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Biomedical subjects

D Janowsky

Publications and source records attributed to D Janowsky.

At least 19 recordsLinked to original sources
PubMed1997

Evidence of preference for a high-concentration sucrose solution in alcoholic men.

OBJECTIVE: The purpose of this study was to test in humans the finding from animal studies indicating an association between preference for more concentrated sweet solutions and excessive alcohol drinking. METHOD: The hedonic response to five different concentrations of sucrose solution was evaluated in 20 detoxified alcoholic and 37 nonalcoholic Caucasian men. All subjects repetitively tasted solutions with 0.05, 0.10, 0.21, 0.42, and 0.83 M sucrose concentrations and rated themselves on two scales measuring the intensity of sweetness and the likability of the solutions. RESULTS: A bimodal distribution of responses to the sweet solutions occurred in the nonalcoholic comparison group, with peaks at 0.05 M and 0.42 M. In the alcoholic group, 65% of the subjects preferred the highest sucrose concentration (0.83 M), compared with only 16% of the nonalcoholic group. CONCLUSIONS: The results of this exploratory study support the hypothesis suggesting a positive association between the preference for stronger sweet solutions and alcohol dependence.

Adult↗
PubMed1993

Reduction of spontaneous alcohol drinking and physical withdrawal by levemopamil, a novel Ca2+ channel antagonist, in rats.

Neuronal Ca2+ channels have been shown to be involved in both alcohol drinking behavior in rats and nonhuman primates and in the manifestation of alcohol withdrawal symptoms in rodents. Experiments were performed to determine the effect of a single injection of levemopamil, a novel Ca2+ channel antagonist with antiserotonergic [5-hydroxytryptamine2 (5-HT2)] properties, on alcohol preference and alcohol withdrawal symptoms in alcohol-preferring (P) and Wistar rats, respectively. P rats were individually housed and provided free access to food, water, and a solution of 10% (v/v) ethanol. Ethanol, food, and water intakes were measured daily. After establishing a stable baseline, P rats were injected with levemopamil (0, 3.3, 10, 15, and 20 mg/kg) and their food, water, and alcohol intakes measured 24 h later. In a separate experiment, the ability of acute and chronic (12 consecutive days) administrations of levemopamil to suppress alcohol withdrawal symptoms in chronically alcohol-treated rats was studied. In addition, the effects of levemopamil on the level of monoamines in different areas of the brain, as well as its action in alcohol metabolism, were examined. Our findings showed that a single administration of levemopamil (10, 15, and 20 mg/kg) significantly and dose-dependently attenuated alcohol intake and increased water intake in P rats. Both acute and chronic treatment with levemopamil reduced the alcohol withdrawal symptoms, overall seizure scores, and proportion of rats seizing. A single injection of levemopamil produced a clear, but not significant, trend to increase the 5-HT turnover rate in certain brain areas. This drug did not influence the pharmacokinetics of alcohol.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1991

The effects of scopolamine on sleep and mood in depressed patients with a history of alcoholism and a normal comparison group.

In order to determine the effect of an anticholinergic agent on mood and sleep, scopolamine (0.4 mg IM) was administered before bedtime for three consecutive nights to 10 depressed patients (8 with a history of alcohol abuse) and 10 normal comparison subjects. The patients had a small, statistically significant antidepressant response on the second morning of treatment. Scopolamine inhibited rapid eye movement (REM) sleep and prolonged REM latency equally in depressed patients and the normal comparison group. Partial tolerance to the REM inhibiting effect of scopolamine developed between the first and third night of treatment. A REM rebound occurred during recovery nights. These results are consistent with concepts relating central cholinergic mechanisms to the control of REM sleep. Compared with controls, patients showed a greater increase in Stage 2 and Stage 2% and a lesser and increase in Delta (Stage 3 and 4) sleep % and Stage 4% on the first night of treatment. Further, well-controlled studies are needed to determine whether anticholinergic drugs possess clinically significant antidepressant effects.

Adult↗
PubMed1991

The effects of physostigmine infusion on patients with panic disorder.

Nine patients who met both DSM-III and RDC criteria for panic disorder and nine age-matched normal controls received infusions of physostigmine. The patients and normal controls did not differ in either their self-reported or the observer-reported ratings of anxiety, mood, or activation. The two subject groups also did not differ in blood pressure, pulse, or cortisol responses to physostigmine. Physostigmine did not provoke panic attacks in either the control or patients groups.

Adult↗
PubMed1991

The cholinergic rapid eye movement induction test with arecoline in depression.

The cholinergic rapid eye movement (REM) induction test using arecoline hydrobromide, a cholinergic muscarinic receptor agonist, was studied in patients with affective disorder and in normal controls to determine whether or not depression is associated with enhanced induction of REM sleep by muscarinic agonists. Arecoline induced REM sleep in a dose-dependent fashion in both patients and controls compared with placebo infusions. Compared with normal controls, patients entered REM sleep significantly more rapidly following intravenous administration of 1.0 mg of arecoline hydrobromide than they did following administration of 0.5 mg of arecoline hydrobromide or placebo. These results, as well as those of previous studies, support the hypothesis that patients with affective disorder show a functional supersensitive induction of REM sleep in response to muscarinic receptor agonists and may be consistent with the hypothesis that functional muscarinic receptor "up regulation" is associated with depression.

Arecoline↗
PubMed1991

Clinical and biochemical aspects of depressive disorders: II. Transmitter/receptor theories.

The present document is the second of three parts in a review that focuses on recent data from clinical and animal research concerning the biochemical bases of depressive disorders, diagnosis, and treatment. Various receptor/transmitter theories of depressive disorders are discussed in this section. Specifically, data supporting noradrenergic, serotonergic, cholinergic, dopaminergic, GABAergic, and peptidergic theories, as well as interactions between noradrenergic and serotonergic, or cholinergic and catecholaminergic systems are presented. Problems with the data and future directions for research are also discussed. A previous publication, Part I of this review, dealt with the classification of depressive disorders and research techniques for studying the biochemical mechanisms of these disorders. A future publication, Part III of this review, discusses treatments for depression and some of the controversies in this field.

Animals↗
PubMed1989

Central nervous system side effects of beta-adrenergic blocking agents with high and low lipid solubility.

beta-adrenergic blocking agents have undesirable effects believed to be mediated through the central nervous system (CNS). If these effects are due to direct CNS action, less lipid soluble agents ought to have fewer effects. Accordingly, several formal psychological tests of items such as mood, motivation, and anxiety were used in a double-blinded crossover study in 17 hypertensive subjects taking equipotent beta blocking agents with high (propranolol) and low (atenolol) lipid solubility. Patients had less negative effects (p less than 0.05) on 12 of 21 items evaluated with atenolol compared to propranolol while peripheral beta blockade [beta 1, exercise heart rate (HR), and blood pressure (BP)] was equivalent. These results suggest that the mental changes which accompany beta blockade therapy are mediated directly in the CNS and that less soluble drugs can be expected to have fewer CNS effects.

Adult↗
PubMed1987

Efficacy and safety of fezolamine in depressed patients.

Forty-two outpatients with major depressive disorder were treated with oral fezolamine in a 6-week, three-center open-label study. Therapy was initiated at 100 mg/day; thereafter dosage was increased based on the response of the patient. Maintenance dosage usually ranged between 100 and 450 mg/day. Clinically significant improvement relative to the patient's prestudy state was observed after 2 weeks in both patient and physician-rating scales. Fifty-five percent of patients improved their Hamilton Psychiatric Rating Scale for Depression (HAM-D) scores by more than 50%. The median dose associated with a clinically significant response was 245 mg/day. Five of the 6 patients who dropped out did so because of gastrointestinal adverse effects. The most common adverse effects were nausea (36%), headache (29%), constipation (26%), and dry mouth (24%).

Adult↗
PubMed1983

Bright white light alleviates depression.

Studies of biological rhythm disorders among manic-depressive patients have suggested that depressed patients may have an early photosensitive interval. If so, exposure to bright light during the photosensitive interval might relieve depressive symptoms. As a test of this hypothesis, 12 depressed patients were exposed to bright white light from roughly 5 to 6 a.m. On the afternoon following this treatment, depressive symptoms were reduced in comparison to baseline ratings and as compared to afternoons following similar exposures to dim red light.

Arousal↗
PubMed1981

Rapid treatment of acute psychotic symptoms with high- and low-dose haloperidol. Behavioral considerations.

Twenty acutely psychotic male psychiatric inpatients were assigned to two groups and treated with high- and low-dose haloperidol using a rapid neuroleptization technique. A six-day maintenance phase followed. Both groups improved at one hour, one day, and seven days after starting treatment, and neither group differed as to degree or rapidity of symptom alleviation. Therefore, the results of the study do not give experimental support for the administration of high doses of haloperidol to young, acutely psychotic inpatients with relatively good prognoses.

Acute Disease↗
PubMed1981

Adult psychiatric diagnosis and symptoms compatible with the hyperactive child syndrome: a retrospective study.

Characteristics of the hyperactive child syndrome have been described extensively. More recently, reports have indicated that manifestation of the hyperactive child syndrome may persist into adulthood, both as a continuation of childhood symptoms and as psychopathologic entities. This study evaluated 100 adult psychiatric inpatient Veterans for self-report of symptoms of childhood and adulthood hyperactivity, attentional deficit, and impulsivity. Psychotic and non-psychotic psychiatric patients reported a significantly higher incidence of childhood hyperactive syndrome symptoms than did age and sex matched controls. In both childhood and adulthood, character disorder patients reported the highest incidence of target symptoms.

Adult↗
PubMed1980

Flurazepam effects on methylphenidate-induced stereotyped behavior.

The effects of flurazepam (0.0, 0.5, and 3.0 mg/kg) on methylphenidate-induced increases in stereotypy, gnawing, sniffing, and locomotion were evaluated in Swiss-Webster mice in daytime and nighttime experiments. Methylphenidate (50 mg/kg) increased overall stereotypy and stereotyped gnawing behavior; two doses of methylphenidate (25 mg/kg and 50 mg/kg) increased locomotion and sniffing behavior. Flurazepam 3.0 mg/kg augmented methylphenidate-induced stereotyped gnawing behavior and stereotypy. Flurazepam significantly decreased locomotion and sniffing, but did not interact with methylphenidate's effects on locomotion and sniffing.

Animals↗
PubMed1979

Naloxone effects on serum growth hormone and prolactin in man.

Endogenous and exogenous opiate-like compounds have been found to cause increased serum growth hormone and prolactin levels in animals, and, in some cases, humans. Naloxone, a relatively specific narcotic antagonist, decreases serum prolactin and growth hormone levels in animals. Naloxone (20 mg IV) did not significantly alter serum prolactin levels and, minimally but not significantly, increased growth hormone levels in humans to whom it was administered.

Growth Hormone↗