Prostatic steroid binding protein

The suggested dosage for androgens varies depending on the age, and diagnosis of the individual patient. Dosage is adjusted according to the patient’s response and the appearance of adverse reactions. The dosage guideline for the testosterone pellets for replacement therapy in androgen-deficient males is 150mg to 450mg subcutaneously every 3 to 6 months. Various dosage regimens have been used to induce pubertal changes in hypogonadal males; some experts have advocated lower doses initially, gradually increasing the dose as puberty progresses, with or without a decrease in maintenance levels. Other experts emphasize that higher dosages are needed to induce pubertal changes and lower dosages can be used for maintenance after puberty. The chronological and skeletal ages must be taken into consideration, both in determining the initial dose and in adjusting the dose.

The  Journal of American Medical Association released a 1998 review stating that s aw palmetto is effective in improving urological symptoms and urine flow . For the review, 18 randomized trials with almost 3,000 male participants were analyzed; 28 percent of the men taking saw palmetto showed fewer urinary tract symptoms, 24 percent showed improvement in peak urine flow and overall urine flow improved for 43 percent of the participants. The results were comparable to the group taking Proscar — a prescribed medication — and they were much more promising than the men taking a placebo.

Prostatic neoplasms were studied for estrogen binding using four methods. Two employed fluorescent estrogen histochemical ligands, one was a new immunocytochemical technique using specific monoclonal antibodies to human estrophilin, and the last procedure was conventional biochemical dextran-coated charcoal assay. Results indicated that the fluorescent ligands recognized closely associated but separate estrogen-binding sites (putative type II sites) which in turn differed from the binding site measured biochemically. Studies with the monoclonal antibodies were nearly always negative, suggesting that prostatic estrogen receptor might vary antigenically from that present in breast and endometrium. Histochemical and biochemical androgen-binding studies were also compared and showed a close association. In the prediction of hormonal response in advanced prostate cancer both showed high sensitivity and low specificity. The addition of estrogen-binding data did not improve the predictive value of the androgen-binding histochemical assay. However, combining results of the biochemical and histochemical androgen-binding assays resulted in significant improvement of the specificity without loss of sensitivity, suggesting that there is a degree of positive interaction between the binding sites assayed by the two methods.

The function of regulatory regions of DNA, which flank the genes for prostatic steroid binding protein, is being analysed by introducing the cloned genes into heterologous cells. Two non-allelic genes for the C3 polypeptide, C3(1) and C3(2) have been transfected into androgen-responsive S115 cells using SV2-gpt vectors. The genes have been introduced either intact or as so-called fusion genes consisting of putative C3 promoters plus human β-interferon cDNA. Both genes for C3 were accurately transcribed and their expression was stimulated 5–10-fold with 10 −8 M testosterone. Thus we should be able to define at least one region of DNA which confers androgen sensitivity to the genes. Although both genes were expressed similarly in S115 cells only C3(1) is responsible for C3 in vivo and C3(2) is transcribed poorly, if at all. The most likely explanation for the difference is that in vivo the C3(2) gene remains hypermethylated whereas the DNA which was introduced into S115 cells was unmethylated. This result supports the notion that the state of DNA methylation is important for controlling the transcription of genes.

Prostatic steroid binding protein

prostatic steroid binding protein

The function of regulatory regions of DNA, which flank the genes for prostatic steroid binding protein, is being analysed by introducing the cloned genes into heterologous cells. Two non-allelic genes for the C3 polypeptide, C3(1) and C3(2) have been transfected into androgen-responsive S115 cells using SV2-gpt vectors. The genes have been introduced either intact or as so-called fusion genes consisting of putative C3 promoters plus human β-interferon cDNA. Both genes for C3 were accurately transcribed and their expression was stimulated 5–10-fold with 10 −8 M testosterone. Thus we should be able to define at least one region of DNA which confers androgen sensitivity to the genes. Although both genes were expressed similarly in S115 cells only C3(1) is responsible for C3 in vivo and C3(2) is transcribed poorly, if at all. The most likely explanation for the difference is that in vivo the C3(2) gene remains hypermethylated whereas the DNA which was introduced into S115 cells was unmethylated. This result supports the notion that the state of DNA methylation is important for controlling the transcription of genes.

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