Serum estradiol fluctuations in women may influence the response of urothelial carcinoma to intravesical bacillus Calmette-Guerin treatment.”
“Purpose: Androgen independent prostate cancer growth and metastasis are a major cause of prostate cancer death. Aberrant androgen receptor activation check details due to androgen receptor mutation is an important
mechanism of androgen independence. We determined the effectiveness and mechanism of 17 alpha-estradiol (Sigma(R)) in blocking aberrant androgen receptor activation due to androgen receptor mutation.
Materials and Methods: We used LNCaP and MDA Pca-2b prostatic tumor cells (ATCC(R)) containing a mutated androgen receptor and WT estrogen receptor beta to test 17 alpha-estradiol inhibition of aberrant androgen receptor activation of prostate specific antigen gene expression and cell growth. Cotransfection analysis was used to further elucidate the mechanism of 17 alpha-estradiol action. Xenograft animals with an LNCaP prostate tumor were prepared to study the in vivo effect of 17 alpha-estradiol on tumor growth inhibition.
Results:
In LNCaP cells 17 alpha-estradiol produced a dose dependent inhibition of cyproterone acetate (Sigma) or dihydrotestosterone induced prostate specific antigen gene expression. In MDA Pca-2b cells 17 alpha-estradiol inhibited cortisol FG-4592 (Sigma) induced prostate specific antigen
expression and blocked dihydrotestosterone and cortisol induced cell proliferation in LNCaP and MDA Pca-2b cells, respectively. Cotransfection analysis showed that 17 alpha-estradiol inhibition of aberrant androgen receptor activation of prostate specific antigen gene expression was medicated via estrogen receptors. In xenograft mice with LNCaP prostate cancer 17 alpha-estradiol but not 17 beta-estradiol (Sigma) significantly inhibited tumor growth, although each estrogen tended to decrease tumor growth.
Conclusions: Results suggest that 17 alpha-estradiol with less classic estrogenic activity is a potential therapeutic agent for androgen independent prostate cancer selleck kinase inhibitor due to androgen receptor mutation.”
“Introduction. – In Alzheimer’s disease (AD), transcranial magnetic stimulation (TMS) studies have been limited to test motor cortical excitability. The aim of this study was to investigate the inhibitory circuits of the motor cortex and to relate these to measures of cognitive function in AD patients. Results were compared with those of a control group of healthy subjects matched for age, sex and education.
Patients and methods. – Forty-five AD patients and 37 healthy volunteers were included in the study. Each participant received a neurological evaluation, Mini-Mental State Examination (MMSE), and Clinical Dementia Rating (CDR).