Pathologic features of the epididymis in patients with epididymal obstructive azoospermia: Observation of 11 cases / 中华男科学杂志

<p><b>Objective</b>To search for potential therapeutic targets for epididymal obstructive azoospermia (EOA) secondary to epididymal infection by observing the pathologic features and analyzing the possible pathophysiologic mechanisms of the disease.</p><p><b>METHODS</b>Eleven 28－53 years old infertile men with the history of epididymal infection were enrolled in this study, all diagnosed with azoospermia by routine semen examination and centrifugation. EOA was confirmed by further examinations of reproductive hormones and seminal plasma biochemical markers and scrotal ultrasonography, followed by surgical exploration and observation of the pathological characteristics of the epididymis.</p><p><b>RESULTS</b>The gross epididymal specimen showed fluid accumulation in the epididymal tube to be the main pathologic feature. Under the microscope, the epididymal duct lumen was structurally intact but distended and with no sperm. Most of the cases revealed no inflammatory cell invasion in the wall of the duct. A small number of the patients with a longer course of disease exhibited cell infiltration in the lumen, hyperblastosis and glassy degeneration of the interstitial fibers, and scattered infiltration of lymphocytes and acidocytes in addition to expansion of the epididymal duct.</p><p><b>CONCLUSIONS</b>EOA secondary to epididymal infection is pathologically characterized mainly by fluid accumulation in the epididymal duct, and its pathogenesis remains to be further studied.</p>

Expression of hypoxia-inducible factor 1 alpha and vascular endothelial growth factor in prostate cancer and its significance / 中华男科学杂志

<p><b>OBJECTIVE</b>To study the expression of hypoxia-inducible factor 1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF) in prostate cancer (PCa) and its biological significance.</p><p><b>METHODS</b>Specimens from 75 patients with PCa (32 cases), benign prostatic hyperplasia (BPH, 16 cases), high-grade prostate intraepithelial neoplasia (PIN, 15 cases) and normal prostate (NP, 12 cases) were comprised in the study. The PCa was divided into high Gleason score group (Gleason score > or = 7) and low Gleason score group (Gleason score < 7). Immunohistochemistry was performed with antibodies against HIF-1 alpha, VEGF and CD34. Microvessel density (MVD) was analyzed by staining with antibodies to CD34.</p><p><b>RESULTS</b>The positive rates of HIF-1alpha were significantly higher in PCa (62.5%) and PIN (60.0%) than those in BPH (6.3%) and NP(0) (P < 0.05), respectively. The positive rates of VEGF were significantly higher in PCa (78.1%) and PIN (73.3%) than those in BPH (18.7%) and NP (8.3%) (P < 0.05), respectively. A higher concentration of MVD was observed in PCa (66.9 +/- 18.0) compared with those in BPH (28.3 +/- 6.9) and NP (15.3 +/- 2.9) (P < 0.05). MVD and the positive rates of HIF-1alpha and VEGF were significantly higher in high Gleason score group than those in low Gleason score group.</p><p><b>CONCLUSION</b>The results suggest that the overexpression of HIF-1alpha and VEGF are closely related to PCa, and the son score group. up-regulation of HIF-1alpha and VEGF are early events in PCa.</p>

Changes of pulmonary tissue area density and their mechanisms in rats with hypoxic pulmonary hypertension / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the changes of pulmonary tissue area density and their mechanisms in rats with hypoxic pulmonary hypertension (HPH).</p><p><b>METHODS</b>54 Wistar rats were divided into hypoxia 10 d (n = 12), 20 d (n = 12), 30 d (n = 12) groups and control group (n = 18). The rats in hypoxia groups were exposed to a simulated hypoxia environment at a height of 5 km above sea level to establish HPH models. The changes in pulmonary tissue area density and pathological morphology were determined by image analysis, optical microscope, electron microscope and histochemistry.</p><p><b>RESULTS</b>After hypoxia, the pulmonary tissue area density markedly increased on 10 d (27.08% +/- 1.29%, P < 0.05), especially on 20 d (31.33% +/- 0.27%) and 30 d (31.10% +/- 1.95%) while that in control group was 22.78% +/- 1.17% (P < 0.01). The area density on 20 d was higher than that on 10 d (P < 0.05) but there wasn't significantly different between 10 d and 30 d (P = 0.057) after hypoxia. Pathological examination showed: edema and collapse of pulmonary tissue, swelling and degeneration of type II alveolus epithelial cells (PII); congestion, accumulation of polymorphonuclear neutrophils and platelets in capillaries; swelling and degeneration of endothelial cells, thickening of basement membranes.</p><p><b>CONCLUSIONS</b>Hypoxia can induce increase in pulmonary tissue area density and decrease in aerial exchange area in alveoli. These changes may be related to the pulmonary collapse caused by the damage of PII and pulmonary surfactant system, structural remodeling of small pulmonary arteries, increase in blood cells and protein granules in alveolar cavity.</p>