Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 81-year-old man with a history of chronic pulmonary disease due to heavy smoking and ischemic heart disease had been suffering for the past few years from chronic constipation and urinary incontinence and was receiving medication for cardiopulmonary symptoms and urinary incontinence. He was admitted for repeated falling for a few months prior to admission. When put in the supine position, his blood pressure fell. He had bilateral pulmonary rales, consistent with lung disease, eccentricity of the left pupil (after cataract surgery), constriction of the right pupil, and absence of the pupillary light reflex. There was generalized hyperreflexia and a bilateral Babinski sign. He had normocytic, normochromic anemia; B12, folic acid and ferritin were within normal ranges, ESR was rapid, there was hyperglobulinemia (IgA and IgG), urea nitrogen and creatinine were increased but returned to normal after rehydration. ECG and chest X-ray were consistent with his cardiopulmonary status. Bone-marrow biopsy showed hypocellularity. IVP and barium enema were normal. Echocardiography revealed a possible old posterior wall myocardial infarction. CT-scan showed moderate cerebral and cerebellar atrophy, calcifications in the carotid and vertebral arteries, and small infarcts in both hemispheres. At this point, after an extensive survey of the literature, the diagnosis of Shy-Drager syndrome was proposed and proved by monitoring ECG and serum levels of noradrenaline during postural changes. He was treated with Fluorinef and there were no more episodes of postural hypotension. Several weeks after discharge he reported that he was feeling well and had not fallen since discharge.
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PMID:[Shy-Drager syndrome]. 775 2

We assessed components of lenticular short-circuit current in adult hypertensive Dahl salt-sensitive rats (DS) during chronic control (0.4% sodium) versus high (3% sodium) dietary NaCl intake begun at the age of 4 weeks until rats were studied. We also evaluated the influence of barium, a potassium channel blocker, and ouabain, a specific inhibitor of Na+, K(+)-ATPase activity, by adding them to the anterior lens surface, thus measuring barium-sensitive, ouabain-sensitive, and barium- and ouabain-in-sensitive short-circuit currents. During control NaCl intake, short-circuit current in DS and their control group, Dahl salt-resistant rats (DR), did not differ significantly. DS were subclassified into cataract-prone rats and rats unlikely to develop cataracts on the basis of their initial pressor response to the change from a normal to high NaCl diet during the first weeks of age. Although only transparent lenses were studied, total lens short-circuit current was already markedly decreased in the cataract-prone subgroup compared with DS unlikely to develop cataracts and control DR. This was in sharp contrast to the increase in short-circuit current previously reported in Sprague-Dawley rats and now observed in control DR in response to high dietary NaCl. The decrease in lens short-circuit current in cataract-prone rats was associated with lower absolute values of barium- and ouabain-sensitive short-circuit currents as well as with low barium- and ouabain-insensitive short-circuit current. Although the barium- and ouabain-sensitive components of the short-circuit current were similar in DS unlikely to develop cataracts and DR, the barium- and ouabain-insensitive component of the short-circuit current was lower in DS unlikely to develop cataracts than values in DR. Interestingly, this component of lens short-circuit current also increased in DR during chronic high NaCl, whereas the opposite change occurred in cataract-prone DS and DS unlikely to develop cataracts. Thus, the barium- and ouabain-insensitive short-circuit current may be a mechanism that protects the normal lens from developing cataracts. Possible candidates for this short-circuit current component are voltage-dependent potassium channels, calcium-activated potassium channels, or both. Our studies show altered lens short-circuit current in response to high NaCl intake in cataract-prone DS and suggest the possibility of altered lens potassium transport during sustained hypertension but before loss of lens transparency.
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PMID:Altered lens short-circuit current in adult cataract-prone Dahl hypertensive rats. 879 30