Adult ; Diagnosis, Differential ; Genital Neoplasms, Male ; pathology ; surgery ; Hernia, Inguinal ; pathology ; Humans ; Male ; Myxoma ; pathology ; surgery ; Scrotum ; pathology

PURPOSE: The aim of this study was to analyze patterns of sensory protein expression and urothelial dysfunction in ketamine-related cystitis (KC) in humans. METHODS: Biopsies of bladder mucosa were performed in 29 KC patients during cystoscopy. Then specimens were analyzed for tryptase, zonula occludens-1 (ZO-1), E-cadherin, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) with immunofluorescence staining and quantification. In addition, 10 healthy control bladder specimens were analyzed and compared with the KC specimens. Another 16 whole bladder specimens obtained from partial cystectomy were also analyzed for the muscarinic receptors M2 and M3, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), β-3 adrenergic receptors (β3-ARs), and the P2X₃ receptor by western blotting. In addition, 3 normal control bladder specimens were analyzed and compared with the KC specimens. RESULTS: The KC bladder mucosa revealed significantly less expression of ZO-1 and E-cadherin, and greater expression of TUNEL and tryptase activity than the control samples. The expression of M3 and β3-AR in the KC specimens was significantly greater than in the controls. The expression of iNOS, eNOS, M2, and P2X3 was not significantly different between the KC and control specimens. CONCLUSIONS: The bladder tissue of KC patients revealed significant urothelial dysfunction, which was associated with mast-cell mediated inflammation, increased urothelial cell apoptosis, and increased expression of the M3 and β3-AR.
Apoptosis ; Biopsy ; Blotting, Western ; Cadherins ; Cystectomy ; Cystitis* ; Cystoscopy ; Fluorescent Antibody Technique ; Humans* ; In Situ Nick-End Labeling ; Inflammation ; Ketamine ; Mucous Membrane ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Receptor, Muscarinic M2 ; Receptors, Adrenergic ; Tryptases ; Urinary Bladder ; Urothelium

INTRODUCTIONThe purpose of this study was to explore whether diabetes mellitus (DM) correlates with the risk of kidney cancer in Taiwan.

MATERIALS AND METHODSWe designed a population-based case-control study from the Taiwan National Health Insurance Database, which consisted of 116 patients with newly diagnosed kidney cancer as cases and 464 subjects without kidney cancer as controls in 2000 to 2009. Both cases and controls were aged ≥20 years. Baseline comorbidities were compared between kidney cancer cases and controls.

RESULTSMultivariable analysis showed no association was detected between DM and kidney cancer (OR 1.06, 95% CI, 0.58 to 1.94). Hypertension (OR 2.05, 95% CI, 1.23 to 3.42), chronic kidney diseases (OR 2.57, 95% CI, 1.23 to 5.37), cystic kidney diseases (OR 18.6, 95% CI, 1.84 to 187.6) and kidney stones (OR 4.02, 95% CI, 2.43 to 6.66) were significant comorbidities associated with increased risk of kidney cancer. Use of alpha-glucosidase inhibitor was associated with increased risk of kidney cancer (OR 4.31, 95% CI, 1.07 to 17.3).

CONCLUSIONDM does not correlate with the risk of kidney cancer. Hypertension, chronic kidney diseases, cystic kidney diseases, kidney stones and use of alpha-glucosidase inhibitors are associated with kidney cancer.

Carcinoma, Renal Cell ; etiology ; Case-Control Studies ; Diabetes Complications ; Female ; Humans ; Hypoglycemic Agents ; therapeutic use ; Kidney Neoplasms ; etiology ; Male ; Middle Aged ; Risk Factors