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Biomedical subjects

G Langer

Publications and source records attributed to G Langer.

At least 55 records · Page 3Linked to original sources
PubMed1984

Chromosomes for molecular hybridization. Assignment of repetitive and single copy genes using a rapid filter-fixation method.

Specific recombinant DNA sequences (5S rRNA, B1, albumin) were assigned to flow sorted chromosomes of the Chinese hamster cell line CHV79. For this purpose, a rapid protocol was developed using filterbound chromosomal DNA and probing with various nucleic acids, that allows sequence identification in chromosomes. A flow histogram and a flow karyogram of the CHV79 cell line were established by flow analysis in order to calculate the amount of DNA per CHV79 cell and their chromosomes. Subsequently, metaphase chromosomes or chromosomal groups were fractionated by electronic sorting and a defined number of chromosomes was directly bound to nitrocellulose filters for sequence homology analysis by a dot blot hybridization procedure. This procedure not only allows the assigning of specific DNA sequences to particular chromosomes, it is also applicable to studies of changes in karyotypes, for example translocations of given sequences.

Animals↗
PubMed1984

TSH-response patterns to TRH stimulation may indicate therapeutic mechanisms of antidepressant and neuroleptic drugs.

The study was designed to investigate, by weekly thyrotropin-releasing hormone tests, possible patterns of thyroid-stimulating hormone (TSH) responses which may indicate therapeutic mechanisms of antidepressant and neuroleptic drugs in patients with depressive and paranoid-hallucinatory syndrome during their process of recovery (3-9 weeks). 65 depressed women and 33 paranoid-hallucinatory women have been studied while on antidepressant (clomipramine) or neuroleptic (haloperidol) treatment, respectively. Four patterns of TSH response were observed. Patients with a pattern of a 'disblunting TSH response' (normalization of an abnormal low response) during drug treatment had a significantly higher chance to recover compared to patients with other TSH response patterns. This finding was independent of psychopathological features and drugs used for treatment. A hypothesis of 'malactivation' as a pathogenetic indicator of various psychotic states is being presented.

Adult↗
PubMed1983

[Therapy with neuroleptics and antidepressive agents: a fundamental and critical discussion from a biological viewpoint].

This paper presents a critical discussion on fundamental questions of treatment with neuroleptic and antidepressant drugs on the basis of current knowledge in the biological psychiatry and clinical psychopharmacology. The issues raised are some problems in the definition of the terms "neuroleptic" and "antidepressant" drugs, the indications for treatment with neuroleptic and antidepressant drugs and a definition of the term "therapeutic efficacy" of neuroleptic and antidepressant drugs.

Antidepressive Agents↗
PubMed1983

The TSH-response to TRH: A possible predictor of outcome to antidepressant and neuroleptic treatment.

This study was designed to investigate the possible common patterns of neuroendocrine mechanisms, which may be involved in the therapeutic effects of antidepressant drugs in depressive and of neuroleptic drugs in schizophrenic patients. Sixty-three depressed women (major depressive disorder) and 21 paranoid-hallucinatory women have been studied while on antidepressant (clomipramine) or neuroleptic (haloperidol) treatment, respectively. The neuroendocrine test (TRH-test) was performed at weekly intervals. The change of TSH-response to TRH during treatment, i.e. the treatment associated normalization of a former blunted TSH-response, can tentatively be regarded as a predictor of outcome for depressive and paranoid-hallucinatory patients to their respective drug treatments. Antidepressant and neuroleptic drugs appear to involve the normalization of the TSH-response in their therapeutic effects in that proportion of patients (40%) which showed a blunted TSH-response at admission.

Adolescent↗
PubMed1981

Effects of antidepressant treatment with clomipramine on hormonal responses to thyrotropin-releasing hormone and insulin-induced hypoglycemia: implications for the "monoamine-hypothesis".

Neuroendocrine test were carried out to study effects of clomipramine treatment in 24 unipolar depressed women. Clomipramine (50-150 mg/day) increased the response of prolactin and thyrotropin to stimulation by thyrotropin-releasing hormone (TRH), while no response of growth hormone (HGH) to TRH was seen. Clomipramine decreased the response of HGH to insulin, while the responses of prolactin and cortisol to insulin were not affected. The findings suggest that the neuroendocrine and antidepressant effects of clomipramine cannot be accounted for entirely on the basis of monoaminergic mechanisms.

Biogenic Amines↗
PubMed1979

Normal prolactin responses in tardive dyskinesia.

Tardive dyskinesia has been hypothesized to be caused by a neuroleptic-induced dopamine hypersensitivity in the nigrostriatal system. This study evaluated with dopamine antagonists the possibility that such dopamine hypersensitivity extends to the tuberoinfundibular dopamine (TIDA) system, which regulates, by inhibition, pituitary prolactin secretion. Plasma prolactin concentrations in six patients with tardive dyskinesia were assessed in four conditions: During chronic haloperidol therapy; serially after abrupt haloperidol withdrawal; while unmediated; and in response to an acute dose of 0.5 mg IM haloperidol. In all four conditions, prolactin responses did not differ from those observed in normal subjects and schizophrenic patients without tardive dyskinesia. It is concluded that there is no evidence for post-synaptic dopamine hypersensitivity in the TIDA-pituitary pathway in patients with tardive dyskinesia, consistent with other reports assessing hormonal responses to dopamine agonists in such cases. It is further suggested that neuroleptic-induced dopamine hypersensitivity does not occur in the TIDA-pituitary system in humans, since it was not manifest in these tardive dyskinesia patients who would be thought particularly prone to develop it.

Adult↗
PubMed1979

Dopaminergic factors in human prolactin regulation: a pituitary model for the study of a neuroendocrine system in man.

This study in normal male subjects further investigates the effects of dopaminergic-antidopaminergic interactions as manifested by the prolactin response to dopamine and neuroleptic drugs. Incremental doses of dopamine hydrochloride (4 microgram/min, 15 microgram/min, 60 microgram/min, 300 microgram/min) were infused at a constant rate over 90-120 min after a fixed dose of a neuroleptic drug (sufficient for about half of the maximal prolactin response) had been given IV. A dose of dopamine in the order of 15-60 microgram/min appeared to match the "loss" of endogenous dopaminergic inhibition due to the antidopaminergic effect of the neuroleptic drug. The lactotrophic cells of the pituitary gland are suggested to serve as a model in man for the study of some basic neurohormonal mechanisms.

Adult↗
PubMed1979

Diurnal variation in the response of plasma prolactin, cortisol, and growth hormone to insulin-induced hypoglycemia in normal men.

Plasma PRL, cortisol, and GH responses to a standard iv dose of regular insulin were studied during the morning and evening in seven normal young men. Hypoglycemia achieved during morning and evening in the same aubjects was equal. There was a substantially greater maximal increment in PRL in the evening compared to the morning (P less than 0.01). The peak levels of cortisol achieved in the morning and evening were equal, but the evening maximal increase was greater (P less than 0.05) because of the significantly lower evening basal cortisol level. Evening increases in GH were greater than in the morning in five subjects and were essentially the same in two subjects; for the group, the evening maximal increment in GH was significantly greater (p less than 0.05 after log transformation). Since serotonergic mechanisms appear to be involved in the PRL, GH, and cortisol responses to hypoglycemia, we suggest the possibility of a diurnal variation in hypothalamic serotonin activity which may partly mediate these differential diurnal hormonal responses to hypoglycemia (although other neurotransmitters may also be involved). The data on cortisol are discussed with regard to the reset hypothesis of feedback inhibition.

Circadian Rhythm↗
PubMed1978

Prolactin responses to neuroleptics in normal and schizophrenic subjects.

The prolactin response to neuroleptics can serve as an index of dopamine blockade in humans. Plasma prolactin increments to single doses of chlorpromazine, and prolactin decrements to single doses of levodopa, were similar in normal and schizophrenic subjects. Antischizophrenic drugs of all chemical classes stimulated prolactin release,while chemically related drugs and other psychotropic agents ineffective in schizophrenia did not. The prolactin response to neuroleptic therapy occurred in all patients, and tolerance did not develop. Within subjects, prolactin responses were graded according to neuroleptic dose, but the upper limit of sensitivity of the response curve was achieved at doses below the therapeutic range. Relative prolactin-stimulating potency in humans of chlorpromazine, thioridazine, trifluoperazine, butaperazine, and haloperidol correlated well with their relative clinical potencies.

Chlorpromazine↗