Respiratory syncytial virus activates epidermal growth factor receptor to suppress interferon regulatory factor 1-dependent interferon-lambda and antiviral defense in airway epithelium.

Respiratory syncytial virus (RSV) persists as a significant human pathogen that continues to contribute to morbidity and mortality. In children, RSV is the leading cause of lower respiratory tract infections, and in adults RSV causes pneumonia and contributes to exacerbations of chronic lung diseases. RSV induces airway epithelial inflammation by activation of the epidermal growth factor receptor (EGFR), a tyrosine kinase receptor.

Distinguishing primary from secondary Δ(4) -3-oxosteroid 5β-reductase (SRD5B1, AKR1D1) deficiency by urinary steroid analysis.

Objective: Deficiency of Δ(4) -3-oxosteroid 5β-reductase (5β-reductase), a bile acid synthesis disorder, presents findings of neonatal cholestasis and hyper-3-oxo-Δ(4) bile aciduria. The 5β-reductase enzyme participates in not only bile acid synthesis but also hepatic steroid metabolism. Deficiency of 5β-reductase includes 2 types: primary deficiency, with an SRD5B1 gene mutation; and secondary deficiency, lacking a mutation.

EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production.

Airway epithelial cells are the primary cell type involved in respiratory viral infection. Upon infection, airway epithelium plays a critical role in host defense against viral infection by contributing to innate and adaptive immune responses. Influenza A virus, rhinovirus, and respiratory syncytial virus (RSV) represent a broad range of human viral pathogens that cause viral pneumonia and induce exacerbations of asthma and chronic obstructive pulmonary disease.

Sequential elevation of autoantibodies to thyroglobulin and glutamic acid decarboxylase in type 1 diabetes.

We have previously reported the high levels of glutamic acid decarboxylase 65 autoantibodies (GAD65A) in patients with type 1 diabetes and autoimmune thyroid disease. Here we describe a 32-year-old Japanese female with a thirteen-year history of type 1 diabetes whose levels of GAD65A were elevated just after the emergence of anti-thyroid autoimmunity. At 19 years of age, she developed diabetic ketoacidosis and was diagnosed with type 1 diabetes.

Moderate to severe nausea in radioactive iodine (RAI) therapy is associated with the RAI dose per body weight and was not prevented by ramosetron.

To retrospectively analyze the individual risk factors for radioactive iodine (RAI)-associated nausea and vomiting, and to examine the anti-emetic effect of ramosetron (5-hydroxytryptamine-3 receptor antagonist) in RAI therapy. Patients with differentiated thyroid carcinoma who underwent first-time RAI therapy at Nagasaki University Hospital between January 2009 and 2013 were included (N = 81). As a routine treatment, all patients were administered 30 mg of domperidone per day.