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Biomedical subjects

G Zerek-Mełeń

Publications and source records attributed to G Zerek-Mełeń.

15 recordsLinked to original sources
PubMed1994

Influence of interleukin 1 and antihuman interleukin 1 receptor antibody on the growth and function of the thyroid gland in rats.

Cytokines seem to influence the hypothalamo-pituitary-thyroid axis. We have studied the effect of different doses of interleukin 1 alpha (IL-1 alpha) and IL-1 beta (given twice daily ip) alone or together with antihuman IL-1 receptor antibody (aIL-1ra) on the proliferation of thyroid follicular cells and thyroid hormone levels in male Wistar rats. We have examined the influence of IL-1 alpha and IL-1 beta at doses of 10.0, 1.0 and 0.1 micrograms/kg body wt of animal and aIL-1ra at a dose of 10.0 micrograms/kg body wt of animals. The incorporation of bromodeoxyuridine into thyroid follicular cell nuclei was used as an index of cell proliferation (labeling index: LI) and measured 24 h after the last of two injections of interleukin. Interleukin 1 beta, at all examined doses, increased thyroid follicular cell proliferation when compared to controls (p < 0.05), and a positive correlation between log of the dose of IL-1 beta used and LI (r = 0.62, p < 0.05) using Student's t-test was found. The administration of aIL-1ra alone also enhanced the thyroid follicular cell proliferation, whereas aIL-1ra used together with IL-1 beta exerted a less pronounced effect than each of these substances used separately (p < 0.05). Interleukin 1 alpha at the dose of 10.0 micrograms/kg body wt increased the proliferation of thyroid follicular cells (p < 0.05). Thyroid hormone levels did not change in any of the experiments. These results suggest a regulatory role of IL-1 upon the proliferation of thyroid cells.

Animals↗
PubMed1993

Effects of new somatostatin analogs on the cell proliferation of colonic crypts and colonic cancers in rats.

The antiproliferative activity of two new somatostatin (SS) analogs: ASS-51 and ASS-52 have been tested in this study. We assessed their ability to inhibit the DNA synthesis in normal colon crypt cells and in the cells of chemically (dimethylhydrazine)-induced colon cancer in the rats. The incorporation of bromodeoxyuridine (BrDU) into appropriate cell nuclei was used as an index of DNA synthesis. It was found that: 1) Only ASS-51 significantly decreases the colon crypt cell proliferation in the rat when compared to controls. Since both analogs were previously shown to inhibit GH release, these data indicate that the antiproliferogenic effect of ASS-51 is independent of the inhibition of GH release. 2) Both examined analogs did not significantly effect the BrDU incorporation into cell nuclei of chemically-induced colon cancer.

Adenocarcinoma↗
PubMed1993

Failure of tripeptide colon mitosis inhibitor to suppress the cell proliferation of dimethylhydrazine-induced colonic cancers in rats.

The effects of tripeptide colon mitosis inhibitor (CMI, pGlu-His-Gly-OH) on the proliferation of tumoral cells of dimethylhydrazine (DMH)-induced colonic cancers in rats were studied. Additionally, the effects of CMI on hyperplastic colonic crypts in DMH-treated rats and on normal colonic crypts in carcinogen-untreated rats were estimated. As an index of the cell proliferation the incorporation of bromodeoxyuridine (BrDU) into cell nuclei was used. It was found that the tripeptide significantly suppressed the proliferation of the colonic crypts in normal, carcinogen-untreated rats. However, it failed to suppress the cell proliferation of DMH-induced colonic adenocarcinomas or adenomas and produced only a slight, statistically insignificant decrease of the BrDU labelling index in hyperplastic colonic mucosa of DMH-treated rats. These findings suggest that the process of carcinogenesis might 'switch off' the local negative control of the colonic cell proliferation exerted by endogenous CMI.

Adenocarcinoma↗
PubMed1992

Thyroliberin (TRH) increases thymus cell proliferation in rats.

The effects of thyroliberin (TRH), a TRH-like tripeptide colon mitosis inhibitor (CMI), a somatostatin analog SMS 201-995 and metoclopramide (dopamine receptor antagonist enhancing prolactin secretion) on rat thymus cell proliferation were investigated. The incorporation of bromodeoxyuridine (BrDU) into thymic cell nuclei was used as an index of the proliferation. It was found that TRH, but not other compounds investigated herein, increased the thymus cell proliferation 12 hours after the injection.

Amino Acid Sequence↗
PubMed1992

Chronic metoclopramide treatment stimulates T lymphocyte proliferation in the spleen but not in the thymus.

The effect of chronic metoclopramide administration (for 10 days at a daily dose of 5 mg/kg body weight subcutaneously) on cell proliferation in spleen and in thymus was investigated. Cell proliferation was evaluated by the stathmokinetic method with the use of vincristine. It was found that metoclopramide administration results in a statistically significant increase in the value of the mean mitotic activity rate index (MMAR) of splenocytes in the areas around arteries. At the same time no statistically significant changes were demonstrated in the MMAR index values obtained for splenocytes present in the germinal centers of the spleen. No significant changes in the MMAR index could also be found for thymocytes.

Animals↗
PubMed1991

Inhibitory effect of bombesin and SMS 201-995 on DNA synthesis in the rat thyroid lobes incubated in vitro.

The effects of 4-h incubation in the presence of bombesin on the incorporation of [3H]-thymidine into DNA of the rat thyroid lobes, collected from animals treated in vivo with a long-acting somatostatin analog (SMS 201-995) or with 0.9% NaCl, were investigated. It was shown that not only in vivo injections of SMS 201-995, but also, unexpectedly, in vitro incubation with bombesin inhibited [3H]-thymidine incorporation. The two examined substances did not reveal any additive action in their inhibitory effects on the thyroid growth.

Animals↗
PubMed1990

Influence of somatostatin and epidermal growth factor (EGF) on the proliferation of thyroid follicular cells in organ culture.

The aim of the present study has been to examine the effects of various concentrations of somatostatin (SS), epidermal growth factor (EGF), as well as of interactions among SS, EGF and thyrotropin (TSH) in their influence upon the mitotic activity of thyroid follicular cells (TFC) in organ culture. The stathmokinetic method was employed. It was shown that: (1) SS, at the concentration of 10(-7) M, suppressed the mitogenic effect of TSH, as well as of TSH and EGF employed together, on TFC; (2) EGF, at the concentration of 10 and 100 ng/ml, increased the mean mitotic activity rate of TFC; (3) TSH and EGF revealed an additive action on TFC proliferation. The obtained results evidently suggest an antiproliferative effect of SS and mitogenic action of EGF on TFC in organ culture.

Animals↗
PubMed1989

Influence of melatonin and N-acetylserotonin on the cyclic AMP concentration in the rat thyroid lobes incubated in vitro.

Effects of melatonin and N-acetylserotonin on the cyclic AMP (cAMP) concentration in the organ-cultured rat thyroid gland were investigated. Exposure of the thyroid explants to melatonin (10(-8) M) resulted in a decrease of cAMP levels. Melatonin at higher concentrations (10(-7) M and/or 10(-6) M) failed to influence the thyroid cAMP level. N-acetylserotonin (10(-6) M), like melatonin in the lowest concentration employed, reduced cAMP concentrations in the thyroid explants when compared with controls. Unexpectedly, melatonin (at a concentration of 10(-7) M) added to the incubation medium with TSH (60 mU/ml), decreased the cAMP concentration in the thyroid compared with the group exposed to melatonin (10(-7) M) alone.

Animals↗
PubMed1989

Melatonin-induced suppression of human lymphocyte natural killer activity in vitro.

One of the important immune functions influenced by neuroendocrine factors is natural killer (NK) activity, which is directed against neoplastic and virus-infected cells. The effects of melatonin (Mel) and N-acetylserotonin (NAc-5HT) on NK activity of human peripheral blood lymphocytes were investigated. Leukocytes of healthy human subjects were used in the experiment. NK activity was estimated by measurement of radioactive chromium (51Cr) release from human leukemia cells K 562 (target cells). The previous exposure of human lymphocytes (effector cells) to Mel in concentrations of 10(-6) M and 10(-10) M resulted in an inhibition of NK activity (P less than 0.01) for all the examined effector-target cell ratios (10:1; 20:1, 40:1). NK activity was also suppressed by Mel (10(-8) M), but only if effector-target ratio equal to 20:1 was used (P less than 0.02), and by Mel (10(-12) M) for effector-target ratio equal to 40:1 (P less than 0.05). In none of the examined concentrations did NAc-5HT inhibit NK activity of human lymphocytes. On the basis of the data reported above, a direct suppressive effect of Mel (but not of NAc-5HT) on NK activity of human peripheral blood lymphocytes can be assumed.

Cells, Cultured↗
PubMed1988

Inhibitory effect of somatostatin on the basal and TSH-stimulated 3H-thymidine incorporation into rat thyroid lobes incubated in vitro.

The effects of somatostatin on the spontaneous and TSH--stimulated incorporation of tritiated thymidine into the rat thyroid lobes incubated in vitro were investigated. The rate of 3H-thymidine incorporation was used as an index of thyroid follicular cells (TFC) proliferation. It was shown that: 1) somatostatin, at a concentration of 10(-7)M, decreased 3H-thymidine incorporation into DNA of TFC, 2) the highest somatostatin concentration, as tested in this study (10(-6)M), produced a similar decreasing effect; the decrease, in this case, did not attain significance vs. controls, 3) somatostatin, when employed together with TSH, suppressed the stimulatory effect of the latter hormone on 3H-thymidine incorporation into DNA of thyroid lobes.

Animals↗
PubMed1988

Influence of sympathetic denervation of the thyroid by superior cervical ganglionectomy on the growth processes in the gland in basal conditions and after hemithyroidectomy.

The aim of the present study has been to examine the effects of superior cervical ganglionectomy (SCGx) on the hypertrophic (thyroid lobe weight) and hyperplastic (thyroid mitotic activity) response of the rat thyroid gland in basal conditions or after hemithyroidectomy (hemiTx), both being assessed 14 days after the surgeries. It has been shown that: 1) Ipsilateral and/or bilateral SCGx brought about the growth (both hypertrophy and hyperplasia) of thyroid lobes in the animals with intact thyroid; the strongest hypertrophic reaction occurred after ipsilateral SCGx and the strongest hyperplastic response followed bilateral SCGx. 2) Unilateral SCGx, when performed ipsilaterally to the remaining thyroid lobe after hemiTx amplified the hypertrophic, but not hyperplastic response of this lobe. Both contralateral and bilateral SCGx had no effect on the hypertrophy of the remaining thyroid lobe. Unexpectedly, both bilateral and contralateral SCGx exerted the suppressive effect on the hyperplastic response of the thyroid lobe following hemiTx. These results indicate that the sympathetic innervation plays an important role in the control of thyroid growth of intact animals and/or after hemiTx.

Animals↗