This study was designed to evaluate the protective effects of hydrogen sulphide (H2 S) against NG-Nitro l-Arginine Methyl Ester (l-NAME)-induced hypertension and its possible effects on the inflammatory process, oxidative stress, and vascular remodelling in rats. Forty male Wistar Albino rats were assigned to four equal groups: the control group, the H2 S control group, the hypertensive group, and the treated group, which received concomitant treatment with sodium hydrosulphide (NaHS) and l-NAME. Systolic blood pressure (SBP) was measured weekly. Serum levels of nitric oxide (NO), total peroxide, and total antioxidant capacity (TAC) were measured and the oxidative stress index (OSI) was calculated. Aortic weight and length were measured and the aortic weight/length ratio determined. Aortic fold expression of interferon-γ (IFN-γ) and vascular cell adhesion molecule-1 (VCAM-1) mRNA was measured using qPCR. Aortic media thickness and elastin content were measured morphometrically. l-NAME administration increased SBP, serum levels of total peroxide and OSI, but reduced serum levels of NO and TAC. Aortic fold expression of IFN-γ and VCAM-1 mRNA, aortic weight, aortic weight/length ratio, aortic media thickness, and elastin area percentage were increased in the hypertensive group. Concurrent administration of l-NAME and H2 S attenuated these changes. Thus, H2 S could attenuate the increase in ABP through restoration of the NO level, reduction in the oxidative state, and attenuation of the inflammatory process, thereby reduced vascular remodelling.

This study was designed to evaluate the protective effects of hydrogen sulphide (H2 S) against NG-Nitro l-Arginine Methyl Ester (l-NAME)-induced hypertension and its possible effects on the inflammatory process, oxidative stress, and vascular remodelling in rats. Forty male Wistar Albino rats were assigned to four equal groups: the control group, the H2 S control group, the hypertensive group, and the treated group, which received concomitant treatment with sodium hydrosulphide (NaHS) and l-NAME. Systolic blood pressure (SBP) was measured weekly. Serum levels of nitric oxide (NO), total peroxide, and total antioxidant capacity (TAC) were measured and the oxidative stress index (OSI) was calculated. Aortic weight and length were measured and the aortic weight/length ratio determined. Aortic fold expression of interferon-γ (IFN-γ) and vascular cell adhesion molecule-1 (VCAM-1) mRNA was measured using qPCR. Aortic media thickness and elastin content were measured morphometrically. l-NAME administration increased SBP, serum levels of total peroxide and OSI, but reduced serum levels of NO and TAC. Aortic fold expression of IFN-γ and VCAM-1 mRNA, aortic weight, aortic weight/length ratio, aortic media thickness, and elastin area percentage were increased in the hypertensive group. Concurrent administration of l-NAME and H2 S attenuated these changes. Thus, H2 S could attenuate the increase in ABP through restoration of the NO level, reduction in the oxidative state, and attenuation of the inflammatory process, thereby reduced vascular remodelling.

Aim: This study was designed to assess the impact of sofosbuvir/daclatasvir on vitamin D and iron status in chronic HCV patients (CHC). Methods: Sixty-five CHC patients registered for sofosbuvir/daclatasvir based regimen were recruited. Serum vitamin D, total iron, total iron binding capacity, and serum hepcidin were measured prior the treatment and 12 weeks after the stoppage of the treatment. Transferrin saturation was calculated. Results: The present study showed that a great majority of CHC patients had vitamin D deficiency or insufficiency, high total serum iron, and high transferrin saturation. Vitamin D was negatively correlated ALT. 12 weeks after completion of treatment, patients who had vitamin D deficiency or insufficiency reduced and the median value of vitamin D significantly increased compared to the pretreatment value. Total serum iron, transferrin saturation tended to decrease, however, there were no significant differences. The number of patients who had concurrently vitamin D deficiency or insufficiency and high transferrin saturation was reduced. Serum hepcidin significantly increased 12 weeks after completion of the antiviral therapy. Despite there were no significant correlations between hepcidin and total serum iron, vitamin D, and transferrin saturation before treatment, a significant positive correlation between hepcidin and serum iron and a significant negative correlation between hepcidin and vitamin D were noted after treatment. Conclusion: CHC is associated with vitamin D deficiency and iron overload, which could be attributed to reduced hepcidin level. Treatment with sofosbuvir/daclatasvir increases hepcidin and thereby reduces iron level and its harmful effect on the liver, thus increases vitamin D.

Aim: This study was designed to assess the impact of sofosbuvir/daclatasvir on vitamin D and iron status in chronic HCV patients (CHC). Methods: Sixty-five CHC patients registered for sofosbuvir/daclatasvir based regimen were recruited. Serum vitamin D, total iron, total iron binding capacity, and serum hepcidin were measured prior the treatment and 12 weeks after the stoppage of the treatment. Transferrin saturation was calculated. Results: The present study showed that a great majority of CHC patients had vitamin D deficiency or insufficiency, high total serum iron, and high transferrin saturation. Vitamin D was negatively correlated ALT. 12 weeks after completion of treatment, patients who had vitamin D deficiency or insufficiency reduced and the median value of vitamin D significantly increased compared to the pretreatment value. Total serum iron, transferrin saturation tended to decrease, however, there were no significant differences. The number of patients who had concurrently vitamin D deficiency or insufficiency and high transferrin saturation was reduced. Serum hepcidin significantly increased 12 weeks after completion of the antiviral therapy. Despite there were no significant correlations between hepcidin and total serum iron, vitamin D, and transferrin saturation before treatment, a significant positive correlation between hepcidin and serum iron and a significant negative correlation between hepcidin and vitamin D were noted after treatment. Conclusion: CHC is associated with vitamin D deficiency and iron overload, which could be attributed to reduced hepcidin level. Treatment with sofosbuvir/daclatasvir increases hepcidin and thereby reduces iron level and its harmful effect on the liver, thus increases vitamin D.

Aim: This study was designed to assess the impact of sofosbuvir/daclatasvir on vitamin D and iron status in chronic HCV patients (CHC). Methods: Sixty-five CHC patients registered for sofosbuvir/daclatasvir based regimen were recruited. Serum vitamin D, total iron, total iron binding capacity, and serum hepcidin were measured prior the treatment and 12 weeks after the stoppage of the treatment. Transferrin saturation was calculated. Results: The present study showed that a great majority of CHC patients had vitamin D deficiency or insufficiency, high total serum iron, and high transferrin saturation. Vitamin D was negatively correlated ALT. 12 weeks after completion of treatment, patients who had vitamin D deficiency or insufficiency reduced and the median value of vitamin D significantly increased compared to the pretreatment value. Total serum iron, transferrin saturation tended to decrease, however, there were no significant differences. The number of patients who had concurrently vitamin D deficiency or insufficiency and high transferrin saturation was reduced. Serum hepcidin significantly increased 12 weeks after completion of the antiviral therapy. Despite there were no significant correlations between hepcidin and total serum iron, vitamin D, and transferrin saturation before treatment, a significant positive correlation between hepcidin and serum iron and a significant negative correlation between hepcidin and vitamin D were noted after treatment. Conclusion: CHC is associated with vitamin D deficiency and iron overload, which could be attributed to reduced hepcidin level. Treatment with sofosbuvir/daclatasvir increases hepcidin and thereby reduces iron level and its harmful effect on the liver, thus increases vitamin D.

Aim: This study was designed to assess the impact of sofosbuvir/daclatasvir on vitamin D and iron status in chronic HCV patients (CHC). Methods: Sixty-five CHC patients registered for sofosbuvir/daclatasvir based regimen were recruited. Serum vitamin D, total iron, total iron binding capacity, and serum hepcidin were measured prior the treatment and 12 weeks after the stoppage of the treatment. Transferrin saturation was calculated. Results: The present study showed that a great majority of CHC patients had vitamin D deficiency or insufficiency, high total serum iron, and high transferrin saturation. Vitamin D was negatively correlated ALT. 12 weeks after completion of treatment, patients who had vitamin D deficiency or insufficiency reduced and the median value of vitamin D significantly increased compared to the pretreatment value. Total serum iron, transferrin saturation tended to decrease, however, there were no significant differences. The number of patients who had concurrently vitamin D deficiency or insufficiency and high transferrin saturation was reduced. Serum hepcidin significantly increased 12 weeks after completion of the antiviral therapy. Despite there were no significant correlations between hepcidin and total serum iron, vitamin D, and transferrin saturation before treatment, a significant positive correlation between hepcidin and serum iron and a significant negative correlation between hepcidin and vitamin D were noted after treatment. Conclusion: CHC is associated with vitamin D deficiency and iron overload, which could be attributed to reduced hepcidin level. Treatment with sofosbuvir/daclatasvir increases hepcidin and thereby reduces iron level and its harmful effect on the liver, thus increases vitamin D.

Introduction: Induction of autophagy could protect against acetaminophen (APAP)-induced hepatotoxicity; however, little is known about the role of autophagy in APAP-induced encephalopathy (APAP-E). This study aimed to evaluate the effects of coenzyme Q10 (CoQ10) and captopril on APAP-E. Material and methods: Forty-eight rats were randomly allotted to 4 equal groups: control, an APAP-E, coenzyme Q10-treated (CoQ10-treated), and captopril-treated groups. Behavioral tests were conducted. Serum ammonia and total antioxidant capacity (TAC) and hippocampal Na+/K+ ATPase activity were measured. The expression levels of hippocampal microtubule-associated protein light chain 3 (LC3-II) and beclin-1 mRNA were detected using quantitative polymerase chain reaction (qPCR). General histological, immunohistochemical staining for glial fibrillary acid protein (GFAP) and electron microscopy (EM) of the hippocampus were performed. Results: In the APAP-E group, serum ammonia was increased significantly, hippocampal LC3-II and beclin-1 mRNA were elevated insignificantly, while serum TAC and the activity of hippocampal Na+/K+ ATPase were reduced significantly compared with the control group. APAP-E rats showed remarkable degenerative changes in CA1 pyramidal neurons in the form of electron- dense cytoplasm with ill-defined nuclei and accumulation of lysosomal structure-like dense bodies. Increased immunoreactivity of astrocytes for GFAP was observed. Treatment with either CoQ10 or captopril significantly reduced ammonia levels, increased hippocampal LC3-II and beclin-1 mRNA, increased serum TAC and Na+/K+ ATPase activity, and noticeably ameliorated the hippocampal neuronal changes. EM revealed restoration of the normal structure of pyramidal neurons. These effects were more obvious in CoQ10-treated than captopril-treated rats. Conclusions: CoQ10 and captopril have neuroprotective effects on APAP-E via enhancing LC3-II, beclin-1 mRNA expression, serum TAC level and hippocampal Na+/K+ ATPase activity.

Introduction: Induction of autophagy could protect against acetaminophen (APAP)-induced hepatotoxicity; however, little is known about the role of autophagy in APAP-induced encephalopathy (APAP-E). This study aimed to evaluate the effects of coenzyme Q10 (CoQ10) and captopril on APAP-E. Material and methods: Forty-eight rats were randomly allotted to 4 equal groups: control, an APAP-E, coenzyme Q10-treated (CoQ10-treated), and captopril-treated groups. Behavioral tests were conducted. Serum ammonia and total antioxidant capacity (TAC) and hippocampal Na+/K+ ATPase activity were measured. The expression levels of hippocampal microtubule-associated protein light chain 3 (LC3-II) and beclin-1 mRNA were detected using quantitative polymerase chain reaction (qPCR). General histological, immunohistochemical staining for glial fibrillary acid protein (GFAP) and electron microscopy (EM) of the hippocampus were performed. Results: In the APAP-E group, serum ammonia was increased significantly, hippocampal LC3-II and beclin-1 mRNA were elevated insignificantly, while serum TAC and the activity of hippocampal Na+/K+ ATPase were reduced significantly compared with the control group. APAP-E rats showed remarkable degenerative changes in CA1 pyramidal neurons in the form of electron- dense cytoplasm with ill-defined nuclei and accumulation of lysosomal structure-like dense bodies. Increased immunoreactivity of astrocytes for GFAP was observed. Treatment with either CoQ10 or captopril significantly reduced ammonia levels, increased hippocampal LC3-II and beclin-1 mRNA, increased serum TAC and Na+/K+ ATPase activity, and noticeably ameliorated the hippocampal neuronal changes. EM revealed restoration of the normal structure of pyramidal neurons. These effects were more obvious in CoQ10-treated than captopril-treated rats. Conclusions: CoQ10 and captopril have neuroprotective effects on APAP-E via enhancing LC3-II, beclin-1 mRNA expression, serum TAC level and hippocampal Na+/K+ ATPase activity.

Introduction: Induction of autophagy could protect against acetaminophen (APAP)-induced hepatotoxicity; however, little is known about the role of autophagy in APAP-induced encephalopathy (APAP-E). This study aimed to evaluate the effects of coenzyme Q10 (CoQ10) and captopril on APAP-E. Material and methods: Forty-eight rats were randomly allotted to 4 equal groups: control, an APAP-E, coenzyme Q10-treated (CoQ10-treated), and captopril-treated groups. Behavioral tests were conducted. Serum ammonia and total antioxidant capacity (TAC) and hippocampal Na+/K+ ATPase activity were measured. The expression levels of hippocampal microtubule-associated protein light chain 3 (LC3-II) and beclin-1 mRNA were detected using quantitative polymerase chain reaction (qPCR). General histological, immunohistochemical staining for glial fibrillary acid protein (GFAP) and electron microscopy (EM) of the hippocampus were performed. Results: In the APAP-E group, serum ammonia was increased significantly, hippocampal LC3-II and beclin-1 mRNA were elevated insignificantly, while serum TAC and the activity of hippocampal Na+/K+ ATPase were reduced significantly compared with the control group. APAP-E rats showed remarkable degenerative changes in CA1 pyramidal neurons in the form of electron- dense cytoplasm with ill-defined nuclei and accumulation of lysosomal structure-like dense bodies. Increased immunoreactivity of astrocytes for GFAP was observed. Treatment with either CoQ10 or captopril significantly reduced ammonia levels, increased hippocampal LC3-II and beclin-1 mRNA, increased serum TAC and Na+/K+ ATPase activity, and noticeably ameliorated the hippocampal neuronal changes. EM revealed restoration of the normal structure of pyramidal neurons. These effects were more obvious in CoQ10-treated than captopril-treated rats. Conclusions: CoQ10 and captopril have neuroprotective effects on APAP-E via enhancing LC3-II, beclin-1 mRNA expression, serum TAC level and hippocampal Na+/K+ ATPase activity.

Background and Aim. We studied through flow cytometry the expression of CD146 on different T cells, and B-cell ALL blasts trying to correlate its expression with different prognostic factors of B-cell ALL and treatment outcomes. Patients and Methods. All pediatric patients with B-cell ALL were subjected to bone marrow examination and cytochemistry, flow cytometric immunophenotyping using monoclonal antibodies utilized for diagnosis of B-ALL including CD34, CD19, CD10, CD22, and intracellular IgM. The diagnosis was based on standard morphologic, cytochemical, and immunophenotypic followed by flow cytometric detection of CD146 expression on blast cells, CD4+, and CD8+ T cells. Results. Significant accumulations of CD146+CD4+ cells, CD146+CD8+ cells, CD4+, CD8+, and lymphocytes in patients were compared to controls, the mean percentages of CD146+CD4+ cells, CD146+CD8+ cells, and CD146+ blasts were significantly higher in patients than controls, and in addition, these cells were associated with poor overall survival and disease-free survival. The median OS for patients with complete response was 22 ± 1:633 (95%CI = 18:799‐25:201), while for those without complete response, it was 13 ± 3:928 (95%CI = 5:301‐25:699), with log‐rank = 5:71, P = 0:017. Conclusion. CD146 was expressed significantly in children’s B-ALL and associated with poor prognostic features including poor response and treatment outcomes and could be a possible poor prognostic factor in pediatric B-cell ALL.