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老年性白内障晶狀體上皮細胞超微結構觀察
目的研究老年性白内障晶狀體上皮細胞的超微結構,探討老年性白内障舆晶狀體上皮細胞凋亡關系.方法用透射電鏡對20例老年白内障及10例正常透明晶狀體上皮細胞的超微結構進行觀察,拍照.結果老年白内障組晶狀體上皮細胞中發現了典型的凋亡小體,正常對照組未見凋亡細胞.結論老年性白内障的發生舆晶體上皮細胞的凋亡有關.
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羊膜貼敷術的改進和臨床應用
羊膜貼敷術(amniotic membrane patching,AMP)在文獻上通稱羊膜移植術(amnioticmembrane transplantation,AMT).它和結、角膜移植本質上的區别在于,羊膜不是也不可能作為結膜和角膜上皮的替代物,它祗是作為一種上皮化的底物或保持膜,通過一系列羊膜生物學特性的發揮,促進相鄰的結膜和角膜上皮細胞的分化、增殖和移行,重建健康的眼表架構.從這個意羲上說,以羊膜貼敷術命名似比羊膜移植術更為貼切.本文述及的AMP是在學習傳統AMT實踐過程中,着眼于我國廣大城鄉的現有條件,對羊膜保存、手術方式和術後處理作了若幹簡化和改良,適應證有所擴大,特别對急性眼表燒傷病例,力求盡早手術.我們從1999年6月開始采用改良的AMP對各種眼表疾患的術後結果作了追踪觀察,發現其技術操作簡捷易行,療效確切.
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老年性白内障的氧化損傷與酶組織化學觀察
目的研究老年性白内障晶狀體上皮酶活性變化和氧化損傷對培養的牛晶狀體上皮細胞酶活性的影響.方法1取老年性白内障晶狀體和正常透明晶狀體進行酶組織化學染色,觀察SDH、LDH、G6PD、ATPase活性的變化.2觀察培養牛晶狀體上皮細胞氧化損傷后及維生素C治療后SDH、LDH、G6PD活性的改變. 結果1老年性白内障SDH、LDH、G6PD、ATPase活性降低.2培養的牛晶狀體上皮細胞經過氧化損傷后SDH、LDH、G6PD活性顯著降低,維生素C可使酶活性顯著提高.結論氧化損傷使能量産生减少,可能是白内障發生的原因之一,維生素C對氧化損傷具有部分保護作用.
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于福興實驗室研究計劃
1 Molecular regulation of corneal wound healing Rapid healing of the corneal epithelium in response to injury is essential for maintenance of its barrier function. The long-term goal of this project is to obtain basic information about the molecular and cell biology of corneal wound healing. The project will test the hypotheses that amyloid β/A4 precursor-like protein controls serine proteinase activity, mediates cell adhesion, and promotes cell migration during corneal reepithelialization. This study should provide the basis to begin constructing a detailed nap of the molecular pathways and interconnecting networks of proteins functioning in wound repair and to develop therapeutics for treatment of corneal diseases like recurrent erosions and persistent defects of the epithelium.2 Developing an ex vivo model for ocular irritation testThe objective of this project is to develop an ex vivo assay system to predict ocular irritation potential of test chemicals and consumer products. Our hypothesis has been that activation of these transcription factors and disruption of corneal integrity can be used as endpoints/ markers for evaluating ocular toxicity in organ culture. Our goal is to develop a sensitive, efficient, economical and reliable ex vivo model for predicting irritation potential of a chemical or consumer product with mechanistic basis.3 Modulation of epithelial barrier function during corneal infectionThe long-term goal of this project is to understand the mechanisms underlying the induction of the inflammatory reaction and breakdown of the epithelial barrier in the cornea upon infection. We will test the hypothesis that in the cornea TLRs confer responsiveness of HCE cells to pathogens, and PA challenge-induced TLR signaling, through activation of NF-?B and/ or mitogen-activated protein kinase (MAPK), contributes to infection-induced epithelial barrier breakdown. The following studies will be carried out. An understanding of how TLRs transmit signals that lead to epithelial response, including modulation of barrier function,may allow the development of therapeutic agents that prevent breakdown or enhance recovery of barrier function during infection and, as an adjuvant therapy, eliminate the corneal scarring and vision loss associated with bacterial keratitis.4 Developing an adjuvant therapy to reduce inflammatory response induced by bacterial infection of the cornea (bacterial keratitis).
