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Biomedical subjects

E Keller

Publications and source records attributed to E Keller.

At least 343 records · Page 19Linked to original sources

[Adrenoleukodystrophy (author's transl)].

A report on clinical course and morphological findings of a case of adrenoleukodystrophy in a 10-years-old boy is given. The brain showed the typical changes of a sudanophilic, inflammatory leukodystrophy in all lobes. Pathognomic intracytoplasmatic inclusions in the perivascular macrophages were found by electron microscopic examination. The adrenal glands showed a severe atrophy, but it was impossible to detect typical cytolpasmatic inclusions within the adrenocortical cells. By thin-layer chromatography an accumulation of cholesterol esters with very long chain fatty acids was found in the demyelinated areas. Findings diagnostic facilities and theories of pathogenesis are discussed.

Addison Disease↗

Postcoital contraception with an injectable estrogen preparation (Org 369 - 2).

In one-hundred women age 15 to 45, postcoital contraception was attempted with a "morning-after" injection consisting of 12.5 mg estradiol-benzoate and 10 mg of estradiol-phenylpropionate. Plasma estradiol-178, progesterone, LH, FSH and Prl were measured by specific radioimmunoassays and BBT was recorded. In 97.8% the injection was given within 48 hours after unprotected coitus. The medication induced minimal cycle and bleeding pattern changes. The rate of side effects was low. The incidence of pregnancies due to medication failure was 3%. The plasma hormone patterns before and under therapy are demonstrated and drug-induced changes discussed.

Adolescent↗

Cyclic AMP enhancement of depolarization-induced NAD(P)H changes in brain cortical slices.

The increased levels of NAD(P)H effected by electrical depolarization are markedly augmented in the presence of cyclic AMP, isoproterenol, or RO 20-1724, agents known to elevate cyclic AMP in rat brain slices. The data presented indicate that the cyclic AMP effect on an important component of intermediate metabolism is not an enhancement of a basal response but a separate response that is activated by depolarization, is Ca2+-dependent, regulates cytochrome a-a3 independently of its effects on NAD(P)H levels, and is dependent on a substrate other than glucose.

Animals↗

Plasma cAMP in normal and abnormal human pregnancy.

Plasma cAMP was determined using the method of Tovey et al. in normal pregnant women with a mean concentration of 18.9 +/- 0.8 pmol/ml (x- +/- SEM). Between weeks 9-12 and 33-36 of gestation, there were two peaks, with a mean cAMP of 22.5 +/- 2.4 which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12-28) which terminated in abortion (11.6 +/- 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 +/- 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 +/- 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 +/- 6.9; p < 0.0005). There was a negative linear regression between T3 and cAMP (2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 +/- 3.8 p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE2 alpha was followed by a decrease of plasma cAMP.

Abortion, Threatened↗

Plasma c-AMP during the normal menstrual cycle and under different hormonal treatment.

There is a highly significant difference between the plasma c-AMP value of the first and the second half of the normal menstrual cycle (days 1-12: 10.5 +/- 2.0 pmol, x +/- SEM; days 13-16: 21.9 +/- 4.5; days 17-28: 19.9 +/- 2.0; p less than 0.001). In amenorrheic patients plasma c-AMP levels were nearly the same as in normal women during the first half of the menstrual cycle (11.1 +/- 2.5). Plasma c-AMP of amenorrheic women was significantly higher under HMG treatment (16.7 +/- 2.5; p less than 0.01). Under oral contraception with estrogens (alone) or with low doses of gestagens the plasma c-AMP values were comparable to those of the amenorrheic women, but there was a dose-dependent increase of plasma c-AMP under gestagen application. It is concluded that the midcyclic plasma c-AMP increase is mainly caused by the gonadotropin effect, and is followed by the progesterone effect during the second half of the menstrual cycle. Therefore, plasma c-AMP levels are in accordance to the stages of the menstrual cycle reflecting their different endocrine pattern.

Contraceptives, Oral↗