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Biomedical subjects

F Kern

Publications and source records attributed to F Kern.

At least 127 records · Page 7Linked to original sources
PubMed1976

Effects of ethinyl estradiol and phenobarbital on bile acid synthesis and biliary bile acid and cholesterol excretion.

Bile acid synthesis calculated from respiratory (14)CO2 derived from the catabolism of [26 or 27-(14)C]cholesterol to bile acids in rats with intact enterohepatic circulations decreased 50% after 5 days of ethinyl estradiol treatment (5 mg per kg per day). Maximal derepressed bile acid synthesis, measured as biliary bile acid excretion after bile acid pool depletion, was also reduced 50% by ethinyl estradiol treatment. Because ethinyl estradiol did not alter biliary cholesterol excretion, bile contained less bile acid relative to cholesterol. Hepatic bile acid concentration was not increased by ethinyl estradiol treatment. Because the inhibitory effect of ethinyl estradiol on bile acid synthesis required 5 days of treatment it is concluded that bile acid synthesis probably was not reduced by negative feedback repression of 7alpha-hydroxylase, the rate-limiting enzyme in bile acid synthesis, which has a half-life of 2 to 3 hr. During the first 14 hr after bile duct cannulation, before bile acid pool depletion, ethinyl estradiol-treated rats excreted less than one-half as much bile acid and the same amount of cholesterol as controls. The bile acid to cholesterol ratio was therefore decreased. Rats treated simultaneously with phenobarbital and ethinyl estradiol excreted significantly more bile acid than rats treated with ethinyl estradiol alone, but biliary cholesterol excretion was not increased. The proportion of biliary bile acid relative to cholesterol was thereby restored to the control value. In contrast, after 14 hr of bile drainage and depletion of the bile acid pool, rats treated with ethinyl estradiol and those treated with phenobarbital-ethinyl estradiol excreted the same amount of bile acid. Thus, when phenobarbital is administered with ethinyl estradiol, it increases the bile acid pool size and biliary bile acid excretion, but it does not increase bile acid synthesis. The increase in pool size and biliary bile acid excretion might be due to the phenobarbital-induced increase in ileal absorption of bile acids.

Animals↗
PubMed1976

Prednisone therapy for alopecia areata. A follow-up report.

Eighteen patients treated with prednisone on alternate days for varying degrees of alopecia areata (AA) were examined a mean of 15 months after discontinuation of the drug. Despite an initial response to the therapy, long-term benefit was not thought to be substantial. Numerous side effects related either to systemic corticosteroids or to AA were apparent during the course of therapy, as well as at the time of the evaluation reported herein. Acne, obesity, lenticular opacities, mild hypertension, and impaired adrenocorticotropic hormone (ACTH) reserve were among the findings noted. Long-term treatment was not accompanied by an obvious beneficial change in the natural course of AA. Because of the potentially serious side effects and the lack of substantial improvement in the eventual course, alternate-day prednisone therapy is not recommended for long-term use in AA.

Adolescent↗
PubMed1975

Measurement of bile acid synthesis by 14CO2: the metabolism of propionyl CoA.

The relationship between 14CO2 evolution from the catabolism of [26 or 2714C] cholesterol to bile acids was studied in rats with biliary fistulae. When equal quantities of [26 or 2714C] cholesterol and [414C] cholesterol were administered, there was a significant linear relationship between 14CO2 expiration in the breath and [414C] bile acid excreted in the bile. Bile acid synthesis calculated as the ratio of 14CO2: molar specific activity of biliary cholesterol correlated highly with biliary bile acid excretion in the bile acid depleted rat. Phenobarbital, a known inducer of gamma-amino levulenic acid formation from succinyl CoA did not alter the relationship between the 14CO2 estimation of bile acid synthesis and biliary bile acid excretion, indicating that the relationship between [26 or 2714C] cholesterol side chain cleavage and 14CO2 formation was not altered. Phenobarbital, however, did cause a reduction in bile acid synthesis measured by 14CO2 evolution and by biliary bile acid excretion. The 14CO2 method underestimated bile acid excretion. 8.7% in untreated and phenobarbital treated rats respectively. Since 11% of the radioactivity which was expired as 14CO2 was isolated as bile acids, radioactivity cleaved as [1 or 314C] propionyl CoA may enter cholesterol-bile acid biosynthesis resulting in the underestimation of bile acid synthesis. To test whether radioactivity from propionyl CoA enters steroid biosynthesis [114C] propionate and [214C] propionate were given to untreated biliary fistula rats and the biliary lipids excreted in 60 hours were analyzed. Incorporation of radioactivity into cholesterol and bile acids was greater after the administration of [214C] propionate than after [114C] propionate than after [114C] propionate, suggesting that radioactivity from propionyl CoA may enter steroid biosynthesis by metabolic events in which the methylene and carboxyl carbon atoms are differentiated. Although the use of 14CO2 expiration from [26 or 2714C] cholesterol catabolism underestimates the rate of bile acid synthesis, it should have many applications because of the constant relationship between 14CO2 formation and cholesterol side chain cleavage.

Animals↗
PubMed1975

Persistent hypotension and intestinal infarction in a patient with primary amyloidosis.

A patient with primary amyloidosis and the nephrotic syndrome had diarrhea and gastrointestinal bleeding probably due to intestinal ischemia. He died with extensive intestinal infarction. The infarction was most likely caused by decreased splanchnic perfusion secondary to the chronic hypotension of the nephrotic syndrome and to amyloid deposition within the walls of the small blood vessels supplying the gut. Although amyloidosis was suspected prior to death, a fixation artifact probably prevented the correct antemortem biopsy diagnosis.

Aged↗
PubMed1975

In vivo effect of bile salts and cholestyramine on intestinal anaerobic bacteria.

In vitro studies have shown that some bile salts inhibit the growth of intestinal bacteria. We investigated the possibility that bile salts might have a similar action in vivo in the ileum by performing serial anaerobic cultures and bile salt analyses on postprandial ileal fluid obtained anaerobically via intestinal tube. Five subjects were studied under control conditions, and after a 1-week course of orally administered cojugated bile salts in a dose shown to increase the bile salt pool. Three of the subjects were also studied after a 1-week course of cholestyramine. The numebr of ileal anaerobic microorganisms decreased significantly after both bile salt and cholestyramine treatment. Ileal bile salt concentrations were generally high (mean 9.2 mM) and did not change significantly after either bile salt or cholestyramine treatment. The results of this study are unexplained. Although it is possible that bile salts play a role in the regulation of small intestinal anaerobic flora, the lack of a relationship between ileal bile salt concentration and population levels of anaerobic organisms is puzzling and raises further questions about such a role for bile salts.

Adult↗
PubMed1974

The treatment of retained stones in the common bile duct with sodium cholate infusion.

Six patients with stones retained in the common bile duct after cholecystectomy and common duct exploration were treated by intraductal infusion of a sodium cholate solution. In the five patients whose stones were between the T-tube and the duodenum the treatment was successful within a few days. A stone became transiently impacted in the ampullary region soon after beginning therapy in three patients and produced mild pancreatitis in two. The only failure was in a patient whose stone was between the T-tube and the liver.

Adult↗