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BackgroundAn outbreak of COVID-19 in Iran has spread throughout the country. Identifying the epidemiological characteristics of this disease will help to make appropriate decisions and thus control the epidemic. The aim of this study was characterization of the epidemiological features of COVID-19 in Iran.MethodsIn this retrospective study, data related to the epidemiological characteristics of COVID-19 patients admitted to Baqiyatallah Hospital in Tehran, Iran, from 19 February 2020 to 15 April 2020 have been analyzed and reported. Patient characteristics including age, gender and underlying diseases were investigated. Data were collected through patient records. Sex ratio, Case Fatality Rate (CFR) and daily trend of cases were also determined. A multiple logistic regression analysis was also performed to assess affecting factors on mortality.ResultsFrom February 19, 2020 to April 15, 2020, 12870 patients referred to the hospital emergency department, of which 2968 were hospitalized with COVID-19 diagnosis. The majority of cases were in the age group of 50 to 60 years of old. The male-to-female ratio was 1.93:1. A total of 239 deaths occurred among all cases for an overall CFR of 1.85% based on the total number of patients (both outpatient and inpatient) and 8.06% among hospitalized patients. Out of all patients 10.89% had comorbidity. Diabetes, chronic respiratory diseases, hypertension, cardiovascular diseases, chronic Kidney diseases and cancer were the most common comorbidities with 3.81, 2.02 , 1.99 , 1.25, 0.60 and 0.57 %, respectively. Male gender (OR=1.45, 95% CI: 1.08-1.96), older age (OR=1.05, 95% CI: 1.04-1.06) and having underlying diseases (OR=1.53, 95% CI: 1.04-2.24) were significantly associated with mortality.ConclusionsThe results of this study showed that Male gender, older age and having comorbidities were significantly associated with the risk of death among COVID-19 patients. It is important to pay special attention to male elderly patients with underlying diseases.

Aim: Respiratory disease (RD) is one of the most common diseases characterized by lung dysfunction. Many diagnostic mechanisms have been used to identify the pathogenic agents of responsible for RD. Among these, proteomics emerges as a valuable diagnostic method for pinpointing the specific proteins involved in RD pathogenesis. Therefore, in this study, for the first time, we examined the protein markers involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), asthma, bronchiolitis obliterans (BO), and chemical warfare victims exposed to mustard gas, using the proteomics method as a systematic study. Materials and Methods: A systematic search was performed up to September 2023 on several databases, including PubMed, Scopus, ISI Web of Science, and Cochrane. In total, selected 4246 articles were for evaluation according to the criteria. Finally, 119 studies were selected for this systematic review. Results: A total of 13,806 proteins were identified, 6471 in COPD, 1603 in Asthma, 5638 in IPF, three in BO, and 91 in mustard gas exposed victims. Alterations in the expression of these proteins were observed in the respective diseases. After evaluation, the results showed that 31 proteins were found to be shared among all five diseases. Conclusion: Although these 31 proteins regulate different factors and molecular pathways in all five diseases, they ultimately lead to the regulation of inflammatory pathways. In other words, the expression of some proteins in COPD and mustard‐exposed patients increases inflammatory reactions, while in IPF, they cause lung fibrosis. Asthma, causes allergic reactions due to T‐cell differentiation toward Th2. [ABSTRACT FROM AUTHOR]

Background: Semen hyperviscosity is a threatening cause of abnormal spermatozoa and infertility in men. We aimed to evaluate oxidative stress, antioxidants depletion and sperm apoptosis as main reasons for poor quality of spermatozoa in men with hyperviscous semen. Materials and Methods: In this cross-sectional study, ejaculate specimens were collected from fertile (n=102) and infertile men with hyperviscous semen (n=123) and without semen hyperviscosity (n=143). Total antioxidant capacity (TAC), glutathione (GSH), malondialdehyde (MDA), protein carbonyl (PC), 8-hydroxydeoxyguanosine (8-OHdG), and were measured in semen samples to estimate oxidative stress status. Gene expression pattern of BAX, CASPASE-9, CASPASE-3, and BCL2 was assessed to estimate sperm apoptosis. Results: The average of sperm count, normal morphology, normal motility, and sperm vitality in men with hyperviscous semen was significantly lower than infertile subjects without hyperviscous semen (P<0.01). Men with hyperviscous semen exhibited higher levels of PC (8.34 ± 1.03 nmol/mg vs. 6.01 ± 0.93 nmol/mg, P=0.008), MDA (1.14 ± 0.27 nmol/ ml vs. 0.89 ± 0.22 nmol/ml, P=0.031), 8-OHdG (259.71 ± 24.59 ng/ml vs. 197.13 ± 18.47 ng/ml, P=0.009), but lower TAC contents (1250.44 ± 66.23 μM/L vs. 1784.31 ± 89.87 μM/L, P=0.018) and GSH (3.82 ± 1.05 μM vs. 5.89 ± 0.87 μM, P=0.021) than men with non-viscous semen. The expression of BAX, CASPASE-3 and CASPASE-9 genes in men with hyperviscous semen was significantly increased by 1.39-fold (P=0.041), 1.47-fold (P=0.046), 1.29-fold (P=0.048), respectively, as compared with the infertile subjects without hyperviscous semen. However, BCL2 expression in infertile men without hyperviscous semen was higher compared to those with hyperviscous semen (1.36-fold, P=0.044). Conclusion: Hyperviscous semen is markedly associated with depletion of seminal plasma antioxidants, sperm membrane lipid peroxidation, DNA and protein oxidation, and sperm apoptosis. Antioxidant therapy might be considered as a valuable strategy to protect sperm cells against oxidative damage in cases with seminal fluid hyperviscosity. [ABSTRACT FROM AUTHOR]

Background: One of the recommended treatment methods for covid-19 is herbal treatments, which, if used, can be used as an effective preventive or supportive treatment in the treatment plan of patients with covid-19. PHR160 spray is a combination of cineole, menthol, Safran, safranal, and crocin each of these substances affects respiratory diseases alone. Aim: Investigating the effectiveness of PHR-160 spray, in the treatment of Covid-19. Methods: The present study is a multicenter, double-blind, randomized clinical trial study, which was conducted in 4 medical centers. The study population includes all hospitalized patients with covid-19 who met the study inclusion criteria. The data collection tool was a checklist including 1- demographic information, 2- vital signs, symptoms, CT scan changes, and drug side effects (neural, cardiac, and respiratory) at the beginning of admission and from the first to the 10th day. Result: There was no significant difference between the intervention and control groups in the study of demographic variables, vital signs, symptoms, CT scan changes, and drug side effects before using PHR-160 spray (P>0.05). Also, after using PHR-160 spray for ten days, there was no significant difference in the admission to the intensive care unit, and patient mortality in the two groups (P>0.05) Conclusion: Based on the results, PHR-160 spray has no beneficial effects in controlling the symptoms of patients with covid-19 and cannot play an effective role in improving the patient's condition and reducing the complications caused by the disease. [ABSTRACT FROM AUTHOR]

Introduction:Among various proposed pathologic mechanisms during the coronavirus disease 2019 (COVID-19) pandemic, overproduction of autoantibodies is not widely studied. Antiphospholipid antibodies (aPLs) are target proteins that have affinity toward charged phospholipids. APLs are thought to have pro-thrombotic potentials that increase during thromboembolism. The present systematic review and meta-analysis aimed to evaluate the relationship between serum aPLs level and COVID-19 mortality, severity, and thrombotic events. Methods: This systematic review and meta-analysis was conducted on all open access published articles in Medline, Scopus and Google Scholar. Studies evaluating individuals over the age of 18 years who were diagnosed with COVID-19 and had positive aPLs; and provided data on mortality or thrombotic events were included. Results: Of the initially identified 512 articles, 22 studies (overall 1462 patients) were finally included in the analysis. The prevalence of positive aPLs was 48.1%. Among the 372 patients with positive aPLs, 156 patients (41.9%) had severe COVID-19 that indicated a significant relationship between COVID-19 severity and aPLs positivity (p<0.05). The prevalence of thrombotic events in aPLs positive patients was 26.3% that indicated a significant relationship between aPLs positivity and the development of thrombotic events (p=0.03). APLs positivity was related to anytime mortality in COVID-19 patients (p=0.01). Conclusion: The present review demonstrated that aPLs are linked to COVID-19 severity and thrombotic events but not short-term mortality. Further studies with longer follow up periods are warranted. [ABSTRACT FROM AUTHOR]

Human papillomavirus (HPV) is a causative agent of cervical cancer among women worldwide. Serological and molecular tests are commonly used to detect and identify HPV, but all the detection methods for HPV have some limitations. Nowadays, considerable advancements in nanosensors have enabled monitoring of hybridization procedures dynamically for HPV detection. Biosensors, as effective, quick, economical, and highly sensitive tools, can be used in the diagnosis of HPV as an alternative technique instead of other detection methods. Biosensor detection methods of HPV in use from 2000 to 2021 were investigated using several databases such as Google Scholar, Scopus, PubMed, and the Scientific Information Database. Furthermore, a manual search of the references of the retrieved articles was performed. On analyzing the most recently developed biosensors for HPV identification, we observed that three biosensor systems, electrochemical, optical, and piezoelectric systems, are the main transducers used in the development of HPV biosensors. The aim of this review is to examine recent research on biosensors for the detection of HPV and perform a comparison with other diagnostic methods. Considering the importance of rapid HPV detection in the control of infection and development of public health measures, improvement of biosensors as an economical and quick method can be very useful in the diagnosis of HPV. [ABSTRACT FROM AUTHOR]

Recent studies have indicated that epigenetic alterations are critical for normal function and development of spermatozoa during the fertilization process. This review will focus on the latest advances in epigenome profiling of the chromatin modifications during sperm development, as well as the potential roles of epigenetic mechanisms in the context of male infertility. In this review, all data were collected from published studies that considered the effect of epigenetic abnormalities on human spermatogenesis, sperm parameters quality, fertilization process, embryo development and live births. The database PubMed was searched for all experimental and clinical studies using the Keywords "epigenetic modifications", "male infertility", "spermatogenesis", "embryo development" and "reproductive function". Post-translational modifications of histone, DNA methylations and chromatin remodeling are among the most common forms of epigenetic modifications that regulate all stages of spermatogenesis and fertilization process. Incorrect epigenetic modifications of certain genes involved in the spermatogenesis and sperm maturation may be a main reason of male reproductive disorder and infertility. Most importantly, abnormal patterns of epigenetic modifications or transgenerational phenotypes and miRNAs expression may be transmitted from one generation to the next through assisted reproductive techniques (ART) and cause an increased risk of birth defects, infertility and congenital anomalies in children. Epigenetic modifications must be considered as a one of the main factors of unexplained male infertility etiology. Due to high risk of transmitting incorrect primary imprints to offspring, there is a need for more research into epigenetic alterations in couples who benefit of ART support. [ABSTRACT FROM AUTHOR]

Cornea injury of sulfur mustard (SM) is considered as the most devastating injuries to the eye. This study aimed to evaluate the single and combined effects of N-acetyl cysteine (NAC) and doxycycline on the inflammatory pathway and cornea neovascularization (CNV) in the rat model of SM-injured cornea. The right cornea of male Sprague–Dawley rats was subjected to 2-chloroethyl-ethyl sulfide (CEES). Rats were topically treated with a single and combined of 0.5% NAC and 12.5 μg/ml doxycycline and examined at 3rd, 15th, and 21st days. The activity of three antioxidant enzymes was analyzed in the cornea of different groups. Real-time PCR was performed to measure gene expression of inflammatory factors (tnf-α, rel-a & cxcl-1) and angiogenesis factors (vegf-a, mmp2,9) in the cornea lysates. The histological and opacity assessments were also carried out. The activity of antioxidant enzymes significantly declined 3 days after the CEES damage. NAC eye drop recovered the enzyme activity on the 21st day of treatment (p-value <.05). The expression of tnf-α and rel-a genes significantly increased after CEES cornea exposure, while NAC declined their expression on the 7th and 21st days. The CNV score and angiogenesis factor expression were decreased in the long term by single and combined treatments (p-value <.05), but the infiltration of inflammatory cells was not completely amended. NAC and doxycycline eye drop could improve the CNV complication. Also, NAC was an effective treatment against the inflammatory pathway involved in CEES-injured cornea. [ABSTRACT FROM AUTHOR]

Sulfur Mustard (SM) induces cell injury via exerting oxidative stress, protease-anti protease imbalance, and inflammation. Inflammasome as one part of innate immunity has a critical role in the recognition of cell injuries and the initiation of the inflammation process by releasing IL-1β. Hence, the present study investigated the effects of the sub-lethal doses of 2-chloroethyl ethyl sulfide (CEES) as SM analog on the gene expression level of inflammasome-related genes as well as the potential protective effects of curcumin on this process. The effects of sub-lethal doses (500, 1000, and 2500 mM) of CEES on pulmonary epithelial cell line (A549) were determined at various time points (12, 24, and 48 h). Following the treatment of cells with CEES, the kinetic alterations of the expression levels of nuclear factor kappa-light-chainenhancer of activated B cells (NF-ĸB1), NLR family pyrin domain containing 1 (NLRP1), Caspase-1 (Casp1), and Interleukin-1β (IL-1β) genes were analyzed; using real-time PCR. In addition, the concurrent protective effects of different doses of curcumin (20, 40, 80, and 160 mM) on modulating the effects of CEES were studied. Although it was found that the lowest sub-lethal dose of CEES (500 mM) was able to upregulate the inflammasome-related genes, the maximum alterations occurred 48 h after the treatment with the higher sub-lethal dose (2500 mM) of CEES. The maximum alteration occurred in Casp1 (38 fold), IL-1β (19 fold), and NLRP1 (~4 fold) genes (p<0.0001). However, the NF-ĸB gene expression level did not alter following CEES exposure. Even though low doses of curcumin (20, 40, and 80 mM) were able to down-regulate the studied genes, it was found that the treatment of cells with 160 mM of curcumin for 48 h was able to normalize the expression level of all genes. The present study concludes that curcumin as an anti-inflammatory agent may have beneficial immunomodulatory effects following CEES exposure. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged as a health problem worldwide. It seems that COVID-19 is more lethal for Iranian veterans with a history of exposure to mustard gas. There are some similarities in the pathogenesis of SARS-CoV-2 and mustard gas in immune system disruption and pulmonary infection. SARS-CoV-2 and mustard gas inducing oxidative stress, immune system dysregulation, cytokine storm, and overexpression of angiotensin-converting enzyme II (ACE2) receptor in lungs that act as functional entry receptors for SARS-CoV-2. Moreover, Iranian survivors of mustard gas exposure are more susceptible and vulnerable to COVID-19. It is suggested that the principles of COVID-19 infection prevention and control be adhered to more stringently in Iranian survivors of mustard gas exposure than others who have not been exposed to mustard gas. Therefore, in this review, we discuss the different pathologic aspects of lung injury caused by mustard gas and also the relationship between this damage and the increased susceptibility of Iranian mustard gas exposed survivors to COVID-19. [ABSTRACT FROM AUTHOR]

Zinc (Zn) is necessary for the normal function of the male reproductive system and spermatozoa. Although influences of zinc deficiency on impaired spermatogenesis and male infertility have been widely considered, the molecular and cellular mechanisms of these abnormalities are not well understood. General abnormalities, including hypogonadism, Leydig cells damage, deficiency of sex hormone production and impaired spermatogenesis, as well as inflammation, antioxidant depletion, sperm death and male infertility can be observed during zinc deficiency. However, it is not obvious which pathways are relevant to the pathogenesis of zinc deficiency. Oxidative stress (OS) induced by reactive oxygen species is likely as the main mechanism of zinc deficiency which is associated with sperm DNA fragmentation, decrease in sperm membrane integrity, apoptosis, depletion of antioxidants, and consequently poor sperm quality and male infertility. Therefore, identification of these pathways will give valuable information regarding the mechanisms of zinc deficiency on the male reproductive system and the potential way for developing a better clinical approach. In this review, we aim to discuss the proposed cellular and molecular mechanisms of zinc deficiency on the male reproductive system, the importance of OS and mechanisms by which zinc deficiency induces OS and depletion of other antioxidants. [ABSTRACT FROM AUTHOR]

Dysregulation of matrix metalloproteinases (MMPs) is now considered as one of the main toxicity effects of sulfur mustard (SM). Numerous studies have found overexpression of MMPs, but the mechanism is unclear. Accumulation of leukocytes, downregulation of tissue inhibitors of metalloproteinases (TIMPs), increase of pro-inflammatory mediators, as well as massive production of reactive oxygen species (ROS) and oxidative stress (OS) are possible mechanisms by which SM induces MMPs expression long-years after exposure. We aim to discuss cellular and molecular mechanisms of SM toxicity, the importance of MMPs and mechanisms by which SM enhances expression of these proteases in SM-victims. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease is mainly specified by progressive and selective death of dopaminergic neurons. Crocus sativus L. (saffron) has been widely used to cure a diverse range of diseases in herbal medicine. Aim: The aim of the present study is to investigate the neuroprotective effects of saffron on arsenic-induced neurotoxicity, which was performed in human neuroblastoma SH-SY5Y cell line as an in vitro model of Parkinson's disease and to confirm whether the neuroprotective effects of saffron on Parkinson's disease are mainly due to their interactions with antioxidant systems. Moreover, as the antioxidant effect of N-acetylcysteine and its effectiveness as an antioxidant agent are proven, we compared saffron with NAC to control saffron extract. Materials and Methods: The induction of cell damage was done by arsenic and the survival of the cells was measured using the MTT assay. In addition, the assessment of the generation of intracellular reactive oxygen species (ROS) and mitochondrial membrane potential was done using fluorescence spectrophotometry method. Furthermore, immunoblotting analysis was performed to precisely determine the biomarkers level for apoptosis in the cells. Results: Our study indicated that arsenic had the ability to decrease cells survival rate, enhance the loss of mitochondrial membrane potential and increase the levels of intracellular ROS, c-Fos ratio and caspease-3. Pretreatment of cells with NAC (5 mM) and saffron aqueous extract (10mg/ml) significantly attenuated the mentioned effects in arsenic-treated cells. Conclusion: The outcome of the study has shown that the protective effects of NAC and saffron aqueous extract are produced by their antioxidant and antiapoptotic properties and their therapeutic potential is demonstrated in the treatment of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Sulfur mustard (SM) is a chemical compound that preferentially targets ocular, cutaneous and pulmonary tissues. Although pathologic effect of SM has been extensively considered, molecular and cellular mechanism of its toxicity, especially at the chronic phase of injury is not well-understood. Excessive production of reactive oxygen species (ROS) and oxidative stress (OS) appears to be involved in SM-induced injuries. SM may trigger several molecular and cellular pathways linked to OS and inflammation that can subsequently result in cell death and apoptosis. At the acute phase of injury, SM can enhance ROS production and OS by reducing the activity of antioxidants, depletion of intercellular glutathione (GSH), decreasing the productivity of GSH-dependent antioxidants, mitochondrial deficiency, accumulation of leukocytes and pro-inflammatory cytokines. Overexpression of ROS producing enzymes and down-regulation of antioxidant enzymes are probably the major events by which SM leads to OS at the chronic phase of injury. Therefore, antioxidant therapy with potent antioxidants such as N-acetylcysteine and curcumin may be helpful to mitigate SM-induced OS damages. This review aims to discuss the proposed cellular and molecular mechanisms of acute and delayed SM toxicity, the importance of OS and mechanisms by which SM increases OS either at the acute or chronic phases of injuries along with research on antioxidant therapy as a suitable antidote. [ABSTRACT FROM AUTHOR]

Sulfur mustard (SM) is a mutagenic compound that targets various organs. Although it causes a wide range of abnormalities, cellular and molecular mechanisms of its action are not-well-understood. Oxidation of DNA, proteins, lipids, as well as depletion of cellular nicotinamide adenine dinucleotide (NAD), antioxidants and increase of intracellular calcium are the hypothesized mechanisms of its action at the acute phase of injury. In this review, the proteome analysis of SM toxicity has been considered. We selected articles that considered proteomics analysis of SM toxicity with two-dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our search yielded nine related articles, four original in vitro and five human studies. The results of these studies have revealed a change in expression pattern of various proteins such as haptoglobin, amyloid A1, surfactant proteins, S100 proteins, apolipoprotein, Vit D binding protein, transferrin, alpha 1 antitrypsin, protein disulfide isomerase and antioxidant enzymes in patients who were exposed to SM about 30 years ago. Most of these proteins are up- or down-regulated in response to excessive production of reactive oxygen species (ROS) and oxidative stress (OS). There is a tight link between the expression pattern of these proteins with accumulation of leukocytes, inflammatory conditions, antioxidant depletion, mitochondrial deficiency, as well as increased expression or activity of several proteases such as caspases and matrix metalloproteinases (MMPs). Therefore, excessive production of ROS and OS along with chronic inflammatory may be the long-term toxic effects of SM following acute exposure. [ABSTRACT FROM AUTHOR]

Calcium (Ca) is a significant element that acts as an intracellular second messenger. It is necessary for many physiological processes in spermatozoa including spermatogenesis, sperm motility, capacitation, acrosome reaction and fertilization. Although influences of Ca deficiency on sperm function and male infertility have been widely studied, mechanisms for these abnormalities are not well considered. Poor sperm motility, impairment of chemotaxis, capacitation, acrosome reaction and steroidogenesis are the major mechanisms by which Ca deficiency induces male infertility. Therefore, an optimal seminal Ca concentration is required to strengthen sperm function and all steps leading to successful fertilization. Furthermore, identification of these mechanisms provides valuable information regarding the mechanisms of Ca deficiency on male reproductive system and the way for developing a better clinical approach. In this review, we aim to discuss the proposed cellular and molecular mechanisms of Ca deficiency on male reproductive system, sperm function and male fertility. Also we will discuss the valuable information currently available for the roles of Ca in male reproduction. [ABSTRACT FROM AUTHOR]

Sulfur mustard (SM) is a toxic compound that can target human spermatozoa. SM induces a wide variety of pathological effects in human reproductive organs, including sexual hormone disturbance, testicular atrophy, impaired spermatogenesis, poor sperm quality, defects in embryo development, childhood physical abnormalities, and severe fertility problems. However, the molecular and cellular mechanisms of SM action on male reproductive health and human sperm function are unclear. Excessive production of reactive oxygen species and the resulting oxidative stress is likely a significant mechanism of SM action, and could be associated with sperm DNA damage, membrane lipid peroxidation, reduced membrane fluidity, mitochondrial deficiency, apoptosis, and poor sperm quality. In this review, we aim to discuss the cellular and molecular mechanisms of SM action on sperm and reproductive health, the significance of OS, and the mechanisms through which SM enhances the infertility rate among SM-exposed individuals. [ABSTRACT FROM AUTHOR]

Diazinon (DZN) is an organophosphate insecticide that has cytotoxic and pathological effects on the reproductive system. It causes a wide variety of pathological effects on the reproductive system such as testicular atrophy, disturbance in sex hormones, impaired spermatogenesis, low quality of sperm, and fertility problems. However, molecular and cellular mechanisms of its adverse effects are not well understood. General events such as testicular damage, inflammation, mitochondrial deficiency, DNA fragmentation, disintegration of sperm plasma membrane, apoptosis, and cell death are observed in DZN-exposed animals. Oxidative stress (OS) induced by reactive oxygen species may be a main mechanism, which can be associated with sperm DNA fragmentation, reduced integrity of sperm cell membrane, apoptosis, depletion of antioxidants, and subsequently poor sperm quality and male infertility. Therefore, identification of these pathways may provide valuable information regarding the mechanisms of DZN action on the male reproductive system. In this review, we aim to discuss the proposed cellular and molecular mechanisms of DZN action on male reproductive system, the importance of OS and mechanisms by which DZN induces OS and depletion of other antioxidants. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard (SM) is a lipophilic and reactive chemical compound that targets human airway system. Objective: Glutathione (GSH) depletion, oxidative stress (OS) status, and changes in expression of GSH-dependent antioxidant enzymes were considered in human mustard lungs. Materials and methods: Lung biopsies and bronchoalveolar lavage (BAL) were collected from non-exposed (n = 10) individuals and SM-exposed patients (n = 12). Alterations in expression of GSH-dependent enzymes were studied using RT2 Profiler™ PCR array. OS was evaluated by determining BAL fluid levels of total antioxidant capacity (TAC), malondialdehyde (MDA), and GSH. Results: Mean TAC (0.142 ± 0.027 µmol/l) and GSH (4.98 ± 1.02 nmol/l) in BAL fluids of control group was significantly higher (p < .05) than those in SM-exposed patients (TAC = 0.095 ± 0.018 µmol/l and GSH= 3.09 ± 1.02 nmol/l), while MDA level in BAL fluids of these patients (0.71 ± 0.06 nmol/l) was significantly (p = .001) higher than that in controls (0.49 ± 0.048 nmol/l). Glutathione peroxidases (GPXs), glutathione-s-transferases (GSTs), and glutathione synthetase (GSS) enzymes were overexpressed in mustard lung biopsies, while glutathione reductase (GSR) was significantly downregulated (14.95-fold). Conclusions: GSH depletion induced by GSR downregulation may be a major mechanism of SM toxicity on human lung. Despite overexpression of GSTs and GPXs genes, GSH depletion may decline the productivity of these enzymes and total antioxidants capacity, which is associated with OS. [ABSTRACT FROM AUTHOR]

Introduction: The chronic systemic inflammation is a result of releasing inflammatory cytokines from the cells relating to the body immunity system and chronic activation of the innate immunity system. Aim: To evaluate the relationship among serum levels of interleukin 6 (IL-6), interleukin 8 (IL-8), C-reactive protein (CRP) with forced expiratory volume in 1st s (FEV1) in patients with mustard lung (ML) and chronic obstructive pulmonary diseases (COPD). Material and methods: A published literature search was performed through SID, web of science, ISI, Science Direct, Scopus, Medline, and PubMed databases for articles published in English. The correlation coefficient (r) and 95% confidence intervals (95% CIs) were calculated using random or fixed effects models. Heterogeneity was assessed using χ² and I² statistics. Results: In total, 4 published studies were included in the final analysis. Using the random-effect model, metaanalysis showed that the r was -0.052 (95% CI: -0.14-0.049, p = 0.28) at serum level of IL-8, serum levels of CRP and FEV1 in these results were r = -0.13, p = 0.012, serum levels of tumor necrosis factor (TNF) and FEV1 levels were r = -0.39, p = 0.03 in the conducted studies on mustard lung patients. The IL-6 serum level was explored in COPD patients. The results of the given studies in these patients are r = -0.006, 95% CI: -0.37-0.15, and p = 0.44. Conclusions: In this meta-analysis, there was evidence that serum levels of CRP and TNF have been significantly increased in chronic obstructive pulmonary diseases compared to the healthy control group, which signifies the presence of systemic inflammation in ML and COPD patients. [ABSTRACT FROM AUTHOR]

Pulmonary complications of exposure to sulfur mustard (SM) gas range from no effect or mild symptoms to severe bronchial stenosis. In the present study, the protective effect of vitamin E on the lung inflammation of SM-exposed guinea pigs was examined. Guinea pigs (n = 5 for each group) were exposed to ethanol (control group), 40 mg/m3 inhaled SM (SME group), SME treated with vitamin E (SME + E), SME treated with dexamethasone (SME + D), and SME treated with both treatments (SME + E + D). Pathological evaluation of the lung was done 14 days postexposure. The epithelial desquamation of trachea and other pathologic changes in the lung of the SME group were significantly higher than those in the control group. Furthermore, the pathological changes of trachea and lung in the SME + E and SME + E + D groups were significantly improved compared with those of SME group. In addition, the pathological changes of trachea and lung of SME + E and SME + E + D animals were significantly less than those of SME + D group. [ABSTRACT FROM AUTHOR]

Mustard lung is a major pulmonary complication in individuals exposed to sulfur mustard (SM) gas during the Iran–Iraq war. It shares common pathological and clinical features with some chronic inflammatory lung disorders, particularly chronic obstructive pulmonary disease (COPD). Airway remodeling, which is one of the main causes of lung dysfunction and the dominant phenomenon of chronic pulmonary diseases, is seen in the mustard lung. Among all mediators involved in the remodeling process, the transforming growth factor (TGF)-β plays a pivotal role in lung fibrosis and consequently in the airway remodeling. Regarding the high levels of this mediator detected in mustard lung patients, in the present study, we have discussed the possible roles of TGF-β in airway remodeling (including epithelial layer damage, subepithelial fibrosis and angiogenesis). Finally, based on TGF-β targeting, we have reviewed new airway remodeling therapeutic approaches. [ABSTRACT FROM AUTHOR]

Despite the attention to the different systems damaged by sulfur mustard(SM), little attention has been paid to the immune system. But, after years following the injury, the immune system dysfunction is discussed as the main cause of death in veterans. Also, the study of inflammatory and pro-inflammatory markers in these patients has not been evaluated at the time of exposure and the acute phase of the disease. Therefore, to gain more information about the inflammatory mechanisms of SM, we proposed to examine the patients in the acute phase and evaluate the inflammatory and pre-inflammatory factors at the beginning of exposure. [ABSTRACT FROM PUBLISHER]

Respiratory disorders in sulfur mustard (SM)-exposed and chronic obstructive pulmonary disease (COPD) patients are mostly associated with neutrophilic inflammation, severe airflow limitation, and oxidative stress. The objective of this study was to establish whether neutrophil (PMN) proteomes in these diseases were similar or differed. Blood neutrophil proteomes from healthy, SM-exposed, and COPD subjects were analyzed using two-dimensional gel electrophoresis followed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI TOF MS). Elastase activity was determined kinetically. The results showed that levels of S100 calcium-binding protein (CBP) A12, S100 CBP A8, glyceraldehyde-3-phosphate dehy-drogenase, superoxide dismutase, and protein disulfide isomerase proteins - as well as elastase activity - were significantly increased in PMN from 'diseased' hosts compared to in cells from healthy controls. In contrast, coactosin-like protein, RhoGDP dissociation inhibitor, and actin isoforms were significantly decreased in diseased subjects' PMN compared to PMN of healthy controls. Moreover, serpin B1 and coronin-1A were expressed only in PMN of the healthy subjects. Lastly, S100 CBP A9, endoplasmic reticulum (ER)-60 protease, and glutathione- S-transferase isoforms were differentially expressed in the cells from the SM-exposed and COPD subjects. These results show that serpin B1, an efficient inhibitor of neutrophil serine proteases, was not detectable, and elastase activity significantly increased in PMN from both SM-exposed and COPD patients. It seems that, apart from inflammation and oxidative stress, a protease:anti-protease imbalance exists within PMN of both COPD and SM-exposed patients. [ABSTRACT FROM AUTHOR]

Objective: Biological effects of sulfur mustard (SM) on various systems have been investigated in both humans and animals. However, few studies are available on the effect of SM on the peripheral nervous system. In the present study, long-term effects of a single dose of SM on nerve conduction velocity and electromyography (EMG) pattern is evaluated in hindlimb of adult male rats. Methods: SM poisoning was induced by two means: subcutaneous injection of I and 3.5 mg/kg SM in two experimental groups (1 and 2) and cutaneous application of 8 and 13 mg/kg SM in groups 3 and 4. Sham and control groups received SM vehicle, isopropyl alcohol, and nothing, respectively. Electrophysiological assessments were performed after 26 weeks as follows: sciatic nerve conduction study that included measuring, amplitude, duration, and latency of M-wave, F-wave latency, and EMG study in resting and minimal contraction states. Results: Results indicate that sciatic nerve conduction velocity did not significantly change in any experimental groups. However, resting EMG records showed some abnormalities very similar to positive sharp waves and fasciculation reported in humans. These abnormalities were observed in 6 of 36 intoxicated rats. Conclusions: Although the present data are in favor of axonal degeneration, to rule out the possibility of other types of degeneration, additional thorough studies at ultrastructural level are suggested. [ABSTRACT FROM AUTHOR]

Although tremendous advancements in cancer therapy over the last several years, cancer still is a complex illness to cure. Traditional cancer treatments, including chemotherapy, radiotherapy, and surgery, have a poor therapeutic effect, emphasizing the significance of employing innovative treatments like activated cell therapy. Chimeric antigen receptor T cell is one of the most prevalent types of activated cell therapy have been developed to direct T lymphocytes toward cancers (CAR-T cells). CAR-T cells therapy has illustrated poor impact versus solid tumors despite the remarkable success in patients suffering from hematological malignancies. CAR-T cells must overcome various hurdles to obtain full responses to solid tumors, including growth, stability, trafficking, and destiny inside tumors. As a result, novel treatment methods will entail overcoming the challenges that CAR-T cells face in solid tumors. The use of CAR-T cells in combination with other therapeutic approaches such as chemotherapy, radiotherapy, immuno-checkpoint inhibitors, and oncolytic viruses can promote the effectiveness of CAR-T cell therapy for the treatment of solid tumors. However, more research is needed to determine the safety and effectiveness of these therapies. CAR-T cell treatment success rates vary by type of disease, but are predicted to reach up to 90% in patients with leukemia. However, since this kind of immunotherapy is still in its infancy, there is much to learn about its efficacy. This review provided an in-depth examination of CAR-T cell therapy and its success and failure as a cancer treatment approach. We also discuss combination therapies with CAR-T Cell. [Display omitted] • CAR-T cell therapy is one of several treatments included in cancer immunotherapy. • CAR T cells have been categorized into fifth distinct generations. • CAR-T cell therapy is not entirely safe, and this strategy has notable limitations. • Combination therapies improve the function of CAR-T cell efficiency in solid tumors. [ABSTRACT FROM AUTHOR]

Coronavirus (SARS-CoV-2) is spreading rapidly in the world and is still taking a heavy toll. Studies show that cytokine storms and imbalances in T-helper (Th)1/Th2 play a significant role in most acute cases of the disease. A number of medications have been suggested to treat or control the disease but have been discontinued due to their side effects. Melatonin, as an intrinsic molecule, possesses pharmacological anti-inflammatory and antioxidant properties that decreases in concentration with age; as a result, older people are more prone to various diseases. In this study, patients who were hospitalized with a diagnosis of coronavirus disease 2019 (COVID-19) were given a melatonin adjuvant (9 mg daily, orally) for fourteen days. In order to measure markers of Th1 and Th2 inflammatory cytokines (such as interleukin (IL)-2, IL-4, and interferon (IFN)-γ) as well as the expression of Th1 and Th2 regulatory genes (signal transducer and activator of transcription (STAT)4 , STAT6 , GATA binding protein 3 (GATA3) , and T-box expressed in T cell (T-bet)), blood samples were taken from patients at the beginning and end of the treatment. Adjuvant therapy with melatonin controlled and reduced inflammatory cytokines in patients with COVID-19. Melatonin also controlled and modulated the dysregulated genes that regulate the humoral and cellular immune systems mediated by Th1 and Th2. In this study, it was shown for the first time that melatonin can be used as a medicinal adjuvant with anti-inflammatory mechanism to reduce and control inflammatory cytokines by regulating the expression of Th1 and Th2 regulatory genes in patients with COVID-19. [ABSTRACT FROM AUTHOR]

Aim: Chemical injuries can potentially lead to the necrosis anterior segment of the eye, and cornea in particular. Inflammatory cytokines are the first factors produced after chemical ocular injuries. Inflammation via promoting the angiogenesis factor tries to implement the wound healing mechanism in the epithelial and stromal layer of the cornea., Methods: Narrative review., Results: In our review, we described the patterns of chemical injuries in the cornea and their molecular mechanisms associated with the expression of inflammatory cytokines. Moreover, the effects of inflammation signals on angiogenesis factors and CNV were explained., Conclusion: The contribution of inflammation and angiogenesis causes de novo formation of blood vessels that is known as the corneal neovascularization (CNV). The new vascularity interrupts cornea clarity and visual acuity. Inflammation also depleted the Limbal stem cells (LSCs) in the limbus causing the failure of normal corneal epithelial healing and conjunctivalization of the cornea.

Recent studies have indicated that epigenetic alterations are critical for normal function and development of spermatozoa during the fertilization process. This review will focus on the latest advances in epigenome profiling of the chromatin modifications during sperm development, as well as the potential roles of epigenetic mechanisms in the context of male infertility. In this review, all data were collected from published studies that considered the effect of epigenetic abnormalities on human spermatogenesis, sperm parameters quality, fertilization process, embryo development and live births. The database PubMed was searched for all experimental and clinical studies using the Keywords "epigenetic modifications", "male infertility", "spermatogenesis", "embryo development" and "reproductive function". Post-translational modifications of histone, DNA methylations and chromatin remodeling are among the most common forms of epigenetic modifications that regulate all stages of spermatogenesis and fertilization process. Incorrect epigenetic modifications of certain genes involved in the spermatogenesis and sperm maturation may be a main reason of male reproductive disorder and infertility. Most importantly, abnormal patterns of epigenetic modifications or transgenerational phenotypes and miRNAs expression may be transmitted from one generation to the next through assisted reproductive techniques (ART) and cause an increased risk of birth defects, infertility and congenital anomalies in children. Epigenetic modifications must be considered as a one of the main factors of unexplained male infertility etiology. Due to high risk of transmitting incorrect primary imprints to offspring, there is a need for more research into epigenetic alterations in couples who benefit of ART support., Competing Interests: The authors declare no conflicts of interest., (Copyright© by Royan Institute. All rights reserved.)

Aim: We aimed to describe the epidemiological and clinical characteristics of Iranian patients with COVID-19., Methods: In this single-center and retrospective study, patients with confirmed COVID-19 infections were enrolled. Univariate and multivariate logistic regression methods were used to explore the risk factors associated with outcomes., Results: Of 179 patients with confirmed COVID-19 infection, 12 remained hospitalized at the end of the study and 167 were included in the final analysis. Of these, 153 (91.6%) were discharged and 14 (8.38%) died in hospital. Approximately half (50.9%) of patients suffered from a comorbidity, with diabetes or coronary heart disease being the most common in 20 patients. The most common symptoms on admission were fever, dyspnea, and cough. The mean durations from first symptoms to hospital admission was 8.64 ± 4.14 days, whereas the mean hospitalization time to discharge or death was 5.19 ± 2.42 and 4.35 ± 2.70 days, respectively. There was a significantly higher age in non-survivor patients compared with survivor patients. Multivariate regression showed increasing odds ratio (OR) of in-hospital death associated with respiratory rates >20 breaths/min (OR: 5.14, 95% CI: 1.19-22.15, p = 0.028) and blood urea nitrogen (BUN) >19 mg/dL (OR: 4.54, 95% CI: 1.30-15.85, p = 0.017) on admission. In addition, higher respiratory rate was associated with continuous fever (OR: 4.08, 95% CI: 1.18-14.08, p = 0.026) and other clinical symptoms (OR: 3.52, 95% CI: 1.05-11.87, p = 0.04)., Conclusion: The potential risk factors including high respiratory rate and BUN levels could help to identify COVID-19 patients with poor prognosis at an early stage in the Iranian population.

The exaggerated host response to Sars-CoV-2 plays an important role in COVID-19 pathology but provides a therapeutic opportunity until definitive virus targeted therapies and vaccines become available. Given a central role of endothelial dysfunction and systemic inflammation, repurposing ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), statins, and aspirin has been of interest. In this retrospective, single-center study, we evaluated the primary outcomes of mortality and ICU admission in 587 hospitalized patients with documented COVID-19 with or without ACEIs, ARBs, statins, and aspirin. Atorvastatin was associated with reduced mortality, which persisted after adjusting for age, lockdown status, and other medications (OR: 0.18. 95% CI: 0.06-0.49, P = 0.001). ACEIs were also associated with reduced mortality in the crude model (OR: 0.20, CI: 0.06-0.66, P = 0.008), as ACEIs and ARBs were combined as a single group (OR: 0.35, CI: 0.16-0.75, P = 0.007), although ARBs alone did not reach statistical significance. There was no association between any medications and risk of ICU admission. Aspirin only achieved a significant association of reduced mortality in a subgroup of patients with diabetes in the crude model (OR: 0.17, CI: 0.04-0.80, P = 0.02). The reduced mortality observed with atorvastatin is consistent with other literature, and consideration should be given to atorvastatin as a COVID-19 treatment. While there was suggested benefit of ACEIs and ARBs in the present study, other studies are varied and further studies are warranted to recommend employing these medications as a treatment strategy. Nevertheless, this study combined with others continues to give credibility that ACEIs and ARBs are safe to continue in the setting of COVID-19., (© 2021. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Following the outbreaks of SARS-CoV in 2002 and MERS-CoV in 2012, the COVID-19 pandemic caused by the SARS-CoV-2 virus has become an increasing threat to human health around the world. Numerous studies have shown that SARS-CoV-2 appears similar to the SARS-CoV as it uses angiotensin converting enzyme 2 (ACE2) as a receptor to gain entry into cells. The main aims of this scoping review were to identify the primary hosts of coronaviruses, the relationship between the receptor binding domain of coronaviruses and ACE2, the organ specificity of ACE2 expression compared with clinical manifestations of the disease, and to determine if this information can be used in the development of novel treatment approaches for the COVID-19 pandemic.

There is data from individual clinical trials suggesting that procalcitonin (PCT) may be a prognostic factor in the severity of COVID-19 disease. Therefore, this systematic review and meta-analysis was performed to investigate PCT levels in severe COVID-19 patients. We searched Embase, ProQuest, MEDLINE/PubMed, Scopus, and ISI/Web of Science for studies that reported the level of PCT of patient with severe COVID-19. We included all studies regardless of design that reported the level of PCT in patients with severe COVID-19. We excluded articles not regarding COVID-19 or not reporting PCT level, studies not in severe patients, review articles, editorials or letters, expert opinions, comments, and animal studies. Nine studies were included in the analysis. The odds of having more severe COVID-19 disease was higher in subjects with elevated PCT (≥0.05 ng/mL) compared with those having low procalcitonin (<0.05 ng/mL) [n = 6, OR(95% CI) = 2.91(1.14, 7.42), p = 0.025). After estimating the mean and standard deviation values from the sample size, median, and interquartile range, a pooled effect analysis indicated higher serum PCT concentrations in patients with severe versus less severe disease [n = 6, SMD(95% CI) = 0.64(0.02, 1.26), p = 0.042]. The results of this study showed that PCT is increased in patients with severe COVID-19 infection.

Background: An outbreak of COVID-19 in Iran has spread throughout the country. Identifying the epidemiological characteristics of this disease will help to make appropriate decisions and thus control the epidemic. The aim of this study was characterization of the epidemiological features of COVID-19 in Iran., Methods: In this retrospective study, data related to the epidemiological characteristics of COVID-19 patients admitted to Baqiyatallah Hospital in Tehran, Iran, from 19 February 2020 to 15 April 2020 have been analyzed and reported. Patient characteristics including age, gender and underlying diseases were investigated. Data were collected through patient records. Sex ratio, Case Fatality Rate (CFR) and daily trend of cases were also determined. A multiple logistic regression analysis was also performed to assess affecting factors on mortality., Results: From February 19, 2020 to April 15, 2020, 12870 patients referred to the hospital emergency department, of which 2968 were hospitalized with COVID-19 diagnosis. The majority of cases were in the age group of 50 to 60 years of old. The male-to-female ratio was 1.93:1. A total of 239 deaths occurred among all cases for an overall CFR of 1.85% based on the total number of patients (both outpatient and inpatient) and 8.06% among hospitalized patients. Out of all patients 10.89% had comorbidity. Diabetes, chronic respiratory diseases, hypertension, cardiovascular diseases, chronic Kidney diseases and cancer were the most common comorbidities with 3.81, 2.02 , 1.99 , 1.25, 0.60 and 0.57 %, respectively. Male gender (OR=1.45, 95% CI: 1.08-1.96), older age (OR=1.05, 95% CI: 1.04-1.06) and having underlying diseases (OR=1.53, 95% CI: 1.04-2.24) were significantly associated with mortality., Conclusions: The results of this study showed that Male gender, older age and having comorbidities were significantly associated with the risk of death among COVID-19 patients. It is important to pay special attention to male elderly patients with underlying diseases., Competing Interests: Declaration of Competing Interest The authors declare that there are no competing interests., (Copyright © 2020 Elsevier B.V. All rights reserved.)