Nocardia seriolae causes chronic nocardiosis in various marine and freshwater aquatic animals; however, grouper species have rarely been investigated. This study evaluated the pathogenicity of nocardiosis following N. seriolae infection in the orange‐spotted grouper Epinephelus coioides. Nine identified genetic isolates of N. seriolae were tested in vivo using the intraperitoneal method and observed daily for 35 days. The most virulent isolate was then used to evaluate transmission through different routes (intraperitoneal IP, intramuscular IM, oral OR, and immersion IS) in the same fish model and was observed daily for 42 days. The results showed mild variation in virulence among N. seriolae isolates. AOD107132‐2 K and OT103003‐N11 strains displayed the highest and lowest risk virulence, respectively, based on the accumulation and kinetics of mortality. IM and IP administrations showed an early phase response with early mortality by 5 dpc (30%–100%), while slower kinetics of nocardiosis occurred in the OR and IS routes with slow mortality at 35 dpc (4%–8%). Histopathology revealed typical granulomas, confirming the progression of nocardiosis in the diseased fish. These results provide the basis for further studies on the virulence profile of N. seriolae in Taiwan and a well‐suited route of administration in orange‐spotted groupers for further prevention development.

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Type 1 diabetes mellitus is a degenerative disease that often occurs, that is caused by impaired insulin production and damage to the cell β pancreas. This disease is characterized by increased levels of glucose in the blood, which interferes with insulin production in the body. Rattus norvegicus was used as an animal model of diabetes mellitus with streptozotocin 20 mg/kg and five experimental groups with three therapeutic doses of 2.3 mg/kg, 4.6 mg/kg, and 9.2 mg/kg. The total flavonoid equivalent contained in Ulomoides dermetoides was 1.48 g/mL. Immunohistochemistry results showed therapeutic doses of 2.3 mg/kg and 4.6 mg/kg can reduce TNF-α expression in kidney tissue, but a dose of 9.2 mg/kg had no effect when compared to the positive control. Necrosis and protein deposits were seen in the renal tubules in the four treatment groups compared with the negative control. A dose of 2.3 mg/kg was the best treatment with high TNF-α expression and can repair kidney tissues.