Cellular and humoral immunity and IgG subclass distribution after omicron XBB.1.5 monovalent vaccination in Japan.

Background: Up to seven doses of coronavirus disease 2019 (COVID-19) mRNA vaccines (BNT162b2) were administered to Japanese healthcare workers, until February 2024. The monovalent Omicron XBB.1.

Humoral response against spike protein enhanced by fifth and sixth COVID-19 mRNA vaccine in the uninfected and infected subjects.

Antibody obtained by the coronavirus disease-19 (COVID-19) mRNA vaccine declines over time, and additional vaccinations are offered. It is not clear how repeated vaccination affects humoral immunity in uninfected individuals. We analyzed immunoglobulin G for spike protein (S-IgG) titers in COVID-19 uninfected and infected individuals vaccinated up to six times.

[A case of pulmonary Mycobacterium kansasii infection with pleural effusion, distinguished from pulmonary tuberculosis].

A case of pulmonary Mycobacterium kansasii infection with pleural effusion is very rare. We report a case of pulmonary Mycobacterium kansasii infection with pleural effusion, distinguished from pulmonary tuberculosis. A 44-year-old man presented to a clinic with a productive cough, sputum, and loss of appetite for several months.

[A clinical investigation of seven patients with pulmonary tuberculosis who developed mixed liver injury during oral anti-tuberculosis treatment].

Background: Liver injury is the most common and clinically significant adverse reaction to anti-tuberculosis drugs, sometimes resulting in a fatal outcome. It has been reported that liver injury induced by isoniazid and pyrazinamide, which has the potential to cause hepatocellular injury, has a risk of becoming severe; while an injury induced by rifampicin, which has the potential to cause cholestatic injury, rarely becomes severe. However, mixed liver injury has not been studied thoroughly.

Selective silencing of a mutant transthyretin allele by small interfering RNAs.

Familial amyloidotic polyneuropathy (FAP) is a hereditary systemic amyloidosis caused by dominantly acting missense mutations in the gene encoding transthyretin (TTR). The most common mutant TTR is of the Val30Met type, which results from a point mutation. Because the major constituent of amyloid fibrils is mutant TTR, agents that selectively suppress mutant TTR expression could be powerful therapeutic tools.