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This study retrospectively investigated the impact of interleukin-1 receptor-associated kinase-3 (IRAK-3/IRAK-M) silencing by methylation on the likelihood of multiple sclerosis (MS) activity. This cross-sectional study included 90 patients with MS: 45 with active disease (Group 1), 45 in remission (Group 2), and 45 healthy controls. The study included quantitation of IRAK-3 methylation index (MI%), IRAK-3 mRNA, and myeloid differentiation factor88 (MyD88) and assessment of NF-κB activity. IRAK-3 MI% was significantly higher in group 1 compared to group 2, accompanied by lower IRAK-3 mRNA expression, elevated circulating MyD88, and increased NF-κB activity. IRAK-3 MI% correlated negatively with its transcript and positively with MyD88 and NF-κB activity. A logistic regression model was created to predict active demyelination. The C-index was 0.924, which indicates a very strong prediction model. Within the limitations of current work, IRAK-3 methylation level seems to be a promising candidate biomarker for identifying MS patients at risk of relapse.

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In previous studies, the inhibitory effect of chloroquine on NLRP3 inflammasome and heme production was documented. This may be employed as a double-bladed sword in schistosomiasis (anti-inflammatory and parasiticidal). In this study, chloroquine's impact on schistosomiasis mansoni was investigated. The parasitic load (worm/egg counts and reproductive capacity index [RCI]), i-Nos/Arg-1 expression, splenomegaly, hepatic insult and NLRP3-immunohistochemical expression were assessed in infected mice after receiving early and late repeated doses of chloroquine alone or dually with praziquantel. By early treatment, the least RCI was reported in dually treated mice (41.48 ± 28.58) with a significant reduction in worm/egg counts (3.50 ± 1.29/2550 ± 479.58), compared with either drug alone. A marked reduction in the splenic index was achieved by prolonged chloroquine administration (alone: 43.15 ± 5.67, dually: 36.03 ± 5.27), with significantly less fibrosis (15 ± 3.37, 14.25 ± 2.22) than after praziquantel alone (20.5 ± 2.65). Regarding inflammation, despite the praziquantel-induced significant decrease in NLRP3 expression, the inhibitory effect was marked after dual and chloroquine administration (liver: 3.13 ± 1.21/3.45 ± 1.23, spleen: 5.7 ± 1.6/4.63 ± 2.41). i-Nos RNA peaked with early/late chloroquine administration (liver: 68.53 ± 1.8/57.78 ± 7.14, spleen: 63.22 ± 2.06/62.5 ± 3.05). High i-Nos echoed with a parasiticidal and hepatoprotective effect and may indicate macrophage-1 polarisation. On the flip side, the chloroquine-induced low Arg-1 seemed to abate immune tolerance and probably macrophage-2 polarisation. Collectively, chloroquine synergised the praziquantel-schistosomicidal effect and minimised tissue inflammation, splenomegaly and hepatic fibrosis.

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BACKGROUND AND AIM: Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) affects most of the cells involved in cardiac fibrosis like inflammatory cells, cardiomyocytes and fibroblasts. CD163, the receptor of TWEAK on the surface of type 2 macrophages, is shed into plasma upon macrophages activation. This work aimed to evaluate serum TWEAK and its decoy receptor CD163 as probable biomarkers to monitor myocardial iron overload (MIO) in transfusion dependent thalassemia major (TDTM) patients and to predict iron-induced cardiac decompensation (IICD). METHODS: A total of 140 TDTM patients were enrolled. Patients were categorized into two groups; group I (n = 70) diagnosed with IICD while group II (n = 70) had no evidence of IICD. sTWEAK and sCD163 were quantitated utilizing Enzyme-linked-immunosorbent- assay. RESULTS: sTWEAK was evidently lower in group I than group II (medians, 412 and 1052 pg/mL respectively). sCD163 was higher in group I than group II (medians, 615.5 and 323.5 ng/mL respectively). sTWEAK positively correlated with cardiac MRI-T2 mapping and ventricular ejection fractions and negatively correlated with B-Natriuretic peptide and cardiac troponin. An inverse relationship between TWEAK and CD163 was documented throughout the study. sTWEAK, sCD163 and TWEAK/CD163 ratio proved to be significant predictors of IICD in TDTM patients. TWEAK/CD163 ratio < 1.04 discriminated IICD in TDTM patients with 100 % clinical sensitivity and specificity. CONCLUSION: Circulating TWEAK and CD163 appears to be promising biomarkers for monitoring MIO and predicting IICD in TDTM patients.

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BACKGROUND: Deregulated autophagy in diabetes has been a field of many experimental studies recently. Impaired autophagy in diabetic kidneys orchestrates every step of diabetic nephropathy (DN) pathogenesis. This study aimed to evaluate three autophagy regulators; RUBCN, mTOR, and SESN2 as clinically applicable indicators of DN progression and as early predictors of DN. METHODS: This retrospective study included 120 participants in 4 groups; G1: diabetic patients without albuminuria, G2: diabetic patients with microalbuminuria, G3: diabetic patients with macroalbuminuria and G4: healthy controls. RUBCN and SESN2 genes expression were tested by RT-qPCR. RUBCN, mTOR, and SESN2 serum proteins were quantitated by ELISA. RESULTS: RUBCN mRNA was over-expressed in diabetic patients relative to controls with the highest level found in G3 followed by G2 then G1; (9.04 ± 0.64, 5.18 ± 0.73, 1.94 ± 0.41 respectively. P < 0.001). SESN2 mRNA expression was at its lowest level in G3 followed by G2 then G1 (0.1 ± 0.06, 0.48 ± 0.11, 0.78 ± 0.13 respectively. P < 0.001). Similar parallel reduction in serum SENS2 was observed. Serum RUBCN and mTOR were significantly elevated in diabetic patients compared to controls, with the increase parallel to albuminuria degree. RUBCN expression, serum RUBCN and mTOR strongly correlated with albuminuria (r = 0.912, 0.925 and 0.867 respectively). SESN2 expression and serum level negatively correlated with albuminuria (r = - 0.897 and -0.828 respectively); (All p < 0.001). Regression analysis showed that serum RUBCN, mTOR, RUBCN and SESN2 mRNAs could successfully predict DN. CONCLUSIONS: The study proves the overexpression of RUBCN and mTOR in DN and the down-expression of SESN2. The three markers can be clinically used to predict DN and to monitor disease progression.

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The present study aimed to detect the prevalence of NOTCH1 c.7541-7542delCT mutation in Egyptian CLL patients using HRM assay and to assess its relation to patients' survival. The study included 50 newly diagnosed treatment-naïve CLL patients and 50 age and sex matched healthy controls. NOTCH1 c.7541-7542delCT mutation was detected using High-resolution melting (HRM) assay and direct Sanger sequencing. Outcome parameters included progression free survival (PFS) and overall survival (OS). NOTCH1 c.7541-7542delCT mutation was detected in 5 (10.0%) of CLL patients. No controls had NOTCH1 c.7541-7542delCT mutation. Similar results were obtained by direct Sanger sequencing yielding a sensitivity and specificity of 100.0% for HRM in detection of NOTCH1 c.7541-7542delCT mutation in the studied patients. In univariate analysis, predictors of OS included Trisomy 12, high LDH, presence of NOTCH1 c.7541-7542delCT mutation and lack of CR. In multivariate analysis, only lack of CR was found as a significant predictor of OS. HRM analysis is a sensitive method for detection of NOTCH1 c.7541-7542delCT mutation in CLL patients. This mutation may be linked to poor disease prognosis.

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PURPOSE: Mitochondrial isocitrate dehydrogenase (IDH2) is a major contributor to cellular redox control. The aim of this study was to preliminary link IDH2 genetic variations to redox imbalance, atherogenesis and risk of acute myocardial infarction (AMI). METHODS: This case-control study included 120 AMI patients and 120 healthy controls. IDH2 genetic variations were tested using direct sequencing. IDH2 enzyme activity was measured spectrophotometrically. Malondialdehyde (MDA) and Oxidized low density lipoproteins (ox-LDL) concentrations, as biomarkers of oxidative stress, were quantitated using ELISA. RESULTS: Four missense heterozygous mutations were detected within IDH2 gene. The variant forms of the enzyme showed a markedly reduced enzymatic activity (2.22 ± 0.56 mU/mL in wild type compared to 0.65 ± 0.35 mU/mL in mutant enzyme). IDH2 enzyme activity correlated negatively with MDA and ox-LDL concentrations (r = -80.875 and -0.891 respectively). There was a strong association between IDH2 mutations and elevated MDA and ox-LDL (rpb = 0.764 and 0.652, both p < 0.001). After adjustment of other risk factors, IDH2 genetic variations showed to be an independent risk factor for AMI (ß=1.792, p = 0.019). CONCLUSIONS: The study proved that IDH2 genetic variations lead to impaired enzyme activity, redox imbalance, accumulation of lipid-peroxides and coronary atherogenesis. However, because such gene association has not been studied before, further studies are recommended.

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BACKGROUND: Diabetic retinopathy (DR) signifies a frequent serious diabetic complication influencing retinal structure and function. Dysregulation of lncRNAs drives a wide array of human diseases especially diabetes; thus, we aimed to study lncRNA HIF1A-AS2 role and its interplay with hypoxia, oxidative stress (OS), and angiogenesis in DR. MATERIALS AND METHODS: 60 DM patients in addition to 15 healthy subjects. were enrolled. LncRNA HIF1A-AS2 mRNA relative gene expression was assessed. Hypoxia inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), mitogen activated protein kinase (MAPK), and endoglin levels were assessed. Detection of DNA damage using comet assay, and Redox status parameters were also detected. RESULTS: LncRNA HIF1A-AS2 expression was significantly increased in diabetic patients with the highest levels in proliferative DR patients. Moreover, HIFα, VEGF, MAPK, and Endogolin levels were significantly higher in the diabetic patients compared to control group with the highest levels in in proliferative DR patients. Significant DNA damage in comet assay was observed to be the highest in this group. CONCLUSION: We observed for the first time the imminent role of long noncoding RNA HIF1A-AS2 in DR throughout its stages and its interplay with hypoxia, OS, and angiogenesis via MAPK/VEGF-dependent pathway.

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Thromboembolic complications are the most reported cause of death in coronavirus disease-2019 (COVID-19). Hypercoagulability, platelets activation and endotheliopathy are well-recognized features in COVID-19 patients. The aim of this work was to evaluate circulating soluble selectins P, E and L at the time of hospital admission as predictors for upcoming thrombosis. This retrospective study included 103 hospitalized COVID-19 patients and 50 healthy volunteer controls. COVID-19 patients were categorized into two groups; group 1 who developed thrombosis during hospitalization and group 2 who did not. Soluble selectins were quantitated using ELISA technique. Higher levels of sP-selectin, sE-selectin and sL-selectin were detected in COVID-19 patients compared to controls. Furthermore, significantly higher levels were found in group 1 compared to group 2. Their means were [5.86 ± 1.72 ng/mL vs. 2.51 ± 0.81 ng/mL]; [50 ± 8.57 ng/mL vs. 23.96 ± 6.31 ng/mL] and [4.66 ± 0.83 ng/mL vs. 2.95 ± 0.66 ng/mL] for sP-selectin, sE-selectin and sL-selectin respectively. The elevated selectins correlated with the currently used laboratory biomarkers of disease severity. After adjustment of other factors, sP-selectin, sE-selectin and sL-selectin were independent predictors for thrombosis. At sP-selectin ≥ 3.2 ng/mL, sE-selectin ≥ 32.5 ng/mL and sL-selectin ≥ 3.6 ng/mL thrombosis could be predicted with 97.1%, 97.6% and 96.5% sensitivity. A panel of the three selectins provided 100% clinical sensitivity. Admission levels of circulating soluble selectins P, E and L can predict thrombosis in COVID-19 patients and could be used to identify patients who need prophylactic anticoagulants. E-selectin showed a superior clinical performance, as thrombo-inflammation biomarker, to the most commonly studied P-selectin.

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Aims: Non-alcoholic fatty liver disease (NAFLD) is a broad category for a disease spectrum that includes simple steatosis, which can proceed to non-alcoholic steatohepatitis, cirrhosis, and, finally, hepatocellular carcinoma. Owing to the invasive nature of liver biopsy, the need for non-invasive tools were required for diagnosis. Objective: To compare the performance of simple biochemical scores (fibroblast) FIB-5 and (fibrosis-4) FIB-4 with fibroscan to differentiate mild to moderate fibrosis (MF; F0 to F2) from advanced fibrosis (AF; F3 to F4) in patients with NAFLD. Patients and methods: This cross-sectional study was done on 116 NAFLD patients. All patients were scanned with the FibroScan examination. FIB-5 and FIB-4 were calculated for all patients. Results: The mean kPa score (liver stiffness measurement score) of the patients belonging to advanced fibrosis [9.53 ± 1.05]. The FIB-4 score was significantly higher in patients with advanced fibrosis (1.54 ± 0.38) compared with patients with mild to moderate fibrosis (1.18 ± 0.44), p-value = 0.001, whereas the FIB-5 score was insignificant between patients. Conclusion: FIB-4 is superior to FIB-5 as a non-invasive simple marker in diagnosing advanced fibrosis in NAFLD patients.

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BACKGROUND: Screening of ß thalassemia among close relatives is more feasible in highly prevalent countries with limited resources. The purpose of this study is to determine the prevalence of ß thalassemia carriers and iron deficiency anemia among relatives of ß thalassemia patients in Mid Delta, Egypt. METHODS: This is a cross-sectional multi-center study conducted on 2118 relatives of patients with ß thalassemia from different Egyptian governorates in the Mid Delta region. They were subjected to history taking with precise determination of geographic location, general examination, and the following investigations: complete blood counts, serum ferritin for those who showed microcytic hypochromic anemia, and high-performance liquid chromatography for those who were not diagnosed as iron deficiency anemia. RESULTS: The total prevalence of iron deficiency anemia among close relatives of confirmed ß thalassemia patients in the Nile Delta region was 17.19%. The highest prevalence of iron deficiency anemia (45.05%) was reported in Al-Gharbia Governorate, followed by Al-Menoufia Governorate (21.67%), and the lowest prevalence was that of Al-Sharkia Governorate (4.91%). The differences were highly statistically significant (p < 0.001). ß thalassemia carrier prevalence rate in the studied relatives was 35.84%, with the highest prevalence detected in Al-Sharkia Governorate (51.32%), followed by Kafr-Alsheikh and Al-Dakahilia Governorates (41.78%, 37.13%) respectively, while Al-Menoufia Governorate had the lowest prevalence rate (25.00%). These differences were also highly statistically significant (p < 0.001). CONCLUSION: More than one-third of relatives of patients with ß thalassemia are carriers of the disease, while 17.19% suffer from iron deficiency anemia. This study demonstrates the importance of tracing the high number of beta thalassemia carriers among relatives of patients with ß thalassemia in Egypt.

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Type 2 Diabetes Mellitus (T2DM) is well known to include an inflammatory component that has been considered to be related to diabetic complications. Diabetic nephropathy (DN) is one of the significant complications as it constitutes the most frequent cause of end-stage renal disease. Tumor Necrosis Factor-α (TNF-α) is known as a multifunctional proinflammatory cytokine which is associated with some pathological processes such as immunoregulation, proliferation, inflammation, and apoptosis. The aim was to explore the association between the TNF-α promoter -1031T/C single nucleotide polymorphism (SNP) and the serum TNF-α level in addition to nephropathy among type 2 diabetic patients. The study included 38 T2DM subjects without nephropathy (DM group), 40 subjects with DN, and 20 controls. Identification of TNF-α promoter gene polymorphism -1031T/C was done by PCR-RFLP, and genotyping was confirmed by direct sequencing. The serum TNF-α level was assessed by ELISA. Correlations were tested by Pearson's correlation analysis. Logistic regression was used to detect the most independent factor for development of DN. The serum level of TNF-α in the DM group was significantly higher than controls (p < 0.001); also, the DN group was considerably higher than controls and DM without nephropathy (p < 0.001). Also, there was a significant positive correlation between serum levels of TNF-α with FBG (fasting blood glucose), creatinine, total cholesterol, LDL-C, HbA1c, and microalbumin/creatinine ratio (ACR) among the DN group (p = 0.042, <0.001, <0.001, <0.001, 0.027, and 0.043, respectively). Mutant homozygous CC and heterozygous TC genotypes were higher in DN than in DM and controls. C allele was more represented in DN than in DM and controls (p = 0.003) while T allele was higher in controls than in DM and DN patients. The levels of TNF-α were higher in subjects who had mutant CC than the wild TT genotype among DN (p < 0.001). C allele was more risky for DN than T allele between DN and controls by 5.4-fold (CI: 1.75-16.68) as well as between DN and DM by 2.25-fold (CI: 1.1-4.59). Conclusion. Serum levels of TNF-α were higher in individuals with mutant CC genotype of -1031T/C TNF-α gene, and C allele could be associated with increased risk for nephropathy among patients with T2DM.

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The correct spelling of the 7th authors' name is Mona Watany.

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PURPOSE: This case-control study aimed to evaluate the ability to use a panel of IL-31, IL-1ß and NLRP3 to differentiate sepsis from systemic inflammatory response syndrome (SIRS) and to predict septic shock. METHODS: Serum levels of IL-31, IL-1ß and NLRP3 were measured by ELISA in 149 participants; 38 with sepsis, 51 with SIRS, 30 with septic shock and 30 healthy controls. RESULTS: Lower levels of IL-31 were found in sepsis (10.21 ± 4.34 pg/ml) compared to SIRS (16.74 ± 3.18 pg/ml) and to controls with the lowest levels detected in septic shock (6.26 ± 2.72 pg/ml). IL-1ß and NLRP3 levels were higher in sepsis (54.99 ± 14.11 pg/ml and 9.93 ± 2.38 ng/ml) compared to SIRS (27.8 ± 6.94 pg/ml and 4.86 ± 1.33 ng/ml) with the highest levels seen in septic shock (125.1 ± 32.79 pg/ml and 19.43 ± 6.48 ng/ml) respectively. IL-31 discriminated sepsis in patients showing SIRS with 80% sensitivity and 70% specificity and, identified septic shock with 78.6% sensitivity and 60.3% specificity. IL-1ß identified sepsis from SIRS with 93.3% and 83.3% specificity. NLRP3 discriminated sepsis from SIRS with 94.5% sensitivity and 93.3% specificity. And, with sensitivity 99.1% and 90.1% and specificity 98.9% and 80% IL-1ß and NLRP3 could respectively define septic shock. A panel of combined markers provided 100% sensitivity and specificity. The three biomarkers proved to be independent prognostic biomarkers. At 95% CI, IL-31 hazard ratio (HR) was 0.716, p = 0.001; IL-1ß HR was 1.023, p ≤ 0.001; and NLRP3 HR was 1.114, p ≤ 0.001. Additionally, IL-1ß proved to be an independent predictor of septic shock (ß = 0.355; p = 0.035). CONCLUSION: The cross-relation between IL-31, IL-1ß and NLRP3 in sepsis can provide a promising diagnostic and prognostic panel.

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BACKGROUND & OBJECTIVES: Prevalence of hepatitis B virus in patients with rheumatic diseases has been reported differently among studies. The loss of immune control in these patients may result in the reactivation of HBV replication within hepatocytes. Considering the lifelong use of multiple anti-rheumatic drugs, screening for HBV is recommended before starting immunosuppressive or immunomodulatory therapy. The aim of this study was to select the best and simplest test for screening of HBV in rheumatic patients. METHODS: This study was carried out in 102 patients with different rheumatic diseases. Screening to all patients for hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) antibodies and human immune deficiency virus antibodies (HIV) was done. HBV core antibodies and real time PCR to detect HBV DNA were done. RESULTS: The mean age of the patients was 37.18 ± 12.37 years, 3.9% of them were males and 96.1% were females. HBsAg had 100% Sensitivity, 100% Specificity, 100% PPV, 100% NPV and 99.0% accuracy. While, anti-HBc had 100% Sensitivity, 78% Specificity, 8% PPV, 100% NPV and 78% accuracy in the screening of HBV. CONCLUSIONS: HBs Ag was found to be superior to antiHBc for screening for HBV infection in rheumatic patients.

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BACKGROUND: Diagnosis of Spontaneous Bacterial Peritonitis (SBP) depends mainly on ascetic fluid culture which may be negative in spite of the clinical suggestion of SBP and high ascetic fluid neutrophilic count. AIMS: This study aimed to evaluate the biological importance of amyloid A biomarker in both serum and ascetic fluid to diagnose SBP as early as possible and to compare it to other markers (C-reactive protein (CRP), and the neutrophil-to-lymphocyte ratio (NLR)). METHODS: This study included 37 patients with hepatic ascites; twenty-two of them had SBP, and 15 patients did not have SBP. Serum and ascetic fluid amyloid A, ascetic fluid neutrophil, C-reactive protein, and neutrophil-to-lymphocyte ratio were measured in all subjects before the start of antimicrobial chemotherapy to the infected ones. RESULTS: Both the serum and ascetic fluid amyloid and also, CRP were significantly higher in patients infected with ascetic fluid than others. The cut-off point of serum amyloid A for early detection of SBP was 9.25ug/ml with the high sensitivity and specificity. For ascetic amyloid A, the sensitivity and specificity were 90.09% and 60% at cut-off point 2.85ug/ml, respectively. CONCLUSION: Amyloid A in serum and ascitic fluid can be considered as a good biomarker for early diagnosis of SBP.

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INTRODUCTION: Diabetic nephropathy (DN) represents one of the main causes of end-stage renal disease in type 2 diabetes mellitus (DM) patients. Galectin-3 has been implicated in pathogenesis of many pathological conditions. To date, there are limited data regarding the relationship between galectin-3 and DN. AIM OF THE STUDY: Evaluation of serum galectin-3 as a novel prognostic biomarker in patients with DN. PATIENTS AND METHODS: This prospective study was carried out in the Internal Medicine and Clinical Pathology Departments, Tanta University Hospital, Egypt, from March 2015 to March 2018 on 300 patients with type 2 DM. Patients were divided into three groups: group I included 100 patients with albumin/creatinine ratio (ACR) <30 mg/g (normoalbuminuria), group II included 100 patients with ACR within 30-300 mg/g (microalbuminuria), and group III included 100 patients with ACR >300 mg/g (macroalbuminuria). All patients were subjected to the following: full history taking, clinical examination, and laboratory evaluation (HbA1c, creatinine, estimated glomerular filtration rate, ACR, and serum galectin-3). RESULTS: The mean levels of galectin-3 were significantly higher in patients with macroalbuminuria than in those with microalbuminuria and normoalbuminuria. Galectin-3 was a significant predictor for progression to microalbuminuria, macroalbuminuria, dialysis, and death among patients with type 2 DM. CONCLUSION: Based on this single center prospective study, serum galectin-3 is considered a significant predictor for DN progression among patients with type 2 DM.

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AIM: Diabetic peripheral neuropathy (DPN) is a frequent and debilitating complication of diabetes mellitus. The low-density lipoprotein receptor-related protein-1 (LRP-1) is a multifunctional cell surface receptor playing critical roles in lipoprotein metabolism and several cell signaling processes. C/EBP homologous protein (CHOP) is a main conduit to endoplasmic reticulum stress-induced apoptosis. We aimed to investigate LRP1 and CHOP gene expression in peripheral blood cells of type 2 diabetes mellitus (T2DM) subjects to clarify its possible relation to DPN pathogenesis. METHOD: The study included 20 non-complicated T2DM subjects, 20 subjects with DPN and 20 healthy controls. Quantitative real time PCR was used to study gene expression. RESULTS: There was a significant reduction in LRP1 mRNA expression and a significant increase in CHOP mRNA expression in subjects with DPN compared to non-complicated group and healthy controls. Both LRP1 and CHOP expression levels were inversely correlated, and both showed significant correlation with HbA1c, hyperlipidemia, hs-CRP, and different electrophysiological parameters. Receiver operating characteristics (ROC) analysis suggested that both LRP1 and CHOP mRNA expression and hs-CRP levels had great potential advantages to predict the progression of DPN. CONCLUSION: LRP1 and CHOP might be involved in DPN pathogenesis and progression, thus providing opportunities for early detection and treatment.

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AIM: This study aimed at investigating the presence of intestinal parasitic infections in inflammatory respiratory diseases patients during the disease attack, and measuring the acidic mammalian chitinase (AMCase) gene expression in blood before and after infection eradication. METHODOLOGY: This case-control study included 123 inflammatory respiratory diseases patients and 120 apparently healthy individuals. Repeated stool examination was done, while total and specific IgE were measured. AMCase gene expression was analysed by real time-polymerase chain reaction (RT-PCR). RESULTS: Infection was detected in 32.5% of the diseased and 23.25% of the healthy individuals. Higher rate of the helminthic infection was detected (23.57) in comparison to the protozoal (12.19%) in the patients. A significantly higher rate of infection with the chitin-rich helminths "Enterobius vermicularis & Hymenolepis nana" and level of anti-Dermatophagoide-IgE were reported in the patients (14.63%, 6.5% and 23.57%, respectively). AMCase expression was significantly higher in helminths-infected patients than the noninfected, or protozoa infected. After infection eradication, AMCase expression significantly declined in the previously helminth-infected patients (mean ± SD = 13.9 ± 3.918 before and 4.515 ± 1.93 after), but insignificantly affected in the protozoa infected (mean ± SD = 2.095 ± .285 before and 2.675 ± 1.181 after). CONCLUSION: Chitin-rich intestinal helminths are suspected to precipitate Th2-immune response in remote tissues by enhancing systemic AMCase expression through intestinal mucosa and macrophages irritation.

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Steroid-resistant nephrotic syndrome represents about 10-20% of pediatrics' nephrotic syndrome. The regeneration of glomerular barrier seems pivotal for cessation of proteinuria. Nephronectin (NPNT) plays a major role in nephrogenesis, signal transduction, and epithelial-mesenchymal interactions. This study aims to preliminary assess NPNT as potential noninvasive biomarker of glomerular regeneration and its ability to identify steroid resistance. In this case control study, 80 retrospectively selected patients with nephrotic syndrome were enrolled in addition to 40 healthy controls. Forty patients were steroid sensitive (SSNS) and the other 40 patients were steroid-resistant (SRNS), NPTN concentration was measured using ELISA and NPNT mRNA expression was assayed using real-time PCR. NPTN concentrations were significantly higher in SSNS than both SRNS and controls (The means were 4.64 ± 3.05, 0.69 ± 0.44, and 1.63 ± 0.59, respectively). Moreover, NPTN concentrations were significantly lower in SRNS than controls. NPTN was significantly overexpressed in SSNS compared to both SRNS and controls (the means were 10.82 ± 7.39, 1.19 ± 0.94, and 1.04 ± 0.10, respectively) with no statistically significant difference between SRNS and controls. ROC curves analysis showed that both NPNT expression and NPNT serum level are of promising diagnostic performance (ROCAUC 0.948 and 0.896, respectively). Regression analysis showed that both NPNT expression and NPNT serum level can be independent predictors of steroid resistance. The present study shows for the first time an enhanced expression of NPNT in steroid-sensitive nephrotic syndrome patients suggesting NPNT as a marker of glomerular regeneration. Also, serum NPNT can be a useful noninvasive biomarker of steroid resistance.

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