rh accumulate in normal and UPL cataract rat lenses. The rates of uptake of trace elements differ among species and also differ between normal and UPL rat lenses. The uptakes of V and Sr are greater in normal rat lenses, while the uptakes of Mn and Co are greater in UPL rat lenses. High concentrations of Zn are transported into normal rat lenses in comparison with other elements. However, the uptake of Se was highest in the lenses of UPL cataract rats. In addition, the difference in Se uptake between the normal and UPL rat lenses was greatest among the tested trace elements. The present study suggests that the transport characteristics of trace elements are different in the lenses of normal and UPL cataract rats. The different transport characteristics of trace elements in the lenses of normal and UPL cataract rats, especially the higher accumulation of Se in UPL rat lenses, may be implicated in cataract development.     

Involvement of DNase II-like acid DNase in the cataract formation of the UPL rat and the Shumiya cataract rat

The loss of organelles and DNA is important to ensure transparency of the lenses, and DNase II-like acid DNase (also called DNase IIbeta, DLAD) is related to the loss of organelles and DNA in the lenses. We investigated the relation between the degradation of DNA and DLAD mRNA expression in the lenses of two hereditary cataract rats, the UPL rat (UPLR) and the Shumiya cataract rat (SCR), during cataract development. Undigested DNA was detected in the lens cortexes of normal UPLRs and SCRs, and undigested DNA was degraded in the lens nuclei of normal UPLRs and SCRs. DLAD does not affect common cataract formation, since DLAD mRNA expression levels in the lenses of cataractous SCRs were not changed with an increase in age, and undigested DNA was degraded in the lens nuclei of cataractous SCRs. On the other hand, an accumulation of undigested DNA was found in the lens nuclei of cataractous UPLRs at 46 and 53 d of age with opaque lenses, and the decrease in DLAD mRNA expression levels occurred prior to the accumulation of undigested DNA in the lens nuclei. It is possible that UPLRs are a good model for cataract caused by a decrease of DNA degradation in the lenses.     

Comparison of the mechanisms of cataract development involving differences in Ca2+ regulation in lenses among three hereditary cataract model rats

We previously found that the increases in Ca2+ content in the lenses of three hereditary cataract model rats, UPL rat (UPLR), Shumiya cataract rat (SCR) and Ihara cataract rat (ICR), are inhibited by aminoguanidine, a selective inhibitor of inducible nitric oxide synthase, and that the mechanisms of Ca2+ enhancement in these rat models differ. In this study, we compare the mechanisms for dysfunction in Ca2+ regulation in UPLR, SCR and ICR. Decreases in the activity of Ca2+-ATPase were found in the lenses of SCR and ICR concurrent with cataract development. In contrast, the Ca2+-ATPase activity in UPLR with opaque lenses was higher than in those with transparent lenses. On the other hand, ATP levels were markedly decreased in UPLR with opaque lenses. The expression of cytochrome c oxidase (CCO)-1 mRNA and CCO activity in UPLR lenses was found to decrease during cataract development. The nitric oxide (NO) and lipid peroxide levels were also increased in the lenses of UPLR, SCR and ICR with opaque lenses. In UPLR, excessive NO may cause damage to the mitochondrial genome, resulting in a decrease in ATP production and increase in Ca2+-ATPase activity. The decrease in ATP content may cause the decrease in Ca2+-ATPase function resulting in the elevation in lens Ca2+. In SCR and ICR, excessive NO may cause an enhancement of lipid peroxidation resulting in the oxidative inhibition of Ca2+-ATPase. The decrease in Ca2+-ATPase activity may cause the elevation in the level of lens Ca2+, thus leading to lens opacification. Our findings show that the Ca2+ contents in the cataractous lenses of all three model rats are increased, the mechanisms for this Ca2+ enhancement is different in each rat model.     

正常和老年性白内障晶体VE Vc含量的测定

测定正常和老年性白内障晶体ＶＥ、Ｖｃ含量，发现老年性白内障晶体ＶＥ、ＶＣ含量比正常晶体明显减少，并讨论了这些改变的意义。