The dataset presented here was created by combining surveys conducted by Open Sourcing Mental Illness, a non-profit organization, from 2017 to 2021. The primary objective of the surveys was to assess the prevalence of mental health concerns among individuals employed in the technology sector and to gauge their attitudes toward mental health in the workplace. The dataset is filtered to include only those respondents with a primary tech role, and descriptive questions are removed, ensuring data consistency and validity of survey responses for effective analysis.
View Article and Find Full Text PDFFront Bioeng Biotechnol
October 2023
Type I interferon-beta (IFN-β) is a crucial component of innate and adaptive immune systems inside the host. The formation of bacterial biofilms on medical implants can lead to inflammatory diseases and implant failure. Biofilms elicit IFN-β production inside the host that, in turn, restrict bacterial growth.
View Article and Find Full Text PDFBackground Smartphone applications have become popular tools in clinical educational environments, particularly because they enhance learning in any setting through their accessibility. Despite students utilizing these apps in their daily learning, Pakistan's medical education system has yet to strongly endorse them. Given the rising usage of medical applications among clinical year medical students and the wide range of apps accessible on contemporary devices aimed specifically at the student population, there is a lack of literature addressing the use of these apps on clinical learning in low- and middle-income countries (LMIC) such as Pakistan.
View Article and Find Full Text PDFBackground: Congenital ISG15 deficiency is a rare autoinflammatory disorder that is driven by chronically elevated systemic interferon levels and predominantly affects central nervous system and skin.
Methods And Results: We have developed induced pluripotent stem cell-derived macrophages and endothelial cells as a model to study the cellular phenotype of ISG15 deficiency and identify novel treatments. ISG15 macrophages exhibited the expected hyperinflammatory responses, but normal phagocytic function.
Excessive inflammation is a major cause of morbidity and mortality in many viral infections including influenza. Therefore, there is a need for therapeutic interventions that dampen and redirect inflammatory responses and, ideally, exert antiviral effects. Itaconate is an immunomodulatory metabolite which also reprograms cell metabolism and inflammatory responses when applied exogenously.
View Article and Find Full Text PDFUlcerating skin lesions are manifestations of human ISG15 deficiency, a type I interferonopathy. However, chronic inflammation may not be their exclusive cause. We describe two siblings with recurrent skin ulcers that healed with scar formation upon corticosteroid treatment.
View Article and Find Full Text PDFAutosomal recessive (AR) complete interferon-γ receptor 1 (IFN-γR1) deficiency, also known as one genetic etiology of Mendelian susceptibility to mycobacterial disease (MSMD), is a life-threatening congenital disease leading to premature death. Affected patients present a pathognomonic predisposition to recurrent and severe infections with environmental mycobacteria or the bacillus Calmette-Guérin (BCG) vaccine. Current therapeutic options are limited to antibiotic treatment and hematopoietic stem cell transplantation, however with poor outcome.
View Article and Find Full Text PDFActivation of signal transducer and activator of transcription 6 (STAT6) is a key signaling pathway in macrophage function, and is required for the so-called alternative (M2) activation of macrophages. Interleukin (IL)-4 and IL-13 are important M2 polarizing cytokines that act through STAT6 by inducing its phosphorylation and promoting transcription of STAT6-responsive genes. Inactivation of STAT6 signaling in macrophages has not been fully explored; however, a recent model suggests that inactivation of STAT6 signaling can occur via ubiquitination and proteasomal degradation.
View Article and Find Full Text PDFThe quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine.
View Article and Find Full Text PDF