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Biomedical subjects

F Kohen

Publications and source records attributed to F Kohen.

At least 127 records · Page 7Linked to original sources
PubMed1978

Plasma progesterone levels during pregnancy and pseudo-pregnancy in the hare (Lepus europaeus syriacus).

A triphasic pattern of progesterone secretion was observed in female hares sampled throughout pregnancy and pseudopregnancy. After injection of hCG and artificial insemination (Day 1), progesterone values rose to a peak of 41.4 ng/ml about Day 14, remained at this level, then declined around Day 20 before increasing sharply to maximum levels of 67.7 ng/ml after midpregnancy (Day 28). Levels remained high for several days, then declined until Day 38, increased again until Day 41, before decreasing towards parturition. Progesterone levels were still high (37.5 ng/ml) 24h before parturition. The progesterone pattern during pseudopregnancy closely resembled that observed during the first half of pregnancy: levels rose from Day 2 to a peak at Days 11--18, then declined sharply to baseline levels around Day 22. It is suggested that the control of progesterone secretion might be transferred from the pituitary to the placenta at the beginning of the second half of pregnancy.

Animals↗
PubMedDate not supplied

Inhibitors of protein tyrosine phosphorylation: preliminary assessment of activity by time-resolved fluorescence.

Epidermal growth factor (EGF) receptor (ErbB1)-associated tyrosine kinase inhibitors may act as potential chemotherapeutic agents. In order to assess the inhibitory activity of these compounds, we developed a simple and sensitive assay based on time-resolved fluorescence. In this technique, crude cell lysates bearing the ErbB1 receptor were captured in microtitre plates immobilized with monoclonal anti-ErbB1 antibody SG 565. Subsequently, the phosphotyrosine content of the cell lysates was quantified by a europium-labelled anti-phosphotyrosine antibody. Thus, genistein, a tyrosine kinase inhibitor, was capable of reducing by half the tyrosine phosphorylation caused by the binding of EGF to A431 cells, whereas 6-carboxymethyl genistein did not inhibit protein tyrosine phosphorylation. This assay is simple to perform, does not use radioactive substrates, and can be useful for screening EGF receptor tyrosine kinase inhibitors from natural products or synthetic compounds. Moreover, the assay has a high signal:noise ratio and is suitable for large-scale screening.

Animals↗
PubMedDate not supplied

Isoluminol as a marker in direct chemiluminescence immunoassays for steroid hormones.

We have used isoluminol steroid hormone conjugates in competitive heterogeneous chemiluminescence immunoassays (CIA) for estradiol, progesterone and estriol in body fluids. The assays did not require prior extraction of the steroid hormone with an organic solvent. Polyclonal or monoclonal antibodies, covalently coupled to polyacrylamide microspheres or adsorbed onto the plastic surface of microtritation plates via an intermediate second antibody, were used as solid-phase. The latter solid-phase system allows rapid processing of incubation mixtures. Sensitive and reliable direct CIAs for estradiol in serum, progesterone in serum and in saliva and for estriol in saliva have been developed and their clinical utility has been assessed. Sensitivities ranged from 0.54 to 0.04 nmol/l, and precision (% CV) ranged from 10% to 16%.

Estradiol↗
PubMedDate not supplied

Synergistic effect of testosterone and of a luteinizing hormone-releasing hormone agonist on androgen receptor content in the ventral prostate of castrated rats.

The aim of the present experiment was that of studying the effect of an LHRH agonist analog on the prostatic content of cytosol and nuclear salt-extractable and salt-resistant androgen receptors (AR). Castrated rats were treated for six days with the LHRH agonist WY 40972 (A), with testosterone enanthate (T) or with A plus T. Intact adult male rats and castrated rats treated with the vehicle served as controls. The animals were sacrificed 18 h after the last subcutaneous injection. The ventral prostates were quickly removed and submitted to subcellular fractionation for the determination of cytosol and nuclear AR content. In addition, the weights of the prostates and of the seminal vesicles were recorded, and serum levels of LH and FSH were evaluated by radioimmunoassay. The dissociation constants (Kd) of cytosol and nuclear AR, on the order of 1 x 10(-9) M, were not affected by the various treatments. Conversely, the combined treatment with T and A induced a significant increase of nuclear AR in the prostatic tissue, when compared to the levels found in castrated rats treated with T alone and in intact rats. The treatment with T was able to restore the reproductive organs to their normal weights. The treatment with A inhibited the hypersecretion of gonadotropins induced by castration. The results show that, under the conditions of the present experiment, A exhibits a synergistic effect with T on nuclear AR content in the rat ventral prostate. The results also suggest that A acts directly on this androgen-dependent structure.

Animals↗
PubMedDate not supplied

Anabolic effects of estrogen and parathyroid hormone on skeletal tissues: the use of creatine kinase B activity as a response marker.

The rapid stimulation of the specific activity of the brain type isozyme of creatine kinase (CK BB) is an almost universal marker of cell stimulation. We have studied its stimulation in skeletal-derived cells and shown that the increase in its activity is closely correlated with the biochemical parameter of cell proliferation - [(3)thymidine incorporation into DNA - and with the morphological parameters of bone growth, increase in thickness of cortical bone and of the number of cells in the proliferating zone of the epiphyseal growth plate. We have used the increase in CK activity to demonstrate sex specific stimulation of diaphyseal bone, exclusively by estrogens in females and by androgens in males, and the dependence of sex steroid stimulation on an adequate level of vitamin D. After finding that parathyroid hormone can act as a mitogen via a phospholipase-C-phosphoinositide turnover pathway, we collaborated with colleagues at the GBF in Braunschweig to find that mid-region fragments of PTH could act exclusively as mitogens, without stimulating cAMP production leading to bone resorption. hPTH (28-48) variants designed to be resistant to proteolysis were efficient in stimulating CK specific activity in vitro and in vivo and increased cortical bone thickness and the number of proliferating epiphyseal cartilage cells in rat long bones. These results are put into an historical context and compared with recent studies, in this short, selective review.

Journal Article↗
PubMedDate not supplied

Regulation of fas ligand expression in breast cancer cells by estrogen: functional differences between estradiol and tamoxifen.

During neoplastic growth and metastasis, the immune system responds to the tumor by developing both cellular and humoral immune responses. In spite of this active response, tumor cells escape immune surveillance. We previously showed that FasL expression by breast tumor plays a central role in the induction of apoptosis of infiltrating Fas-immune cells providing the mechanism for tumor immune privilege. In the present study, we showed that FasL in breast tissue is functionally active, and estrogen and tamoxifen regulate its expression. We identified an estrogen recognizing element like-motif in the promoter region of the FasL gene, suggesting direct estrogen effects on FasL expression. This was confirmed by an increase in FasL expression in both RNA and protein levels in hormone sensitive breast cancer cells treated with estradiol. This effect is receptor mediated since tamoxifen blocked the estrogenic effect. Interestingly, tamoxifen also inhibited FasL expression in estrogen-depleted conditions. Moreover, an increase in FasL in breast cancer cells induces apoptosis in Fas bearing T cells and, tamoxifen blocks the induction of apoptosis. These studies provide evidence that tamoxifen inhibits FasL expression, allowing the killing of cancer cells by activated lymphocytes. This partially explains the protective effect of tamoxifen against breast cancer.

Breast Neoplasms↗