Abstract Background: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. Aim: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methods: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using etraamplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. Results: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P = 0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA + AA, P = 0.004 and TT + TA vs AA, P = 0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P 0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P 0.001each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMAIR, insulin, and ALT values (P 0.05 each) and a negative correlation with HDL-C (P 0.01). Conclusion: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

Abstract Background: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. Aim: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methods: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using etraamplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. Results: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P = 0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA + AA, P = 0.004 and TT + TA vs AA, P = 0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P 0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P 0.001each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMAIR, insulin, and ALT values (P 0.05 each) and a negative correlation with HDL-C (P 0.01). Conclusion: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

Abstract Background: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. Aim: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methods: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using etraamplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. Results: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P = 0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA + AA, P = 0.004 and TT + TA vs AA, P = 0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P 0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P 0.001each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMAIR, insulin, and ALT values (P 0.05 each) and a negative correlation with HDL-C (P 0.01). Conclusion: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

Abstract Background: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. Aim: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methods: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using etraamplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. Results: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P = 0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA + AA, P = 0.004 and TT + TA vs AA, P = 0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P 0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P 0.001each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMAIR, insulin, and ALT values (P 0.05 each) and a negative correlation with HDL-C (P 0.01). Conclusion: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

Abstract Background: Vaspin is an adipokine that is potentially linking obesity, insulin resistance, metabolic syndrome and type-2 diabetes. Aim: The present study aimed to investigate the impact of vaspin rs2236242 gene polymorphism on the risk of obesity, diabetes, their metabolic traits, and serum vaspin levels in a sample of Upper Egyptian women. Subjects and methods: A total of 224 subjects, 112 obese (62 non diabetics, 50 diabetics) and 112 controls were included in this case control study. Vaspin gene rs2236242 polymorphism was performed using etraamplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) and serum vaspin levels were estimated by ELISA. Results: The minor (A) allele of vaspin rs2236242 gene polymorphism was significantly lower in obese (30.8%) than controls (43.7%) (P = 0.005). The protective effect was evident in dominant and recessive inheritance models (TT vs TA + AA, P = 0.004 and TT + TA vs AA, P = 0.036). After adjusting genotypes for diabetes there were no significant association between vaspin rs2236242 gene polymorphism and obesity but significant association was maintained in the obese diabetics. Vaspin serum levels were found to be lower in minor protective (AA) genotype carriers than the other two genotypes (P 0.001). In the mean-time serum vaspin levels were significantly higher in obese diabetics and non-diabetics than controls (P 0.001each).There were significant positive correlations between vaspin levels and hs-CRP, cholesterol, LDL-C, fasting glucose, HOMAIR, insulin, and ALT values (P 0.05 each) and a negative correlation with HDL-C (P 0.01). Conclusion: The minor A allele of vaspin rs2236242 polymorphism plays a protective role against obesity and diabetes but this relation is largely ascribed to its effect on insulin resistance. The serum vaspin concentration was lower in minor protective allele carriers. To the best of our knowledge, this is the first study of vaspin SNP in Upper Egyptian women. The entire understanding of vaspin intimate mechanistic action might enable the development of novel etiology-based treatment strategies for obesity, the complex genetic trait.

Abstract: Introduction: Chronic kidney disease is associated with increased morbidity and mortality in cardiovascular disease. Apart from traditional risk factors, chronic inflammation, and increased left-ventricular wall tension related to hypervolemia are important in cardiovascular disease development in renal patients. B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted by cardiac ventricles in response to volume expansion and pressure overload. High sensitivity C-reactive (hsCRP) have been found to reflect chronic inflammation and significantly elevated in hemodialysis patients. Aim of the work: To assess the relationship between left ventricular filling pressure (using plasma BNP levels) and inflammation (using plasma hsCRP levels) in patients with chronic renal failure and their relationship with renal echogenisity detected by ultrasonography. Patients and methods: Plasma BNP and hs CRP were measured on the same day in 38 pre-dialysis patients. Patients were classified into 5 groups according to ultrasonographic renal echogenisity into Group 1(no=3) with grade 0, group 2 (no=2) with grade I, group 3 (no=15) with grade II, group 4 (no=14) with grade III renal echogenisity and group 5 (no=4) with complete loss of the medulla and cortex of the kidney. Result: Plasma levels of BNP and hsCRP were significantly higher in patients with chronic renal failure in comparison with controls (274.3±97.1 pg/ml versus 33.7±8.0 pg/ml and 11.4±3.9 mg/L versus 2.7±1.0 mg/L respectively P 0.0001 for each). Comparing plasma levels of BNP and hsCRP with ultrasonograghic renal echogenisity, which reflect severity of renal disease, showed that the plasma levels of BNP were 104.7±15.0 pg/ml, 148.0±67.9 pg/ml, 248.5±72.0 pg/ml, 310.1±39.2 pg/ml and 436.0±10.0 pg/ml in the five groups of patients respectively and hsCRP were 4.7±0.6 mg/L, 5.5±0.7 mg/L, 10.3±3.2 mg/L, 13.6±1.8 mg/L and 16.0±0.8 mg/L in the same previous groups respectively. It was clear that the plasma levels of both biomarkers were significantly higher in patients with more severe renal affection (P 0.0001 for each). There was also, highly significant positive correlation between plasma levels of BNP and hsCRP in all groups of patients (r= 0.9, P0.0001) and significant negative correlation between both markers and serum albumin (r=-0.4, P0.001 and r=-0.5, P 0.0001 respectively) and significant negative correlation between both markers and hemoglobin levels (r=-0.8, P 0.0001 and r=-0.8, P 0.0001 respectively).Conclusion: The present results suggest a link between left ventricular pressure and inflammation in patients with chronic renal failure. The importance of strict volume control in these patients, in order to reduce left ventricular pressure and therefore inflammation, should be considered. Both BNP and hs CRP could provide complementary diagnostic and prognostic information regarding future cardiovascular disorders in renal patients.

Abstract: Introduction: Chronic kidney disease is associated with increased morbidity and mortality in cardiovascular disease. Apart from traditional risk factors, chronic inflammation, and increased left-ventricular wall tension related to hypervolemia are important in cardiovascular disease development in renal patients. B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted by cardiac ventricles in response to volume expansion and pressure overload. High sensitivity C-reactive (hsCRP) have been found to reflect chronic inflammation and significantly elevated in hemodialysis patients. Aim of the work: To assess the relationship between left ventricular filling pressure (using plasma BNP levels) and inflammation (using plasma hsCRP levels) in patients with chronic renal failure and their relationship with renal echogenisity detected by ultrasonography. Patients and methods: Plasma BNP and hs CRP were measured on the same day in 38 pre-dialysis patients. Patients were classified into 5 groups according to ultrasonographic renal echogenisity into Group 1(no=3) with grade 0, group 2 (no=2) with grade I, group 3 (no=15) with grade II, group 4 (no=14) with grade III renal echogenisity and group 5 (no=4) with complete loss of the medulla and cortex of the kidney. Result: Plasma levels of BNP and hsCRP were significantly higher in patients with chronic renal failure in comparison with controls (274.3±97.1 pg/ml versus 33.7±8.0 pg/ml and 11.4±3.9 mg/L versus 2.7±1.0 mg/L respectively P 0.0001 for each). Comparing plasma levels of BNP and hsCRP with ultrasonograghic renal echogenisity, which reflect severity of renal disease, showed that the plasma levels of BNP were 104.7±15.0 pg/ml, 148.0±67.9 pg/ml, 248.5±72.0 pg/ml, 310.1±39.2 pg/ml and 436.0±10.0 pg/ml in the five groups of patients respectively and hsCRP were 4.7±0.6 mg/L, 5.5±0.7 mg/L, 10.3±3.2 mg/L, 13.6±1.8 mg/L and 16.0±0.8 mg/L in the same previous groups respectively. It was clear that the plasma levels of both biomarkers were significantly higher in patients with more severe renal affection (P 0.0001 for each). There was also, highly significant positive correlation between plasma levels of BNP and hsCRP in all groups of patients (r= 0.9, P0.0001) and significant negative correlation between both markers and serum albumin (r=-0.4, P0.001 and r=-0.5, P 0.0001 respectively) and significant negative correlation between both markers and hemoglobin levels (r=-0.8, P 0.0001 and r=-0.8, P 0.0001 respectively).Conclusion: The present results suggest a link between left ventricular pressure and inflammation in patients with chronic renal failure. The importance of strict volume control in these patients, in order to reduce left ventricular pressure and therefore inflammation, should be considered. Both BNP and hs CRP could provide complementary diagnostic and prognostic information regarding future cardiovascular disorders in renal patients.

Abstract: Introduction: Chronic kidney disease is associated with increased morbidity and mortality in cardiovascular disease. Apart from traditional risk factors, chronic inflammation, and increased left-ventricular wall tension related to hypervolemia are important in cardiovascular disease development in renal patients. B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted by cardiac ventricles in response to volume expansion and pressure overload. High sensitivity C-reactive (hsCRP) have been found to reflect chronic inflammation and significantly elevated in hemodialysis patients. Aim of the work: To assess the relationship between left ventricular filling pressure (using plasma BNP levels) and inflammation (using plasma hsCRP levels) in patients with chronic renal failure and their relationship with renal echogenisity detected by ultrasonography. Patients and methods: Plasma BNP and hs CRP were measured on the same day in 38 pre-dialysis patients. Patients were classified into 5 groups according to ultrasonographic renal echogenisity into Group 1(no=3) with grade 0, group 2 (no=2) with grade I, group 3 (no=15) with grade II, group 4 (no=14) with grade III renal echogenisity and group 5 (no=4) with complete loss of the medulla and cortex of the kidney. Result: Plasma levels of BNP and hsCRP were significantly higher in patients with chronic renal failure in comparison with controls (274.3±97.1 pg/ml versus 33.7±8.0 pg/ml and 11.4±3.9 mg/L versus 2.7±1.0 mg/L respectively P 0.0001 for each). Comparing plasma levels of BNP and hsCRP with ultrasonograghic renal echogenisity, which reflect severity of renal disease, showed that the plasma levels of BNP were 104.7±15.0 pg/ml, 148.0±67.9 pg/ml, 248.5±72.0 pg/ml, 310.1±39.2 pg/ml and 436.0±10.0 pg/ml in the five groups of patients respectively and hsCRP were 4.7±0.6 mg/L, 5.5±0.7 mg/L, 10.3±3.2 mg/L, 13.6±1.8 mg/L and 16.0±0.8 mg/L in the same previous groups respectively. It was clear that the plasma levels of both biomarkers were significantly higher in patients with more severe renal affection (P 0.0001 for each). There was also, highly significant positive correlation between plasma levels of BNP and hsCRP in all groups of patients (r= 0.9, P0.0001) and significant negative correlation between both markers and serum albumin (r=-0.4, P0.001 and r=-0.5, P 0.0001 respectively) and significant negative correlation between both markers and hemoglobin levels (r=-0.8, P 0.0001 and r=-0.8, P 0.0001 respectively).Conclusion: The present results suggest a link between left ventricular pressure and inflammation in patients with chronic renal failure. The importance of strict volume control in these patients, in order to reduce left ventricular pressure and therefore inflammation, should be considered. Both BNP and hs CRP could provide complementary diagnostic and prognostic information regarding future cardiovascular disorders in renal patients.

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Abstract: HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n = 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs in vitro. The HEV viral load was comparable in HEV-1- and HEV-3-infected cells, but HEV-1 induced more inflammatory responses. In conclusion, HMOs, HMACs, and human BMDMs are permissive to HEV infection and these cells could be the source of chronic and recurrent infection, especially in immunocompromised patients. Replication of HEV in human BMDMs could be related to hematological disorders associated with extrahepatic manifestations.