No abstract

A high prevalence of advanced hepatic fibrosis was observed in patients with hypertension. Hypertension was an independent risk factor, and creatinine level and SGLT2i were divergence variables for advanced hepatic fibrosis. Thus, hypertension with chronic kidney injury may exacerbate hepatic fibrosis, while SGLT2i treatment may ameliorate hepatic fibrosis.

As an approach to the mechanism of myalgia and myositis observed frequently in human influenza, virological and morphological studies were carried out on experimental influenza in mice. Influenza virus A/PR8/34 (HoNi) was inoculated by the intranasal or intramuscular route. Muscle was examined histologically, by electron microscopic and immunofluorescent techniques. Virus isolation was also carried out from muscle, lung, spleen and blood. Myositis was induced predominantly when virus was inoculated into the hamstring muscles of young mice (three-week-old, DDy strain). In mice inoculated intranasally, myositis was not observed. Significant changes in muscle were observed neither in congenitally athymic nude mice inoculated with active virus nor in DDy mice inoculated with inactivated virus. On the other hand, the degree of myositis in adult mice (seven-week-old) was milder than that in younger mice. Myositis developed from the epimydium surrouding muscle cells, and healed approximately 14th days after inoculation. In spite of obviousmyositis, no evidence for multiplication of virus in muscle was obtained by virus isolation and immunofluorescent studies. The virus was stained by fluorescent antibody method mainly in fibroblasts and adipose tissues near muscle cells. A similar outcome was seen in the muscle of nude mice. Thus, host factors such as age, species and immune system might play a role in the susceptibility of muscle to influenza virus. The results obtained from these studies suggest that viral toxicity and T cell function, rather than the virus itself, may induce inf luenzal myositis.

No abstract

No abstract