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Biomedical subjects

J G Bellows

Publications and source records attributed to J G Bellows.

At least 55 records · Page 3Linked to original sources
PubMed1977

[Preferential screening to prevent glaucoma blindness (author's transl)].

The chief barrier to formulating an effective program of preventing glaucoma blindness is the difficulty of identifying those individuals in the population who have glaucoma but do not know it and those who are likely to develop the disease. Primary open-angle glaucoma (POAG), the most common tupe of glaucomatous disease, is an inherited disease. Fifty percent of all patients who have POAG also have a family history of glaucoma. Further, it is estimated that six to seven percent of the first degree relatives of POAG patients will develop POAG. This information suggests that for ophthalmologists who are likely to have limited time available for glaucoma screening, the most practical glaucoma screening program is that which is directed at those individuals who are first degree relatives of patients known to have glaucoma. For these people, the minimal screening tests should include tonometry, perimetry, and a meticulous examination of the optic discs. If tonometric testing reveals an intraocular pressure of 21-23 mmHg, tonometry should be repeated at different hours of the day. If results of these tests are negative, the patient then should be tested for increased sensitivity to corticosteroids and epinephrine. If all tests are negative, the patient still should be tested periodically. A relationship between HLA antigens and primary open-angle glaucoma has not been confirmed.

Glaucoma↗
PubMed1977

[Anthropogenic catatacts (author's transl)].

The traditional theories of senile cataract formation have one common denominator. Nearly all the agents and factors heretofore ascribed as causes of cataract formation have some element involving a potent crosslinking agent. The factors considered in this paper include endocrine and metabolic factors, involutional and hereditary influences, nutritional deficiencies, osmotic changes, ionizing radiation, ultraviolet light, altered capsular permeability, and the cumulative effects of subliminal exposure to noxae. Throughout life, the human lens is exposed to the influence of numerous potent crosslinking agents and it now appears that the cumulative actions of crosslinkage is the chief cause of senile cataracts. If this theory proves to be correct, it will offer some hope that cataract formation can be retarded by agents which counteract crosslinkage or by avoidance of excessive exposure to crosslinking agents.

Aging↗
PubMed1976

Crosslinkage theory of senile cataracts.

The theory of crosslinkage as a cause of aging of all living organic tissues has withstood the test of time. Nearly all the past theories of senile cataract formation contain elements involving a potent crosslinking agent. Therefore crosslinkage may now be recognized as the common denominator in past theories of senile cataracts. This paper proposes that crosslinkage is the mechanism for senile cataract formation.

Aged↗