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Introduction: Aspergillus is one of the most ubiquitous airborne saprophytic fungi. Humans constantly inhale numerous conidia of this fungus. The conidia are normally eliminated in the immunocompetent host by innate immune mechanisms. With increase in the number of immunocompromised patients, there has been a dramatic increase in severe and fatal invasive aspergillosis (IA). The present study was aimed to know the clinico-mycological profile of suspected pulmonary aspergillosis cases. Methods: The present study was a prospective study conducted over a period of 1 year in the department of microbiology in admitted cases with clinical suspicion of pulmonary aspergillosis. Samples such as sputum, bronchoalveolar lavage, endotracheal secretions, fine-needle aspiration or biopsy and blood (for serological analysis) were collected and processed as per standard protocol. Results: Over a period of 1 year, 89 cases were included in the study. Their mean age was 58.7 years. Majority were male (60.6%). The most common presentation was cough (89.9%), followed by chest pain (57.3%) and fever (56.2% most common chest X-ray finding was homogeneous haziness (40.4%). Fungal smear was positive in 55.1% and 61.8% showed fungal growth. Galactomannan (GM) and (1-3)-β-D glucan positivity were 56% and 83.3%, respectively. The mortality was observed in 21.4% of patients. Conclusions: The study demonstrated that GM assay and (1-3)-β-D glucan assay are useful diagnostic modalities with a high sensitivity and specificity for the detection of pulmonary aspergillosis in high-risk patients along with positive fungal culture. Thus, these tests are early markers for IA. [ABSTRACT FROM AUTHOR]

Pemphigus vulgaris (PV) is a potentially fatal autoimmune blistering disease characterised by cell‐cell detachment or acantholysis. The mechanisms which follow antibody (Ab) binding and culminate in acantholytic changes and skin/mucosal blistering have not been fully clarified. Current treatment strategies are not specific to PV pathophysiology and although life‐saving, harbour considerable side effects. We aimed to systematically assess the molecules amenable to targeted treatments that follow Ab binding and are associated with PV acantholysis. The resulting scoping review was conducted under PRISMA‐ScR guidelines with clear inclusion and exclusion criteria and focused specifically on kinases, caspases, proteases, hydrolytic enzymes and other molecules of interest postulated to take part in the pathophysiology of PV. The review process resulted in the identification of 882 articles, of which 56 were eligible for qualitative synthesis. From the included articles, the majority (n = 42) used PV‐IgG as the pathogenic agent, mainly via in vitro (n = 16) and in vivo (n = 10) models. Twenty‐five molecules were found to play a pathogenic role in PV, including uPA, ADAM10, EGFR, Src, PKC, cdk2, ERK, PLC, calmodulin, NOS, p38MAPK and caspase‐3. Selective inhibition of these molecules resulted in varying degrees of reduction in acantholysis and blistering. The pathogenic molecules identified in this review represent potential candidates for clinical translation. [ABSTRACT FROM AUTHOR]