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Biomedical subjects

F Eisenberg

Publications and source records attributed to F Eisenberg.

At least 19 recordsLinked to original sources
PubMed1981

Selective hormonal control of myo-inositol biosynthesis in reproductive organs and liver of the male rat.

myo-Inositol biosynthesis has been examined in hypophysectomized and thyroidectomized male rats. After hypophysectomy, inositol-1-phosphate synthase [1L-myo-inositol-1-phosphate lyase (isomerizing), EC 5.5.1.4] in the reproductive organs and liver decreased markedly. At the same time, testicular acid phosphatase [orthophosphoric-monoester, phosphohydrolase (acid optimum), EC 3.1.3.2] and beta-glucuronidase (beta-D-glucuronide glucuronosohydrolase, EC 3.2.1.31) increased. Thyroidectomy caused a similar decrease in inositol-1-phosphate synthase in the liver but not in the reproductive organs. Follicle-stimulating in the liver but not in the reproductive organs. Follicle-stimulating hormone (follitropin) and luteinizing hormone (lutropin) restored the activity to at least normal levels in the testis, prostate, and seminal vesicle but not in the liver of hypophysectomized animals. Triiodothyronine and thyroxine stimulated liver synthase 30-fold in hypophysectomized animals. We conclude that inositol-1-phosphate synthase in the reproductive organs is under more or less direct control of the pituitary; in the liver, the control is mediated through the thyroid.

Acid Phosphatase↗
PubMed1978

A longitudinal analysis of artificial insemination with donor semen.

A longitudinal analysis of artificial insemination with donor semen (AID) in 114 consecutive couples revealed a 37% over-all pregnancy rate. The 45 pregnancies occurred in 39 patients, and approximately 90% of these pregnancies occurred within six cycles of AID. Pregnancy rates were higher in the age group 25 to 30, in those who received only fresh semen, and in those with a history of a previous pregnancy. Lower pregnancy rates were observed in patients age 31 or older, in those with pelvic disease, and in those randomly receiving freshly thawed semen or fresh semen. The use of a vaginal device for retaining semen, the use of patient positioning, or the duration of infertility did not appear to affect the success rate. When surgically correctable pelvic disease was treated, a pregnancy rate of 22% was obtained.

Adolescent↗
PubMed1977

Unequivocal demonstration of fructose-1,6-bisphosphatase in mammalian brain.

Fructose-1,6-bisphosphatase (D-fructose-1,6-bisphosphate 1-phosphohydrolase; EC 3.1.3.11) has been found in rat brain and identified unequivocally. The enzyme has been purified to 95% homogeneity by standard procedures, including adsorption to a phosphocellulose column followed by elution with substrate. The purified enzyme exhibits a broad optimum above pH 7.6. Both fructose 1,6-bisphosphate and sedoheptulose 1,7-bisphosphate are substrates of this enzyme; the hydrolysis of the latter occurs at about 20% of the rate of the former, and the Km for fructose 1,6-bisphosphate is approximately 1.32 X 10(-4) M. 5'-AMP, an inhibitor of other mammalian-fructose-1,6-bisphosphatases, is without effect, and in further contrast with the other enzymes there is no metal requirement for activity. Purified brain enzyme fails to crossreact with the antibody prepared against the purified liver fructose-1,6-bisphosphatase. On the other hand, antiserum produced against the brain fructose-1,6-bisphosphatase quantitatively precipitates the enzyme activity and forms precipitin bands with preparations of brain fructose-1,6-bisphosphatase.

Animals↗
PubMed1976

Inhibition of glycolysis in brain by a phospholipid effect on interconversion of fructose phosphates. A possible regulatory control on utilization of glucose 6-phosphate.

Glucose 6-phosphate accumulation in 10,000 X g supernatant of rat brain was enhanced up to 16-fold by the addition of phosphatidylcholine, other common phospholipids, or linoleate. This glucose 6-phosphate is of endogenous origin via UDP-glucose and glucose 1-phosphate but not glucose. The accumulation is the result of inhibition of glycolysis by an effect of phospholipid on the interconversion of fructose 6-phosphate and fructose 1,6-bisphosphate. Brain is therefore capable of gluconeogenesis from fructose 1,6-bisphosphate. A regulatory function for phospholipid which coordinates glycolysis and other major routes of utilization of glucose 6-phosphate in brain, e.g. inositol synthesis, is proposed.

Animals↗
PubMed1975

Myoinosose-2 1-phosphate: an intermediate in the myoinositol 1-phosphate synthase reaction.

Partially purified testicular myoinositol 1-phosphate synthase was incubated with glucose 6-phosphate and NAD+. After 2 min the reaction was stopped by the addition of NaB3H4. Phosphorylated reduced sugars were isolated by ion exchange and dephosphorylated enzymatically. Scylloinositol and myoinositol, added as carriers, were re-isolated and purified to constant specific radioactivity. Since scylloinositol phosphate is uniquely related to myoinosose-2 1-phosphate, the finding of labeled scylloinositol and myoinositol is considered strong evidence for the presence of myoinosose-2 1-phosphate, an intermediate which has been postulated in the synthase-catalyzed isomerization of glucose 6-phosphate to myoinositol 1-phosphate. About one-half the amount of intermediate was demonstrable with boiled synthase, indicating firm binding of myoinosose-2 phosphate to the enzyme.

Animals↗
PubMed1973

The defect in the Hunter syndrome: deficiency of sulfoiduronate sulfatase.

Skin fibroblasts cultured from patients affected with the Hunter syndrome are deficient in the activity of a protein, named the "Hunter corrective factor," that is required for degradation of dermatan and heparan sulfates. We now show that this factor, purified from human urine, removes about 2% of the sulfate residues from [(35)S]mucopolysaccharide accumulated within Hunter fibroblasts; these groups are derived from "oversulfated" regions of the polymer. Acetone-powder extracts of fibroblasts derived from patients with the Hunter syndrome are deficient in this sulfatase, in contrast to similar extracts from fibroblasts of individuals of other genotype. Hunter corrective factor coupled to alpha-L-iduronidase (or alternatively, mixed extracts from Hurler and Hunter fibroblasts) release iduronic acid from 4-O-alpha-L-sulfoiduronosyl-D-sulfoanhydromannose. We conclude that the Hunter corrective factor is a sulfatase for sulfated iduronic acid residues.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1968

[Avilamycin].

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Anti-Bacterial Agents↗