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かぐらおか 第172号
Get PDF平成30年度入学生への学長挨拶 2/ 医学教育の昔と今 14/ 病院長挨拶｢働きがいのある職場の構築｣ 15/ 教授就任のご挨拶 16/ 教授就任のご挨拶 17/ 旭川医科大学に入学してもう4ヶ月 18/ 旭川医科大学に入学して 18/ 旭川医科大学に入学して19 / 旭川医科大学に入学して 19/ 旭川医科大学に入学して 20/ 医学生として地域と向き合うこと 20/ 旭川医科大学に入学して 21/ 旭川医科大学に入学して 21/ 旭川医科大学に入学して 22/ 平成30年度入学式を挙行しました 23/ 平成30年度医学科・看護学科新入生合同研修会が実施されました 24/ 学生海外留学助成制度を利用して 26/ 学生海外留学助成制度を利用して 26/ アメリカで学んだこと 27/ 学生海外留学助成制度を利用して 27/ 医大祭2018｢医子奮迅｣を終えて 28/ 授業評価(平成29年度後期) 30/ 教員の異動 55/ 今後のスケジュール 55/ 第172号表紙 55
Lock-in transition of charge density waves in quasi-one-dimensional conductors: Reinterpretation of McMillan's theory
Get PDFWe investigated the lock-in transition of charge density waves (CDWs) in quasi-one-dimensional conductors, based on McMillan's free energy. The higher-order umklapp terms play an essential role in this study. McMillan's theory was extended by Nakanishi and Shiba to treat multiple CDW vectors. Although their theories were aimed at understanding CDWs in quasi-two-dimensional conductors, we applied them to the quasi-one-dimensional conductors, including K0.3MoO3, NbSe3, and m−TaS3, and confirmed its validity for these cases. Then we discussed our previous experimental result of o−TaS3, which revealed the coexistence of commensurate and incommensurate states. We found that the coexistence of multiple CDW vectors is essential for the lock-in transition to occur in o−TaS3. The even- and odd-order terms in the free energy play roles for amplitude development and phase modulation, respectively. Moreover, consideration of the condition of being commensurate CDWs allowed us to relate it with that of the weak localization in random media
Thrombin-Induced Responses Via Protease-Activated Receptor 1 Blocked by the Endothelium on Isolated Porcine Retinal Arterioles
Get PDFPURPOSE:
Thrombin, a serine protease, causes organ-specific responses to vessels. However, the mechanism by which thrombin affects the retinal microcirculation remains unclear. We examined the effects of thrombin on the retinal microvasculature and signaling mechanisms.
METHODS:
Porcine retinal arterioles were isolated, cannulated, and pressurized (55 cmH2O) without flow in this in vitro study. Videomicroscopy techniques recorded changes in diameter in the retinal arterioles in response to thrombin at concentrations ranging from 0.001 to 20 mU/ml.
RESULTS:
Extraluminal administration of thrombin induced concentration-dependent vascular responses, that is, vasoconstriction at low concentrations less than 5 mU/ml and vasorelaxation with high concentrations greater than 5 mU/ml. However, intraluminal administration of thrombin (5 mU/m) did not constrict the retinal arterioles; in denuded vessels, intraluminal administration constricted the retinal arterioles. Thrombin-induced vasoconstriction was significantly (p < 0.01) suppressed by pretreatment with a protein kinase C (PKC) inhibitor and a protease-activated receptor (PAR)-1 inhibitor but not by PAR-2 and PAR-4 inhibitors or denudation. A rho kinase (ROCK) inhibitor also suppressed thrombin-induced vasoconstriction (5 mU/ml) compared with sodium nitroprusside. Endothelial denudation and pretreatment with an endothelial nitric oxide (NO) synthase inhibitor suppressed vasorelaxation caused by a high concentration of thrombin.
CONCLUSIONS:
A low concentration of thrombin causes vasoconstriction of smooth muscles via PAR-1, PKC, and ROCK, and a high concentration of thrombin possibly causes vasorelaxation of the retinal arterioles via nitric oxide synthase activation in the endothelium. The vascular endothelium might block signaling of thrombin-induced vasoconstriction in the retinal arterioles when administered intraluminally.博士（医学）旭川医科大
Targeting phosphorylated p53 to elicit tumor-reactive T helper responses against head and neck squamous cell carcinoma
Get PDFThe human T cell receptor is capable of distinguishing between normal and post-translationally modified peptides. Because aberrant phosphorylation of cellular proteins is a hallmark of malignant transformation, the expression of the phosphorylated epitope could be an ideal antigen to combat cancer without damaging normal tissues. p53 activates transcription factors to suppress tumors by upregulating growth arrest and apoptosis-related genes. In response to DNA damage, p53 is phosphorylated at multiple sites including Ser33 and Ser37. Here, we identified phosphorylated peptide epitopes from p53 that could elicit effective T helper responses. These epitope peptides, p5322-41/Phospho-S33 and p5322-41/Phospho-S37, induced T helper responses against tumor cells expressing the phosphorylated p53 protein. Moreover, chemotherapeutic agents augmented the responses of such CD4 T cells via upregulation of phosphorylated p53. The upregulation of phosphorylated p53 expression by chemotherapy was confirmed in in vitro and xenograft models. We evaluated phosphorylated p53 expression in the clinical samples of oropharyngeal squamous cell carcinoma and revealed that 13/24 cases (54%) were positive for phosphorylated p53. Importantly, the lymphocytes specific for the phosphorylated p53 peptide epitopes were observed in the head and neck squamous cell cancer (HNSCC) patients. These results reveal that a combination of phosphorylated p53 peptides and chemotherapy could be a novel immunologic approach to treat HNSCC patients