In this paper we investigate the existence of positive solutions of the q-difference equation −D 2 q u(t) = a(t) f (u(t)) with some boundary conditions by applying a fixed point theorem in cones.
To compare the expression of two promising circulating micro-ribonucleic acids (miRNAs 21 and 221) in patients with prostate cancer to subjects without cancer and to evaluate their potential role as specific noninvasive molecular biomarkers for prostate cancer diagnosis, circulating miRNAs 21 and 221 expression profiles were analyzed in 20 men aged 50-75 years, presenting with lower urinary tract symptoms (LUTSs) and undergoing transrectal ultrasound (TRUS)-guided prostate biopsy based on either elevated serum prostate-specific antigen (PSA) (>4.0 ng/ml) or suspicious digital rectal examination (DRE). The performance of miRNAs 21 and 221 in differentiating prostate cancer from nonmalignant cases was evaluated and compared to DRE and elevated PSA. miRNA 21 was overexpressed in 90 % of group A vs. 10 % of group B, while miRNA 221 was overexpressed in 80 % of group A vs. 20 % of group B (p = 0.001). MiRNA 21 overexpression had the highest performance as a diagnostic test with a sensitivity of 90 % and a specificity 90 % (p = 0.02). No correlations were noted between Gleason score of prostate cancer cases and relative quantity (RQ) 21 (r = -0.355, p = 0.292) or RQ 221 (r = -0.044, p = 0.892). Our study showed that serum miRNAs 21 and 221 expression profiling tests may be used as specific noninvasive molecular biomarkers for prostate cancer diagnosis due to their higher sensitivity and specificity with a high negative predictive value leading to a decrease in the biopsies taken for patients with elevated serum PSA values.
Disorders/differences of sex development (DSD) comprise a group of congenital disorders that affect the genitourinary tract and usually involve the endocrine and reproductive system. The aim of this work was to identify genetic variants responsible for disorders of human urogenital development in a cohort of Egyptian patients. This three‐year study included 225 patients with various DSD forms, referred to the genetic DSD and endocrinology clinic, National Research Centre, Egypt. The patients underwent thorough clinical examination, hormonal and imaging studies, detailed cytogenetic and fluorescence in situ hybridization analysis, and molecular sequencing of genes known to commonly cause DSD including AR, SRD5A2, 17BHSD3, NR5A1, SRY, and WT1. Whole exome sequencing (WES) was carried out for 18 selected patients. The study revealed a high rate of sex chromosomal DSD (33%) with a wide array of cytogenetic abnormalities. Sanger sequencing identified pathogenic variants in 33.7% of 46,XY patients, while the detection rate of WES reached 66.7%. Our patients showed a different mutational profile compared with that reported in other populations with a predominance of heritable DSD causes. WES identified rare and novel pathogenic variants in NR5A1, WT1, HHAT, CYP19A1, AMH, AMHR2, and FANCA and in the X‐linked genes ARX and KDM6A. In addition, digenic inheritance was observed in two of our patients and was suggested to be a cause of the phenotypic variability observed in DSD.
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