大鼠半乳糖性白内障晶状体上皮细胞的病理变化

目的　探讨半乳糖性白内障大鼠晶状体上皮细胞的改变。方法　２４只ＳＤ雌性大鼠,分为正常对照组和白内障组,每组１２只。白内障组大鼠用半乳糖饲料喂养,正常对照组大鼠用普通颗粒饲料喂养。裂隙灯显微镜下观察大鼠晶状体混浊程度变化,观察至３０ｄ处死大鼠后取晶状体,在光镜和电镜下观察晶状体病理组织和超微结构改变。结果　观察至３０ｄ时,正常对照组大鼠晶状体保持透明,白内障组大鼠９眼（３７．５％）出现均一的皮质性混浊,１５眼（６２．５％）出现核混浊。白内障组光镜下可见晶状体皮质和核部大量纤维细胞水肿、崩解,前囊膜下及后囊膜下出现纤维细胞样的有核细胞堆积;透射电镜下可见晶状体上皮细胞变性、增生并突破晶状体上皮层向浅层皮质移行。结论　半乳糖性白内障不仅有晶状体纤维细胞水肿及结构破坏,还存在晶状体上皮细胞的异常增生、分化和移行。     

老年性和糖尿病性白内障晶状体上皮细胞的超微结构改变

目的 观察正常人，老年性白内障、糖尿病性白内障晶状体上皮细胞的超微结构，探讨细胞凋亡在白内障发生中的作用。方法 收集正常人、老年性白内障、糖尿病性白内障晶状体前囊膜送透射电镜扫描，取老年性白内障和糖尿病性白内障前囊膜各15例，用脱氧核苷酸末端转移酶缺口标记原位细胞检测法，检测晶状体上皮细胞的凋亡细胞。结果 老年性和糖尿病性白内障晶状体上细胞的超微结构在形态上为扁平状，胞浆出现空泡变性，胞核出现固缩，染色质边聚，浓缩等改变。糖尿病性白内障晶状体上皮细胞的胞浆空泡变性更加严重。在光镜下老年性和糖尿病性白内障的晶状体上皮均有凋亡细胞。结论 老年性白内障和糖尿病性白内障的发生与晶状体上皮的细胞凋亡密切相关。     

核性白内障中的核空泡

空泡或空泡样改变是囊膜下白内障的典型表现,偶可见于正常晶体皮质。本文作者注意到,在高压氧诱发的核性白内障和老年性灰白色核性白内障中也可见到空泡样改变,并用裂隙灯光学照像技术和显微放射照像技术(MRG,Microradiography)对这些空泡进行了定量研究。研究包括三组:一是老年性白内障组,从白内障患者的术前裂隙灯检查中,连续选出100例核性白内障以研究其核的颜色,混浊程度及是否存在空泡等。二是高压氧治疗组,25人,在12个     

老年性和糖尿病性白内障晶状体上皮细胞的超微结构改变

目的 观察正常人,老年性白内障、糖尿病性白内障晶状体上皮细胞的超微结构,探讨细胞凋亡在白内障发生中的作用。方法 收集正常人、老年性白内障、糖尿病性白内障晶状体前囊膜送透射电镜扫描,取老年性白内障和糖尿病性白内障前囊膜各15例,用脱氧核苷酸末端转移酶缺口标记原位细胞检测法,检测晶状体上皮的凋亡细胞。结果 老年性和糖尿病性白内障晶状体上皮细胞的超微结构在形态上为扁平状,胞浆出现空泡变性,胞核出现固缩,染色质边聚,浓缩等改变。糖尿病性白内障晶状体上皮细胞的胞浆空泡变性更加严重。在光镜下老年性和糖尿病性白内障的晶状体上皮均有凋亡细胞。结论 老年性白内障和糖尿病性白内障的发生与晶状体上皮的细胞凋亡密切相关。     

猕猴白内障晶体上皮细胞超微结构研究

目的 探讨猕猴白内障晶体上皮细胞的超微结构,为将猕猴白内障作为人类白内障理想的动物模型提供病理学研究资料。方法 采用透射电镜对猕猴正常眼和猕猴白内障眼的晶体上皮细胞超微结构进行观察。结果 猕猴白内障眼晶体上皮细胞发生明显的变化：线粒体肿胀、空化、嵴消失,甚至形成凹空细胞;细胞水肿,细胞质溶解,甚至细胞崩解破坏;细胞核固缩、畸形,核膜间隙与核孙消失,核内异染色质浓集、周边化。结论 猕猴白内障上皮细胞     

正常晶状体及年龄相关性白内障晶状体的超微结构观察

目的：探讨正常晶状体和年龄相关性白内障晶状体的超微结构变化。

方法：采用飞利浦208型透射电镜及日本产JSM-6380LV扫描电镜对3例正常的透明晶状体及5例行白内障囊外摘出的囊膜及晶状体核进行超微结构观察,并进行比较。

结果：透射电镜下白内障上皮细胞与正常组晶状体上皮细胞相比出现大量的异性核,染色质凝集,线粒体肿胀,减少,呈现空泡化; 白内障晶状体核区纤维细胞界限不明显,出现明显溶解、坏死改变。扫描电镜下白内障晶状体皮质纤维细胞失去光滑,晶状体核区纤维细胞表面因挤压而变形,细胞间的连接出现变化。

结论：白内障晶状体中上皮细胞及纤维细胞均发生了超微结构改变,这些变化可能是晶状体混浊的原因之一。     

Nd:YAG激光乳化白内障手术后兔角膜和视网膜超微结构的变化

目的观察激光乳化白内障术后兔角膜和视网膜急性超微结构的变化并确定安全的激光能量范围。方法新西兰白兔18只，分为（A、B、C）3组，每组6只，行Nd：YAG激光乳化白内障手术。A组使用300个脉冲（3J能量）；B组使用600个脉冲（6J能量）；C组使用900个脉冲（9J能量）。术后0．5h内取中央角膜和后极部视网膜做透射电镜检查。结果A组未见角膜内皮细胞超微结构的异常；B组角膜内皮细胞线粒体肿胀，粗面内质网嵴断裂，内皮细胞空泡变性；C组角膜后弹力层脱离、内皮细胞空泡变性、线粒体肿胀、角膜基质水肿和后弹力层变性。3组均未见视网膜超微结构改变。结论在兔眼Nd：YAG激光乳化白内障手术中，较少的脉冲和低能量的激光对兔角膜无明显损伤，随着脉冲次数和能量的增加，对角膜内皮细胞的损伤加重。使用9J以下的激光能量，Nd：YAG激光乳化白内障手术对兔视网膜无急性损伤。     

世界卫生组织（WHO）新白内障分级系统临床试用的初步报告

本文应用世界卫生组织（ＷＨＯ）新的白内障分级系统对１０７名患者２１３眼晶体混浊，包括核部，皮质及后囊下混浊进行了白内障的分级。初步试点证明通过散瞳在裂隙灯下检查，并将检查结果与标准照片对照，以确定检查或分级结果，以此方法较单纯用文字描述检查结果更易于掌握。检查结果通过一致性ｋａｐｐａ值的分析表明ＷＨＯ白内障分级系统在皮质及后囊下混浊一致性较好，而在核性混浊一致性较差，因此对核性混浊的分级需进一步研究     

人晶体上皮细胞密度及形态学观察

本文对正常及白内障晶体上皮细胞的密度及形态学进行了观察，对比分析了晶体上皮细胞形态学特点与白内障类型的关系，结果证明核性白内障晶体上皮细胞密度较高，且形态规则，是其晶体混浊发展缓慢的形态学基础，后囊下型白内障发生与晶体上皮存在的增生活跃的重叠细胞有关。     

先天性白内障的分类及致病基因研究进展(续)

4.皮质性白内障(cortical cataract) 由于周边部晶体纤维层变性、分解、液化,在囊膜产生半透明的乳状液体,核失去支撑,棕色的胚胎核在液化的皮质中浮动,有时核亦液化.皮质性白内障中常会出现Morgagnian小体,为大小不等的圆形小体,是晶状体皮质纤维破裂形成的细胞碎片,如果这种小体和异常蛋白取代了整个皮质并且液化,就形成了过熟期白内障或称莫干尼白内障(Morgagnian cataract),此时晶体核失去支撑而下沉,晶体内水分逐渐丢失而使晶体体积缩小,囊膜皱缩可受到损害而减少通透性.     

American Uveitis Society Meeting October 30, 1995 Marriott Marquis Hotel, Atlanta, GA, USA

1 Retinal vascular occlusion and scleroderma. Tessler H, Flores-Guevara J, Goldstein D, Chicago, IL, USA. 2 MHC Class II antigen expression in ciliary body in spontaneous and experimental uveitis. Kalsow C, Zhavoronkova M, Dwyer A, Rochester, NY & Scottsville, NY, USA. 3 IL-10 in the vitreous of patients with intraocular lymphoma. Whitcup S, Solomon D, Nussenblatt R, Chan C-C, Bethesda, MD, USA 4 Iris juvenile xanthogranuloma studied by immunohistochemistry. Shields J, Shields C, Eagle R, DePotter P, Collins M, Philadelphia, PA, USA. 5 Outcomes analysis in with JRA-associated uveitis. Dana M-R, Merayo-Lloves J, Foster C, Boston MA, USA. 6 Persistent glaucoma secondary to periocular steroids. Akduman L, Conway M, Burchfield J, Kolker A, Black D, DelPriore L, Kaplan H, St. Louis, MO, USA 7 The use of itraconazole in ocular histoplasmosis Callanan D, Fish G, Dallas, TX, USA 8 Succesful treatment of macular hole secondary to sympathetic ophthalmia. Cano J, Diaz M, Navea A, Ruiz C, Castilla M. Barcelona, Spain. 9 HLA-DR2+ intermediate uveitis. Pulido J, Tang W, Han D, Mieler W. Milwaukee, WI, USA. 10 Vein occlusion in AIDS misdiagnosed as CMV retinitis. Park K, Marx J, Rao N. Los Angeles, CA, USA. 11 HIV-associated foveal hemorrhage. Crews K, Zimmerman P, Lohner S. Salt Lake City, UT, USA. 12 Cytomegalovirus papillitis in patients with AIDS. Patel S, Rutzen A, Marx J, Thach A, Chong L, Rao N, Los Angeles, CA, USA. 13 Recurrence rate of CMV retinitis following the ganciclovir implant and pars plans vitrectomy and silicone oil. Marx J, Thach A, Rao N, Chong L. Los Angeles, CA, USA.     

American uveitis society meeting october 31, 1994 san francisco, california

1 Ophthalmic manifestations of presumed rifabutin-related uveitis. Arevalo JF, Freeman WR, La Jolla, CA, USA. 2 Diagnosis of toxoplasmosis acute anterior uveitis by PCR. Cano J, Diaz M, Navee A, Maldonado M, Barcelona, Spain. 3 Neuroretinits in patients with AIDS. Berger B, Austin TX, USA. 4 Presumed varicella zoster retinitis in a pediatric patient with AIDS. El Baba F, Nachman S, Stony Brook, NY, USA. 5 ARN with hypopyon caused by EVB and herpes type VI viruses. Cano J, Diaz M, Navea A, Maldonado MJ, Barcelona, Spain. 6 CD8(+) T-lymphocytes and ocular infections in HIV(+) patients. Lowder CY, Butler CP, Dodds EM, Recillas-Gispert C, Cleveland, OH, USA. 7 Intravitreal foscanet for persistent CMV. Lieberman RM, Orellana J, New York, NY, USA. 8 Perfluorocarbon liquid versus air-fluid exchange during surgical repair of retinal detachment caused by cytomegalovirus retinitis in patients with AIDS. Sery T, Gomes J, Sando R, Dua H, Donoso L, Vrabec T, Philadelphia, PA, USA. 9 Endogenous ophthalmitis simulating retinoblastoma: a report of six cases. Shields J, Shields C, Eagle R, Barrett J, DePotter P, Philadelphia, PA, USA. 10 Ocular lymphoma resembling chronic postoperative endophthalmitis. Fox G, Chan CC, Whitcup SM, Nussenblatt R, Bethesda, MD, USA. 11 A phase II trial of combination chemotherapy for primary central nervous system lymphoma. Whitcup SM, Stark-Vanes V, Nussenblatt RB, Heiss H, Witte R, Bethesda, MD, USA. 12 Cancer-induced autoimmune retinopathy. Thirkill C, Sacramento, CA, USA. 13 Leukocytoclastic vasculitis. Tessler H. Chicago, IL, USA. 14 Bilateral choroidal neovascular membranes after Candida albicans chorioretinitis. Dodds E, Townsend-Pico W, Lowder CY, Lewis H, Cleveland, OH, USA. 15 An unusual complications of Toxoplasma retinochoroiditis. Gormley PD, Flaxel CJ, Pavesio CE, Conrad DK, Lightman S, London, UK. 16 Surgical removal of a choroidal neovascular membrane in sympahtetic ophthalmia. Conrad DK, McCluskey PJ, Schwartz S, Gregor Z. Lightman S, London, UK. 17 Peripheral laser scatter ablation in pars planitia. Park SE, Mieler WF, Pulido JS, Milwaukee, WI, USA.     

The Protocol for the Early vs. Late Infantile Strabismus Surgery Study

The Early vs. Late Infantile Strabismus Surgery Study Group is a group of strabismologists and orthoptists who investigate whether early or late surgery is preferable in infantile strabismus, in a non-randomized, prospective, multi-centre trial. Infants between 6 and 18 months of age will receive a standardized entry examination and then be operated either before their second anniversary in clinics A, or between their 32nd and 60th month of age in clinics B. The children will be evaluated at age six. After completion of the study, the two groups can then be compared regarding degree of binocular vision, angle of strabismus and visual acuity of the worse eye relative to the better. Zentrum zur methodischen Betreuung von Therapiestudien, Mrs H. Dinkel, Universit?t Heidelberg, Im Neuenheimer Feld 305, W-69120 Heidelberg. 49.6221.565500. fax: 564195 Germany PD Dr. H.J. Simonsz, Orthoptics & Neuroophthalmology, Afdeling Oogheelkunde, University Hospital Dijkzigt, Dr. Molewaterplein 40, NL 3015 GD Rotterdam. 3 i. 10.4639222, ask for beeper 3394 fax: 4635105 The Netherlands PD Dr. med. G.H. Rolling, Schule für Orthoptik, Universit?ts-Augenklinik, Im Neuenheimer Feld 400, W-69047 Heidelberg. 49.6221.566627/34/39 fax: 565422 Germany Dipl.-Inform. Med. U. Haag, Universit?t Heidelberg, Zentrum zur methodischen Betreuung von Therapiestudien, Im Neuenheimer Feld 305, W-69120 Heidelberg. 49.6221.564192 fax: 564195 Germany Dr. A. Deák, Augenklinik, Korányi Fasor, U-6720 Szeged. 36.62.12321/10822 fax: 22826 Hungary Mr P. Fells, F.R.C.S., F.C. Ophth., Lower Corridor Suite, Moorfields Eye Hospital, City Road, ECIV 2PD London. 44.71.2533411 fax: 2534696 (lower corridor suite) England Prof. R. Frosini, Istituto di Clinica Oculista dell' Universita di Firenze, Insegnamento di Ottica Fisiopatologica, Viale Morgagni 85,1-50134 Florence. Dr. R. Gomez de Lia?o, Nu?ez de Balboa 81, E-28006 Madrid. 34.1.5763229/72318 Spain Dr. O. Haugen, Orthoptic Department, Department of Ophthalmology, University of Bergen, N-3021 Bergen. Norway Dr. med. G. Klainguti, Clinique Ophtalmique, 15 Av. de France, CH-1004 Lausanne. 41.21.9637696/250211 Switzerland Prof.Dr. K. Krzystkowa, Ophthal. Clinic Medical Acad., 38 Copernika Str, P-31501 Krakow. 4812.223272/215210/210460/214577/220411 Poland M.C.M.E. van Lammeren, Afdeling Orthoptie, Dienst Oogziekten, U.Z. St. Rafa?l, Kapucijnenvoer 33, B-3000 Leuven. Prof. G. Lennerstrand, Institutionen for Oftalmiatrik, Huddinge sjukhus, S-14186 Huddinge. 46.8.7461000/3854/3418 Sweden Dr. med. H. Luka, Abt. f. Schielen, Schwachsichtigkeit und Bewegungsst?rungen des Auges, Allgem. ?ffentl. Krankenhaus der Landeshauptstadt St. P?lten, A-3100 St. P?lten. 43.512.85597/5040 43.2742.62521 (Klappe 2869) Dr. V. Paris, Rue de Luxembourg, 48, B-6900 Marche-en-Famenne. 32.84314749 Belgium Dr. L.J.J.M. Prick-Wenniger, Afdeling Oogheelkunde, A.M.C., Meibergdreef 9, NL 1105 AZ Amsterdam. 31.20.5663881/6715637 The Netherlands Prof. M.A. Quéré, 19, Rue Voltaire, F-44000 Nantes. 33.40.738370/083406 fax: 084649 France Dr. F. Reich-d'Almeida, Rua Castilho, No 65.z:Dto, P-1200 Lissabon. 351.1520619 Dr. med. R. Weidlich, Universit?ts-Augenklinik, Leninallee 8, O-4020 Halle. 37.4684.9878/81 Germany.     

Cochlin及其编码基因凝血因子C同源物（COCH）在形觉剥夺性近视豚鼠眼球后极部组织的表达

目的　探讨Cochlin及其编码基因凝血因子C同源物（coagulation factor C homology，COCH）在形觉剥夺性近视（form-deprived myopia，FDM）豚鼠眼球后极部组织的表达。方法　选取3周龄的雄性健康三色豚鼠46只，随机分为2组，每组23只，饲养6周。正常对照组的双眼不予任何处理，FDM组的右眼为实验眼，左眼为自身对照，遮盖FDM组豚鼠的右眼，但不压迫右眼角膜和眼睑，保证右眼能自由瞬目。在遮盖后0周、2周、4周及6周时，分别测量两组豚鼠的屈光度、眼轴长度和角膜曲率半径；HE染色观察两组豚鼠后极部巩膜的厚度及形态变化；进行高通量蛋白质组学分析；实时荧光定量PCR检测COCH mRNA的表达量；Western blot检测Cochlin的蛋白表达水平。结果　遮盖前，两组豚鼠眼球的屈光度和眼轴长度双眼间差值（右眼-左眼）差异均无统计学意义（均为P>0.05）。遮盖后2周，相比对侧的左眼，FDM组右眼诱导出近视，眼轴相对延长；与正常对照组相比，FDM组右眼的屈光度下降，眼轴长度增加，差异均有统计学意义（均为P<0.05）。遮盖后4周和6周，FDM组的右眼相对左眼近视进一步加深，眼轴相对更加延长，近视度数和眼轴长度双眼间差值较正常对照组差异进一步加大，差异均有统计学意义（均为P<0.05）。遮盖前，遮盖后2周、4周及6周，两组豚鼠眼球的角膜曲率半径双眼间差值差异均无统计学意义（均为P>0.05）。遮盖后6周，HE染色结果显示，正常对照组右眼后极部巩膜的厚度正常，胶原纤维排列致密规则，未见断裂现象。然而FDM组右眼的后极部巩膜变薄，胶原纤维变细，变稀疏，间隙变大，且部分纤维出现断裂现象。蛋白质组学分析结果显示，正常对照组和FDM组间表达差异在1.3倍以上的蛋白共221种，其中100种上调，121种下调。其中Cochlin在FDM组豚鼠眼球后极部组织的表达量是正常对照组的3.77倍，升高趋势最明显。实时荧光定量PCR检测结果显示，遮盖后6周，在正常对照组和FDM组右眼后极部组织中，COCH mRNA的相对表达量分别为0.38±0.15和1.86±0.35。FDM组的相对表达量明显高于正常对照组，差异有统计学意义（P<0.05）。Western blot检测结果显示，在正常对照组和FDM组右眼后极部组织中，Cochlin与GAPDH的灰度比值分别为0.37±0.14和0.73±0.15。FDM组Cochlin的表达水平显著高于正常对照组，差异有统计学意义（P<0.05）。结论　FDM豚鼠眼球后极部组织中可检测到COCH mRNA和蛋白Cochlin的表达上调，提示COCH可能在FDM的发生发展中起到重要作用。     

American Uveitis Society Meeting, May 13,1995 Fort Lauderdale, FL, USA

1 Confirmation of Bartonella henselae as the cause of cat scratch related acute neuroretinitis and prospective observation to its response to oral doxycycline and rifampin. Reed B, Smith R, Dolan M, Wong M, Scales D, Department of Ophthalmology & Infectious Disease, Wilford Hall Medical Center, Lackland AFB, TX, USA. 2 Recurrence rate of CMV retinitis in patients following pars plana vitrectomy and silicone oil injection. Marx JL, Thach AB, Reingold W, Terry B, Rao NA, Chong LP. Doheny Eye Institute, Los Angeles, CA, USA. 3 A PCR based assay for the diagnosis of AIDS related VZV retinitis. Margolis T, Short G, Schwartz D, Irvine A, Martin D, Francis I. Proctor Foundation, San Francisco, CA, USA. 4 Presumptive ocular sarcoidosis. Dodds EM, Lowder CY, Meisler DM. Division of Ophthalmology, Cleveland, OH, USA. 5 Prevalence of uveitis in an outpatient juvenile arthritis clinic. Akduman L, Tychsen L, Kaplan HJ, Washington University, St. Louis, MO, USA. 6 The role of choroidal dendritic cells in the pathogenesis of experimental autoimmune uveoretinitis. Choudhury A, Padhye NS, Caspi RR, Bowers WE, University of South Carolina School of Medicine, Columbia, S.C. and The National Eye Institute, Bethesda, MD, USA.     

BOOK REVIEWS

Book reviewed in this article:
THE MYOPIAS: Basic Science and Clinical Management Brian J. Curtin. Philadelphia: Harper and Row, 1985 .
CHANDLER & GRANT'S GLAUCOMA David L. Epstein, 3rd edition, Philadelphia: Lea & Febiger, 1986, pp. 539, $118–25. ISBN 08121 0972 4 .
THYROID EYE DISEASE Devron H. Char, 1st edition, Baltimore: Williams and Wilkins, 1985, pp, 227, $134.00 .
POCKET CONSULTANT. OPHTHALMOLOGY Patrick D. Trevor-Roper. 2nd edition, Oxford: Blackwell, 1985, pp. 95, $19.50 .
THE EYE IN SYSTEMIC DISEASES Jack J. Kanski. London: Butterworths, 1986, pp. 249 $75.00 .
MICROPIGMENTATION Zwerling, Christiansen, Goldstein et al. Slack Inc, 1986, pp. 234 .
REFRACTIVE CORNEAL SURGERY Edited by Donald R. Sanders, Robert F. Hofman and James J Salz. Slack Inc, $129.00 .     

BOOK REVIEWS

Book reviewed in this article:
EYE DISEASES IN HOT CLIMATES John Sandford-Smith. Bristol: John Wright & Sons, 1986. ISBN 0 7236 0749 4. Also available in paperback .
PERIPHERAL IRIDECTOMY. SURGICAL: ARGON: YAG Arthur Lim Siew Ming. Singapore: PG Publishing, 1987, pp. 86, 100 colour illustrations, £54.00. ISBN 9971 973 86 3 .
RADIAL KERATOTOMY: SURGICAL TECHNIQUE R. F. Hofmann, R. L. Lindstrom, A. C. Neumann, J. J. Salz, G. W. Tate, S. P. Thornton. Thorofare, New Jersey: Slack, 1986, pp. 137, £67.75 .
TEXTBOOK OF GLAUCOMA M. Bruce Shields. Baltimore: Williams and Wilkins, 1987, pp. 549,£240.00. ISBN 0 683 07694 9 .
GLAUCOMA Edited by J. A. McAllister FRCS and Richard P. Wilson MD. London: Butterworths, 1986, pp. 278, £190.00. ISBN 0 407 02343 7 .
NEURO-OPHTHALMOLOGY REVIEW MANUAL Frank J. Bajandas, Lanning B. Kline. Second Edition Thorofare, New Jersey: Slack 1987, pp. 176, £A44.95. ISBN 0 943432 96 0 .
OPHTHALMIC NURSING Rosalind Stollery. Southampton: Blackwell Scientific, 1987, pp, 261, £A38.95. ISBN 0 632 01S15 2 .
ADLER'S PHYSIOLOGY OF THE EYE: CLINICAL APPLICATION Edited by Robert A. Moses and William Hart, Jr. Eighth edition. St Louis, CV. Mosby, 1987, pp, 709 .     

American Uveitis Society Meeting October 31, 1994 San Francisco,California

1 Ophthalmic manifestations of presumed rifabutin-related uveitis. Arevalo JF, Freeman WR, La Jolla, CA, USA.

2 Diagnosis of toxoplasmosis acute anterior uveitis by PCR. Cano J, Diaz M, Navee A, Maldonado M, Barcelona, Spain.

3 Neuroretinits in patients with AIDS. Berger B, Austin TX, USA.

4 Presumed varicella zoster retinitis in a pediatric patient with AIDS. El Baba F, Nachman S, Stony Brook, NY, USA.

5 ARN with hypopyon caused by EVB and herpes type VI viruses. Cano J, Diaz M, Navea A, Maldonado MJ, Barcelona, Spain.

6 CD8⁺ T-lymphocytes and ocular infections in HIV⁺ patients. Lowder CY, Butler CP, Dodds EM, Recillas-Gispert C, Cleveland, OH, USA.

7 Intravitreal foscanet for persistent CMV. Lieberman RM, Orellana J, New York, NY, USA.

8 Perfluorocarbon liquid versus air-fluid exchange during surgical repair of retinal detachment caused by cytomegalovirus retinitis in patients with AIDS. Sery T, Gomes J, Sando R, Dua H, Donoso L, Vrabec T, Philadelphia, PA, USA.

9 Endogenous ophthalmitis simulating retinoblastoma: a report of six cases. Shields J, Shields C, Eagle R, Barrett J, DePotter P, Philadelphia, PA, USA.

10 Ocular lymphoma resembling chronic postoperative endophthalmitis. Fox G, Chan CC, Whitcup SM, Nussenblatt R, Bethesda, MD, USA.

11 A phase II trial of combination chemotherapy for primary central nervous system lymphoma. Whitcup SM, Stark-Vanes V, Nussenblatt RB, Heiss H, Witte R, Bethesda, MD, USA.

12 Cancer-induced autoimmune retinopathy. Thirkill C, Sacramento, CA, USA.

13 Leukocytoclastic vasculitis. Tessler H. Chicago, IL, USA.

14 Bilateral choroidal neovascular membranes after Candida albicans chorioretinitis. Dodds E, Townsend-Pico W, Lowder CY, Lewis H, Cleveland, OH, USA.

15 An unusual complications of Toxoplasma retinochoroiditis. Gormley PD, Flaxel CJ, Pavesio CE, Conrad DK, Lightman S, London, UK.

16 Surgical removal of a choroidal neovascular membrane in sympahtetic ophthalmia. Conrad DK, McCluskey PJ, Schwartz S, Gregor Z. Lightman S, London, UK.

17 Peripheral laser scatter ablation in pars planitia. Park SE, Mieler WF, Pulido JS, Milwaukee, WI, USA.     

复方血栓通胶囊联合氪激光治疗糖尿病性视网膜病变的疗效观察

目的观察应用复方血栓通胶囊联合氪激光治疗糖尿病性视网膜病变的疗效。方法对300例 (420只眼)随机分组、对照治疗。根据FFA造影结果分型,行视网膜次全光凝、全光凝。光凝能量、范围及光斑大小视病情而定。治疗组200例(286只眼),光凝后口服复方血栓通胶囊每日3次,每次3片,维生素C 200mg每日3 次,维生素E 100mg每日3次;而对照组100例(286只眼)口服维脑路通300mg每日3次,维生素C 200mg每日3 次,维生素E 100rng每日3次,持续服药一年。治疗前常规检查视力、眼底、FFA及眼压。结果治疗组用药后每隔半月复查视力、眼底。显效56只眼(19．5％),有效182只眼(63．6％),总有效率达83．1％。无效48只眼(16． 9％)。对照组:显效15只眼(15％),有效47只眼(47％),总有效率达62％。无效38只眼(38％)。眼底表现远不如治疗组理想,经卡方检验P<0．05,两组差异有显著性。结论复方血栓通胶囊联合氪激光治疗糖尿病视网膜病变有较好疗效,能改善视力,减少视网膜光凝量,缩短病程,提高疗效。     

Toxoplasmosis

Toxoplasmosis is the most common cause of posterior uveitis in immunocompetent subjects. The infection can be congenital or acquired. Ocular symptoms are variable according to the age of the subject. For instance, young children present with reduced visual acuity, strabismus, nystagmus, and leucocoria, while teenagers and adults complain of decreased vision, floaters, photophobia, pain, and hyperemia. Toxoplasmic retinochoroiditis typically affects the posterior pole, and the lesions can be solitary, multiple or satellite to a pigmented retinal scar. Active lesions present as grey-white focus of retinal necrosis with adjacent choroiditis, vasculitis, hemorrhage and vitreitis. Cicatrization occurs from the periphery towards the center, with variable pigmentary hyperplasia. Anterior uveitis is a common finding, with mutton-fat keratic precipitates, fibrine, cells and flare, iris nodules and posterior synechiae. Atypical presentations include punctate outer retinitis, neuroretinitis, papillitis, pseudo-multiple retinochoroiditis, intraocular inflammation without retinochoroiditis, unilateral pigmentary retinopathy, Fuchs'-like anterior uveitis, scleritis and multifocal or diffuse necrotizing retinitis. The laboratory diagnosis of toxoplasmosis is based on detection of antibodies and T. gondii DNA using polymerase chain reaction (PCR). Toxoplasmosis therapy includes specific medication and corticosteroids. There are several regimens, with different drug combinations. Medications include pirimetamine, sulfadiazine, clindamycin, trimethoprime-sulphamethoxazol, spiramycin, azithromycin, atovaquone, tetracycline and minocycline. The prognosis of ocular toxoplasmosis is usually good in immunocompetent individuals, as long as the central macula is not directly involved.