Boys with cryptorchidism with an insufficient testosterone surge after HCG risk infertility despite early and successful surgery. The testicular biopsy assists in identifying those who might benefit from hormonal treatment following successful orchiopexy.
Human platelet-derived growth factor (PDGF) is mainly composed of two polypeptide chains (PDGF-AB). All three possible dimeric forms of PDGF-i.e., PDGF-AA, PDGF-BB and PDGF-AB-exist in nature. We have used two recombinant PDGF homodimers to determine the roles of each isoform in the activation of phosphatidylinositol turnover in vascular smooth muscle cells (VSMC) isolated from rat thoracic aorta, their mitogenic effect on VSMC, and their vasoconstrictor effect on intact strips of aortic vascular tissue. Three Ca2 -channel blockers, nifedipine, verapamil, and diltiazem, were used as antagonists for investigating the PDGFdependent changes mediated by the homodimers. PDGF-BB had a greater efficacy than PDGF-AA on inositol 1,4,5-trisphosphate release, on the formation of diacylglycerol, and on Ca2+ mobilization, which was also associated with vasoconstrictor activity and effective mitogenicity. PDGF-AA, on the other hand, was more potent than PDGF-BB in stimulating protein kinase C. In all instances, the activation of the phosphatidylinositol turnover by the two homodimers was inhibited by the Ca2+-channel blockers.
Manidipine, a Ca2+-channel blocker, at concentrations that lower elevated blood pressure, modulates the transcription rates of cytokine genes in the mesangial cells of humans that had been stimulated with platelet-derived growth factor BB isomer; although the transcription for mRNA of interleukin 1p3 and granulocyte/monocyte colony-stimulating factor was inhibited, the transcription of mRNA for interleukin 6 was enhanced. Additionally, the induction of c-fos, c-jun, and 3-hydroxy-3-methylglutaryl-coenzyme A reductase transcription was inhibited by manidipine. We conclude that manidipine, at nanomolar concentrations, is efficacious in modulating gene transcriptions that are involved in proinflammatory changes of mesangial cells. Thus, manidipine, at pharmacological concentrations that are one to two orders of magnitude lower than those required for inhibition of agonist-or depolarization (K+)-induced vasoconstriction, causes changes in the activity of the genes that code for inflammatory mediators.
Extensive apoptosis is a phenomenon that occurs regularly in the germinal epithelium of the contralateral testis in testicular torsion. Specifically primary and secondary spermatocytes are predominantly affected. Notably spermatogonia, capillary endothelium, connective tissue and peritubular fibroblasts are rarely involved. A selection strategy has seemingly evolved that precludes the possibility of the perpetuation of genetic mutations. We hypothesize that trauma to the blood-testis barrier initiated by testicular torsion induces the release of apoptotic activating factors (cytokines), which subsequently cause extensive apoptosis in the germinal epithelium of the contralateral testis. Therefore, it is probable that repeat apoptotic episodes may explain the high incidence of infertility in these patients.
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