Degeneration of the seminiferous epithelium with ageing is a cause of spermatoceles?

A spermatocele refers to the cystic accumulation of semen in the male reproductive tract. Although it is thought to be caused by narrowing of the lumen of the excurrent duct with resultant cystic dilatation of the duct, the pathogenesis of the narrowing remains unknown. In the present study, we histologically examined spontaneous spermatoceles in C3H/He mice to elucidate the pathogenesis of the lesions. Testes, efferent ducts, epididymides and vas deferens obtained from young and aged C3H/He mice were embedded in plastic for histological observation at the light microscopic level. It was found that spontaneous spermatoceles were localized in the rete testis and efferent ducts of aged mice, as seen in man. The dilated rete testis and efferent ducts contained many degenerated and aggregated germ cells derived from the exfoliated seminiferous epithelium in the aged testis. In particular, it was noted that the agglutinated germ cells obstructed the narrow lumen of the efferent ducts, resulting in the failure of transport of germ cells to the caput epididymis, and spermatoceles were consistently found in the region between the rete testis and the obstructed site in the efferent ducts. However, no inflammatory cell infiltration, traumatic injury or spermatic granulomas were found in the occluded region. These results suggest that agglutinated germ cells may occupy the narrow lumen of the efferent ducts, resulting in the formation of a spermatocele. It may be that a senile change to the seminiferous epithelium, which releases immature germ cells into the lumen of the seminiferous tubules, is the cause of this type of spermatocele.     

Hemodialysis access graft failure: time to revisit an unmet clinical need?

Hemodialysis (HD) access complications constitute a major cause of morbidity in HD patients. The failure of HD access grafts is predominantly due to progressive intimal hyperplasia (IH) at the venous anastomosis, resulting in a graft flow decline, which ultimately gives rise to graft thrombosis. To date, all tested pharmacological and surgical interventions have not resulted in increased arteriovenous (AV) graft patency rates in HD patients. In this review, we address the mechanisms contributing to AV graft failure and discuss several "emerging" strategies, which could hold promise for optimizing AV graft patency rates. In view of the failure of systemic therapies and the predictable localization of IH, local therapeutic strategies comprise the most promising interventions to improve AV graft patency rates. Based on the large number of promising candidates including drug-eluting stents and brachytherapy, the unmet clinical need for AV graft failure in HD patients is likely to be revisited in the very near future. The biggest challenge, however, remains to translate basic experimental findings into clinical benefits. Simultaneously, continuous efforts should be undertaken to increase the percentage of patients utilizing AV fistulas, which remains the best form of permanent vascular access (VA) for HD.     

Misplacement of dysplastic epithelium in Peutz-Jeghers Polyps: the ultimate diagnostic pitfall?

Peutz-Jeghers syndrome is characterized by multiple polyps throughout the gastrointestinal tract in association with mucocutaneous pigmentation. Small bowel polyps in the syndrome may exhibit epithelial misplacement, into the submucosa, the muscularis propria, and even the subserosa. The authors demonstrate two patients in whom there is also misplacement of dysplastic epithelium into the submucosa and muscularis propria of the small bowel. Epithelial misplacement is recognized to mimic invasive malignancy. Such mimicry is heightened substantially when the misplaced epithelium is dysplastic. Correct interpretation of the histologic changes is aided by the use of special stains, which demonstrate the associated lamina propria and the lack of a desmoplastic response, and immunohistochemistry, which shows that the misplaced dysplastic epithelium is accompanied by non-neoplastic mucosa. There is an increased prevalence of gastrointestinal malignancy in Peutz-Jeghers syndrome. However, the presence of perplexing histologic features, caused by epithelial misplacement, especially when some of that epithelium is dysplastic, in small bowel polyps at least has the potential for the overdiagnosis of malignancy in the syndrome.     

The patients less than 50 years: is there a need to lower the PSA cutoff point?

The aim of this study was to study the incidence and possibility of prostate cancer detection in patients <50 years with prostate-specific antigen (PSA) <4 ng ml(-1). Between January 2006 and January 2008, 355 men were subjected to radical cystoprostatectomy for bladder cancer. Among 162 cases without pathological prostatic invasion, random selection of two groups with serum PSA <4 ng ml(-1) was carried out. According to the age, 56 pairs in group A (< or =50 years) and group B (>50 years) were selected randomly. The resected prostate glands of each group were examined pathologically for evidence of prostatic adenocarcinoma. Correlation of the age groups with pathological findings, PSA, digital rectal examination (DRE) and body mass index (BMI) was carried out. The mean age of the groups (A and B) was 46.17+/-4.3 and 58.42+/-4.4 years, respectively. Mean PSA was 1.9+/-1.6 ng ml(-1) in group A and 2+/-1.6 ng ml(-1) in group B. Prostatic adenocarcinoma was detected in 1.8 and 10.7% in groups A and B, respectively (P=0.051). High-grade prostatic intraepithelial neoplasia (PIN) was higher in group A than in group B, 11 cases versus 4 (P=0.079). DRE was not significantly associated with pathological findings in those groups of patients. BMI was directly correlated with PSA in patients of group A (mean: 27.8+/-4.4, CC: 0.5, P=0.015), but not with that of group B (mean: 27.5+/-4.8, CC: 0.16, P=0.239). A new PSA cut-off point for younger patients (<50 years) is warranted. Serum PSA 2 ng ml(-1) is recommended as a cut-off point to screen and biopsy advice for nonsymptomatic patients <50 years. High-grade PIN was higher among the younger patients with low serum PSA, which indeed needs a meticulous follow-up.     

The inflammatory response to ischemic acute kidney injury: a result of the 'right stuff' in the 'wrong place'?

PURPOSE OF REVIEW: Ischemic acute kidney injury may be exacerbated by an inflammatory response. How injury elicits inflammation remains a major question in understanding acute kidney injury. The present review examines the hypothesis that molecules released by injured cells elicit inflammation. RECENT FINDINGS: After necrotic death, intracellular molecules find their way into the extracellular space. These molecules include heat shock proteins and HMGB1. Receptors for these proteins include TLR4, TLR2, CD91 and RAGE. These proinflammatory mechanisms may be so useful that nature has evolved mechanisms for programming necrotic death via poly(ADP-ribose) polymerase and cyclophilin D. In addition, apoptosis may also elicit inflammation. SUMMARY: The concepts discussed in this review are important for clinical medicine. Drugs and genetic manipulation may ameliorate ischemic kidney injury by regulating the inflammatory response to cell injury.     

Editorial Commentary: The Importance of Capsular Closure in Hip Arthroscopy: Is There a Limit to the Benefit?

Capsular closure is an important concept in hip arthroscopy and should be performed in nearly all patients. However, in patients with stiff hips and borderline arthritic changes, leaving the capsule unrepaired or performing a partial repair in the setting of a T-capsulotomy could result in successful outcomes.