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Biomedical subjects

S H Koslow

Publications and source records attributed to S H Koslow.

At least 55 records · Page 3Linked to original sources
PubMed1982

Insulin tolerance test: human growth hormone response and insulin resistance in primary unipolar depressed, bipolar depressed and control subjects.

Preliminary data from the National Institute of Mental Health-Clinical Research Branch Collaborative Program on the Psychobiology of Depression dealing with the human growth hormone (hGH) response to the Insulin Tolerance Test (ITT) during the pre-treatment (drug-free) period of the study are presented in this paper. Data are reported for 54 unipolar depressed, 21 bipolar depressed, and 40 normal control subjects, who represent approximately 50% of the final subject sample to be studied. In this population the unipolar depressed subjects showed a significantly greater resistance to insulin-induced hypoglycaemia than bipolar and control subjects. After applying the inclusion/exclusion criteria necessary to interpret hGH responses accurately, the data from only 54 subjects were acceptable. Mean peak hGH concentrations were not significantly different among the three groups. There was, however, a significant difference in the distributions of the hGH peak response, with the bipolar depressed population demonstrating greater variability in response than unipolar and control populations. These findings are discussed as they relate to previous reports and theoretical considerations.

Adult↗
PubMed1980

Biological component of the NIMH clinical research branch collaborative program on the psychobiology of depression: I. Background and theoretical considerations.

There are many reports which suggest that patients with effective illness (mania and/or depression) have abnormalities in the functioning of one or more neurobiological systems. At a conference convened by the Clinical Research Branch, Division of Extramural Research Programs, National Institute of Mental Health, these findings were reviewed and some of the factors impeding movement towards a more complete and integrated view of the functioning of neurobiological systems in patients with mania or depression were identified. As a result, a multi-research centre, collaborative approach to the study of the psychobiology of affective disorders was developed. In this collaborative programme, which has now been underway for several years, the focus has been upon: (a) the assessment of the functioning of several different types of biological systems in the same patient, both before and during treatment; (b) obtaining a reasonably large number of patients and comparison subjects; and (c) the use within and across centres of standardized diagnostic categories and behavioural rating methodologies. In this paper the history, background, and rationale for this collaborative effort are reviewed. Those biological systems chosen for study are noted, and issues such as reliability and validity of diagnoses, measurement of state variables, assessment of change with treatment, and logistical and coordinating problems are discussed.

Affective Disorders, Psychotic↗
PubMed1980

Biological component of the NIMH clinical research branch collaborative program on the psychobiology of depression: II. Methodology and data analysis.

A preceding paper has reviewed the history, background, and rationale for this collaborative effort exploring the biologic basis of the affective disorders. This paper details the "flow" of a subject through the experimental protocol, the instrumentation used to obtain the clinical and behavioural data, and the biologic methodologies employed in the analysis of the body fluids. Data management and analysis techniques developed for this study are also examined.

Adrenocorticotropic Hormone↗
PubMed1979

NIMH clinical research branch collaborative program on the psychobiology of depression.

This is a report on the history and implications of the collaborative effort that evolved from the 1969 National Institute of Mental Health conference on the psychobiology of depression. The major issues identified at that time were the need to (1) assess relative validities of current systems of nosology and (2) retest critical biological hypotheses concerning the etiology and nature of the depressive disorders. Research was required that would be multidisciplinary and involve clinical settings treating diverse types of depression. The objectives and the nature of the biological and clinical collaborative programs that were designed to address these problems are described. These unique programs, initiated in the early 1970s, currently span research on nosology, genetics, neurochemistry, neuroendocrinology, and psychosocial factors. Although these studies are still in the early stages, they have resulted in significant methodologic developments in diagnosis, descriptive psychopathology, and biological measurements.

Adrenocorticotropic Hormone↗
PubMed1979

Biogenic amine metabolism in Tourette syndrome.

Biogenic amine metabolism in the central nervous system of 9 children with Tourette syndrome was evaluated by quantitation of their metabolites in cerebrospinal fluid by a gas chromatographic/mass spectrometric method. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) were measured in CSF before and after oral administration of probenecid. Dopamine metabolism appeared defective, as both baseline and accumulated levels of HVA after probenecid were decreased. Serotonin metabolism also appeared defective in some patients with low baseline and low accumulated levels of 5-HIAA after probenecid. Taken together with other clinical features of this disease, the results suggest an underlying disorder of dopamine and serotonin metabolism in Tourette syndrome.

Biogenic Amines↗
PubMed1978

A disorder of biogenic amines in dihydropteridine reductase deficiency.

A severe deficiency of dihydropteridine reductase (DHPR) in liver, brain, and cultured skin fibroblasts was demonstrated in a child with hyperphenylalaninemia and an atypical form of phenylketonuria. DHPR is required for regeneration of the cofactor, tetrahydrobiopterin. The cofactor is essential in hydroxylation of aromatic amino acid precursors in the biosynthesis of neurotransmitters, serotonin, dopamine, and norepinephrine. In gray tissue at brain biopsy, dopamine was low at 3 ng per gram of tissue, serotonin was barely detected, and norepinephrine appeared high at 1600 ng per gram. In cerebrospinal fluid, homovanillic acid (HVA) was low normal at 33 ng/ml, 5-hydroxyindoleacetic acid (5-HIAA) was low at 4.2 ng/ml, and after a high dose of oral probenecid there was impaired accumulation of HVA to 128 ng/ml and 5-HIAA to 22.4 ng/ml. When the patient was 22 months of age, treatment with hydroxylated aromatic amino acid precursors was initiated, and after three months HVA and 5-HIAA levels were increased in CSF. The apparent restoration of biogenic amines in brain appears to have delayed the rate of neurological deterioration. DHPR activity in cultured skin fibroblasts of children with persistent hyperphenylalaninemia should permit early diagnosis and early treatment of this disorder.

5-Hydroxytryptophan↗
PubMed1977

Biogenic amine synthesis defect in dihydropteridine reductase deficiency.

In the enzymatic hydroxylation of aromatic amino acids, tetrahydrobiopterin is the essential cofactor. Regeneration of tetrahydrobiopterin requires dihydropteridine reductase, without which there should be a deficiency of hydroxylated amino acids and their products, biogenic amines. Assay of biopsied brain cortex of a patient with a deficiency of dihydropteridine reductases showed low concentrations of serotonin and dopamine, and this was reflected in the concentrations of their major metabolites measured in cerebrospinal fluid from lumbar, ventricular, and subarachnoid spaces. The metabolite concentrations were restored to normal, or above normal, by treatment with specific amino acids which bypass the metabolic block at the hydroxylation step. It is postulated that the seizures and neurological deterioration of the patient were related to a deficiency in the synthesis of biogenic amine neurotransmitters.

5-Hydroxytryptophan↗
PubMed1976

Effects of glucocorticoid treatment on catecholamine content and ultrastructure of adult rat carotid body.

Carotid bodies of dexamethasone-treated (daily injections, 10 days) adult male rats were analyzed with respect to catecholamine content and ultrastructure. Gas chromatographic-mass spectrometric assays demonstrated that norepinephrine (NE) and dopamine (DA) concentrations more than doubled after dexamethasone treatment. The increase in NE was relatively greater than that of DA. No epinephrine (E) could be detected. Morphometry revealed, as for the control carotid bodies, two subclasses of type I cells on the basis of the diameters of their dense-cored vesicles. These groups of cells were termed small vesicle cells (SVC) and large vesicle cells (LVC). Dexamethasone treatment resulted in significantly increased volume densities and diameters of the dense-cored vesicles in both SVC and LVC. The greatest increase occurred in the SVC. If these morphological changes do reflect the change in amine concentrations then it is possible to speculate that the type of cells with the greatest increase of amine storage capacity may store the kind of catecholamine most increased. Thus NE may presumably be stored in the SVC and DA in the LVC. Furthermore, these effects of administered glucocorticoids may also indicate a regulatory function for endogenous glucocorticoids on the carotid body catecholamines.

Animals↗
PubMed1976

Nocturnal elevation of plasma melatonin and urinary 5-hydroxyindoleacetic acid in young men: attempts at modification by brief changes in environmental lighting and sleep and by autonomic drugs.

In order to determine whether the human pattern of circulating melatonin resembles that previously described in lower animals, men 19-32 years old were exposed to a light-dark cycle with 14 hours of light per day (L:D 14:10). In whites and blacks, nocturnal (dark phase, sleeping) melatonin levels were almost always elevated to 0.05-0.1 ng/ml plasma compared with lower or undetectable levels during the day, measured by the tadpole bioassay. Thin-layer migration of bioactive material was identical to that for melatonin standard. A rhythm with nocturnal elevation of urinary 5-hydroxyindoleacetic acid (5-HIAA) was observed. Nocturnal (sleep phase) rise in blood melatonin (but not urinary 5-HIAA) continued during 21/2 day-night cycle lengths after the onset of constant light. Though the dark phase plasma melatonin rise was less marked after reversal of the sleep-wake cycle (no change in the light cycle), dark phase rise in urinary 5-HIAA continued. Though marked cardiovascular and other effects were produced by intravenous isoproterenol or scopolamine, no definite effect on melatonin levels was observed after either drug during the light phase in waking subjects.

Adult↗
PubMed1976

Reduction of tryptophan hydroxylase activity and 5-hydroxytryptamine concentration in certain rat brain nuclei after p-chloroamphetamine.

High-pressure liquid chromatography and mass fragmentography have been used to determine tryptophan hydroxylase activity and 5-hydroxytryptamine (5-HT) concentration, respectively, in certain rat brain nuclei. (+/-)-p-Chloroamphetamine (100 mumol/kg i.p.) decreased enzyme activity in 5-HT terminals of the caudate, hippocampus and septum to a minimum level within 3 days. In hippocampus, but not in septum, the enzyme activity and 5-HT content remained maximally depleted (about 80%) for as long as 2 months after the p-chloroamphetamine injection. Of the 5-HT cell body areas investigated, only in the B9 nucleus was the tryptophan hydroxylase activity and 5-HT content still significantly reduced (about 25-50%) at 21 and 60 days after the drug injection. The enzyme activity and 5-HT content of the B7 and B8 nuclei were not significantly different from control values at these times. These results suggest that the primary site of action of p-chloroamphetamine is on nerve terminals followed by secondary effects on serotonergic cell bodies.

Amphetamines↗