Search PubMed⌕ Search

Biomedical subjects

D S Janowsky

Publications and source records attributed to D S Janowsky.

At least 73 records · Page 4Linked to original sources
PubMed1988

Cellular immunity and the hypothalamic-pituitary axis in major affective disorder: a preliminary study.

To assess cellular immune status and the hypothalamic-pituitary axis in patients with major depression, we examined peripheral blood mononuclear cells and measured the plasma levels of four neurohormones. Eleven patients with major depression had increased % of T4 lymphocytes and decreased concanavalin (Con A) stimulated T lymphocyte proliferation when compared with 11 age-, sex-, and race-matched control subjects. Percent of total lymphocytes labeled as all T lymphocytes, all B lymphocytes, and natural killer cells did not differ in the two groups, nor did mitogen-induced interleukin-2 production. These findings support theories of interaction between depression and immune cell function.

Adrenocorticotropic Hormone↗
PubMed1988

Human growth hormone releasing factor infusion effects on plasma growth hormone in affective disorder patients and normal controls.

In a preliminary, prospective pilot study, five patients with major depressive disorder and eleven age and sex matched normal controls received intravenous human growth hormone releasing factor (hGRF) (1 microgram/kg in 5 cc of normal saline infused over five minutes) and placebo. Thirty minutes after insertion of the catheter, blood was sampled every 15 minutes for thirty minutes prior to and for 2 hours subsequent to intravenous infusion of hGRF or placebo. hGRF but not placebo caused significant elevations of plasma growth hormone levels in all subjects. Of interest, the depressed patients had a significantly attenuated rise in plasma growth hormone concentrations when compared with the normal controls. These results must be considered preliminary awaiting replication with a larger subject population.

Adult↗
PubMed1988

Age, cellular immunity and the HP axis in major depression.

1. To assess the effect of age on cellular immune status and the HP axis in patients with major depression, we examined peripheral blood mononuclear cells (PBMC) and measured the plasma level of four neurohormones. 2. In 36 subjects, decreasing T lymphocyte response to con A covaried with age. Percent of lymphocytes labeled as T8 lymphocytes tended to decrease and T4/T8 ratio tended to increase with increasing age. 3. Hamilton and Beck scores were significantly different between the two sex and race matched groups of 18 depressed patients and 18 control subjects, and plasma prolactin was significantly higher in depressed subjects. 4. Increasing age correlated with decreasing T lymphocyte response to con A in the combined group of all subjects, and in the control group, but not in the patient group. 5. Hamilton and Beck scores correlated inversely with T lymphocytes response in the combined group of all subjects. 6. Differences in mitogen responsiveness between patient and control groups were not found, having been obscured by the effect of age. 7. These findings indicate the need to age match subjects when studying the interaction between depression and immune cell function.

Adult↗
PubMed1988

Differential diagnosis of pseudodementia in the elderly.

When depression occurs in the elderly, it may mimic dementia. The identification of depressive pseudodementia is important because this syndrome, unlike true dementia, often responds to antidepressant treatment. In this paper, the authors present strategies for differentiating pseudodementia, dementia, and coexisting depression and dementia. The treatment of depression in the elderly is also discussed.

Aged↗
PubMed1987

Cardiovascular, catecholamine and psychological responses to TRH in four types of affective disorder patients.

When 500 micrograms of TRH is given intravenously, an increase in TSH, blood pressure, plasma catecholamines and positive emotions follows. Four groups of patients with major, minor or bipolar depression or schizoaffective disorder increased their TSH levels by similar amounts after TRH. The neurohormone also significantly increased diastolic blood pressure by 5.5 +/- 1.6 mm Hg, and decreased heart rate by 7.6 +/- 1.3 beats/min. There was a weak trend for bipolar depressives to have less cardiovascular response to TRH than the other groups. Plasma norepinephrine (NE) was higher after TRH than after placebo. The NE response differed between patient groups (P = .0023) because of a smaller response by major depressives. TRH decreased anger, tension and depression, and increased friendliness. Positive emotional responses were significantly greater in the bipolar depressives than in other groups. Forty-one other studies have found a subnormal TSH response does not distinguish between subtypes of the affective disorders, but cardiovascular, catecholamine and mood responses may do so.

Adult↗
PubMed1987

Measurement of ACTH and prolactin in the dexamethasone suppression test.

Plasma concentrations of ACTH and prolactin were measured in psychiatric inpatients at 8 a.m. and 4 p.m. before and after the standard 1 mg overnight Dexamethasone Suppression Test (DST). Plasma concentrations of cortisol were measured at 8 a.m. and 4 p.m., and 11 p.m. before and after 1 mg dexamethasone. Dexamethasone suppressed plasma concentrations of ACTH, prolactin and cortisol in the subject group as a whole. "Cut Points" obtained using Fisher's Exact Test identified plasma ACTH values at 8 a.m. baseline, 4 p.m. baseline and 8 a.m. post-dexamethasone and plasma prolactin values at all four times that significantly differentiated patients with bipolar depressive disorder and major depressive disorder from other psychiatric patients. There were no cut points found at any of the six times for plasma levels of cortisol that significantly differentiated between these two diagnostic groups. Of interest in this subject population, basal (pre-dexamethasone) plasma concentrations were of more diagnostic information than post-dexamethasone values. These pilot findings suggest that monitoring plasma prolactin and ACTH concentrations before and after dexamethasone might increase the sensitivity and specificity of this laboratory test for depression.

Adrenocorticotropic Hormone↗
PubMed1986

Specific [3H]-N-methyl scopolamine binding without cholinergic function in cultured adult skin fibroblasts.

Cultured adult skin fibroblasts were studied for binding and functional evidence of muscarinic receptors in order to assess their utility as a model of cholinergic function in affective illness. Saturable, specific, high affinity binding could be demonstrated in intact cells from some cell lines with [3H]-NMS, but not [3H]-QNB, presumably because of intracellular trapping of unbound [3H]-QNB. [3H]-NMS specific binding indicated a single site with a KD of approximately 210 pM. [3H]-NMS was displaced by cholinergic agonists and antagonists with relative affinities similar to muscarinic receptors in brain. Many cell lines, however, showed no specific binding. No functional response to carbachol could be demonstrated with respect to inhibition of isoproterenol-stimulated cyclic AMP formation, stimulation of cyclic GMP formation or stimulation of phosphoinositide hydrolysis in any cell line regardless of either high or no specific [3H]-NMS binding.

Adult↗
PubMed1986

Enhanced elevation of corticosterone following arecoline administration to rats selectively bred for increased cholinergic function.

Serum corticosterone levels were determined following administration of the cholinergic agonist arecoline (4 mg/kg) to rats selectively bred for differences in cholinergic function. The Flinders Sensitive Line (FSL) of rats exhibited both greater suppression of behavioural activity and enhanced elevation fo serum corticosterone than the Flinders Resistant Line of rats. These enhanced responses to arecoline in the FSL rats parallel those reported in depressed humans, suggesting that these rats may provide a new animal model of affective disorders.

Animals↗
PubMed1986

Central muscarinic effects of physostigmine on mood, cardiovascular function, pituitary and adrenal neuroendocrine release.

The mechanism by which physostigmine exerts its behavioral, neuroendocrine and cardiovascular effects was explored in two separate experiments. In the first, the centrally-acting cholinesterase inhibitor physostigmine was compared with the non-centrally-acting agent neostigmine. In contrast to physostigmine, neostigmine caused no effects. In the second experiment, pretreatment with scopolamine, in contrast to methscopolamine, attenuated physostigmine's effects. The results suggest that physostigmine exerts its effects via a central muscarinic mechanism.

Adrenal Cortex↗
PubMed1986

Neuroendocrine responses in psychiatric and pain patients with major depression.

Basal and postdexamethasone concentrations of cortisol and prolactin were studied in three groups of male patients: chronic pain patients with no psychiatric diagnosis (n = 12), chronic pain patients with coexisting major depression by Research Diagnostic Criteria (RDC) (n = 24), and pain-free psychiatric patients meeting RDC criteria for major depression (n = 28). Basal cortisol concentrations were significantly higher in pain-major depression and psychiatric-major depression patients compared to pain patients without psychiatric illness. The frequency of cortisol nonsuppression after dexamethasone was significantly greater in pain patients with major depression (41.7%) compared to pain patients without psychiatric disorder (8.3%), and was comparable to that of psychiatric patients (21.4%). Prolactin concentrations, but not cortisol levels, were significantly correlated with observer-rated severity of depression in pain patients. These findings suggest that cortisol and prolactin abnormalities in chronic pain may be related to psychiatric disorder rather than to pain per se, at least in male patients, and may indicate a role for cholinergic mechanisms in the interface of pain and depression.

Adult↗
PubMed1986

Stress-induced immobility in rats with cholinergic supersensitivity.

Immobility during forced swimming or after mild footshock (1 mA for 2 sec) was observed in five groups of rats. The Flinders Sensitive Line (FSL) of rats, known to be more sensitive to cholinergic agonists, exhibited the greatest degree of immobility in the forced swim test. Rats chronically treated with, and subsequently withdrawn from, either scopolamine (2 mg/kg, once daily) or amitriptyline (10 mg/kg, once daily) were also significantly more immobile than either a control group treated chronically with isotonic saline or the Flinders Resistant Line (FRL) of rats in the forced swim test. Similar trends were observed for locomotor depression in the open field following exposure to footshock. Receptor binding studies indicated significantly greater concentrations of muscarinic acetylcholine receptors in the hippocampus of the scopolamine, and amitriptyline, withdrawn rats. These findings indicate that rats with increased cholinergic sensitivity are more sensitive to the immobility-inducing effects of mild stressors. Thus, they may prove to be useful models for studying the relationship between affective disorders and the cholinergic system.

Amitriptyline↗
PubMed1986

A kinetic analysis and replication of decreased platelet serotonin uptake in depressed patients.

Platelet serotonin uptake was kinetically measured in 32 psychiatric inpatients and 32 age- and sex-matched controls. Patients were categorized into four groups: depressed patients, manic bipolars, other affective disorders, and nonaffective psychiatric disorders. A randomized block factorial analysis of variance indicated that the depressed patients had a significantly lower maximal velocity (Vmax) of serotonin uptake in comparison to matched controls, without a statistically significant difference in Km. No statistically significant difference was found for any of the other diagnostic groups in comparison to controls for Vmax or Km. These results are compared with previous studies of platelet serotonin transport in clinically depressed patients and in physostigmine-induced depression.

Bipolar Disorder↗
PubMed1986

Central and peripheral cholinesterase inhibition: effects on anterior pituitary and sympathomimetic function.

Ten physically healthy inpatients of mixed diagnosis received, in a randomized, counterbalanced double-blind paradigm, physostigmine (22 micrograms/kg) and neostigmine (11 micrograms/kg). Infusions were separated by at least 2 days. The differential effects of physostigmine and neostigmine on plasma concentrations of cortisol, prolactin, growth hormone, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, dopamine, norepinephrine, and epinephrine are reported. Administration of physostigmine, unlike that of neostigmine, was associated with statistically significant increases in plasma concentrations of cortisol, prolactin, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, and epinephrine, presumably via central mechanisms. In a separate study, 15 subjects, mostly depressed inpatients, were pretreated with methscopolamine (0.75 mg) on one day and scopolamine (0.5 mg) on another day, at least 2 days apart, in a randomized, counterbalanced double blind paradigm and subsequently on each day received physostigmine (22 micrograms/kg). Scopolamine significantly attenuated the physostigmine-associated increase in plasma concentrations of cortisol, growth hormone, prolactin, ACTH, and dopamine compared to methscopolamine, and a close-to-significant attenuation of epinephrine as well. These results provide further evidence that physostigmine's effects on plasma concentrations of pituitary hormones and epinephrine occur via central mechanisms and are muscarinically mediated.

Adrenocorticotropic Hormone↗
PubMed1986

Patterns of memory failure after scopolamine treatment: implications for cholinergic hypotheses of dementia.

To test the idea that scopolamine provides a suitable pharmacological model of the memory defects associated with cortical or subcortical dementias, we assessed memory on a battery of tasks in healthy young normal subjects who received 0.5 mg scopolamine, 0.1-0.2 mg glycopyrrolate or physiological saline, once each on three separate occasions, and compared the pattern of memory failure induced by scopolamine to that observed on the same tasks in patients with Alzheimer's disease (AD) or Huntington's disease (HD). In agreement with previous reports, scopolamine impaired acquisition and delayed recall of a 14-word list and disrupted retention on the Brown-Peterson distractor task, whereas the peripherally active anticholinergic glycopyrrolate was without effect. However, under scopolamine the pattern of errors made on these memory tasks was quite different from that seen in patients with AD. Scopolamine did not increase the number of false positive errors on delayed recognition of the word list and also failed to increase the number of prior-item intrusions on the Brown-Peterson task. Also, scopolamine did not impair learning of a symbol-digit paired-associate task, and did not reduce the number of words retrieved or increase the number of words repeated on a standardized verbal fluency test. When the effects of scopolamine on memory were compared to the pattern of impairments observed in demented patients with HD, several differences were found. Although scopolamine clearly produces deficits on some measures of anterograde memory, the present findings question whether anticholinergic drugs adequately mimic the full range of memory impairments observed in cortical or subcortical dementias.

Adult↗
PubMed1986

Physostigmine-induced epinephrine release in patients with affective disorder.

Infusion of the cholinomimetic drug physostigmine led to profound increases in serum epinephrine levels and slight increases in serum norepinephrine levels among 38 patients with affective disorder and 22 control subjects. Preliminary results suggest that physostigmine may induce relatively blunted increases in serum epinephrine levels in patients with affective disorders.

Adult↗