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.

NULL

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.

Abstract: Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis worldwide. The tropism of HEV is not restricted to the liver, and the virus replicates in other organs. Not all the extrahepatic targets for HEV are identified. Herein, we found that non-decidualized primary human endometrial stromal cells (PHESCs), which are precursors for the decidua and placenta, are susceptible to HEV infection. PHESCs, isolated from healthy non-pregnant women (n = 5), were challenged with stool-derived HEV-1 and HEV-3. HEV RNA was measured by qPCR, and HEV capsid protein was assessed by flow cytometry, immunofluorescence (IF), and ELISA. HEV infection was successfully established in PHESCs. Intracellular and extracellular HEV RNA loads were increased over time, indicating ecient replication in vitro. In addition, HEV capsid protein was detected intracellularly in the HEV-infected PHESCs and accumulated extracellularly over time, confirming the viral assembly and release from the infected cells. HEV-1 replicated more eciently in PHESCs than HEV-3 and induced more inflammatory responses. Ribavirin (RBV) treatment abolished the replication of HEV in PHESCs. In conclusion, PHESCs are permissive to HEV infection and these cells could be an endogenous source of HEV infection during pregnancy and mediate HEV vertical transmission.

Objective: Expression of certain miRNAs in the primary tumors has been shown to be associated with progression of breast cancer and the initiation of metastasis with poor prognosis leading to death. In this study we compared serum circulating micro RNA21 expression and its correlation to metastases in different stages of human breast cancer as a novel noninvasive biomarker that could be used for early detection. Methods: We analyzed the expression of miRNA-21 by quantitative real-time PCR, in 40 patients at different stages of breast cancer and compare its expression with another 20 healthy volunteers as control group. Results: miRNA-21 was significantly up-regulated in the early stage of breast cancer as compared to healthy control group (p 0.01). miRNA-21 was also higher expressed in patients with metastases as compared to healthy control group (p 0.01). There was positive correlation between miRNA-21 expression and the stage of the disease, and strong association between miR-21 over expression and the degree of invasiveness of the tumor. Conclusion: In the context of other studies that demonstrated the increased miRNA-21 expression in metastatic tumors, our results can mark miR-21 in different stages of breast cancer to be used as a potentially strong diagnostic and prognostic early biomarker and also these results raise the question whether or not miRNA-21 might be involved in the initiation of metastases.

Breast cancer is the most frequent cancer in women; in Egypt it affects 37.7% of all women and accounts for 29.1% of their cancer‑related mortality. Cyclin D1 protein overexpression is found in up to 50% of breast cancers. The aim of this study is to study the correlations between cyclin D1 level and stages of breast cancer (TNM staging) and to study the correlations between cyclin D1 and routine markers used in breast cancer [cancer antigen 15‑3 (CA15‑3) and carcinoembryonic antigen (CEA)]. This study was performed on 80 female breast cancer patients. Ten healthy women served as controls. The patients were referred from the Assiut University Hospital and South Egypt Cancer Institute. None of the healthy women in the control group had elevated cyclin D1 level above the cutoff value. Elevated levels of cyclin D1 was detected in 80, 90, 95, and 100% of patients in groups II, III, IV, and V, respectively. There was a significant positive correlation between cyclin D1 positivity with CEA and CA15‑3 concentrations. The combination of CA15‑3, CEA, and cyclin D1 resulted in the highest sensitivity (95.2%), highest specificity (100%), and highest diagnostic accuracy (96%). The cyclin D1 level in samples obtained from Egyptian women with breast cancer is a good marker for the detection of breast cancer, and in the detection of metastasis as it correlates with the clinical staging of the disease. A combination of CA15‑3, CEA, and cyclin D1 may be used as a panel for the diagnosis of metastasis among those patients.

Background Pleural effusion is considered an interesting clinical problem that is commonly faced by physicians and is caused by several diseases. The ability of computed tomography (CT) to differentiate transudate effusion from exudate effusion is still under research. Objective The aim of this study was to assess the accuracy of the CT in diagnosing the nature of the pleural effusion. Patients and methods In this prospective cross-sectional analytic study, laboratory biochemistry markers were used to classify pleural effusion into exudate or transudate based on Light’s criteria. Chest CT without contrast had been done for all patients, and CTs were diagnosed by the radiologist. Measurement of the pleural fluid density was done and shown using the CT attenuation values [Hounsfield unit (HU)]. Results Of 79 patients with pleural effusion, 60 patients had exudate effusion and 19 patients had transudate. The mean attenuation values were significantly higher in exudate effusion (20.11±7.11 HU) versus transudate effusion (13.8 ±4.11 HU), with P value of 0.03. Receiver operating characteristic curve analysis showed that the cutoff for exudate effusion was optimal at greater than or equal to 15.33 versus less than 15.33 HU for transudate (area under the curve=0.57; 95% confidence interval: 0.45–0.68). This point had 85.71% sensitivity and 46.55% specificity. Conclusion We reasoned the CT attenuation values of the pleural fluid may replace the laboratory tests in characterizing the pleural effusion, either exudate or transudate. However, there was an overlapping HU values in most effusions. So correlation of the CT results with the clinical findings is essential, and further CT studies are highly recommended to confirm and validate these findings.

NULL

NULL