ABSTRACT
This study is principally the first to test a moderated mediation model of COVID-19 fear and job satisfaction in the Quality of Work Life (QWL)-commitment relationship of medical teachers during the pandemic. The conceptual model draws its theoretical tenet from spillover and conservation of resources theories. Cluster sampling was incorporated from four metropolitan cities in India. A mixed-method research design was administered to 378 medical teachers amidst the pandemic. The partial least squares structural equation modeling (PLS-SEM) results indicate a significant positive association between the constructs. Path analyses have highlighted positive associations between QWL, job satisfaction, and affective commitment to medical institutions. Further, a partial mediation effect of job satisfaction in the QWL-commitment relationship is highlighted, adding a new dimension to past studies. Intriguingly, each of the positive associations between QWL, job satisfaction, and commitment was negated and significantly moderated by the fear of COVID-19 experienced by the medical teaching fraternity. The findings offer practical implications to the stakeholders (Ministry of Health and Family Welfare, Department of Higher Education, Government of India, and State Governments) in enriching the QWL, job satisfaction, and medical teachers' commitment induced by psychological stress, anxiety, role conflict, post-traumatic stress disorder, and fear of COVID-19 in the global pandemic.
ABSTRACT
Background: Mucormycosis is a deadly fungal infection that emerges in patients affected with COVID-19. All fungal illnesses are caused by dysregulated adaptive immunity, but Myeloid-derived suppressor cells (MDSC) have added a new di-mension to the chronic inflammatory response. Objective(s): We attempted to enumerate the MDSC immune response in rhino-orbital mucormycosis patients before and after treatment and compared the data with healthy control. Method(s): A total of 3 ml of blood samples were taken in an EDTA vial from 20 patients with mucormycosis and 20 age-matched healthy control. A second blood sample was collected to examine the immune system post three months of treatment. Mycological identification was performed on nasal crust retrieved aftersurgery using KOH/culture.The expression of the MDSC marker was analyzed by immunostaining with the antibodies against CD14, HLA-DR, CD11b, CD33, CD66 (Biolegend). Flu-orescence profiles were recorded by Flow Cytometer (BD FACSAria TM III) and analyzed by Flow Jo s oftware (BD Biosciences). The percentage of positive cells is used to express the results.The GraphPad Prism (version 8, GraphPad s oftware, LaJolla, CA, USA) was used to analyze the data. All of the results were considered significant when P <.05. Result(s): All of the patients tested positive for Rhizopus arrhizus, which was confirmed by the culture. The percentages of Monocytic-MDSC (mMDSC: CD14 + HLA-DR-/low) cells were significantly high in patients compared to healthy control. In post-3-month treatment, the percentages of mMDSC were found significantly low and comparable with healthy control. Granulocytic MDSC (gMDSC: HLA-DR-/low CD33 + CD11b + CD66 +) cell population was higher in patients compared with healthy control and patients with post-3-month treatment. Conclusion(s): MDSC regulates T cells and other immune cells with a different mode of action. The findings in this study imminently indicatethe mechanism of immunedysregulation involvingMDSCpathways inmucormycosis andprovide evidence that restoration of immune balance causes reduction of MDSCcells may be considered a therapeutic option for long-term benefit.
ABSTRACT
Understanding of the genetic basis underlying inflammatory disorders has progressed in recent years. Contribution of proinflammatory cytokines, human leukocyte antigen (HLA), and non-HLA polymorphisms in the pathogenesis of several autoimmune and immune-mediated inflammatory disorder is critical. HLA plays a central role in disease pathology. Harmful stimuli triggering the signaling mechanisms including nuclear factor-kappa B pathway, Janus kinase-signal transducer and activator of transcription pathway, and mitogen-activated protein kinase pathway results in the release of inflammatory mediators. From acute to chronic inflammation, the etiology of various inflammatory disorders is poorly understood. Inflammatory disorder such as COVID 19 is a devastating havoc to the world. As we reach the end of 2020, >1 million people have succumbed to death worldwide. Disease-manifesting clinical features include mild to severe pneumonia, loss of respiratory function progressing to acute respiratory distress syndrome with occasional multiorgan failure. Cytokine storm, decreased T cell count, and insufficient immune response are conducive issues to COVID 19 pandemic. Varied immune responses to the same antigen across different individuals determine the genetic perspective of disease susceptibility. Through genome-wide association studies, next-generation sequencing and other genetic techniques, several genetic risk loci associated with various inflammatory diseases such as inflammatory bowel disease, psoriasis, sclerosis, and systemic lupus erythematosus (SLE) have been identified. Dysregulated inflammatory pathways, gene mutation, or elevated cytokine level may lead to the disease progression. However, the production of autoantibodies against the nuclear antigens is a hallmark of diseases like SLE and rheumatoid arthritis. Moreover, environmental factors like smoking also increase the risk of inflammatory disorders. Understanding the functional aspects of casual genetic factors underlying the disease pathogenesis greatly facilitates the ability to identify the therapeutic targets relevant to disease. The current chapter deals with the idea of genetic perspective associated with various inflammatory disorders and their potential therapeutic targets along with the factors contributing to disease susceptibility. © 2022 Elsevier Inc. All rights reserved.
ABSTRACT
OBJECTIVE: To study the utility of Galactomannan (GM) antigen as a screening marker for diagnosing invasive pulmonary aspergillosis (IPA) in coronavirus disease 2019 (COVID-19) patients. PATIENTS AND METHODS: The serum samples from patients with severe COVID-19 diseases admitted to the Critical Care Unit were collected on the 5th day of admission for GM screening. The samples were analysed by enzyme linked immune sorbent assay (ELISA) and GM index of more than 1 was considered as positive. All GM positive patients were serially followed until discharge or death. RESULTS: The GM was raised in serum of 12 out of 38 patients, indicating an incidence of possible COVID-19 associated IPA (CAPA) in 31.57% of patients. The median age of these CAPA patients was 56.5 years, males were significantly more affected than females. The inflammatory marker serum ferritin was raised in all 12 patients (median value of 713.74 ng/ml), while IL-6 was raised in 9 patients (median value of 54.13 ng/ml). None of these patients received antifungals. Their median length of hospital stay was 20 days (IQR: 12, 34 days). All these patients succumbed to the illness. CONCLUSIONS: The serum GM appears to be sensitive diagnostic tool to identify early IPA in COVID-19 patients and pre-emptive antifungal therapy could play a role in salvaging these patients.