Mechanisms involved in the side effects of glucocorticoids

eMedicine创建于1996年，由近万名临床医师作为作者或编辑参与此临床医学知识库的建设，其中编辑均是来自美国哈佛、耶鲁、斯坦福、芝加哥、德克萨斯、加州大学等各分校医学院的教授或副教授。

eMedicine

The multifunctional choroid.

The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjogren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.

TFOS DEWS II pathophysiology report

Age-related macular degeneration: etiology, pathogenesis, and therapeutic strategies.

Because the organogenesis and physiology of the lens are essentially similar in various mammals, an understanding of the etiology and pathogenesis of the formation of cataract in an animal model will enhance our knowledge of cataractogenesis in man In this review, we summarize the background, etiology, and pathogenesis of cataracts that occur in rodents The main advantages of using rodent mutants include the well-researched genetics of the animals and the comparative ease of breeding of large litters Numerous rodent models of congenital and hereditary cataracts have been studied extensively In mice, the models include the Cts strain, Fraser mouse, lens opacity gene (Lop) strain, Lop-2 and Lop-3 strains, Philly mouse, Nakano mouse, Nop strain, Deer mouse, Emory mouse, Swiss Webster strain, Balb/c-nct/nct mouse, and SAM-R/3 strain The rat models include BUdR, ICR, Sprague-Dawley, and Wistar rats, the spontaneously hypertensive rat (SHR), the John Rapp inbred strain of Dahl salt-sensitive rat, as well as WBN/Kob, Royal College of Surgeons (RCS), and Brown-Norway rats Other proposed models for the study of hereditary cataract include the degu and the guinea pig Because of the ease of making clinical observations in vivo and the subsequent availability of the intact lens for laboratory analyses at different stages of cataract formation, these animals provide excellent models for clinicopathologic correlations, for monitoring of the natural history of the aging process and of metabolic defects, as well as for investigations on the effect of cataract-modulating agents and drugs, including the prospect of gene therapy

Rodent models of congenital and hereditary cataract in man.

A new method for light and electron microscopic localization of fluorescein-labelled dextran in ocular tissue using epoxy-resin embedding.

• We investigated the cytotoxicity of hydrogen peroxide by exposing primary cell cultures of human corneal epithelium to a single dose of this agent at concentrations ranging from 30 to 100 ppm. Hydrogen peroxide, at a concentration as low as 30 ppm, caused cell retraction as well as cessation of cell movement and mitotic activity. Formation of membranous vesicles preceded cell death that occurred by 7 to 8 hours after exposure to 30 ppm. With a concentration of 50 ppm, normal cell activity ceased almost instantaneously. Numerous surface vesicles formed by 1.5 hours of exposure, and the cells died by 4 to 5 hours. Higher concentrations of hydrogen peroxide (70 to 100 ppm) caused cell death within a few minutes. Because neutralization of hydrogen peroxide and patient compliance are critical in the proper use of hydrogen peroxide-based contact lens disinfection systems, users will be well served if the long-term effects of residual peroxide on the cornea are subjected to continued study.

Brenda J. Tripathi

Papers

Rodent models of congenital and hereditary cataract in man.

A new method for light and electron microscopic localization of fluorescein-labelled dextran in ocular tissue using epoxy-resin embedding.

Hydrogen Peroxide Damage to Human Corneal Epithelial Cells In Vitro: Implications for Contact Lens Disinfection Systems

Localization of sialic acid moieties in the endothelial lining of Schlemm's canal in normal and glaucomatous eyes.

Effect of oxygen on the developing retinal vessels of the rabbit: I. Anatomy and development of the retinal vessels of the rabbit