Digoxin-like immunoreactivity detected in cerebrospinal fluid of humans with fever.
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Biomedical subjects
Publications and source records attributed to N Krivoy.
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A nosocomial outbreak of fulminant hepatitis B infection at a medical center in Haifa, Israel, between 7 and 26 June 1986, involved five patients who had been hospitalized previously in the medical ward in late April and early May (first generation). This outbreak had an unusual clinical course, with fulminant hepatic failure associated with acute renal failure from acute glomerulonephritis, leading to death within a few days. The onset dates of hepatitis were tightly clustered temporally and incubation periods were short. Extensive laboratory and epidemiologic evaluation showed that the probable common-source vehicle of transmission was a multiple-dose vial of heparin and normal saline flush solution that may have been contaminated by blood of a known HBsAg carrier, who was positive for anti-HBe, hospitalized at the same time. A sixth patient died in August 1986 (second generation), after his initial admission in June that coincided with the terminal hospitalizations of three first-generation patients. Those patients had marked coagulopathies, and transmission to the sixth patient most probably occurred through environmental contamination by patients or through cross-contamination between patients through staff. The unusually high mortality rate (5 of 6) in this outbreak has not been definitely explained.
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Plasma digoxin-like immunoreactive factor(s) (DLIF) have been reported in various pathophysiological conditions associated with volume expansion and linked to the regulation of blood volume and pressure. We hypothesized that DLIF might be present in rapidly expanding gonadotropin-stimulated ovarian follicles. The mean total and free DLIF concentrations in the follicles (n = 9) studied were 4925 nmol/L and 1885 nmol/L, respectively. These concentrations were substantially higher than the plasma total and free DLIF levels in these women: 1216 nmol/L and 158 nmol/L, respectively (p less than 0.0001). The plasma DLIF levels in the gonadotropin-treated women were comparable to those in term pregnant women, which are known to be higher than those in non-pregnant women. The ovary thus may be a source of DLIF in the plasma of gonadotropin-treated women, and DLIF may have a role in ovarian follicular fluid homeostasis.
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The objective of this study was to measure maternal total digoxin-like immunoreactive factor levels in singleton pregnancies with or without hypertension and in twin pregnancies. Plasma digoxin-like immunoreactive factor was measured in 113 third-trimester patients: 51 normotensives, 20 preeclamptics, 19 with latent or chronic hypertension, and 23 with twin pregnancies. The concentration of total digoxin-like immunoreactive factor in the twin gestations (1143 +/- 249 pg/mL) was significantly higher than that in either the normotensive pregnancies (890 +/- 161 pg/mL) (P less than .001) or in the hypertensive pregnancies (903 +/- 256 pg/mL) (P less than .01). However, there were no significant differences in digoxin-like immunoreactive factor levels between the normotensive and hypertensive groups. A trend of higher, although not statistically significant, levels of digoxin-like immunoreactive factor was noted in the chronic hypertensive group as compared with the preeclamptic patients (957 +/- 212 versus 852 +/- 288 pg/mL). We therefore conclude that digoxin-like immunoreactive factor does not contribute significantly to the pathogenesis or prediction of preeclampsia. The increased amount of digoxin-like immunoreactive factor in twin pregnancies may reflect a contribution from multifetal origin, or might be a physiologic adaptive mechanism allowing higher cardiac output by a possible cardiotropic effect.
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Submaximal histamine dose-response curves were obtained on 34 dogs divided into six groups. These groups were: A (n = 6) untreated; B (n = 6) after atropine (1 mg/kg); C (n = 5) after verapamil inhalation (10 mg total dose); D (n = 5) after verapamil inhalation (100 mg total dose); E and F (n = 6) as for C and D but pre-treated with atropine (1 mg/kg). Total lung resistance (R1) was measured in each case at increasing delivered concentrations of inhaled histamine and expressed as a ratio of baseline valve. For each group a composite mean curve was obtained and the maximal recorded responses (mean maximal resistance ratios) for the various groups were compared. It appears that the combination of verapamil inhalation (low dose) and atropine reduced the anticholinergic effect of atropine causing marked bronchoconstriction. This unexpected result depends on the verapamil dose since it was not present at the higher dose (group F).
The trough steady-state concentration of theophylline in plasma and stimulated saliva of 12 asthmatic children receiving an oral slow-release theophylline preparation was determined after 1 week of treatment. Plasma theophylline concentration ranged from 3.6 to 10.8 microgram/ml and saliva concentration ranged from 3.2 to 7.0 microgram/ml. There was an excellent linear relationship between theophylline concentration in plasma and stimulated saliva (r=0.89, p is less than 0.001). These observations suggest that theophylline therapy could be monitored routinely using stimulated saliva. This may be a convenient, painless and non-invasive alternative for routine monitoring of theophylline levels in asthmatic children.
Different, dose-dependent effects of verapamil inhalation on histamine-induced bronchoconstriction in anaesthetized dogs are reported. Cumulative histamine dose-response curves were obtained on three groups each consisting of six dogs. These groups were: A - after atropine sulphate (1 mg/kg); B - after atropine sulphate and verapamil (approximately 0.5 mg/kg); C - after atropine sulphate and verapamil (approximately 5.0 mg/kg). Total lung resistance (R1) was measured as the indicator of bronchoconstriction. The mean maximal response of R1 in B was significant greater (p less than 0.01) than in A and C, while no significant difference was observed between A and C. A possible mechanism is postulated.
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