Late obstruction after ureteroneocystostomy.
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Biomedical subjects
Publications and source records attributed to M Schiff.
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Probably one of the greatest problems in hearing aid fitting is to try to adapt hearing amplification to the recruiting ear. Sound is not loud enough, and then it is too loud. Microchips have permitted hearing aids to be smaller and smaller. However, they still remain either linear output- or input-compression types. Log-linear amplification permits the "smart aid" to automatically decrease the gain as the input power of speech or noise increases. This together with a patented low-frequency signal processor permits maximum discrimination with minimal violation of the patient's threshold of discomfort. This is a considerable step in ameliorating the major problem of the recruiting ear.
Tympanosclerosis is a preventable disease. Its elimination is more the responsibility of the pediatrician and general practitioner than the otolaryngologist's. The education of our colleagues is the most effective way of possibly eliminating this disease process. Cholesteatoma and tympanosclerosis may have similar causative factors, but certainly have different pathogenic developmental patterns; their occurrence together in otologic disease is coincidental. The mechanism of this disease process shows that the subepidermal and submucosal connective tissue layers of the eardrum are the ones involved. The cure for tympanosclerosis may be achieved more easily than its amelioration. This may seem like a strange paradox, but cure is intimately bound up with prevention which is the key for the clinical significance of this theory of pathogenesis. The pediatrician and the general practitioner, or family physician--the first to see the children with their ear problems--are urged to refer patients to an otologist when fluid is turbid. Development of tympanosclerosis must be prevented in the early but treatable stages. Prevention is less costly than repair.
It has been suggested that immune responses and resultant generation or release of inflammatory mediators play a role in otitis media with effusion (OME). To explore the potential of one such mediator to contribute to OME, the effects of histamine injected into the middle ear cavity were examined. Injection of histamine into the guinea pig middle ear was found to produce dilation and endothelial disjunction in capillaries, leading to striking mucosal edema and effusion which persisted for at least several hours. This response could be partially blocked by pretreatment with either H1 or H2 antihistamines. It is suggested that histamine released during immune responses in the middle ear may contribute to the formation of effusion and submucosal edema as observed in OME.
The immunogenicity of the middle ear constituents is a matter of prime importance. In this work, the authors were interested in the antigenicity of the guinea pig's tymphanic membrane. They reached the conclusion, after developing an antiserum (IgG), that the tympanic membrane of the guinea pig can be antigenic in the rabbit. After purification and absorption, a cross-reactivity remains between the tympanic membrane and the mucosae of the upper respiratory system.
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Renovascular hypertension can result from renal artery lesions involving the main renal artery, or its branches. It is generally felt that the elevation of blood pressure results from excessive systemic vasoconstriction secondary to enhanced renin secretion by one or part of one kidney. Renin secretion is enhanced because of constriction of the renal artery and resultant intrarenal ischemia. Clinically patients cannot be distinguished from those with essential hypertension and diagnosis must be made with arteriography although urography and isotope renography may suggest the diagnosis. Surgical cure can be predicted if differential renal vein renin ratios lateralize but a non-lateralizing study does not necessarily mean that surgery will fail. In properly selected patients, surgical results are excellent.
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