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Biomedical subjects

Z S Herman

Publications and source records attributed to Z S Herman.

At least 55 records · Page 3Linked to original sources
PubMed1995

Antitumor activity of bestatin and thiorphan in mice.

We have investigated the effect of bestatin and thiorphan on growth of murine transplantable tumors, survival time, activity of natural killer (NK) cells and macrophages in mice. The injections of thiorphan at the does of 0.5 or 5 micrograms per mouse retarded tumor growth and prolonged survival period in B16 melanoma bearing animals. Pretreatment with naloxone (an unspecific antagonist of opioid receptors) blocked the tumor growth inhibition induced by the treatment with bestatin and thiorphan what could suggest a contribution of endogenous enkephalin in this antitumor effect. The percentage of mice bearing B16 melanoma tumor in the group treated with thiorphan at doses of 0.5, 5 or 50 micrograms per mouse was lower in comparison with control animals in a dose-dependent manner. The treatment with thiorphan at concentrations of 0.4-1.6 mg/ml inhibited growth of cultured in vitro B16 melanoma cell in comparison with control culture. Thiorphan added to the medium at concentration of 0.5 microgram/ml or administered 4 times at the dose of 0.5 microgram/mouse augmented NK lymphocyte activity.

Animals↗
PubMed1995

Effect of captopril and thiorphan on the proliferation of human neoplastic cell lines and their influence on cytostatic activity of interferon alpha or cytotoxic activity of doxorubicin.

We have assessed the effect of thiorphan or captopril on proliferation of two human tumor cell lines, A549 and HL60 including their influence on the cytostatic activity of interferon alpha or doxorubicin. The results showed that captopril inhibits the proliferation of both A549 and HL60 cells lines but thiorphan has antiproliferative effect only on A549 cells in a dose-dependent manner. However, neither captopril nor thiorphan administered in combination with interferon alpha or doxorubicin enhanced cytotoxic potential of doxorubicin and cytostatic activity of interferon alpha.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

The dihydropyridines modulate neurotensin inotropic action paradoxically.

The interaction of neurotensin and calcium channel modulators is examined in isolated electrically driven guinea pig left atrial appendages. Left guinea pig atria exposed to diltiazem become desensitised to neurotensin. There is no significant influence of verapamil pretreatment on the neurotensin inotropic action. Nifedipine pretreatment causes increase in the inotropic response of guinea pig atria to neurotensin. The regression line of neurotensin after pretreatment with nifedipine compared to the regression line of neurotensin alone has higher slope and is shifted to the left. The ED50 of neurotensin after nifedipine pretreatment compared with the ED50 of neurotensin alone results in potency ratio of 2.24. Bay K8644 significantly decreases the inotropic effect of ED100 of neurotensin. Results suggest that: (1) the mechanism of interaction of calcium channel modulators and neurotensin in the atrium does not depend on the calcium influx through calcium channel nor does it on the calcium channel itself; (2) the interaction of nifedipine and neurotensin is possibly dependent on dihydropyridine receptors, (3) the dihydropyridine binding site, possibly different from voltage-sensitive calcium channel, is somehow involved in the neurotensin action in guinea pig atria.

Animals↗
PubMed1992

Behavioural effects of two dipeptides L-phenyl alanyl-L-arginine (Phe-L-Arg) and L-phenyl alanyl-D-arginine (Phe-D-Arg) after intracerebroventricular or intrathecal injections in mice.

L-phenylalanyl-L-arginine (Phe-L-Arg) and L-phenylalanyl-D-arginine (Phe-D-Arg), dissolved in a physiological saline were injected intrathecally into the lateral brain ventricle, and their behavioural as well as analgesic effects in mice were determined. It was found that a 100 nM dose of either peptide intracerebroventricularly (i.c.v.) injected induced an increase in the locomotor activity and a convulsive effect, whereas the same dose if injected produced a significant analgesic effect. It has been concluded that Phe-L-Arg and Phe-D-Arg have significant but different central effects in mice.

Analgesics↗
PubMed1991

Chronic treatment with chlorpromazine, thioridazine or haloperidol increases striatal enkephalins and their release from rat brain.

The aim of this paper is to study the effect of 1, 2 or 3 months' administration of chlorpromazine (CPZ), thioridazine (TDZ) (2 or 6 mg/kg) or haloperidol (HAL) (0.25 or 1 mg/kg) IP on the level of leu- and met-enkephalin (ENK) in striatum. A dose- and time-dependent increase of striatal ENK level was observed after chronic administration of the neuroleptics (NL), but 8 days after withdrawal of chronically administered NL striatal ENK was decreased. Apomorphine pretreatment significantly attenuated the elevation in ENK produced by chronic injections of NL. In perfusion fluid obtained from the lateral ventricle of animals treated 1 month with HAL a dose-dependent increase of ENK levels was observed, which was augmented by potassium ions. It is concluded that: 1) Chronic administration of neuroleptic drugs that block dopamine receptors increases the level and the release of striatal enkephalins; 2) The results support the hypothesis that activation of dopaminergic neurons tonically inhibits the synthesis of enkephalins in the striatum.

Animals↗
PubMed1989

Criteria for the validity of clinical trials of treatments of cohorts of cancer patients based on the Hardin Jones principle.

With the assumption of the validity of the Hardin Jones principle that the death rate of members of a homogeneous cohort of cancer patients is constant, three criteria for the validity of clinical trials of cancer treatments are formulated. These criteria are satisfied by most published clinical trials, but one trial was found to violate all three, rendering the validity of its reported results uncertain.

Ascorbic Acid↗
PubMed1987

Biological activity of TRH thionalogue and its diastereoisomers.

Binding affinity and TSH-releasing activity of [Prot3] TRH analogue (L-pyroglutamyl-L-histidyl-L-proline thioamide), TRH and their LDL and LLD diastereoisomers were compared in rats. Binding affinity and dose-related increase of TSH secretion were similar for both [Prot3] TRH and TRH. Moreover, similar effect of both peptides on sleeping time and motoric activity of rat was found. Substitution of L- for D-amino acids of TRH and [Prot3] TRH decreased the binding affinity and TSH-releasing activity as well. It was concluded that [Prot3] TRH analogue is as active as native TRH.

Animals↗
PubMed1985

Effect of dietary ascorbic acid on the incidence of spontaneous mammary tumors in RIII mice.

A study of the effect of different amounts of L-ascorbic acid (vitamin C), between 0.076% and 8.3%, contained in the food has been carried out with ten groups of RIII mice (seven ascorbic acid and three control groups), with 50 mice in each group. With an increase in the amount of ascorbic acid there is a highly significant decrease in the first-order rate constant for appearance of the first spontaneous mammary tumor after the lag time to detection by palpation. There is also an increase in the lag time. The mean body weight and mean food intake were not significantly different for the seven ascorbic acid groups. Striking differences were observed between the 0.076% ascorbic acid and the control groups (which synthesize the vitamin): smaller food intake, decreased lag time, and increased rate constant of appearance of the first mammary tumor. This comparison cannot be made experimentally for guinea pigs and primates because the control groups would develop scurvy.

Animals↗
PubMed1985

Central effects of D-Ala2-met-enkephalinamide on the blood pressure of rats after central chemical sympathectomy or serotoninectomy.

D-Ala2-met-enkephalinamide (DAMEA) in ethyl urethane anesthetised rats increased the blood pressure, decreased heart rate and frequency of respirations. DAMEA could act centrally as well as peripherally after the penetration from the cerebro-spinal into the blood stream. These effects were blocked by naloxone. 6-Hydroxydopamine inhibited the circulatory and respiratory action of DAMEA. 5,6-Dihydroxytryptamine reversed this action of DAMEA. It is suggested that central presynaptic catecholamine and serotonin neurons modulate the central effects of DAMEA on the circulatory system and respiration in rats.

Animals↗
PubMed1984

Enkephalin content in rat striatum during prolonged treatment with fluphenazine.

Male Wistar rats were injected with fluphenazine /FLU/ i.p. in doses of 1 or 5 mg/kg for twelve months. Striatal met- and leu-enkephalin contents were determined after 1, 3, 6, 9 and 12 months of treatment, and one week after the drug withdrawal following a 12-month treatment, Enkephalin levels were significantly increased with slight fluctuations in some months and returned to normal one week after the last neuroleptic dose following a 12-month administration. Apomorphine, but not naloxone, prevented elevation of enkephalin levels after a one month FLU administration. Our findings confirm previous observations that prolonged disturbances in functions of the dopaminergic mechanism result in specific disturbances in the endogenous opioid peptide content, release and biosynthesis, and demonstrate that enkephalins are one of the factors with take part in the mechanism of neuroleptic action during a long-term treatment.

Animals↗