Prevalence of concealed and overt chronic renal failure in patients with COPD

AbstractAimTo assess the prevalence of chronic renal failure (concealed and overt) in patients with COPD.Patients and methodsThis study was conducted on 150 patients who were classified into three groups: Group I: 67 patients with COPD, Group II: 33 COPD patients with co morbidities (diabetes mellitus, hypertension and or ischemic heart disease). Group III: (control group): 50 patients with other diseases such as diabetes mellitus, ischemic heart disease and or hypertension. All patients were subjected to: (1) Full history taking. (2) Complete clinical examination. (3) Anthropometric measurements (weight, height and body mass index). (4) Arterial oxygen saturation. (5) Radiological examination (Plain chest X-ray posterior–anterior view and Pelvi-abdominal ultrasound). (6) ECG and Echocardiography. (7) Spirometry. (8) Laboratory investigations (complete blood picture, erythrocyte sedimentation rate, Liver function tests, serum creatinine, blood urea and uric acid and GFR, total cholesterol, sodium, potassium and chloride concentration).ResultsIn group I, there were 8 patients who had CRF (11.94%), 5 patients had overt CRF (7.46%) and 3 patients had concealed CRF (4.48%). In group II, there were 11 patients with CRF (33.33%), 6 patients had overt CRF (18.18%) and 5 patients had concealed CRF (15.15%). In group III, there were 9 patients having CRF (18%), 6 patients had overt CRF (12%) and 3patients had concealed CRF (6%). In COPD (group I and II) the overall prevalence of CRF was 19%.ConclusionCRF either concealed or overt may be associated with COPD patients and should be screened, not only by serum creatinine level but also by the estimated GFR to recognize the cases of concealed CRF who have low GFR despite normal serum creatinine level

Nifuroxazide Mitigates Angiogenesis in Ehlrich’s Solid Carcinoma: Molecular Docking, Bioinformatic and Experimental Studies on Inhibition of Il-6/Jak2/Stat3 Signaling

Nifuroxazide is an antidiarrheal medication that has promising anticancer activity against diverse types of tumors. The present study tested the anticancer activity of nifuroxazide against Ehrlich’s mammary carcinoma grown in vivo. Furthermore, we investigated the effect of nifuroxazide on IL-6/jak2/STAT3 signaling and the possible impact on tumor angiogenesis. The biological study was supported by molecular docking and bioinformatic predictions for the possible effect of nifuroxazide on this signaling pathway. Female albino mice were injected with Ehrlich carcinoma cells to produce Ehrlich’s solid tumors (ESTs). The experimental groups were as follows: EST control, EST + nifuroxazide (5 mg/kg), and EST + nifuroxazide (10 mg/kg). Nifuroxazide was found to reduce tumor masses (730.83 ± 73.19 and 381.42 ± 109.69 mg vs. 1099.5 ± 310.83) and lessen tumor pathologies. Furthermore, nifuroxazide downregulated IL-6, TNF-α, NFk-β, angiostatin, and Jak2 proteins, and it also reduced tumoral VEGF, as indicated by ELISA and immunohistochemical analysis. Furthermore, nifuroxazide dose-dependently downregulated STAT3 phosphorylation (60% and 30% reductions, respectively). Collectively, the current experiment shed light on the antitumor activity of nifuroxazide against mammary solid carcinoma grown in vivo. The antitumor activity was at least partly mediated by inhibition of IL-6/Jak2/STAT3 signaling that affected angiogenesis (low VEGF and high angiostatin) in the EST. Therefore, nifuroxazide might be a promising antitumor medication if appropriate human studies will be conducted

Nifuroxazide Mitigates Angiogenesis in Ehlrich’s Solid Carcinoma: Molecular Docking, Bioinformatic and Experimental Studies on Inhibition of Il-6/Jak2/Stat3 Signaling

Nifuroxazide is an antidiarrheal medication that has promising anticancer activity against diverse types of tumors. The present study tested the anticancer activity of nifuroxazide against Ehrlich’s mammary carcinoma grown in vivo. Furthermore, we investigated the effect of nifuroxazide on IL-6/jak2/STAT3 signaling and the possible impact on tumor angiogenesis. The biological study was supported by molecular docking and bioinformatic predictions for the possible effect of nifuroxazide on this signaling pathway. Female albino mice were injected with Ehrlich carcinoma cells to produce Ehrlich’s solid tumors (ESTs). The experimental groups were as follows: EST control, EST + nifuroxazide (5 mg/kg), and EST + nifuroxazide (10 mg/kg). Nifuroxazide was found to reduce tumor masses (730.83 ± 73.19 and 381.42 ± 109.69 mg vs. 1099.5 ± 310.83) and lessen tumor pathologies. Furthermore, nifuroxazide downregulated IL-6, TNF-α, NFk-β, angiostatin, and Jak2 proteins, and it also reduced tumoral VEGF, as indicated by ELISA and immunohistochemical analysis. Furthermore, nifuroxazide dose-dependently downregulated STAT3 phosphorylation (60% and 30% reductions, respectively). Collectively, the current experiment shed light on the antitumor activity of nifuroxazide against mammary solid carcinoma grown in vivo. The antitumor activity was at least partly mediated by inhibition of IL-6/Jak2/STAT3 signaling that affected angiogenesis (low VEGF and high angiostatin) in the EST. Therefore, nifuroxazide might be a promising antitumor medication if appropriate human studies will be conducted