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Over the past years, the benefits of stem cell therapy approach for treatment of the cardiovascular diseases have been shown through the rebuilding of new cardiomyocytes and blood vessels. while a successful regeneration of the myocardium has been proven on the animal models of acute myocardial injuries resulted from the stem cells transplantation, no significant long-term regenerative with autologous stem cell therapy in patients with acute myocardial infarction have been reported based on recent meta-analyses. It seems that the inflammatory microenvironment of acute myocardial infarction has an inhibitory effect on the stem cells potential for regenerating the injured myocardium. Secretion of critical cytokines with pro-inflammatory properties including tumor necrosis factor-α, interleukin-1β, and interleukin-6 as well as induction of hypoxic condition and finally formation of cytotoxic elements cause the cellular death and hinder the stem cells proliferation and differentiation. Based on the evidence, application of some approaches like co-delivery of mesenchymal stem cells with the other useful cells, using the stem cells derived productions, administration of preconditioned and modified cells, and also using the anti-inflammatory agents besides the cell therapy are hypothesized as the primary developed safe and practical approaches for decreasing destructive effects of the inflammation on the implanted stem/progenitor cells. In this review, we critically discuss the quiddity of the inflammatory microenvironment and its promoted mechanisms as the main elements to hinder the efficacy of stem cell therapy in the cases of acute myocardial infarction. Also, we finally propose some applied solutions to the problem of cardiac regeneration with stem cells therapy.Over the past years, the benefits of stem cell therapy approach for treatment of the cardiovascular diseases have been shown through the rebuilding of new cardiomyocytes and blood vessels. while a successful regeneration of the myocardium has been proven on the animal models of acute myocardial injuries resulted from the stem cells transplantation, no significant long-term regenerative with autologous stem cell therapy in patients with acute myocardial infarction have been reported based on recent meta-analyses. It seems that the inflammatory microenvironment of acute myocardial infarction has an inhibitory effect on the stem cells potential for regenerating the injured myocardium. Secretion of critical cytokines with pro-inflammatory properties including tumor necrosis factor-α, interleukin-1β, and interleukin-6 as well as induction of hypoxic condition and finally formation of cytotoxic elements cause the cellular death and hinder the stem cells proliferation and differentiation. Based on the evidence, application of some approaches like co-delivery of mesenchymal stem cells with the other useful cells, using the stem cells derived productions, administration of preconditioned and modified cells, and also using the anti-inflammatory agents besides the cell therapy are hypothesized as the primary developed safe and practical approaches for decreasing destructive effects of the inflammation on the implanted stem/progenitor cells. In this review, we critically discuss the quiddity of the inflammatory microenvironment and its promoted mechanisms as the main elements to hinder the efficacy of stem cell therapy in the cases of acute myocardial infarction. Also, we finally propose some applied solutions to the problem of cardiac regeneration with stem cells therapy.

Treatment options for viral infections are limited and viruses have proven adept at evolving resistance to many existing therapies, highlighting a significant vulnerability in our defenses. In response to this challenge, we explored the modulation of cellular RNA metabolic processes as an alternative paradigm to antiviral development. Previously, the small molecule 5342191 was identified as a potent inhibitor of HIV-1 replication by altering viral RNA accumulation at doses that minimally affect host gene expression. In this report, we document 5342191 as a potent inhibitor of adenovirus, coronavirus, and influenza replication. In each case, 5342191-mediated reduction in virus replication was associated with altered viral RNA accumulation and loss of viral structural protein expression. Interestingly, while resistant viruses were rapidly isolated for compounds targeting either virus-encoded proteases or polymerases, we have not yet isolated 5342191-resistant variants of coronavirus or influenza. As with HIV-1, 5342191’s inhibition of coronaviruses and influenza is mediated through the activation of specific cell signaling networks, including GPCR and/or MAPK signaling pathways that ultimately affect SR kinase expression. Together, these studies highlight the therapeutic potential of compounds that target cellular processes essential for the replication of multiple viruses. Not only do these compounds hold promise as broad-spectrum antivirals, but they also offer the potential of greater resilience in combating viral infections.

The conditioning of grinding tools is one of the most important factors for achieving an optimal grinding process. It influences the grinding forces and temperatures and, therefore, the achievable material removal rate, dimensional accuracy and the surface integrity of the workpiece. Furthermore, the roundness, profile accuracy and the wear of the grinding tools are strongly influenced by the conditioning process. The conditioning process should be matched to the abrasive type and the bonding of the grinding tool. Laser conditioning is a promising unconventional and non-contact method, which is able to condition all kinds of abrasives and bonding types. The main advantages of this novel method are no tool wear, good repeatability and controllability, high precision and a relatively short process time. Additionally, using this method grinding tools can be micro-structured. This paper reviews the literature on the laser conditioning of grinding tools, covering the associated setups, wheel conditioning and structuring mechanisms, and experimental results. It also discusses the technical barriers that have to be overcome before laser conditioning can be fully integrated into manufacturing.

Laser treatment is a novel and promising non-conventional method to reduce the conditioning costs and time of superabrasive tools. In this study, the thermal effects of picosecond laser radiation on metal-bonded cubic boron nitride (CBN) and diamond superabrasive tool surfaces have been analytically and experimentally investigated. The analytical approach is intended to find threshold process parameters for the selective ablation of the superabrasive grains and the bond material. The laser radiation experiments have been conducted with a picosecond Yb:YAG laser on metal-bonded CBN and diamond honing tools. It has been analytically and experimentally demonstrated that, using suitable parameters, the selective and controlled treatment of superabrasive tool components is possible.

Treatment of bacterial infections with antibiotic resistance is complicated. For this reason, new therapeutic methods are needed to control bacterial infections. Therefore, it is necessary to discover new antibiotics from medicinal plants that can destroy drug-resistant bacteria. Essential oils (EO) of some medicinal plants have antimicrobial effects and can be used as antimicrobial agents in the treatment of infections and food industries. The aim of this study was to determine the EO composition and antimicrobial effects of EO and polyphenols profile of Salvia Sahendica roots for the first time. Chemical compounds and antibacterial activity of EOs against Staphylococcus aureus and Bacillus cereus as gram-positive and Escherichia coli and Pseudomonas aeruginosa as gram- negative bacteria were evaluated using microtiter broth dilution method. Studied organs of S. sahendica showed significant diversity in terms of type and percentage of essential oil and polyphenol compounds. Overall, 44, 46, 42, and 45 compounds were identified in the essential oil of leaves, flowers, stems, and roots of this plant, which constituted 99.6, 99.3, 98.2, and 99.4% of total oil composition, respectively. The current study collectively demonstrated inhibitory effects ranged from strong ( S. aureus ) to low inhibition ( P. aeruginosa ). According to the HPLC result, the amounts of coumaric acid, chlorogenic acid, and gallic acid compounds in the root are higher than in other plant parts, which indicate that the root can be a suitable source for the production of these valuable polyphenol compounds. Due to the results, it is possible to hope for the application of EO from S. sahendica as natural antibacterial in the pharmaceutical and food industries.

Autophagy is a fundamental catabolic process essential for the maintenance of cellular and tissue homeostasis, as well as directly contributing to the control of invading pathogens. Unsurprisingly, this process becomes critical in supporting cellular dysregulation that occurs in cancer, particularly the tumor microenvironments and their immune cell infiltration, ultimately playing a role in responses to cancer therapies. Therefore, understanding “cancer autophagy” could help turn this cellular waste-management service into a powerful ally for specific therapeutics. For instance, numerous regulatory mechanisms of the autophagic machinery can contribute to the anti-tumor properties of oncolytic viruses (OVs), which comprise a diverse class of replication-competent viruses with potential as cancer immunotherapeutics. In that context, autophagy can either: promote OV anti-tumor effects by enhancing infectivity and replication, mediating oncolysis, and inducing autophagic and immunogenic cell death; or reduce OV cytotoxicity by providing survival cues to tumor cells. These properties make the catabolic process of autophagy an attractive target for therapeutic combinations looking to enhance the efficacy of OVs. In this article, we review the complicated role of autophagy in cancer initiation and development, its effect on modulating OVs and immunity, and we discuss recent progress and opportunities/challenges in targeting autophagy to enhance oncolytic viral immunotherapy.

Background There is some evidence of the association between ST‐segment elevation in the V4R chest lead and the likelihood of anterior wall myocardial infarction; however, the link of this phenomenon with the location and the severity of the coronary involvements in such patients remains uncertain. We aimed to investigate the ST‐segment elevation in V4R leads in patients with anterior myocardial infarction and also its effect on prognosis as well as the detection and prediction of the location of arterial stenosis in coronary angiography. Methods Data collection was performed by reviewing the hospital recorded files of 195 patients’ suspicion of acute myocardial infarction who have been referred within 2 h of the onset of cardiac symptoms. The patients were then categorized into two groups with and without ST elevation in the V4R chest lead. Results Comparing two groups showed a significantly higher rate of concurrent ST‐segment elevation in V1 lead in those with ST‐segment elevation in V4R. Echocardiography on the day after anterior myocardial infarction showed LVEF <40% in 74% and 35.2% of patients with and without ST‐segment elevation in V4R, respectively, indicating a significant difference. The lesions on proximal LAD were more common in the group with ST‐segment elevation in V4R. Conclusion Our study emphasized a high likelihood of ST‐segment elevation in V4R lead concurrently with ST‐elevation in V1 lead. Also, the appearance of ST‐segment elevation in V4R lead can be accompanied with a lower LVEF, myocardial infarct size, involvement of proximal part of LAD, and Wrap around LAD.

Hearing loss, one of the most prevalent chronic health conditions, affects around half a billion people worldwide, including 34 million children. The World Health Organization estimates that the prevalence of disabling hearing loss will increase to over 900 million people by 2050. Many cases of congenital hearing loss are triggered by viral infections during different stages of pregnancy. However, the molecular mechanisms by which viruses induce hearing loss are not sufficiently explored, especially cases that are of embryonic origins. The present review first describes the cellular and molecular characteristics of the auditory system development at early stages of embryogenesis. These developmental hallmarks, which initiate upon axial specification of the otic placode as the primary root of the inner ear morphogenesis, involve the stage-specific regulation of several molecules and pathways, such as retinoic acid signaling, Sonic hedgehog, and Wnt. Different RNA and DNA viruses contributing to congenital and acquired hearing loss are then discussed in terms of their potential effects on the expression of molecules that control the formation of the auditory and vestibular compartments following otic vesicle differentiation. Among these viruses, cytomegalovirus and herpes simplex virus appear to have the most effect upon initial molecular determinants of inner ear development. Moreover, of the molecules governing the inner ear development at initial stages, SOX2, FGFR3, and CDKN1B are more affected by viruses causing either congenital or acquired hearing loss. Abnormalities in the function or expression of these molecules influence processes like cochlear development and production of inner ear hair and supporting cells. Nevertheless, because most of such virus–host interactions were studied in unrelated tissues, further validations are needed to confirm whether these viruses can mediate the same effects in physiologically relevant models simulating otic vesicle specification and growth.

Zika virus (ZIKV), a neglected tropical disease until its re-emergence in 2007, causes microcephaly in infants and Guillain-Barré syndrome in adults. Its re-emergence and spread to more than 80 countries led the World Health Organization in 2016 to declare a Public Health Emergency. ZIKV is mainly transmitted by mosquitos, but can persist in infected human male semen for prolonged periods and may be sexually transmitted. Testicular Sertoli cells support ZIKV replication and may be a reservoir for persistent ZIKV infection. Electrical impedance analyses indicated ZIKV infection rapidly disrupted Vero cell monolayers but had little effect upon human Sertoli cells (HSerC). We determined ZIKV-induced proteomic changes in HSerC using an aptamer-based multiplexed technique (SOMAscan) targeting >1300 human proteins. ZIKV infection caused differential expression of 299 proteins during three different time points, including 5 days after infection. Dysregulated proteins are involved in different bio-functions, including cell death and survival, cell cycle, maintenance of cellular function, cell signaling, cellular assembly, morphology, movement, molecular transport, and immune response. Many signaling pathways important for maintenance of HSerC function and spermatogenesis were highly dysregulated. These included IL-6, IGF1, EGF, NF-κB, PPAR, ERK/MAPK, and growth hormone signaling. Down-regulation of the PPAR signaling pathway might impact cellular energy supplies. Upstream molecule analysis also indicated microRNAs involved in germ cell development were downregulated by infection. Overall, this study leads to a better understanding of Sertoli cellular mechanisms used by ZIKV during persistent infection and possible ZIKV impacts on spermatogenesis.

Maternal influenza infection during pregnancy was reported multiple times as the possible cause of many defects and congenital anomalies. Apart from several cases of influenza-related miscarriage during various trimesters of pregnancy, some epidemiological data suggest a link between maternal influenza infection and genetic abnormalities in offspring. However, there are no reports yet describing how maternal influenza alters cellular pathways at early stages of development to result in congenital defects in the fetus. In the present study, using proteomic approaches, we utilized human-induced pluripotent stem cells (hiPSCs) for modeling intrablastocyst infection with influenza virus to not only investigate the vulnerability and responses of pluripotent stem cells to this virus but also to determine the possible impacts of influenza on pluripotency and signaling pathways controlling differentiation and embryogenesis. Our data indicated viral protein production in influenza A virus (IAV)-infected hiPSCs. However, viral replication was restricted in these cells, but cell viability and pluripotency were negatively affected. These events occurred simultaneously with an excessive level of IAV-induced autophagy as well as cytopathic effects. Quantitative SOMAscan screening also indicated that changes in the proteome of hiPSCs corresponded to abnormal differentiation in these cells. Taken together, our results showed that IAV-modulated reduction in hiPSC pluripotency is associated with significant activation of autophagy. Further investigations are required to explore the role of IAV-induced autophagy in leading pluripotent stem cells toward abnormal differentiation and impaired development in early stages of embryogenesis.