Fabry病の分子遺伝学的研究

金沢大学医学部研究課題/領域番号:02770547, 研究期間(年度):1990出典：研究課題「Fabry病の分子遺伝学的研究」課題番号02770547（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-02770547/）を加工して作

ヒト21番染色体の分子遺伝学的研究:ダウン症候群の病因へのアプローチ

金沢大学医学部研究課題/領域番号:63770639, 研究期間(年度):1988出典：研究課題「ヒト21番染色体の分子遺伝学的研究:ダウン症候群の病因へのアプローチ」課題番号63770639（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-63770639/）を加工して作

ヒト21番染色体の分子遺伝学的研究:ダウン症候群の病因へのアプローチ

金沢大学医学部研究課題/領域番号:01770647, 研究期間(年度):1989出典：研究課題「ヒト21番染色体の分子遺伝学的研究:ダウン症候群の病因へのアプローチ」課題番号01770647（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） （https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-01770647/）を加工して作

Acinar Cell Carcinoma of the Pancreas with Colon Involvement

We report a case of acinar cell carcinoma of the pancreas with colon involvement that was difficult to distinguish from primary colon cancer. A 60-year-old man was admitted with a 1-month history of diarrhea. Contrast-enhanced computed tomography (CT) revealed a large tumor (10.6×11.6 cm) at the splenic flexure of the colon. Colonoscopy showed completely round ulcerative lesions, and biopsy revealed poorly differentiated adenocarcinoma. Left hemicolectomy, resection of the jejunum and pancreas body and tail, and splenectomy were performed based on a diagnosis of descending colon cancer (cT4N0M0, stage IIB), and surgery was considered to be curative. Diagnosis was subsequently confirmed as moderately differentiated acinar cell carcinoma of the pancreas by immunohistochemical staining (pT3N0M0, stage IIA). Multiple liver metastases with portal thrombosis were found 8 weeks postoperatively. Despite combination chemotherapy with oral S-1 and gemcitabine, the patient died of hepatic failure with no effect of chemotherapy 14 weeks postoperatively. Correct diagnosis was difficult to determine preoperatively from the clinical, CT, and colonoscopy findings. Moreover, the disease was extremely aggressive even after curative resection. Physicians should consider pancreatic cancer in the differential diagnosis of similar cases

Continuing mind for primary care medicine as total family care mailing list (TFC-ML) group

There were historically two great doctors for primary care (PC) medicine in Japan. They are Dr. Shigeaki Hinohara and Dr. Yoshikazu Tasaka. Tasaka was always active in medical treatment, organizational management, postgraduate education, and information dissemination using the Internet, and started Total Family Care Mailing List (TFC-ML) in 1998. TFC-ML included medical information with his comments every day for long. Even after his death in 2007, TFC-ML activity has been continued by many voluntary PC physicians. His TFC mind has been transmitted to future PC physicians. His inspiration may often come to TFC members for better total family care

Role of interleukin 6 for differential responsiveness of naive and memory CD4+ T cells in CD2-mediated activation

金沢大学大学院医学系研究科血管病態制御学The present study was undertaken to elucidate different requirements for CD2-mediated activation of naive (CD45RO-) and memory (CD45RO+) CD4+ T cells. A mitogenic combination of anti-CD2 (anti-T112 and anti-T113) mAbs could effectively induce the proliferation of memory CD4+ T cells even in the absence of monocytes. In marked contrast, naive CD4+ T cells did not disclose any proliferative responses to antiCD2 mAbs, when monocytes were absent in culture. This differential responsiveness of naive and memory CD4+ T cells appeared to be related largely to a difference in IL-6 - producing ability between both populations. IL-6 among monocyte-derived cytokines could correct unresponsiveness of naive CD4+ T cells to anti-CD2 stimulation. Unlike naive CD4+ T cells, memory CD4+ T cells produced IL-6 by themselves, with its mRNA being expressed on anti-CD2 stimulation. Anti-IL-6R mAb significantly inhibited proliferation of memory CD4+ T cells seen in the anti-CD2-stimulated cultures without monocytes, indicating the involvement of their own production of IL-6 in CD2-mediated activation. The results suggest an essential role of IL-6 for triggering of CD4+ T cells via the CD2 molecule