Previously, it has been demonstrated that the neurotrophins and their receptors are present in human prostate tissue, but neither their functional role nor localization is clearly understood. We studied the expression of neurotrophins and their receptors in prostate cancer. Between 1990 and 1999, 48 prostate cancer specimens were obtained from patients undergoing radical prostatectomy, of whom 25 received neoadjuvant hormonal therapy (NHT) and 23 were untreated. The specimens were analyzed immunohistochemically for neurotrophins (nerve growth factor, brain derived neurotrophic factor, neurotrophin 3, neurotrophin 4/5) and their receptors (TrkA, TrkB, TrkC, p75NTR). Immunohistochemical studies revealed that both benign and malignant prostate gland epithelial cells expressed the neurotrophins and their receptors to various degrees, but no obvious immunopositive reaction was observed in stromal cells. In benign epithelial cells, the neurotrophins were localized to secretory cells and the receptors were localized to basal cells. The neurotrophins, TrkA and TrkC were expressed to a similar extent in prostate cancer specimens obtained from patients both with and without NHT. In contrast, the expression of TrkB was downregulated and the expression of p75NTR was up-regulated in prostate cancer after hormonal therapy. These findings suggest that neurotrophins are secreted by prostate cancer cells in an autocrine fashion. Neurotrophins may be involved, through their receptors, in the escape mechanism from cell death after androgen depletion found in prostate cancer.
Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ender differences in the incidence of various types of ventricular arrhythmias have been reported. Torsades de pointes associated with long QT syndrome is more common in females than males. 1,2 The higher incidence of Brugada syndrome in males than females 3-5 is associated with gender differences in the early phase of ventricular repolarization, that is, the greater transient outward potassium current (Ito)-mediated phase 1 notch in the right ventricular epicardium in males than females. 6 Early repolarization syndrome is characterized by a prominent J wave and by ST-segment elevation in the left precordial leads; it is most commonly seen in young males. 7 Although the mechanisms underlying early repolarization syndrome remain unknown, it has been suggested to share notable cellular and ionic similarities with Brugada syndrome. 7-10Studies on gender-related repolarization differences have focused on the duration of repolarization, such as the longer QT 11,12 and JT intervals 13 in females than in males. While these sex differences in ventricular repolarization are not observed before, they become obvious after puberty, suggesting an important effect of sex hormone. In contrast, gender differences have been reported in the configuration of the ST segment in healthy subjects. 11 Previous studies showed that after puberty, the J point amplitude is higher and the ST segment angle is steeper in males. 14,15 However, little is currently known about age-and gender-related differences in the ST levels in the different leads that represent the right and left ventricles.Androgen-deprivation therapy, 16,17 a neoadjuvant treatment for prostate cancer, might strongly inhibit the hormonal modulation of not only prostate cells but also of cardiac ventricular myocytes. Although this therapy is associated with increased risks of cardiovascular death in patients with prostate cancer, 18,19 its effects on ventricular repolarization including the ST segment remain to be elucidated.We studied healthy subjects to identify age-and gender differences in the ST segments in leads V2 and V5, which are Background: ST-segment elevation in a structurally normal heart is observed in Brugada- and early repolarization syndrome. The incidence of both syndromes is much higher in males than females. Clinical and basic studies suggest that testosterone plays an important role in ventricular repolarization.
Spinal cord injury (SCI) at Thl3 was induced in female Wistar rats, and changes in the urinary bladder were examined during the acute phase of SCI. Wet weights of the spinal bladders increased twofold over controls by 7 days after SCI. Intravesical volumes increased sixfold over control values by day 3, and then decreased 7 days after the injury. Maximal pressure within the bladder decreased in all spinal rats compared with controls. Smooth muscle cells were isolated from the urinary bladder, and their total protein and DNA content were measured by multiparametric cytofluorometry. DNA content of isolated smooth muscle cells decreased by day 3 and remained 7 days after the spinal injury. Total protein content of isolated smooth muscle cells was decreased 1 day after and increased 7 days after the spinal injury, just when spinal reflex of the bladder recovered. These findings suggest that hypertrophy of smooth muscle cells in urinary bladder is related to the activity of peripheral autonomic nerve and that smooth muscle cells already begin to hypertrophy during the spinal shock period to adjust themselves to the new state, that is, the spinal bladder.
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