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1.
BMC Urol ; 18(1): 100, 2018 Nov 09.
Artigo em Inglês | MEDLINE | ID: mdl-30413194

RESUMO

BACKGROUND: Epidermal growth factor receptor (EGFR) overexpression is believed to be associated with bladder cancer (BC) progression and poor clinical outcomes. In vivo studies have linked EGFR subcellular trafficking and chemo-resistance to cisplatin-based chemotherapies. This has not been studied in the clinical adjuvant setting. We aimed to investigate the prognostic significance of EGFR expression in patients receiving cisplatin-based adjuvant chemotherapy following radical cystectomy for advanced BC. METHODS: The database from the Urology and Nephrology Center at Mansoura University was reviewed. BC patients who were treated with radical cystectomy and adjuvant chemotherapy for adverse pathological features or node positive disease were identified. Patients who underwent palliative cystectomy, had histological diagnoses other than pure urothelial carcinoma, or received adjuvant radiotherapy were excluded from the study. Immunohistochemical staining for EGFR expression was performed on archived bladder specimens. The following in vitro functional analyses were performed to study the relationship of EGFR expression and chemoresponse. RESULTS: The study included 58 patients, among which the mean age was 57 years old. Majority of patients had node positive disease (n = 53, 91%). Mean follow up was 26.61 months. EGFR was overexpressed in 25 cystectomy specimens (43%). Kaplan-Meier analysis revealed that EGFR over-expression significantly correlated with disease recurrence (p = 0.021). Cox proportional hazard modeling identified EGFR overexpression as an independent predictor for disease recurrence (p = 0.04). Furthermore, in vitro experiments demonstrated that inhibition of EGFR may sensitize cellular responses to cisplatin. CONCLUSIONS: Our findings suggest that EGFR overexpression is associated with disease recurrence following adjuvant chemotherapy for advanced BC. This may aid in patient prognostication and selection prior to chemotherapeutic treatment for BC.

2.
Can J Physiol Pharmacol ; 94(2): 140-146, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26544923

RESUMO

In this study, we studied the effect of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), an inhibitor of Toll-like receptor 4 (TLR4), in LPS-induced acute lung injury (ALI). Male Sprague-Dawley rats were treated with LPS-RS (0.1 mg/kg body mass, by intraperitoneal (i.p.) injection) 1 h before LPS injection (10 mg/kg, i.p.). Bronchoalveolar lavage fluid (BALF) and lung tissues were collected 24 h later to determine total and differential cell count, total protein content, levels of lactate dehydrogenase (LDH), histopathological changes, markers of oxidative stress, and mRNA expression of the inhibitory protein nuclear factor kappaB-α (NFκBIA) and TLR4. Additionally, rings of pulmonary artery were isolated for measuring vascular reactivity. LPS-induced ALI was indicated by increases in total and differential cell count, total protein, and LDH in BALF, and increased lung levels of malondialdehyde (MDA), as well as decreased activity of reduced glutathione (GSH) and superoxide dismutase (SOD). Moreover, LPS increased pulmonary artery contraction in response to phenylephrine (PE). Additionally, LPS downregulated mRNA expression of NFκBIA and upregulated mRNA expression of TLR4. LPS caused a marked inflammation in the lung tissue, with tubercular granuloma and numerous neutrophils. Pretreatment with LPS-RS protected against LPS-induced ALI by decreasing total and differential cell count, total protein, and LDH in BALF, and increased pulmonary GSH content and SOD activity without affecting MDA content. Additionally, it decreased the elevated PE-induced pulmonary artery contraction. LPS-RS upregulated mRNA expression of NFκBIA and downregulated mRNA expression of TLR4. Moreover, LPS-RS prevented inflammation in lung tissues. In conclusion, pretreatment with LPS-RS protects against LPS-induced ALI in rats through its anti-inflammatory effects, possibly by decreasing the mRNA expression of TLR4 and increasing that of NFκBIA.

3.
Arab J Urol ; 9(4): 235-9, 2011 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26579304

RESUMO

OBJECTIVES: To assess the predictive importance of ultrasonic grade 1 hyperechogenicity in potential live related kidney donors in the absence of urinary abnormalities and with perfect renal function. SUBJECTS AND METHODS: The study included 34 potential living related kidney donors with this abnormality; their mean (SD, range) age was 32.7 (8.45, 23-48) years. Ten matched healthy donors with normal ultrasonographic appearance of the kidneys were studied as controls. All cases were thoroughly investigated, including measuring glomerular filtration rate by isotopic scintigraphy. The renal reserve was estimated by dopamine and amino-acid infusion in all subjects (study and control groups). A percutaneous renal biopsy was taken from 17 subjects in the abnormal echogenicity group and open renal biopsy was taken from eight of the control subjects. RESULTS: The renal reserve was comparable in both groups. Abnormal histopathological changes were found in seven subjects (41%) of the abnormal echogenicity group, i.e. partial glomerulosclerosis in one, mesangial thickening in two, interstitial fibrosis in one, focal tubular atrophy in one, immunoglobulin (Ig M) immune deposits in three and IgA in one. Only one subject in the control group showed mild mesangial thickening. CONCLUSION: Grade 1 echogenicity might be a sign of unrecognized kidney disease. Renal biopsy is mandatory when such related donors are the only available ones. Abnormal histopathology contraindicates donation.

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