Frequency and risk factors for Hepatitis C virus seropositivity in blood transfusion-dependent thalassemic patients in Qena hospitals

Background: Beta-thalassemia major (BTM) is still mostly treated with routine blood transfusions. One of the most prevalent transfusion-transmitted infections (TTI) of clinical significance is the hepatitis C virus (HCV). Objectives: To estimate the prevalence of HCV infection among thalassemic patients in Qena hospitals, and to identify the possible risk factors associated with HCV infection. Patients and methods: a cross-sectional study involving 400 thalassemic patients with an age ranging from 1.5 to 29 years, a mean age of 12.8 ±7.3 years, 176 (44%) were male and 224 (56%) were female, and 75.5% were from rural areas. All are reviewed by a structured questionnaire. Results: The study revealed that the prevalence of HCV infection in the studied thalassemic patients was 9.5%. The most important risk factors were the duration of blood transfusion for more than 15 years, previous surgery, dental procedure, and splenectomy (P<0.001), followed by patient age of more than 18 years (P = 0.001), urban population, and a positive family history of thalassemia (P = 0.001), and frequency of blood transfusion (P = 0.054). Conclusion:The most important risk factors were the duration of blood transfusion for more than 15 years, previous surgery, dental procedure, and splenectomy. Thalassemic patients with older age were at higher risk for HCV infection. The risk increased with patients aged more than 18 years old. A family history of thalassemia was a risk factor for HCV infection

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

The kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis

Erythropoietin Suppresses the Hepatic Fibrosis Caused by Thioacetamide: Role of the PI3K/Akt and TLR4 Signaling Pathways

Erythropoietin (EPO) is recognized for its function in erythropoiesis; however, its potential antifibrotic effect against liver fibrosis remains unknown. This study examined whether EPO affects thioacetamide (TAA)-induced liver fibrosis by concentrating on the Toll-like receptor 4 (TLR4) cascade and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway as possible pathways. Male Wistar rats were randomized into four groups, which included: the negative control group, the TAA group (intraperitoneal; TAA 100 mg/kg three times per week for 2 weeks), and EPO-treated groups (150 and 300 IU/kg, i.p.) for 2 weeks after TAA injections. EPO attenuated hepatic fibrosis in a dosage-dependent way, as manifested by the diminution in serum alanine aminotransferase and aspartate aminotransferase activities, as well as the increase in albumin level. EPO inhibited the increase in tissue levels of tumor necrosis factors-α, interleukin-1β, transforming growth factor-β1, and TLR4 and raised tissue levels of PI3K and p-PI3K. EPO antioxidant properties were demonstrated by restoring hepatic glutathione and superoxide dismutase by preventing the accumulation of hepatic malondialdehyde. Further, EPO increased the protein expression of PI3K and Akt and decreased TLR4 protein expression. Immunohistochemically, EPO treatment altered tissue histology and downregulated mitogen-activated protein kinase protein expression. Overall, the research suggested that EPO could prevent TAA-induced hepatic fibrosis through upregulating the PI3K/Akt signaling cascade and downregulation the TLR4 downstream axis

Burnout among surgeons before and during the SARS-CoV-2 pandemic: an international survey

Background: SARS-CoV-2 pandemic has had many significant impacts within the surgical realm, and surgeons have been obligated to reconsider almost every aspect of daily clinical practice. Methods: This is a cross-sectional study reported in compliance with the CHERRIES guidelines and conducted through an online platform from June 14th to July 15th, 2020. The primary outcome was the burden of burnout during the pandemic indicated by the validated Shirom-Melamed Burnout Measure. Results: Nine hundred fifty-four surgeons completed the survey. The median length of practice was 10&nbsp;years; 78.2% included were male with a median age of 37&nbsp;years old, 39.5% were consultants, 68.9% were general surgeons, and 55.7% were affiliated with an academic institution. Overall, there was a significant increase in the mean burnout score during the pandemic; longer years of practice and older age were significantly associated with less burnout. There were significant reductions in the median number of outpatient visits, operated cases, on-call hours, emergency visits, and research work, so, 48.2% of respondents felt that the training resources were insufficient. The majority (81.3%) of respondents reported that their hospitals were included in the management of COVID-19, 66.5% felt their roles had been minimized; 41% were asked to assist in non-surgical medical practices, and 37.6% of respondents were included in COVID-19 management. Conclusions: There was a significant burnout among trainees. Almost all aspects of clinical and research activities were affected with a significant reduction in the volume of research, outpatient clinic visits, surgical procedures, on-call hours, and emergency cases hindering the training. Trial registration: The study was registered on clicaltrials.gov "NCT04433286" on 16/06/2020

L-carnitine alleviated acute lung injuries induced by potassium dichromate in rats: involvement of Nrf2/HO-1 signaling pathway

The activation of the Nrf2/HO-1 signaling pathway regulates cellular antioxidant stress and exerts anti-inflammatory and cytoprotective effects against acute lung injury (ALI). The present study aimed to evaluate the therapeutic role of L-carnitine (LC) against potassium dichromate (PD) - induced acute lung injury in adult male albino rats via modulation of Nrf2/HO-1 signaling pathway. For this purpose, forty rats were randomly allocated into 5 groups (8 rats each). The normal group received intranasal (i.n.) saline, while the ALI group received intranasal instillation of PD as a single dose of 2 mg/kg. The 3d – 5th groups received PD then after 24 h administered L-carnitine (25, 50 and 100 mg/kg; orally) for 3 consecutive days. The therapeutic effect of L-carnitine was evaluated by assessment of serum levels of glutathione (GSH) and malondialdehyde (MDA) along with measurement of lung contents of transforming growth factor β1 (TGFβ1), protein kinase B (AKT), Nuclear factor erythroid-2 related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase 1 enzyme (NQO1) and glutathione cysteine ligase modifier subunit (GCLM) expression. Post-treatment with L-carnitine effectively increased the levels of GSH and AKT, elevated Nrf2 and its target genes and decreased the levels of MDA and TGFβ1 in comparison with PD control rats. Additionally, L-carnitine effectively reduced the number of goblet cell, inhibited the mucus formation in bronchioles and interstitial inflammatory infiltrate as well as alleviated the destruction of alveolar walls, and the congestion of blood vessels in lung tissue induced by PD. Our findings showed that L-carnitine may be a promising therapeutic agent against PD-induced acute lung injury

The pharmacological effect of apricot seeds extracts and amygdalin in experimentally induced liver damage and hepatocellular carcinoma

Introduction: Apricot (Prunus armeniaca L.) has been widely used for the treatment of several disorders such as liver diseases, but the hepatoprotective and anticancer activities of its seeds were not studied before. In this study, we evaluated the pharmacological effects of apricot seeds extracts and amygdalin on prevention of liver damage and treatment of hepatocellular carcinoma. Methods: Amygdalin contents of apricot seeds in ethanolic extracts were determined using high performance liquid chromatography (HPLC) then, the ethanolic apricot seeds extract and amygdalin were evaluated for its hepatoprotective activity against carbon tetrachloride-induced hepatotoxicity and anticancer activity against N-nitrosodiethylamine (NDEA)-induced hepatocarcinogenesis. Results: The amount of amygdalin was 5.72 g and 10.22 g/100 g extract for 70% and 99.9% ethanolic apricot seeds extracts, respectively. Pretreatment of the rats with 70% and 99.9% ethanolic apricot seeds extracts (100 mg/kg), amygdalin and silymarin (50 mg/kg) prevented elevation in liver function parameters such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) caused by carbon tetrachloride injection with significant increase in albumin, total proteins, and no effect on total direct bilirubin when compared to those in hepatotoxic group. Both extracts also showed anticancer activity against hepatocellular carcinoma via diminishing the elevated serum levels of AST, ALT, ALP, total, direct bilirubin, albumin, total proteins, alpha-fetoprotein, malondialdehyde (MDA) and nitric oxide (NO) and elevating the decreased hepatic reduced glutathione (GSH) level when compared with NDEA- intoxicated group. Conclusion: Apricot seeds possess hepatoprotective and anticancer activities that justify its traditional use, and its potential for the treatment of liver diseases including hepatocellular carcinoma

Miconazole Mitigates Acetic Acid-Induced Experimental Colitis in Rats: Insight into Inflammation, Oxidative Stress and Keap1/Nrf-2 Signaling Crosstalk

Ulcerative colitis (UC) is the most common type of inflammatory bowel disease, characterized by oxidative stress and elevated pro-inflammatory cytokines. Miconazole is an azole antifungal that stimulates the expression of antioxidant enzymes via Nrf2 activation, which consequently inhibits ROS formation and NF-&kappa;B activation. Hence, the present study aimed to investigate the protective effect of miconazole, sulfasalazine (as a reference drug) and their combination on acetic acid (AA)-induced UC in a rat model which was induced by intra-rectal administration of 4% AA. Rats were pretreated with miconazole (20 and 40 mg/kg, orally) or sulfasalazine (100 mg/kg, orally), or their combination (20 mg/kg miconazole and 50 mg/Kg of sulfasalazine, orally). Pretreatment with miconazole significantly reduced wet colon weight and macroscopic scores, accompanied by a significant amelioration of the colonic architecture disorder. Moreover, the treatment also significantly decreased the malondialdehyde (MDA) level and prevented the depletion of superoxide dismutase (SOD) activity and GSH content in inflamed colons. Additionally, the treatment showed suppressive activities on pro-inflammatory cytokines, including tumor necrosis factor-&alpha; (TNF-&alpha;), interleukin-6 (IL-6) and C-reactive protein (CRP), and upregulated the anti-inflammatory cytokine interleukin-10 (IL-10). Moreover, the treatment upregulated the protein levels of Nrf-2 and heme oxygenase-1 (HO-1) in the colon tissue. Taken together, miconazole is effective in alleviating AA-induced colitis in rats, and the mechanism of its action is associated with the activation of Nrf2-regulated cytoprotective protein expression

Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

Abstract The kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis

Serum 25-hydroxyvitamin D level is negatively associated with serum phosphorus level among stage 3a-5 chronic kidney disease patients

Background: Serum 25-hydroxyvitamin D (25(OH)D) negatively correlates with serum phosphorus level of stage 3a-5 chronic kidney disease (CKD) patients. So far, no explanation has been provided for this negative association. Objective: To confirm this negative association and determine if this relationship is mediated through other known co-morbid factors. Cases and methods: One hundred (57 male and 43 female) pre-dialysis stage 3a-5 CKD patients were selected. Estimated glomerular filtration rate (eGFR), serum calcium (Ca), phosphorus (P), 25(OH)D, parathyroid hormone (PTH), and intact fibroblast growth factor-23 (FGF23) were assessed. A correlation analysis between serum 25(OH)D and the different parameters studied was performed. Multivariate linear regression analysis was carried out to determine predictors of 25(OH)D. Results: The negative association between serum 25(OH)D and serum P was confirmed in univariate and multivariate correlation analysis. On the other hand, we failed to detect a significant association between 25(OH)D and serum FGF23. Serum P is the most important independent predictor of 25(OH)D in these patients (partial R2 = 0.15, p < 0.0001). Conclusion: Serum P is likely to have a direct negative impact on serum 25(OH)D. Further studies are needed to determine the underlying mechanism. Resumen: Antecedentes: La 25-hidroxivitamina D (25[OH]D) sérica se correlaciona negativamente con el nivel de fósforo sérico en pacientes con enfermedad renal crónica (ERC) en estadio 3a-5. Hasta la fecha, no se dispone de ninguna explicación sobre esta asociación negativa. Objetivo: Confirmar la asociación negativa y averiguar si esta relación está mediada por otros factores de comorbilidad conocidos. Casos y métodos: Se seleccionaron 100 pacientes (57 varones y 43 mujeres) con ERC en estadio 3a-5 prediálisis. Se evaluaron la tasa de filtración glomerular estimada (TFRe), el calcio sérico (Ca), el fósforo (P), la 25(OH)D, la hormona paratiroidea (HPT) y el factor de crecimiento de fibroblastos 23 intacto (FGF23). Se realizó un análisis de correlación entre la 25(OH)D sérica y los distintos parámetros estudiados. Se llevó a cabo un análisis de regresión lineal multivariable para determinar los factores pronósticos de 25(OH)D. Resultados: Se confirmó la asociación negativa entre la 25(OH)D sérica y el P sérico en análisis de correlación univariable y multivariable. Por otro lado, no detectamos ninguna asociación significativa entre la 25(OH)D y el FGF23 sérico. El P sérico es el factor predictivo independiente más importante de la 25(OH)D en estos pacientes (R2 parcial = 0,15; p < 0,0001). Conclusión: Es probable que el P sérico tenga un impacto negativo directo sobre la 25(OH)D sérica. Es necesario realizar más estudios para averiguar el mecanismo subyacente. Keywords: 25-Hydroxyvitamin D, CKD-MBD, Phosphorus, FGF23, Parathyroid hormone, Palabras clave: 25-Hidroxivitamina D, ERC-TMO, Fósforo, FGF23, Hormona paratiroide

Plasma exchange (PE) versus intravenous immunoglobulin (IVIG) for the treatment of Guillain-Barré syndrome (GBS) in patients with severe symptoms: A systematic review and meta-analysis

Background and purpose: Guillain- Barré syndrome (GBS) is a neuropathic condition that leads to the rapid development of impairments and is characterized by weakness and numbness or tingling sensation in the legs and arms and sometimes loss of movement and feeling in the legs, arms, upper body, and face. Currently, the cure for the disease is yet to be developed. However, treatment options such as intravenous immunoglobulin (IVIG) and plasma exchange (PE) have been used to minimize the symptoms and duration of the disease. Therefore, this systematic review and meta-analysis compared the efficacy of IVIG and PE in treating GBS patients with severe symptoms. Methodology: Six electronic databases, including PubMed, Embase, Scopus, ScienceDirect, Medline, and Google scholar, were scoured for articles related and relevant to our research. Additionally, more studies were obtained through the reference lists of the studies retrieved from these electronic databases. Quality assessment and statistical data analysis were conducted using Review Manager software (RevMan 5.4.1). Results: The search for relevant articles resulted in 3253 articles, of which only 20 were included for review in the current study. A sub-group analysis indicated no significant difference in the curative effect (Hughes score reduces by at least one score 4 weeks after GBS treatment; OR: 1.00; 95% CI: 0.66–1.52; p = 1.00 and Achieving grade 0 or 1 on Hughes scale; OR: 1.03; 95% CI: 0.27–3.94; p = 0.97). Similarly, the statistical showed that the difference in length of hospitalization and duration of mechanical ventilation was insignificant between the IVIG and PE group (Standard Mean Difference (SMD): -0.45; 95% CI: −0.92, 0.02; I2 = 91%; p = 0.06 and SMD: -0.54; 95% CI: −1.67, 0.59; I2 = 93%; p = 0.35, respectively). Moreover, the meta-analysis did not find any significant difference in the risk of GBS relapse (RR: 0.47; 95% CI: 0.20–1.14; p = 0.10) and risk of complications related to the treatment regimens (RR: 1.03; 95% CI: 0.71–1.48; p = 0.89). However, the statistical analysis of outcomes from 3 studies showed that the risk of discontinuation was significantly lower in the IVIG group than in the PE group (RR: 0.22; 95% CI: 0.06–0.88; p = 0.03). Conclusion: Our study suggests that IVIG and PE have similar curative effects. Similarly, IVIG seems easier to use and thus can be preferred for treating GBS