FMD control strategies.
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Biomedical subjects
Publications and source records attributed to J Clapp.
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A placental embolization model in the fetal lamb was used to examine the relationship between acute and chronic alternations in placental vascular resistance and changes in flow velocity waveforms as measured by Doppler and electromagnetic flow probes. The peak systolic to end-diastolic (S/D) ratio measured by these techniques was .885 and the correlations between Doppler S/D ratio and placental vascular resistance in the acute and chronic situations were .86 and .339, respectively. This preliminary data suggest that flow velocity waveforms are independent of the method used and that remarkable differences occur in the placental microcirculation during acute and chronic embolization.
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A 51-year-old man with serologically confirmed Rocky Mountain spotted fever was believed to have inappropriate antidiuretic hormone (ADH) secretion. He was observed for four days in the hospital until the correct diagnosis was made. During this period, he progressively became more hyponatremic, despite a low BUN level and the administration of large amounts of sodium and water. At the time, his serum sodium concentration was 117 mEq/liter, and his urine was hypertonic to that of serum. Thereafter, his serum sodium level rose with fluid restriction. Rickettsia-induced CNS damage may have lead to the inappropriate ADH release that was observed in this patient.
Described are the clinical course and renal morphologic findings in a patient with membranoproliferative glomerulonephritis. intially, the patient had a pure form of membranoproliferative glomerulonephritis but after a 3 year course, it became crescentic. After a renal allograft was performed, membranoproliferative glomerulonephritis recurred within 1 month in a pure form and subsequently developed into the crescentic form. This change occurred in the host kidney as well as in the allograft immediately after immunosuppressive and steroid therapy was discontinued.
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Various drugs brought about a reduction of serum progesterone level irrespective of whether or not a potent inducer (phenobarbital, 4-methyl-coumarin) or a hepatotoxin (carbon tetrachloride, alpha-naphthylisothiocyanate, coumarin) has been administered. The decrease by hepatotoxins was highly significant during the estrus phase of the cycle. These treatments affected the hepatic level of progesterone and altered the uptake of [4-14C]progesterone in vivo. The serum level of progesterone was significantly decreased by phenobarbital and carbon tetrachloride; however, the incorporation into the liver was enhanced by phenobarbital and reduced by carbon tetrachloride. This opposing hepatic action showed selectivity; phenobarbital increased the oxidative pathway of progesterone metabolism (formation of 6 beta-, 16 alpha-, 20 alpha-hydroxyprogesterone) but the reductive pathway remained unaltered (formation of pregnanediol, pregnanolone). Conversely, carbon tetrachloride diminished oxidation and raised reduction of progesterone. These results have been confirmed by measurements of progesterone metabolism in vitro using isolated microsomes. Phenobarbital brought about an induction of progesterone 16 alpha-, 6 beta- and 20 alpha-hydroxylase, did not affect progesterone delta 4-5 alpha-dehydrogenase, whereas carbon tetrachloride inhibited hydroxylase and raised dehydrogenase activities. The action of these test compounds on serum and liver levels of progesterone and on the variation of progesterone metabolism seemed to be related to changes manifest in the function of the hepatic endoplasmic reticulum. Similar changes might be associated with the development of mild hepatic lesions induced by various steroids.