- 著者
- Hikaru Mamizu Takeshi Ohta Kensuke Yanai Ryo Yamazaki Maiko Mamizu Daisuke Ishikawa Hidenori Kawakami Toshiki Furukawa Takashi Ishida
- 出版者
- The Japanese Society of Internal Medicine
- 雑誌
- Internal Medicine (ISSN:09182918)
- 巻号頁・発行日
- pp.1302-22, (Released:2023-02-22)
- 参考文献数
- 22
We herein report a 75-year-old woman who presented with dyspnea and purpura. She was diagnosed with eosinophilic granulomatosis with polyangiitis (EGPA) based on axonal damage observed in the left tibial nerve and skin and lung pathologies. Lung pathology showed IgG4-positive plasma cells, considered a complication of IgG4-related disease (IgG4-RD). Computed tomography revealed thickening of the abdominal aorta and a poor contrast area in the left kidney, which was indicative of IgG4-RD. Steroid administration improved the IgG4-RD. However, the EGPA resisted treatment; therefore, immunosuppressive drugs and mepolizumab were administered. Refractory EGPA complicated with IgG4-RD showed different treatment responses for each organ.
- 著者
- Collins NIMAKO Yoshinori IKENAKA Yuko OKAMATSU-OGURA Jussiaea V. BARIUAN Atsushi KOBAYASHI Ryo YAMAZAKI Kumiko TAIRA Nobuhiko HOSHI Tetsushi HIRANO Shouta M. M. NAKAYAMA Mayumi ISHIZUKA
- 出版者
- JAPANESE SOCIETY OF VETERINARY SCIENCE
- 雑誌
- Journal of Veterinary Medical Science (ISSN:09167250)
- 巻号頁・発行日
- vol.83, no.3, pp.487-500, 2021 (Released:2021-04-03)
- 参考文献数
- 47
- 被引用文献数
- 1 4
Hepatic steatosis is known to precede a continuum of events that lead to hepatic metabolic dysfunction, inflammation and carcinogenesis. Recently, studies have linked xenobiotic exposures to hepatic steatogenesis and its associated metabolic disorders; however, the underlying mechanisms remain elusive. This study aimed to elucidate the mechanistic role of imidacloprid in the prevalence of high fat diet (HFD)-induced liver steatosis, using a C57BL/6J mice model. Mice (3 weeks old) were fed with HFD and treated with 0.6 mg/kg bw/day (one-tenth of the NOAEL) of imidacloprid through water or diet, for 24 weeks. In a controlled group, mice were fed with only HFD. At the end of the study, imidacloprid treatment significantly potentiated HFD-induced body weight gain in mice. Also, imidacloprid increased the liver weights of mice, with complimentary reductions in mesenteric and gonadal white adipose tissue weights. Histopathological analysis of liver revealed a drastic steatosis in imidacloprid treated mice. Following a real-time qPCR analysis, imidacloprid upregulated transcriptions of hepatic fatty acid biosynthesis-related transcription factors and genes. Imidacloprid also induced hepatic expression of the gene encoding pregnane X receptor; but had no significant effect on hepatic expressions of liver X receptor and aryl hydrocarbon receptor. The imidacloprid treatment further enhanced serum alanine aminotransferase levels but downregulated hepatic antioxidant mRNA expressions. Ultimately, this study suggested an imidacloprid-potentiation effects on prevalence of HFD-induced liver steatosis via transcriptional modulations of the hepatic FA biosynthesis pathway.