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BACKGROUND: Ginkgo biloba leaves extract has been widely used worldwide to protect against oxidative stress-induced cell damage and improves blood circulation. METHODS: The potential protective role of the standardized leaf extract of Ginkgo biloba (EGb761) on hypertension-induced renal injury was investigated in rats. Hypertension was induced in rats by L-NAME. RESULT: Repeated treatment with EGb761 produced progressive reductions in the systolic, diastolic and mean arterial blood pressure. Also, EGb761 increased the progressive reductions in blood pressure induced by losartan. Hypertension-induced marked elevation of renal malondialdehyde (MDA) and nitrite levels and reduction of reduced glutathione (GSH) level were inhibited by EGb761. In addition, hypertension-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β)) levels in renal tissues were inhibited by EGb761. Also, treatment with EGb761 inhibited hypertension-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1B in the kidney tissues. EGb761 enhanced losartan effects on renal tissues oxidative stress, nitrite, and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1B. effects. CONCLUSIONS: These results indicate that EGb761 has the ability to protect against hypertension-induced renal injury.

BACKGROUND: Ginkgo biloba leaves extract has been widely used worldwide to protect against oxidative stress-induced cell damage and improves blood circulation. METHODS: The potential protective role of the standardized leaf extract of Ginkgo biloba (EGb761) on hypertension-induced renal injury was investigated in rats. Hypertension was induced in rats by L-NAME. RESULT: Repeated treatment with EGb761 produced progressive reductions in the systolic, diastolic and mean arterial blood pressure. Also, EGb761 increased the progressive reductions in blood pressure induced by losartan. Hypertension-induced marked elevation of renal malondialdehyde (MDA) and nitrite levels and reduction of reduced glutathione (GSH) level were inhibited by EGb761. In addition, hypertension-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β)) levels in renal tissues were inhibited by EGb761. Also, treatment with EGb761 inhibited hypertension-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1B in the kidney tissues. EGb761 enhanced losartan effects on renal tissues oxidative stress, nitrite, and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1B. effects. CONCLUSIONS: These results indicate that EGb761 has the ability to protect against hypertension-induced renal injury.

BACKGROUND: Ginkgo biloba leaves extract has been widely used worldwide to protect against oxidative stress-induced cell damage and improves blood circulation. METHODS: The potential protective role of the standardized leaf extract of Ginkgo biloba (EGb761) on hypertension-induced renal injury was investigated in rats. Hypertension was induced in rats by L-NAME. RESULT: Repeated treatment with EGb761 produced progressive reductions in the systolic, diastolic and mean arterial blood pressure. Also, EGb761 increased the progressive reductions in blood pressure induced by losartan. Hypertension-induced marked elevation of renal malondialdehyde (MDA) and nitrite levels and reduction of reduced glutathione (GSH) level were inhibited by EGb761. In addition, hypertension-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β)) levels in renal tissues were inhibited by EGb761. Also, treatment with EGb761 inhibited hypertension-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1B in the kidney tissues. EGb761 enhanced losartan effects on renal tissues oxidative stress, nitrite, and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1B. effects. CONCLUSIONS: These results indicate that EGb761 has the ability to protect against hypertension-induced renal injury.

BACKGROUND: Ginkgo biloba leaves extract has been widely used worldwide to protect against oxidative stress-induced cell damage and improves blood circulation. METHODS: The potential protective role of the standardized leaf extract of Ginkgo biloba (EGb761) on hypertension-induced renal injury was investigated in rats. Hypertension was induced in rats by L-NAME. RESULT: Repeated treatment with EGb761 produced progressive reductions in the systolic, diastolic and mean arterial blood pressure. Also, EGb761 increased the progressive reductions in blood pressure induced by losartan. Hypertension-induced marked elevation of renal malondialdehyde (MDA) and nitrite levels and reduction of reduced glutathione (GSH) level were inhibited by EGb761. In addition, hypertension-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β)) levels in renal tissues were inhibited by EGb761. Also, treatment with EGb761 inhibited hypertension-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1B in the kidney tissues. EGb761 enhanced losartan effects on renal tissues oxidative stress, nitrite, and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1B. effects. CONCLUSIONS: These results indicate that EGb761 has the ability to protect against hypertension-induced renal injury.

Background: Co-occurrence of carbapenem and fluoroquinolone resistance amongst K. pneumoniae strains created a problem in treating infections caused by these MDR organisms. Objectives: This study was carried out to evaluate the co-existence of carbapenemases and plasmid mediated quinolone resistance (PMQR) determinants in K. pneumoniae isolates in Egypt. Methodology: Forty-three K. pneumoniae isolates were collected from patients admitted to various intensive care units at Assiut University Hospital. Genes encoding for carbapenemases and PMQR were detected by PCR and sequencing. To determine the horizontal transfer of the PMQR and /or carbapenemases positive plasmids, conjugation experiments were performed. Results: Carbapenemases were detected in 34/43 (79.1%) of K. pneumoniae isolates. The positive rates of blaKPC and blaNDM1 were (48.8%) and (74.4%), respectively. PMQR determinants were detected in 100% of K. pneumoniae isolates. The positive rates of qnrB, qnrS and aac(6`)-Ib-cr were (83.7 %), (81.4 %) and (23.3%), respectively. bla NDM1 positive K. pneumoniae positive isolates co-harbored qnr S, qnrB and aac(6`)-Ib-cr at rates of (87.5%), (81.3%) and (25%) respectively, while (90.5%), (85.7%) and (9.5%) of blaKPC positive isolates co-harbored qnrS, qnrB and aac(6`)-Ib-cr, respectively. qnrB and qnrS exhibited statistically significant association with blaKPC and blaNDM1 (p0.001). Conclusion: Our study revealed high rate of co-existence of carbapenemases and PMQR determinants in K. pneumoniae isolates in Egypt. To our best of knowledge, this is the first study to report the presence of a statistically significant relation between carbapenemases and PMQR.

Background: Co-occurrence of carbapenem and fluoroquinolone resistance amongst K. pneumoniae strains created a problem in treating infections caused by these MDR organisms. Objectives: This study was carried out to evaluate the co-existence of carbapenemases and plasmid mediated quinolone resistance (PMQR) determinants in K. pneumoniae isolates in Egypt. Methodology: Forty-three K. pneumoniae isolates were collected from patients admitted to various intensive care units at Assiut University Hospital. Genes encoding for carbapenemases and PMQR were detected by PCR and sequencing. To determine the horizontal transfer of the PMQR and /or carbapenemases positive plasmids, conjugation experiments were performed. Results: Carbapenemases were detected in 34/43 (79.1%) of K. pneumoniae isolates. The positive rates of blaKPC and blaNDM1 were (48.8%) and (74.4%), respectively. PMQR determinants were detected in 100% of K. pneumoniae isolates. The positive rates of qnrB, qnrS and aac(6`)-Ib-cr were (83.7 %), (81.4 %) and (23.3%), respectively. bla NDM1 positive K. pneumoniae positive isolates co-harbored qnr S, qnrB and aac(6`)-Ib-cr at rates of (87.5%), (81.3%) and (25%) respectively, while (90.5%), (85.7%) and (9.5%) of blaKPC positive isolates co-harbored qnrS, qnrB and aac(6`)-Ib-cr, respectively. qnrB and qnrS exhibited statistically significant association with blaKPC and blaNDM1 (p0.001). Conclusion: Our study revealed high rate of co-existence of carbapenemases and PMQR determinants in K. pneumoniae isolates in Egypt. To our best of knowledge, this is the first study to report the presence of a statistically significant relation between carbapenemases and PMQR.

Background: Co-occurrence of carbapenem and fluoroquinolone resistance amongst K. pneumoniae strains created a problem in treating infections caused by these MDR organisms. Objectives: This study was carried out to evaluate the co-existence of carbapenemases and plasmid mediated quinolone resistance (PMQR) determinants in K. pneumoniae isolates in Egypt. Methodology: Forty-three K. pneumoniae isolates were collected from patients admitted to various intensive care units at Assiut University Hospital. Genes encoding for carbapenemases and PMQR were detected by PCR and sequencing. To determine the horizontal transfer of the PMQR and /or carbapenemases positive plasmids, conjugation experiments were performed. Results: Carbapenemases were detected in 34/43 (79.1%) of K. pneumoniae isolates. The positive rates of blaKPC and blaNDM1 were (48.8%) and (74.4%), respectively. PMQR determinants were detected in 100% of K. pneumoniae isolates. The positive rates of qnrB, qnrS and aac(6`)-Ib-cr were (83.7 %), (81.4 %) and (23.3%), respectively. bla NDM1 positive K. pneumoniae positive isolates co-harbored qnr S, qnrB and aac(6`)-Ib-cr at rates of (87.5%), (81.3%) and (25%) respectively, while (90.5%), (85.7%) and (9.5%) of blaKPC positive isolates co-harbored qnrS, qnrB and aac(6`)-Ib-cr, respectively. qnrB and qnrS exhibited statistically significant association with blaKPC and blaNDM1 (p0.001). Conclusion: Our study revealed high rate of co-existence of carbapenemases and PMQR determinants in K. pneumoniae isolates in Egypt. To our best of knowledge, this is the first study to report the presence of a statistically significant relation between carbapenemases and PMQR.

Hepatitis C virus (HCV) is a major cause in development of chronic liver disease worldwide. The course of disease in the transplant setting is accelerated whereas up to 20%–40% of patients transplanted for HCV will develop cirrhosis after 5 years, compared to 3%–20% at 20 years in the non-transplant setting. The degree of fibrosis determines the stage of the disease and subsequently development of complications. Liver fibrosis can regress in patients with chronic hepatitis in whom the cause of liver damage is adequately managed, but most studies assessing the benefits of viral eradication were performed in the era of IFN-based therapy and in pre-transplant settings. Aim To assess noninvasively the effect of sofosbuvir-based antiviral therapy on liver fibrosis in patients with post-transplant recurrent HCV infection. Material and Methods This is a prospective study, in which patients with recurrent HCV infection post-transplant, treated with sofosbuvir plus ribavirin were enrolled. Clinical, biochemical findings (including APRI and FIB-4 scores) and liver stiffness (LS), measured by Fibroscan at baseline and at 3 months after end of therapy, virological data, type of immunosuppression and response to antiviral therapy were evaluated. Patients were further divided into two groups, according to antiviral response. Results From August 2014 till January 2016, sixty patients were enrolled, 78.3% were male, 67.8% had genotype 1 and 61.7% received previous HCV treatment. At baseline, 21 patients (35%) had severe fibrosis according to Ishak score. The median time interval from LT was 51 months (5-284), immunosuppressive therapy was tacrolimus based in 78.4%. The median baseline HCV-RNA was 2.341.172 UI/ml (770-52.330.800 UI/ml). SVR was achieved in 43 patients (71.6%). There was significant decrease in LS, FIB-4 and APRI scores in patients who achieved SVR in comparison to those who did not achieve SVR (Median change of LS, FIB-4 and APRI in SVR vs. NSVR group was 4.9 vs. 2.2 (P=0.000 vs. 0.074), 1.06 vs. 0.6 (P=0.000 vs. 0.177) and 0.97 vs. 0.44 (P=0.000 vs. 0.177) respectively). The percentage of the patients with improved LS, FIB-4 and APRI scores in SVR vs. NSVR group was 86% vs. 58.8%, 79.1% vs. 70.5% and 86% vs. 64.7% respectively. Multiple linear regression was done for patients with SVR and it was found that the change in FIB-4 and APRI was significantly associated with pre-treatment levels of AST, GGT, bilirubin, INR and Child Pugh score, while the change in LS was associated only with high pre-treatment LS values. Conclusion Eradication of HCV with sofosbuvir-based regimen leads to significant regression in Liver fibrosis, assessed by combined non-invasive tests in post-transplant setting as early as 3 months post-therapy.

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