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Biomedical subjects

R Turss

Publications and source records attributed to R Turss.

At least 19 recordsLinked to original sources
PubMed1980

[Diagnosis and treatment of neuroparalytic zoster keratitis (author's transl)].

In severe zoster keratitis many pathogenic factors are involved. In addition to viral manifestations, the cornea is often affected by anterior uveitis or secondary glaucoma. Neuroparalytic keratitis causes lowered blinking frequency and decreased tear secretion. In addition, zoster ulcerations of the upper lid margin mechanically disturb reformation of the tear film and weaken the lipid layer by necrosis of the Meibomian glands. Ointments reduce break-up time and parasympathicolytic mydriatics further decrease tear secretion. When the average time between two blinks is shorter than the tear film break-up time, a "dry eye" condition usually develops. The appropriate treatment in such cases is thorough prevention of evaporation.

Bandages↗
PubMed1979

[The artificial epithelium in chronic corneal diseases and to avoid emergency keratoplasty (author's transl)].

Report on the treatment of 41 patients in the last 10 years. In chronic corneal diseases epikeratoprosthesis is possible when every other therapy failed. With growing experience functional results are better and complications seldom. Since several years we use glued-on contact lenses in acute ulcers too in order to avoid emergency keratoplasty. When suitable donor material is missing or if plastic surgery of the eye lids is necessary the artificial epithelium prevents ulcer perforation as a mechanical collagenase inhibitor. The anterior chamber can be reinstalled in perforated ulcers by sealing with cyanoacrylate glue and covering with artificial epithelium. A corticosteroid therapy of the iritis becomes possible to avoid the frequent complication of anterior synechia in later keratoplasty. By reducing the steroid dosis vascularisation of the ulcer is reached and a corneal grafting can be evaded sometimes if the prognosis of keratoplasty is poor or the central cornea is clear such as in ulcers near the limbus.

Adrenal Cortex Hormones↗
PubMed1979

[Trophic corneal diseases. Their pathogenesis and corneal nutrition (author's transl)].

Experimental research has not provided any proof that "trophic" corneal diseases are caused by nutritional deficiencies. It seems that cases in which the course is chronic, but characterized by an absence of exacerbations of great pain and failure of medical therapy, are said to be trophic. Some of these diseases are dry eye conditions. Sensory disturbances lead to corneal complications by lowering the blinking frequency, but not seem to interfere with nutrition of the tissue. Otherwise keratoplasty would be impossible, since the innervation of the graft is often impaired for months or even years.

Chronic Disease↗
PubMed1978

[Metabolite changes and ulcer formation in the cornea. Experiments with acid burns of varying severity (author's transl)].

Acid burns with 0,25 n H2SO4 constantly cause mild corneal opacities. Burns with 2 n acid are too severe to be investigated for more than one week. Lactate and pyruvate levels drop in the aqueous and, less pronounced, in the cornea. A very similar decrease of glucose levels in aqueous and cornea can be found depending in its degree on the acid concentration used. In milder burns the levels return to normal within 2--3 weeks. The results can be explained by changes of the blood-aqueous barrier and of the rate of aqueous flow. It seems very unlikely that the metabolite changes cause the formation of corneal ulcers, as severe ulcerations can be found along with almost normal metabolite levels.

Animals↗
PubMed1975

[Prenatal chorio-retinitis transmitted by golden hamsters (author's transl)].

Two children of mothers who, in the second half of pregnancy, had been in touch with golden hamsters, had an internal hydrocephalus at birth and extensive chorio-retinitic scars in both eyes. One newborn also had myopia magna, the other severe bilirubinaemia. Increasing titres of neutralizing serum antibodies in both mothers and children and falling titres of complement-binding serum antibodies against the virus of lymphocytic chorio-meningitis argue for a causative role of this micro-organism, apparently transmitted by the hamsters.

Animals↗