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Introduction: Breast cancer is the most commonly occurring cancer in women. It is also one of the most important health issues in many countries. Its high prevalence in women makes it necessary to encourage breast cancer screening behaviours. Aim: To investigate the relationship between breast cancer prevention behaviour and its screening behaviour in Tehranian women. Materials and Methods: This was cross-sectional study conducted on 859 women from November to December 2019 by the Iran University of Medical Sciences in Tehran, Iran. These women were selected by the multistage cluster method among five socio-economic classes living in different districts of Tehran. Structural Equation Modeling (SEM) was used to determine the relationship between breast cancer prevention behaviour and its screening behaviour. Data were analysed by Statistical Package for Social Sciences (SPSS) version 22.0 and Analysis of Moment Structures (AMOS) software. The level of significance was set at 0.05. Results: The mean age of the participants was 42±6.94 years. Also, 137 (15.9%) of the participants were single, and 604 70.3%) were married, 78 (9.08%) were divorced and rest widow. Among the studied subjects, 510 (57%) had unfavourable breast cancer screening behaviour. In Pearson's correlation test, there was a direct and significant relationship between the mean score of breast cancer prevention behaviour and its subscales with breast cancer screening behaviour, except for the dimension of information-seeking (r=0.35, p=0.007). In other words, with the increased breast cancer prevention behaviour, breast cancer screening behaviour also increased. The results of SEM analysis showed that breast cancer prevention behaviour was positively correlated to breast cancer screening behaviour (p<0.001), and about 41% of changes in the breast cancer screening behaviour could be explained by the breast cancer prevention behaviour (ß=0.41, p=0.01). Conclusion: Based on the results, it seems vital to take measures to inform and educate women about breast cancer and its complications, problems, prevention, screening, and diagnostic methods. The findings of this study can be used to increase motivation in the design of interventions in order to improve attitude, strengthen self-efficacy, reduce stress, and improve breast cancer screening behaviour. [ABSTRACT FROM AUTHOR]

Tropisetron, an antagonist of 5-HT3 receptor (5-HT3R), has exhibited a number of beneficial effects on the treatment of several diseases; however, its effect on diabetic cardiomyopathy, which is an important causal factor in morbidity and mortality among diabetic patients, remains to be fully elucidated. Therefore, this study was designed to investigate the effect of tropisetron on diabetes-induced cardiomyopathy and the molecular mediators possibly involved. Twenty-four male wistar rats were assigned into three groups, control, diabetic, and tropisetron--treated diabetic groups. After 14 days of treatment, the results revealed a significant increase in calcium/calmodulin-dependent protein kinaseIIδ (CaMKIIδ) total and isoforms δ2 and δ3 of CaMKIIδ, as well as myosin heavy chain (MHC)-β. Furthermore, it decreased MHC-α gene expression among the diabetic group compared to the control group. Western blot analysis showed a significant increase in Bax and cleaved caspase 3 protein levels and a significant decrease in Bcl-2 contents in heart tissue of diabetic rats in comparison to the control rats. Moreover, the levels of Tumor necrosis factor alpha (TNF-α), ICAM-1, and CaMKII in heart tissue of diabetic rats were significantly higher than those in the control rats. Significant amelioration of alteration in the genes expression and protein changes along with restoration of the elevated levels of TNF-α, ICAM-1, and CaMKII were found in the tropisetron--treated diabetic group compared to the diabetic group. Collectively, our study provided strong evidence that 5-HT3 antagonist tropisetron was capable of attenuating the development of experimental diabetic cardiomyopathy associated with the reduction of intramyocardial MHCs and CaMKIIδ gene expression, inflammation and cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the effect of tropisetron on liver injury induced by diabetes. Thirty-five male Wistar rats were assigned to five groups (n = 7): control (C), tropisetron (T), diabetic (D), diabetic + tropisetron (D + T) and diabetic + glibenclamide (D + G). Diabetic rats were treated with tropisetron (3 mg/kg body weight/day) or glibenclamide (1 mg/kg/day) for two weeks. Liver from diabetic rats exhibited a significant increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), cholesterol (Chol), triglycerides (TG), low-density lipoprotein (LDL), and atherogenic index, and a significant decrease in liver glycogen, serum albumin and high-density lipoprotein. Treatment with tropisetron significantly abrogated diabetes-induced perturbation in these parameters. These effects were equipotent with glibenclamide, suggesting that tropisetron treatment is associated with a hepatoprotective effect against diabetic injury. Therefore, the results of this study manifested the significance of using tropisetron as a promising remedial agent to improve diabetic complications. [ABSTRACT FROM AUTHOR]

Summary: In this paper a novel topology of switched capacitor based multilevel inverters is proposed. In this topology, to increase the output voltage levels and to add the voltage boosting capability, several switched capacitor units are cascaded in series. Having voltage boosting capability and generating maximum number of output voltage levels using minimum number of circuit components, is a merit for this topology. To highlight the attributes of the proposed topology, it is compared with other recently proposed multilevel inverters on number of circuit components such as power electronic switches, diodes and capacitors, voltage boosting capability, total standing voltage, cost and efficiency. The comparison results verify the superiority of the proposed topology over other proposed topologies on number of circuit components, and number of output voltage levels. It is also clear that, this topology has lower voltage stress on power electronic switches, which makes it an appropriate solution for industrial applications. Finally, to show the capabilities of the proposed topology, and to verify the accurate operation of the topology, circuit analysis as well as the experimental results are provided. [ABSTRACT FROM AUTHOR]

• Cerebral IR increased apoptotic index as evidenced by bcl2 and bax alterations in cerebral cortex of rats. • Cerebral IR up-regulated miR-27a gene expression in cerebral cortex tissue in rats. • Cerebral IR increased TNF-α protein level and decreased smurf1 protein expression in the cerebral cortex of rats. • CGA treatment significantly reduced the apoptosis through bax and bcl2 protein alterations in IR rats. • CGA treatment decreased miR-27a and TNF-α level and increased smurf1protein expression in cerebral cortex tissue of rats. Apoptosis may contribute to a considerable proportion of neuron death after acute cerebral ischemia, although the underlying mechanisms remain unknown. The purpose of this research is to investigate the effect of cerebral ischemia–reperfusion on miR-27a/smurf1 axis in rat cerebral cortex alone and in combination with chlorogenic acid. To create a model of ischemic brain injury, nylon monofilament occlusion of the common carotid artery (CCAO) was used for 20 min. Chlorogenic acid (30 mg/kg) was given intraperitoneally (ip) 10 min before ischemia and 10 min before reperfusion. TUNEL staining of cerebral cortex neurons revealed an increase in the number of apoptotic neurons 24 h after reperfusion. At the molecular level, IR damage lowered bcl2 protein expression while simultaneously increasing bax levels and the bax/bcl2 ratio. Also, we observed higher miR-27a gene expression and higher TNF-α protein level as well as lower smurf1 protein expression after 24 h following CCAO. Treatment with chlorogenic acid significantly reduced the apoptotic damage and reversed molecular alterations in cerebral cortex neurons after IR. Our findings indicate that miR-27a/smurf1/TNF-α axis may play a regulatory function in cerebral cortex cell death, providing a new target for novel therapeutic approaches during transit ischemic stroke. It was also shown that chlorogenic acid could restore these molecular changes, demonstrating that it is an effective agent against cerebral cortex apoptotic damage after acute IR injury. [ABSTRACT FROM AUTHOR]

Objectives: There is an association between diabetes and liver disorders. Oxidative stress plays a crucial role in the pathology of hepatic abnormalities in diabetes. In this study, the effect of Tropisetron on the oxidative damage and histological alterations in the liver of type 1 diabetes mellitus (DM) were evaluated. Methods: Thiry-five male Wistar rats were randomly divided into five experimental groups (n = 7): control (C), tropisetron (T), diabetes (D), diabetes + tropisetron (D + T) and diabetes + glibenclamide (D + G). A single injection of streptozotocin (STZ, 50 mg/kg; i.p) was used to induce diabetes. Tropisetron (3 mg/kg; i.p), as a 5-HT3 receptor antagonist and glibenclamide (1 mg/kg; i.p), as a positive control were given once daily for 2 weeks. Finally, animals were euthanized and liver samples were obtained for histopathological examination and biochemical measurements including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx) levels. Results: There is a significant increase in MDA (p < 0.001) level and a significant decrease (p < 0.001) in SOD and GPx contents in diabetic animals. Tropisetron attenuated MDA levels (p < 0.001) and enhanced SOD (p < 0.05) and GPx (p < 0.01) activities accompanied by histopathological improvement in the diabetes liver. Similar results were achieved in the rats treated with the standard drug, namely: glibenclamide. Conclusions: Our findings indicate that tropisetron mitigates liver damage in the diabetes rats in part by attenuation of oxidative stress. [ABSTRACT FROM AUTHOR]

Objectives: Diabetes mellitus is one of the most common metabolic diseases. Tropisetron, as a 5‐HT3 receptor antagonist, has a considerable role in the inflammation and oxidative stress lowering. This study aimed to investigate the effect of this 5‐HT3 receptor antagonist on insulin secretion in male diabetic rats and the possible mechanisms. Methods: Animals were divided into five equal groups; the control, tropisetron, diabetes, tropisetron–diabetes and glibenclamide–diabetes (7 in each group). Tropisetron and glibenclamide were administrated for 2 weeks after inducing type 1 diabetes. Key findings: We demonstrated that insulin secretion improved robustly in diabetes–tropisetron compared with the diabetic group. Oxidative stress biomarkers were lower in a diabetes–tropisetron group than in diabetic rats. Simultaneously, tropisetron administration promoted the expression of ZnT8 and GLUT2 and also beta‐cell mass in pancreatic tissue, while the expression of uncoupling protein 2 (UCP2) was restrained. The histological evaluation confirmed our results. These effects were equipotent with glibenclamide, indicating that tropisetron can protect islets from the abnormal insulin secretion and morphological changes induced by type 1 diabetes. Conclusions: This effect might be partly related to the modulated UCP2/ZnT8 signal pathway and improved oxidative stress‐induced damage. [ABSTRACT FROM AUTHOR]

Background: Sirtuin1 is a regulator of oxidative stress involved in the management of diabetes complications. Due to the beneficial effects of swimming training in diabetes, this study aimed to investigate the effects of swimming training on pancreatic Sirtuin1, oxidative stress and metabolic parameters in type 2 diabetic male rats. Materials and methods: Twenty-eight male Wistar rats (200–250 g) were randomly divided into four groups: control, diabetic, swim trained and swim trained diabetic rats (n = 7). Diabetes was induced by a high-fat diet and streptozotocin injection [35/kg intraperitoneally]. After 72 hours, animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, animals in the exercise groups were subjected to swimming training (60 min/daily, 5 days/week) for 12 weeks. At the end of the intervention, the animals were anesthetized, and tissue/blood samples were prepared for measurements of metabolic parameters, albumin, the Sitruin1 gene and its protein expression levels, oxidative stress and histological study. Results: This study indicated that the diabetic rats had a significant decrease (p < 0.01, p < 0.05) in pancreatic Sitruin1 gene and its protein expression levels, antioxidant enzymes, serum albumin, and the quantitative insulin sensitivity check index, but a significant increase (p < 0.01) in malondialdehyde level. Swimming training resulted in a considerable improvement (p < 0.01, p < 0.05) in pancreatic Sitruin1 gene and its protein expression levels, antioxidant enzymes, serum levels of albumin and metabolic parameters. In addition, histological findings indicated the beta-cells conservation. Conclusions: This study suggested that pancreatic Sitruin1 may be a promising therapeutic target for diabetic complications. [ABSTRACT FROM AUTHOR]

Background and purpose: The present study investigated the role of the prostaglandin I2/peroxisome proliferator activator receptor (PGI2/PPAR) signaling pathway in cardiac cell proliferation, apoptosis, and systemic hemodynamic variables under cyclosporine A (CsA) exposure alone or combined with moderate exercises. Experimental approach: Twenty-four male Wistar rats were classified into three groups, namely, control, CsA, and CsA + exercise. Findings/Results: After 42 days of treatment, the findings showed a significant enhancement in the expression of the β-MHC gene, enhancement in protein expression of Bax and caspase-3, and a significant decline in the protein expression of Bcl-2 expression, as well as increased proliferation intensity in the heart tissue of the CsA group compared to the control group. Systolic pressure, pulse pressure, mean arterial pressure (MAP), QT and QRS duration, and T wave amplitude, as well as QTc amount in the CsA group, showed a significant increase compared to the control group. PPAR-γ and PGI2 showed no significant changes compared to the control group. Moderate exercise along with CsA significantly enhanced the protein expression of PPAR-γ and PGI2 and declined protein expression of Bax, and caspase-3 compared to those in the CsA group. In the CsA + exercise group, systolic pressure, MAP, and Twave showed a significant decrease compared to the CsA group. Moderate exercises along CsA improved heart cell proliferation intensity and significantly reduced β- MHC gene expression compared to the CsA group. Conclusions and implications: The results showed moderate exercise alleviated CsA-induced heart tissue apoptosis and proliferation with the corresponding activation of the PGI2/PPAR-γ pathway. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a debilitating condition that results in impaired sensory and motor function due to the limited self-regenerative ability of the spinal cord. To address this issue, combination therapy has been proposed as an effective treatment strategy for SCI regeneration. In this study, Platelet-Rich Plasma (PRP)-derived exosomes loaded with dexamethasone were utilized in a mouse model of SCI compression. PRP-derived exosomes loaded with dexamethasone (Dex) were prepared using ultracentrifugation and sonication methods and were administered to the mice via intravenous injection. Following a four-week duration, behavioral assessments were administered to assess functional recuperation, and diverse metrics encompassing the expression of genes associated with apoptosis and antiapoptosis, serum cytokine concentrations and tissue sampling were subjected to thorough examination. The results of this study demonstrated that mice treated with PRP-derived exosomes loaded with Dex (ExoDex) exhibited altered levels of TNF-a and IL-10, along with decreased Bax and increased Bcl2 expression in comparison to the model group. Furthermore, intravenously injected ExoDex reduced the size of the lesion site, lymphocyte infiltration, vacuolation, cavity size and tissue disorganization while also improving locomotor recovery. We propose that the utilization of exosome-loaded Dex therapy holds potential as a promising and clinically relevant approach for injured spinal cord repair. However, further extensive research is warranted in this domain to validate and substantiate the outcomes presented in this study. [ABSTRACT FROM AUTHOR]

A simple dry physical grinding and solvent mixing approach was used to prepare tin selenide – multiwalled carbon nanotube (MWCNT) hybrid as an anode material for high performance lithium ion batteries (LIBs). The pure tin selenide and their composites with carbon black or graphene oxides were previously reported, however no other groups have reported tin selenide/MWCNT composite as anode materials for LIBs. The new hybrid had superior electrochemical cycling performance with higher reversible (lithiation) capacity of 882 to 651 mA hg −1 over 50 cycles compared to pure tin selenide (602 to 58 mAhg −1 ) or pure MWCNT (339 to 171 mAhg −1 ) electrodes. The enhanced performance of the tin selenide/MWCNT hybrid was attributed to various factors including alleviation of volume change of tin selenide during lithiation/delithiation by nanoscale network of MWCNT which helped to preserve the electrical connectivity between active particles, reversible decomposition of tin selenide, lithiation/delithiation of MWCNTs and conductive electronic transport pathways provided by MWCNTs. [ABSTRACT FROM AUTHOR]

Purpose: Oxidative stress plays a key role in the onset and development of diabetes complications. In this study, we evaluated whether voluntary exercise could alleviate oxidative stress in the heart and blood of streptozotocin - induced diabetic rats. Methods: 28 male Wistar rats were randomly divided into four groups (n=7): control, exercise, diabetes and exercise + diabetes. Diabetes was induced by injection of streptozotocin in male rats. Rats in the trained groups were subjected to voluntary running wheel exercise for 6 weeks. At the end of six weeks blood and heart tissue samples were collected and used for determination of antioxidant enzymes (including SOD, GPX and CAT activities) and MDA level. Results: Exercise significantly reduced MDA levels both in the heart tissue (p<0.01) and blood samples (p<0.05). In addition, exercise significantly increased SOD (p<0.05), GPX (p<0.001) and CAT (p<0.05) in the heart tissue. Voluntary exercise also significantly increased SOD (p<0.01), GPX (p<0.05) and CAT (p<0.001) in the blood. Conclusion: Voluntary exercise diminishes the MDA level in blood and heart tissue of diabetic rats. It also accentuates activities of SOD, GPX and CAT. Therefore, it may be considered a useful tool for the reduction of oxidative stress in diabetes. [ABSTRACT FROM AUTHOR]

One of the newest analytical methods to solve nonlinear equations is Variational Iteration Method-II which is an accurate and a rapid convergence method in finding the approximate solution for nonlinear equations. In these papers, VIM-II is implemented to solve the initial and boundary value problems of Bratu-type which are widely applicable in fuel ignition of the combustion theory and heat transfer. Several examples are given to confirm the efficiency and the accuracy of the proposed algorithm. [ABSTRACT FROM AUTHOR]

In this study, accurate analytical solution for KDV Equation is derived. This solution is called Reconstruction Variational Iteration Method (RVIM). Numerical results show the efficiency of the proposed algorithm. By using RVIM, only a few iterations lead us to high accuracy of the solutions and it is valid for whole solution domain. [ABSTRACT FROM AUTHOR]

Abstract: We assume that phenylephrine produces late pharmacological preconditioning through the opening of the mitochondrial KATP channels. To test this hypothesis, rat hearts were isolated and perfused with Krebs buffer solution by Langendorff method and subjected to 30min regional ischemia followed by 60min of reperfusion. In this study, phenylephrine as a selective α1-adrenoceptor agonist and 5HD (5-hydroxydecanoate) as a putatively specific blocker of the mitochondrial KATP channels were used. Rats were randomly divided into six groups (n =6): (I) Control: surgical procedure was performed with no ischemia/reperfusion, (II) ischemia/reperfusion: hearts underwent regional ischemia/reperfusion, (III) phenylephrine-early preconditioning: phenylephrine (50µM) was perfused for 5min prior to ischemia/reperfusion, (IV) phenylephrine-late preconditioning: rats were treated with phenylephrine (10mg/kg, i.p) 24h prior to ischemia/reperfusion, (V) 5HD-phenylephrine early preconditioning-: 5HD (100µM) was perfused for 5min prior to phenylephrine as seen in group III, (VI) Phenylephrine late preconditioning-5HD: 5HD (100µM) was perfused for 5min prior to ischemia/reperfusion as seen in group IV and (VII) 5HD- ischemia/reperfusion: 5HD (100µM) was perfused for 5min prior to ischemia/reperfusion. Compared to ischemia/reperfusion group, phenylephrine in early and late phases decreased myocardial infarct size (% of ischemia zone), reduced CK-MB (Creatine Kinase-MB) release in the coronary effluent and improved cardiac function. Pretreatment with 5HD abolished phenylephrine-induced cardioprotection in early and late phases. It is concluded that phenylephrine-induced late cardioprotection was abolished by administration of 5HD in the isolated rat hearts. [Copyright &y& Elsevier]

High-fat diet (HFD) increases the risk of non-communicable inflammatory diseases including pulmonary disorders. Trans-chalcone is a chalcone with antioxidant and anti-inflammatory effects. This study aimed to explore the effect of this natural compound and molecular mechanism of its effect on HFD-induced pulmonary inflammation. Twenty-eight male Wistar rats were randomly divided into four main groups (n = 7 per each group): control, receiving 10% tween 80; Chal, receiving trans-chalcone, HFD, receiving a high-fat emulsion and 10% tween 80; HFD + Chal, receiving a high-fat emulsion and trans-chalcone. After 6 weeks, the lungs were dissected, and the expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and miR-146a were determined using real-time PCR. Moreover, histological analysis was done by hematoxylin and eosin staining. Significant elevations in TNF-α, IL-1β, IL-6, and miR-146a expression levels (P < 0.001) were observed within the lungs of HFD-fed rats compared with the control. However, oral administration of trans-chalcone reduced TNF-α, IL-1β, IL-6 (P < 0.001), and miR-146a (P < 0.05) expression levels and also improved HFD-induced histological abnormalities. These findings indicate that trans-chalcone ameliorates lung inflammatory response and structural alterations. It seems that this beneficial effect is associated with the down-regulation of pro-inflammatory cytokines and miR-146a. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to investigate the role of mitochondrial permeability transition pore (mPTP) in cardioprotection afforded by phenylephrine pretreatment in early and late phases. Methods: Rat hearts were isolated and perfused with Krebs buffer in Langendorff preparation and subjected to 30 min regional ischemia followed by 60 min of reperfusion. Phenylephrine as a selective α1-adrenoceptor agonist and atractyloside as a specific opener of the mPTP were used. Seven groups (n = 6) of rats were randomly studied: (I) control: surgical procedure was performed with no ischemia/reperfusion, (II) ischemia/reperfusion: hearts underwent regional ischemia/reperfusion, (III) early phenylephrine: phenylephrine (50 μM) was perfused for 5 min prior to ischemia/reperfusion, (IV) late phenylephrine: rats were treated with phenylephrine (10 mg/kg, i.p) 24 h prior to ischemia/reperfusion, (V) early phenylephrine+atractyloside: hearts were perfused with phenylephrine as in group III and then atractyloside (20 mM) 5 min before reperfusion for 20 min, (VI) late phenylephrine+atractyloside: hearts were treated with phenylephrine as in group IV and then received atractyloside (20 mM), 5 min before reperfusion for 20 min, (VII) atractyloside-IR group: hearts were perfused with atractyloside (20 mM) 5 min before reperfusion for 20 min. Results: Compared with ischemia/reperfusion group, perfusion of phenylephrine in early and late phases decreased myocardial infarct size (% of ischemia zone), reduced creatine kinase-MB (CK-MB) in the coronary effluent, and improved cardiac function. Administration of atractyloside abolished cardioprotective effects of phenylephrine in both early and late phases and returned infarct size, CK-MB and cardiac function to levels as seen in ischemia/reperfusion group. Conclusion: These results suggest that administration of atractyloside as a specific opener of the mPTP abolishes phenylephrine-induced early and late cardioprotection in the isolated rat hearts. [Copyright &y& Elsevier]

Background: Alcohol consumption in pregnancy is associated with an increased risk of cardiovascular abnormalities, but the mechanisms are unknown. This study evaluated the impact of ethanol exposure on the offspring's aorta structural, functional, and molecular alterations on postnatal (PN) both on days 21 and 90. Methods: This experimental study was conducted at Urmia University of Medical Sciences (Urmia, Iran) in 2019. Twenty Pregnant Wistar rats on the seventh day of Gestation Day (GD) were randomly divided into two groups: control and ethanoltreated groups (n=10 per group). From the seventh day of GD throughout lactation, rats in the ethanol group were fed binge alcohol (4.5 g/Kg body weight) once daily. Systemic hemodynamic variables in the offspring were analyzed using waveform contour analysis 90 days after birth. On postnatal days (PN) 21 and 90, aorta wall histological alterations and the level of inflammatory factors were assessed in the aorta of male offspring. The statistical differences were examined via an independent samples t test. P<0.05 was considered to be statistically significant. Results: The results revealed that offspring in the ethanol group had higher systolic, diastolic, mean arterial pressure, and dicrotic pressure than the control group (P<0.001). The level of aorta tissue tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, nuclear factor (NF)-κ, and endothelin-1 were significantly higher in the ethanol offspring group than in the control group (P<0.001). Histopathological changes such as total aorta thickness, tunica media, tunica adventitia, elastin fiber thickness, fiber interval, and elastin/media ratio significantly increased in the aorta of the offspring of the ethanol group compared to the control group 21 and 90 days after birth. Conclusion: Our findings suggest that prenatal and early postnatal ethanol exposure-induced cardiovascular abnormalities are, in part, due to predisposing the aorta to atherosclerosis, which was mediated through the aorta wall remodeling and inflammation process. [ABSTRACT FROM AUTHOR]

Cytokine storms and extra-activated cytokine signaling pathways can lead to severe tissue damage and patient death. Activation of inflammatory signaling pathways during Cytokine storms are an important factor in the development of acute respiratory syndrome (SARS-CoV-2), which is the major health problem today, causing systemic and local inflammation. Cytokine storms attract many inflammatory cells that attack the lungs and other organs and cause tissue damage. Angiotensin-converting enzyme 2 (ACE2) are expressed in a different type of tissues. inhibition of ACE2 activity impairs renin-angiotensin (RAS) function, which is related to the severity of symptoms and mortality rate in COVID-19 patients. Different signaling cascades are activated, affecting various organs during SARS-CoV-2 infection. Nowadays, there is no specific treatment for COVID-19, but scientists have recognized and proposed several treatment alternatives, including applying cytokine inhibitors, immunomodulators, and plasma therapy. Herein, we have provided the detailed mechanism of SARS-CoV-2 induced cytokine signaling and its connection with pathophysiological features in different organs. Possible treatment options to cope with the severe clinical manifestations of COVID-19 are also discussed. • Potential molecular pathways activated by SARS-CoV-2 in different organs were investigated. • Clinical features and pathophysiological effect of SARS-CoV-2 infection in different organs were indicated. • cytokine-based therapeutic targets during SARS-CoV2 infection were identified. [ABSTRACT FROM AUTHOR]

Apoptosis is the main pathological aspect of neuronal injury after cerebral ischemia–reperfusion (I/R) injury. However the detailed molecular mediators are still under debate. The aim of this study is to explore the effect of cerebral I/R on miR‐23a/TGF‐β‐activated kinase 1 binding protein 3 (TAB3)/nuclear factor kappa B (NF‐κB)/p53 axis in rat hippocampus alone and in combination with chlorogenic acid (CGA). Common carotid artery occlusion (CCAO) was performed by nylon monofilament for 20 min to establish a model of ischemic brain injury. CGA (30 mg/kg) was administered intraperitoneally (ip), 10 min prior to ischemia and 10 min before reperfusion. Examination of hippocampus neurons by terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling staining showed that the number of apoptotic neurons was elevated at 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of p53 with a concomitant upregulation of cleaved‐caspase3/phosphorelated‐caspase3 ratio and cytochrome c level. Further miR‐23b gene expression was significantly downregulated after 24 h of reperfusion. Also, we observed increased TAB3 and NF‐κB protein expressions after 24 h following CCAO. Treatment with CGA significantly reduced the apoptotic damage and also reversed miR‐23b gene expression, TAB3 and NF‐κB protein expressions in hippocampus neurons in I/R rats. In conclusion our data suggest that miR‐23b/TAB3/NF‐κB/p53 axis could play a regulatory role in hippocampus cell death, which provide a new target for novel therapeutic interventions during transit ischemic stroke. It also demonstrated that CGA could reverse these molecular alterations indicating an effective component against hippocampus apoptotic insult following acute I/R injury. [ABSTRACT FROM AUTHOR]

[Display omitted] • COVID-19, a viral immune disease, is defined by a cytokine storm. • COVID-19 is also a diagnostic consideration in patients with various complications. • Interferon-gamma, a cytokine, and Neopterin, produced by macrophages, have an active role in predicting the severity of the disease for COVID-19, as well as being used in the prognosis and diagnosis of various patients. Coronavirus Disease 2019 [COVID-19], caused by severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2], has rapidly evolved into a global health emergency. Neopterin [NPT], produced by macrophages when stimulated with interferon [IFN-]gamma, is an essential cytokine in the antiviral immune response. NPT has been used as a marker for the early assessment of disease severity in different diseases. The leading cause of NPT production is the pro-inflammatory cytokine IFN-. Macrophage activation has also been revealed to be linked with disease severity in SARS-CoV-2 patients. We demonstrate the importance of NPT in the pathogenesis of SARS-CoV-2 and suggest that targeting NPT in SARS-CoV-2 infection may be critical in the early prediction of disease progression and provision of timely management of infected individuals. [ABSTRACT FROM AUTHOR]

Introduction: Consumption of ecstasy (3,4-methylenedioxymethamphetamine, MDMA), a derivative of amphetamine, can results in various undesirable side effects including hematological and serological parameters. This study is intended to examine the effects of curcumin along with MDMA in the early and late phase of consumption on hematological parameters and serum immunoglobins (IgM, IgG and IgA) levels. Methods: We used 56 male rats that are divided into 7 groups: group1 (control), group2 (MDMA+vehicle1), group3 (curcumin), group4 (MDMA+early curcumin), group5 (MDMA+vehicle2), group6 (MDMA+late curcumin) and group7 (MDMA+early&late curcumin). The groups were received MDMA (20mg/kg) orally and curcumin (20μM/kg) intra-peritoneally for 2 and 4 weeks (n=8). After 24h of final dose, rats were anesthetized and blood samples were collected and used for determination of hematological parameters and IgM, IgG and IgA levels using a Coulter Automated Cell Counter and ELISA kit. Results: Our data indicated that either MDMA alone or in combination with curcumin in both early and late phases decreased lymphocytes, platelet, total leukocyte count and RBC, MCHC, RDW, immunoglobin levels, as well as hemoglobin content in comparison with the control group. In contrast, the amount of neutrophils, eosinophils, monocytes, mean cell volume and HCT increased. Furthermore, we observed blood parasites of red blood cells in the MDMA groups with curcumin. Conclusion: In conclusion, MDMA alone and in combination of curcumin altered the hematological parameters. Furthermore, their combination therapy induces toxic effects on hematological parameters and serum immunoglobin levels. This is a serious consequence for recreational drug users. [ABSTRACT FROM AUTHOR]

The association between chronic alcohol consumption and the development of alcpholic liver disease is a very well known phenomenon, but the precise underlying molecular mediators involved in ethanol-induced liver disease remain elusive. This study aimed to characterize the lipid metabolism alterations and the molecular mediators which are related to lipid metabolism in liver under the heavy ethanol exposure alone or combined with ginger extract. Twenty-four male wistar rats were assigned into three groups, namely control, ethanol, and ginger extract treated ethanol (GETE) groups. Six weeks after the treatment, the ethanol group showed a significant increase in fatty acid translocase (FAT)/CD36, protein tyrosine phosphatase 1B (PTP1B) and decrease hepatocyte nuclear factor 4 Alpha (HNF4A) genes expressions compared to the control group. The ethanol administration also significantly increased plasma LDL, cholesterol, triglyceride, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) compared to the control group. Moreover, compared to the control group, the ethanol group showed liver histhological changes, such as fibrosis, focal microvesicular steatosis, some apoptotic hepatocytes, spotty necrosis, portal lymphocytic inflammation, mallory-denk bodies, giant mitochondria, piecemeal necrosis. Consumption of ginger extract along with ethanol, partially ameliorated gene expression alteration and histological changes, improved undesirable lipid profile and liver enzymes changes compare to those in the ethanol group. These findings indicate that ethanol-induced liver abnormalities may in part be associated with lipid homeostasis changes mediated by overexpression of FAT/CD36, PTP1B and downexpressionof HNF4A genes. It also show that these effects can be reduced by using ginger extract as an antioxidant and anti-inflammatory agent. [ABSTRACT FROM AUTHOR]

Background: The interaction of ethanol consumption and sexual behavior has been evaluated over the past three decades; however, some studies have assessed how ethanol consumption affects the general behavioral aspects of the copulatory cycle patterns in male rats. The aim of this study was to investigate the effect of chronic ethanol consumption on adult male Wistar rats' sexual motivation and behavior alteration in precopulatory, copulatory, and executive phases of the copulatory cycle. Methods: Male Wistar rats were randomly allocated to two groups (control and ethanol treated groups). After 42 days of treatment, male rats were given access to adult female rats for 2 hours and their sexual behavior were recorded in a fully dark room using an infrared camera. Findings: Chronic ethanol consumption caused a significant increase in anogenital sniffing and mounting, intermission, and ejaculation latencies periods, as well as a significant decrease in the sexual activity index (SAI) and copulatory efficiency (CE) compared to the control group. Conclusion: It is suggested that chronic ethanol consumption suppresses sexual behavior and reduces male rats' tendency toward sexual interaction with female rats as manifested by the enhanced latency periods in the copulatory phases and reduced SAI of ethanol treated animals. [ABSTRACT FROM AUTHOR]

Solar cells become a viable energy source to charge lithium ion batteries. Here a simple and efficient photocharging design approach is demonstrated, where a promising low cost single junction solar cell such as perovskite solar cell or dye sensitized solar cell efficiently charges a Li4Ti5O12-LiCoO2 Li-ion cell using a DC-DC voltage boost converter. The converter boosts the low input voltage of a single junction solar cell to charge a lithium ion cell and offers advantages including maximum power point tracking of solar photovoltaics and overvoltage protection for the lithium ion cell. This is the first demonstration of this technology. This approach leads to the highest reported overall efficiency of 9.36% and average storage efficiency of 77.2% at 0.5 C discharge for a perovskite solar cell-converter charging. The high efficiency for the perovskite solar cell-converter charging is attributed to maximum power harvesting along with high power conversion efficiency of the perovskite solar cell and low potential polarization between the charge and discharge voltage plateaus for the Li4Ti5O12-LiCoO2 Li-ion cell. [ABSTRACT FROM AUTHOR]

Purpose: Insulin resistance plays a key role in the onset and development of type 2 diabetes mellitus (T2DM) and its complications. In this study, we evaluated the effect of swim training on insulin resistance in diabetic rats. Methods: Forty male Wistar rats were randomly divided into four groups (n=10): sedentary control (Con), sedentary diabetic (Dia), swim trained control (Exe) and swim trained diabetic (Dia+Exe) rats. Diabetes was induced by high fat diet (HFD) and a low dose of streptozotocin (35 mg/kg, i.p). In trained groups, one week after the induction of diabetes, animals were subjected to swimming (60 min/5 days a week) for 10 weeks. At the end of training, fasting blood sugar (FBS), oral glucose tolerance test (OGTT), fasting/basal insulin, glycosylated hemoglobin (HbA1c) levels, insulin resistance index, homeostasis model assessment method (HOMA-IR), triglycerides (TG,) total cholesterol (TCh), and high density lipoprotein (HDL) levels in blood were measured. Results: Swimming significantly improved OGTT (P<0.01) and HOMA-IR (P<0.01). Swim training also significantly decreased FBS (p<0.01), fasting/basal insulin (P<0.01), HbA1C (p<0.01), TG (P<0.05), and TCh (P<0.05) levels. It also significantly increased HDL (p<0.05) level. Conclusion: Our findings indicate that swim training improved glycemic control and insulin sensitivity in type 2 diabetes caused by high fat diet in male rats. [ABSTRACT FROM AUTHOR]

Renal fibrosis is a major cause of renal failure in diabetic nephropathy. Tropisetron is an antagonist of the 5HT3 receptor that exhibits anti-fibrosis effects. The present research aimed to investigate the protected role of tropisetron against renal fibrosis of diabetic nephropathy and its molecular mechanisms. For this purpose, male Wistar rats were allocated into 5 groups of control, tropisetron, diabetes, tropisetron + diabetes, and glibenclamide + diabetes (n = 7). After induction of type 1 diabetes with a single injection of STZ, tropisetron (3 mg/kg) and glibenclamide (1 mg/kg) were given to the rats daily by intraperitoneal injection for 2 weeks. The obtained data revealed that the treatment of diabetic rats with tropisetron led to a significant decrease in the elevated blood glucose, serum cystatin c, and urinary total protein (UTP) level, indicating the improvement of the impaired kidney function. Moreover, the results of Massonʼs trichrome staining showed that fibrosis attenuated in the kidney of diabetic rats after tropisetron treatment. RT-PCR and Western blotting revealed that TGF-β1, the apoptotic mediator, and p53 were considerably declined in the kidney of diabetic rats in response to tropisetron treatment. Meanwhile, the expressions of matrix metalloproteinase-9 (MMP-9) and matrix metalloproteinase-2 (MMP-2) were increased. These notable effects were equipotent with glibenclamide, as a standard drug, suggesting that tropisetron can alleviate renal fibrosis in diabetic nephropathy. Our data indicate that tropisetron could improve kidney function and attenuate renal fibrosis through regulation of TGF-β1, p53, and expression of extracellular matrix metalloproteinases. • Tropisetron alleviated renal fibrosis in diabetic nephropathy. • Tropisetron modulated MMP-9, MMP-2, TGF-β1 gene expressions in diabetic nephropathy. • Tropisetron modulated p53 protein expression in diabetic nephropathy. • Tropisetron modulated serum cyctatin c and UTP level indicating the improvement of the impaired kidney function in diabetes. • The same results were obtained in the glibenclamide treated group. [ABSTRACT FROM AUTHOR]

Testicular damage contributes to cyclosporine A (CsA) induced male infertility. However, the exact underlying molecular mediators involved in CsA-induced testis disorder remains unclear. The present study aimed to characterize the role of mir-34a/sirt-1 in CsA induced testicular injury alone or in combination with curcumin. A total of twenty-eight male Wistar rats were subdivided into four groups: control (Con), sham, cyclosporine A (CsA), cyclosporineA + curcumin (CsA + cur). The animals received cyclosporine A (30 mg/kg) and curcumin (40 mg/kg) for 28 days by oral gavage. At the end of the experiment, CsA administration significantly resulted in a decrease in testis weight and testis coefficient. The molecular analysis demonstrated that CsA exposure increased 8-OHdg and Nox4 protein contents in the testis tissue. TUNEL staining indicated that CsA caused the number of apoptotic cells to increase in the testes of male rats. In addition, exposure to CsA resulted in an increased expression of Bax, and a decreased expresion in that of Bcl-2, with a concomitant up-regulation of the Bax/Bcl-2, c-Caspase-3/p-Caspase-3 ratio and cytochrome c level. Meanwhile, exposure to CsA increased the expression of mir-34a and decreased sirt-1 protein level in the testis tissue samples compared to the control group. Taken together, our findings suggested that CsA can cause damage to testicular germ cells via oxidative stress and mitochondrial apoptotic pathway, and probably mir-34a/sirt-1 play a crucial role in this process. It also demonstrates that these negative effects of CsA can be reduced by using curcumin as an antioxidant and anti-inflammatory agent. Image 1 • Cyclosporine A increased oxidative stress manifestations in testis of rats. • Cyclosporine A increased apoptotic cells by mitochondrial apoptotic pathway in testis of rats. • Cyclosporine A increased the expression of mir-34a and decreased sirt-1 (sirtuin-1) protein level in the testis tissue. • Curcumin alleviated genes and protein expression alterations in testis of rats. [ABSTRACT FROM AUTHOR]

• Diabetes decreased CB1 receptor at both transcriptional and protein levels in the liver of rats. • Diabetes increased FAAH enzyme at both transcriptional and protein levels in the liver of rats. • Tropisetron reversed DM-induced changes of TNF-α, apoptosis, CB1 receptor and FAAH enzyme in rat liver. • Glibenclamide reversed DM-induced changes of TNF-α, IL-6, apoptosis, CB1 receptor and FAAH enzyme in rat liver. Confident relationships between diabetes and liver damage have previously been established. This study was designed to evaluate hepatic inflammation, apoptosis, and endocannabinoid system alterations in diabetes with or without tropisetron treatment. Rats were assigned to five equal groups: control, tropisetron, diabetes, tropisetron+diabetes, and glibenclamide+diabetes (n = 7 in each group). Rats were treated with tropisetron (3 mg/kg) and glibenclamide (1 mg/kg) as a positive control for two weeks after type 1 diabetes induction. Inflammatory cytokines tumor necrosis factor-alpha and interleukin 6 (TNF-α and IL-6) levels, apoptotic cells, and fatty acid amide hydrolase (FAAH) enzyme, at both transcriptional and protein levels increased, while the gene expression of cannabinoid receptor 1 (CB1) and its protein level decreased in the diabetic liver compared to the control. Treatment with tropisetron reversed TNF-α, apoptotic index, and endocannabinoid system components. These effects were equipotent with glibenclamide, indicating that tropisetron can protect liver tissue against diabetic disturbances. These findings strongly support the idea that diabetes-induced liver abnormality is mediated by inflammatory reactions, apoptosis, and endocannabinoid system, and that these effects can be alleviated by using tropisetron as an antioxidant and anti-inflammatory agent. [ABSTRACT FROM AUTHOR]