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4 results on '"Kashiwagi-Takayama, Risa"'

1. Myocardial fat accumulation is associated with cardiac dysfunction in patients with type 2 diabetes, especially in elderly or female patients: a retrospective observational study

Author

Kashiwagi-Takayama, Risa, Kozawa, Junji, Hosokawa, Yoshiya, Kato, Sarasa, Kawata, Satoshi, Ozawa, Harutoshi, Mineo, Ryohei, Ishibashi, Chisaki, Baden, Megu Y., Iwamoto, Ryuya, Saisho, Kenji, Fujita, Yukari, Tamba, Sachiko, Sugiyama, Takuya, Nishizawa, Hitoshi, Maeda, Norikazu, Yamamoto, Koji, Higashi, Masahiro, Yamada, Yuya, Sakata, Yasushi, Matsuzawa, Yuji, and Shimomura, Iichiro

Published
2023
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2. Additional file 1 of Myocardial fat accumulation is associated with cardiac dysfunction in patients with type 2 diabetes, especially in elderly or female patients: a retrospective observational study

Author

Kashiwagi-Takayama, Risa, Kozawa, Junji, Hosokawa, Yoshiya, Kato, Sarasa, Kawata, Satoshi, Ozawa, Harutoshi, Mineo, Ryohei, Ishibashi, Chisaki, Baden, Megu Y., Iwamoto, Ryuya, Saisho, Kenji, Fujita, Yukari, Tamba, Sachiko, Sugiyama, Takuya, Nishizawa, Hitoshi, Maeda, Norikazu, Yamamoto, Koji, Higashi, Masahiro, Yamada, Yuya, Sakata, Yasushi, Matsuzawa, Yuji, and Shimomura, Iichiro

Abstract

Additional file 1: Table S1. Clinical characteristics of older and younger subgroups. Table S2. Clinical characteristics of female and male subgroups. Table S3. Clinical characteristics of patients with complete cases for multiple regression analysis (total). Table S4. Clinical characteristics of older and younger subgroups with complete cases for multiple regression analysis. Table S5. Clinical characteristics of female and male subgroups with complete cases for multiple regression analysis. Figure S1 Flowchart for the recruitment of the patients. Figure S2. Method for measuring myocardial CT values on non-contrasted CT images. Figure S3. Multiple logistic regression analyses (total).

Published
2023
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3. Inflammatory Cell Infiltration into Islets without PD-L1 Expression is Associated with the Development of Immune Checkpoint Inhibitor-Related Type 1 Diabetes in Genetically Susceptible Patients

Author

Kawata, Satoshi, primary, Kozawa, Junji, primary, Yoneda, Sho, primary, Fujita, Yukari, primary, Kashiwagi-Takayama, Risa, primary, Kimura, Takekazu, primary, Hosokawa, Yoshiya, primary, Baden, Megu Y, primary, Uno, Sae, primary, Uenaka, Rikako, primary, Namai, Kazuyuki, primary, Koh, Yoko, primary, Tomimaru, Yoshito, primary, Hirata, Haruhiko, primary, Uemura, Motohide, primary, Nojima, Satoshi, primary, Morii, Eiichi, primary, Eguchi, Hidetoshi, primary, Imagawa, Akihisa, primary, and Shimomura, Iichiro, primary

Published
2023
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4. Inflammatory Cell Infiltration Into Islets Without PD-L1 Expression Is Associated With the Development of Immune Checkpoint Inhibitor–Related Type 1 Diabetes in Genetically Susceptible Patients.

Author

Kawata, Satoshi, Kozawa, Junji, Yoneda, Sho, Fujita, Yukari, Kashiwagi-Takayama, Risa, Kimura, Takekazu, Hosokawa, Yoshiya, Baden, Megu Y., Uno, Sae, Uenaka, Rikako, Namai, Kazuyuki, Koh, Yoko, Tomimaru, Yoshito, Hirata, Haruhiko, Uemura, Motohide, Nojima, Satoshi, Morii, Eiichi, Eguchi, Hidetoshi, Imagawa, Akihisa, and Shimomura, Iichiro

Subjects
TYPE 1 diabetes, IMMUNE checkpoint proteins, GENE expression, PROGRAMMED death-ligand 1, ISLANDS of Langerhans, HYPERGLYCEMIA
Abstract

Immune checkpoint inhibitors (ICIs) could cause type 1 diabetes (T1D). However, the underlying mechanism remains unclear. We immunohistochemically analyzed pancreatic specimens from three individuals with ICI-related T1D, and their histopathological data were compared those from three patients who had received ICI therapy but did not develop T1D (non-T1D) and seven normal glucose-tolerant subjects as control subjects. All ICI-related T1D patients had susceptible HLA haplotypes. In ICI-related T1D, the β-cell area decreased and the α-cell area increased compared with non-T1D and control subjects. The number of CD3-positive cells around islets increased in ICI-related T1D and non-T1D compared with control subjects, while the number of CD68-positive cells around islets increased in ICI-related T1D compared with non-T1D and control subjects. The expression ratios of programmed death-ligand 1 (PD-L1) on islets decreased in non-T1D and almost completely disappeared in ICI-related T1D, while PD-L1 expression was observed in most cells of pancreatic islets in control subjects. This study, therefore, indicates that ICI therapy itself could reduce PD-L1 expression on islets in all subjects, which may be related to β-cell vulnerability. In addition, we showed that absence of PD-L1 expression on β-cells, genetic susceptibility, and infiltration of macrophages as well as T lymphocytes around islets might be responsible for T1D onset. ARTICLE HIGHLIGHTS: Immune checkpoint inhibitors (ICIs) could cause type 1 diabetes (T1D). However, the underlying mechanism remains unclear. Pancreatic histological findings of ICI-related T1D patients were compared with those of patients who had received ICI therapy but did not develop T1D (non-T1D) and control subjects. Programmed death-ligand 1 expression on islets decreased in non-T1D and almost completely disappeared in ICI-related T1D, while it was observed in control subjects. Patients with ICI-related T1D had T1D-susceptible HLA haplotypes and islet inflammation. ICIs may decrease programmed death-ligand 1 expression on islets, and its absence and additional islet inflammation in genetically susceptible patients can lead to development of T1D. [ABSTRACT FROM AUTHOR]

Published
2023
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