Juvenile nasopharyngeal angiofibroma (JNA) is the most common benign tumor of the nasopharynx. For reasons unknown, this tumor is found almost always in male population. However, site of origin of JNA is still an enigma. Previously, JNA was considered to arise from the superior aspect of sphenopalatine foramen. Over last decade, the vidian canal was considered to be the more specific and likely site of origin. However, based on our observations, we believe this hypothesis to be anomalous as it does not explain major blood supply, pattern of skull base erosion in early stage of tumor and newer studies on electron microscopic and immunopathological findings. To explain these anomalies, we hypothesize the site of origin to be palato-vaginal canal.Outbreaks of influenza infections in the past have severely impacted global health and socioeconomic growth. Antivirals and vaccines are remarkable medical innovations that have been successful in reducing the rates of morbidity and mortality from this disease. However, the relentless emergence of drug resistance has led to a worrisome increase in the trend of influenza outbreaks, characterized by worsened clinical outcomes as well as increased economic burden. This has prompted the need for breakthrough innovations that can effectively manage influenza outbreaks. This article provides an insight into a novel hypothesis that describes how the integration of nanomedicine, with the development of drugs and vaccines can potentially enhance body immune response and the efficacies of anti-viral therapeutics to combat influenza infections.Necroptosis is emerging among possible mechanisms underlying cell death in neurodegenerative diseases. In this line, we hypothesize that necroptosis might be implicated in neuronal cell death in amyotrophic lateral sclerosis (ALS). To support this hypothesis, we hereby provide pilot data as well as some findings from the literature about the expression of key markers of the necroptotic pathway in ALS. Our preliminary data indicate the upregulation of key markers of necroptosis activation in lower motor neurons of the spinal cord. These human-derived data combined with some clinical and preclinical findings support our hypothesis testing the involvement of necroptosis in lower motor neurons death in ALS patients. These results pave the way to deepen the role of necroptosis in ALS using both preclinical and clinical approaches. If confirmed, this hypothesis might raise new interventional strategies to alleviate neurodegenerative process in ALS.The factors that may contribute to a COVID-19 patient remaining in the asymptomatic stage, or to the infection evolving into the more serious stages are examined. In particular, we refer to the TMPRSS2 expression profile, balance of androgen and estrogen, blood group-A and/or B, nonsynonymous mutations in ORF3, and proteins NS7b and NS8 in SARS-CoV-2. Also, we review other factors related to the susceptibility and pathogenicity of SARS-CoV-2.In this paper, we raise the hypothesis that Methylene Blue may be a treatment option for Corona Virus Disease of 2019 specially when combined with Non Steroid Anti-Inflammatory Drugs. In previous publications including ours, the role of kininogen system has been postulated. A correlation between clinical findings of the disease and this mechanism has been drawn to denote a pivotal role of kininogen-kallikrein system in pathophysiology of the disease. Therein the possible role of Icatibant, Ecallantide and Aprotinin in the treatment of this disease has been raised. Here we want to emphasize on an important post-receptor mechanism of bradykinin that is Nitric Oxide. We came to this aim because we found out how access to these novel treatment nominees may be expensive and unaffordable. For this reason we are focusing on possible role of an old albeit "mysterious" drug namely Methylene Blue. This medication may abort effects of Bradykinin by inhibition of Nitric Oxide synthase inhibitor and promote oxygen saturation while it is inexpensive and ubiquitously accessible. Clinical studies cannot be over emphasized.Perioperative neurocognitive disorders (PND) are highly prevalent after surgery, especially in aged patients. PND results in long-term morbidity and mortality with unclear pathophysiologic mechanisms.  https://www.selleckchem.com/products/mrtx0902.html  As a key hallmark of PND, surgery-induced neuroinflammation resulted from the invading of exogenous tracers into the cerebral parenchyma, causing hippocampal neuroinflammation and cognitive impairment. IL-32, with different isoforms, played a significant regulatory role in various inflammatory diseases. Its prevalence in peripheral circulating blood was closely associated with the central nervous system (CNS) diseases. Beyond that, specific subtype of IL-32 was reported to involve in the neuroinflammation regulation in cerebral ischemia impairment, multiple sclerosis, Alzheimer's Disease, and so on. Thus, we speculate that IL-32 may participate in the regulation of the surgery-induced neuroinflammation during the parthenogenesis of PND. The isoforms, spatio-temporal regulation of IL-32 may determine its pro- or anti-inflammation properties in parthenogenesis of PND. Therefore, IL-32 could be a putative therapeutic target for the prevention and reversal of PND in the future.The world is experiencing one of the most difficult moments in history with the COVID-19 pandemic, a disease caused by SARS-CoV-2, a new type of coronavirus. Virus infectivity is mediated by the binding of Spike transmembrane glycoprotein to specific protein receptors present on cell host surface. Spike is a homotrimer that emerges from the virion, each monomer containing two subunits named S1 and S2, which are related to cell recognition and membrane fusion, respectively. S1 is subdivided in domains S1A (or NTD) and S1B (or RBD), with experimental and in silico studies suggesting that the former binds to sialic acid-containing glycoproteins, such as CD147, whereas the latter binds to ACE2 receptor. Recent findings indicate that the ABO blood system modulates susceptibility and progression of infection, with type-A individuals being more susceptible to infection and/or manifestation of a severe condition. Seeking to understand the molecular mechanisms underlying this susceptibility, we carried out an extensive bibliographic survey on the subject.