Background: Benign prostatic hyperplasia (BPH) is the most common urogenital condition in aging males, while inflammation and tissue proliferation constitute the main pathophysiological factors. The adverse effects of currently available BPH medications limit patient compliance. We tested the protective effect of aescin against the development of BPH in rats. Methods: A total of 18 male Wistar rats were divided into 3 groups: control (sesame oil 1 mL/kg, s.c.); BPH (testosterone oenanthate 3 mg/kg, s.c., in sesame oil), and BPH-aescin rats (testosterone oenanthate 3 mg/kg, s.c. + aescin 10 mg/kg/day, p.o.). All treatments continued for 4 weeks. Serum and prostatic samples were harvested for biochemical and histopathological examination. Results: Induction of BPH by testosterone increased the prostate weight and prostate weight index, serum testosterone, prostate expression of inflammatory (IL-1β, TNF-α, and COX-2), and proliferative markers (PCNA and TGF-β1). Concurrent treatment with aescin decreased the testosterone-induced increase in prostatic IL-1β, TNF-α, and COX-2 expression by 47.9%, 71.2%, and 64.4%, respectively. Moreover, aescin reduced the prostatic proliferation markers TGF-β1 and PCNA by 58.3% and 71.9%, respectively, and normalized the prostate weight. Conclusion: The results of this study showed, for the first time, that aescin protected against the development of experimental BPH in rats via its anti-inflammatory and antiproliferative effects. These findings warrant further studies to clinically repurpose aescin in the management of BPH.

Background: This study aimed to investigate the expression of epithelial-mesenchymal markers’ E-cadherin, β-catenin, zinc-finger E-box-binding homeobox 1 (ZEB1), zinc-finger E-box-binding homeobox 2 (ZEB2) and p63 in transitional cell carcinoma (TCC) and squamous cell carcinoma (SCC) variants of bladder carcinoma (BC) and their correlation with clinicopathological parameters of prognostic importance. Methods: In this retrospective study, 91 patients were enrolled (66 with TCC and 25 with SCC). All patients had full clinical and follow-up data and available paraffin blocks. Immunohistochemical analysis was performed and correlated with clinicopathological factors. Results: In TCC cases, reduced E-cadherin, β-catenin positivity and p63 expression rate were evident in the sitting of increased expression of ZEB1 and ZEB2. Patients with ZEB2 positive tumors were more likely to die compared to those with negative ZEB2 (P = 0.024). Moreover, in patients with muscle-invasive BCs, an intense p63 expression was associated with poor overall survival (OS) (P < 0.001). For patients with SCC, there was a reduction in E-cadherin and β-catenin positivity with elevated p63 expression and concomitant increased ZEB1 and ZEB2 expression. Poor prognosis was evident in association with reduced E-cadherin, positive nuclear β-catenin/reduced membranous β-catenin, ZEB1 and ZEB2 positive cases as well patients with elevated p63 expression (P < 0.001). TCC and SCC cases showed similar poor prognosis in association with elevated p63 expression (P < 0.001). Conclusions: In both TCC and SCC variants, epithelial-mesenchymal transition (EMT) process is evident; however, its molecular mechanism shows some variations, specifically this notably different p63 expression pattern among two carcinoma variants with the similar impact of elevated p63 expression pattern on prognosis. World J Oncol. 2019;10(6):199-217 doi: https://doi.org/10.14740/wjon1234

This study aims to assess whether the expression of Twist1, Ki-67, and E-cadherin can guide the differential diagnosis of complete hydatidiform mole (CHM), partial hydatidiform mole (PHM), and hydropic abortion (HA). Differential expression of Twist1, Ki-67, and E-cadherin was analyzed in gestational products from 55 cases of CHM, PHM, and HA using immunohistochemistry. Prior to analysis, the studied cases were confirmed for their diagnosis by flow cytometric assessment of DNA ploidy and p57 immunostaining. Twist1 expression can distinguish CHM from PHM and HA with 100% sensitivity, 100%, specificity, 100% positive predictive value (PPV), and 100% negative predictive value (NPV). Furthermore, combined Ki-67 and E-cadherin expression could differentiate PHM and HA with 100% sensitivity, 93.3% specificity, 92.3% PPV, and 100% NPV. Twist1 expression is a highly reliable marker for the diagnosis of CHM, where combined Ki-67 and E-cadherin immunoreactivity can distinguish PHM from nonmolar pregnancies.

Purpose: To assess the frequency of Sjӧgren’s syndrome (SS), either primary or secondary to rheumatic disease, in a cohort of patients with aqueous-deficient dry eye and to determine the most accurate objective test for diagnosis of SS. Methods: A total of 111 patients with dry eye were recruited from Minia University’s ​Ophthalmology Outpatient Clinic (69 patients) and Rheumatology Outpatient Clinic (42 patients). The patients were screened for aqueous tear–deficient dry eye by abnormal test results of Schirmer test I (<10 mm) and tear-film break-up time (<10 seconds) in at least one eye. The diagnosis of SS was made according to the 2012 American College of Rheumatology​ criteria. A complete work up for SS was performed, including clinical examination, serological tests, ocular tests, and labial salivary–gland biopsy (LSGB). Results: Of the 111 patients, 58 had aqueous-deficient dry eye: 23 in the ophthalmology clinic cohort (group I) and 35 in the rheumatology clinic cohort (group II). Three patients had pSS, and its frequency was 13% in group I and 5.2% among all studied patients. The ocular staining score is the most diagnostic ocular test (sensitivity 100% and specificity 90.9%). Anti-SSA/Ro antibody is the most accurate serological method (sensitivity 33.3% and specificity 100%). LSGB histopathology is the most diagnostic method for SS, with sensitivity, specificity, and positive and negative predictive values of 100%. Conclusion: SS was detected with reasonable frequency among dry-eye patients, particularly pSS. Screening of dry eye for SS can select SS patients early in the disease course.