Theoretical study of NMR relaxation due to rattling phonons

We calculate the NMR relaxation rate due to quadrupolar coupling of the nucleus to a local, strongly anharmonic phonon mode. As a model potential for a rattling motion we consider a square-well potential. We calculate the free phonon Green's function analytically and derive the low and high temperature limits of the NMR relaxation rate. It is shown that the temperature dependence of the NMR relaxation rate possesses a peak in contrast to harmonic phonons but in qualitative agreement with a recent NMR study on KOs2O6. We discuss the influence of phonon renormalization due to electron-phonon interaction.Comment: 5 pages, 3 figures, SNS2007 (Sendai, Japan) conference proceedings, accepted for publicatio

小細胞肺癌培養細胞株N231/CDDPにおけるシスプラチン耐性機構の検討

取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1011号,学位授与年月日：平成3年9月30日,学位授与年：199

Detection of EGFR T790M Mutation in Pericardial Effusion from a Non-Small Cell Lung Cancer Patient with Erlotinib Therapy

We report the case of a Japanese male with epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI)-sensitive lung adenocarcinoma, who had an EGFR mutation and presented in the emergency department with acute cardiac tamponade as the recurrence during EGFR-TKI therapy. We could detect a second mutation, T790M in exon 20 in the pericardial effusion. This is the first report to detect the resistant mutation T790M in pericardial effusion. We suggest that the pericardial effusion may therefore be useful as surrogate tissue for detecting EGFR mutation

肺癌細胞のアポトーシスにおける脂質メディエーターの役割

金沢大学附属病院1、肺癌細胞株におけるアポトーシスの検討肺癌細胞株PC-9及びそのシスプラチン耐性細胞株PC-9/CDDPを用い実験を行った。それぞれの細胞株をシスプラチンに2時間接触させて後、24時間培養し、細胞を回収した。シスプラチンにより誘導されるアポトーシスはPC-9において有意に多く、さらに脂質メディエーターであるトロンポキサンA2(TXA2)拮抗薬、合成酵素阻害薬を併用したところ、シスプラチンにより誘導されるアポトーシスは有意に増強した。即ち、TXA2の機能を阻害する事でシスプラチン誘導細胞死が増加した。血小板活性化因子(PAF)拮抗薬についても同様の結果を得た。2、細胞死に関するプロテアーゼの解析TXA2拮抗薬の併用により、シスプラチン誘導アポトーシスの増強が確認されたので、細胞死に関わるシステインプロテアーゼであるカズパーゼについて検討した。ウェスタンブロット法を用い、蛋白量を検討したところ、TXA2拮抗薬の処理によってカスパーゼ2が誘導された。PAF拮抗薬ではカスパーゼ1が誘導された。3、Mitogen-activated proteinキナーゼ(MAPK)の検討TXA2拮抗薬、PAF拮抗薬のシスプラチン誘導細胞死の増強機序を解析するために脂質メディエーターと深く関わりを持つMAPKが果たす役割を検討した。活性化状態のMAPKを確認する抗リン酸化抗体を用いウェスタンブロット法で検討したが、TXA2拮抗薬、PAF拮抗薬、共に影響を与えなかった。以上の結果から、脂質メディエーターであるTXA2、PAFを阻害する事によりシスプラチン誘導アポトーシスが増強し、これはカズパーゼ蛋白を誘導する事に起因すると考えられた。研究課題/領域番号:10770264, 研究期間(年度):1998 – 1999出典：「肺癌細胞のアポトーシスにおける脂質メディエーターの役割」研究成果報告書　課題番号10770264（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-10770264/)を加工して作

Desensitization of delayed-type hypersensitivity in mice: suppressive environment

The systemic injection of high doses of antigen into a preimmunized animal results in transient unresponsiveness of cell-mediated immune responses. This phenomenon is known as desensitization. Serum interleukin 2 (IL-2) activity was found transiently in desensitized mice at 3 h after the antigen challenge. These mice could not reveal antigen nonspecific delayed-type hypersensitivity (DTH) 1 d after the challenge. Specific suppression of DTH was observed at later stages. Sera from 3 h desensitized mice showed suppressive effects on DTH in preo immunized mice. Administration of recombinant IL-2 into preimmunized mice led to the failure of development of DTH to antigens. These observations suggest that IL-2 plays an important role in the suppressive environment

副鼻腔転移をきたした肺腺癌の1例

金沢大学大学院医学系研究科細胞移植学講座Background. Even though the head and neck are common metastatic sites in lung cancer patients, paranasal metastases are rare. We report a patient with lung cancer who had paranasal sinus metastases. Case. A 56-year-old man with lung cancer presented with nasal hemorrhage 1.5 years after the initiation of chemotherapy. On CT, mass shadows were seen in bilateral frontal sinuses, maxillary antra, the left ethmoidal sinus, the sphenoidal sinus, and the nasal cavity. Biopsies of the lesion in the nasal cavity showed adenocarcinoma, confirming that the lesions in the paranasal sinuses were lung cancer metastases. The cranial MRI done at the time of the first admission was reviewed, and a small nodule was found in left ethmoidal sinus. Conclusion. Paranasal sinus metastases are found in a patient with NSCLC who don\u27t have symptoms related to the paranasal sites. Paranasal sites should be carefully evaluated in patients with advanced NSCLC. © 2008 The Japan Lung Cancer Society.　　　[背景]肺癌の頭頸部への転移は比較的高い頻度で認められるが、副鼻腔転移は極めて稀である。今回われわれは、経過中に副鼻腔転移を認めた症例を経験した。[症例]症例は56歳、男性。1年半にわたる肺癌治療経過中に鼻出血が出現した。頭部CTでは両側前頭洞、左側篩骨洞・上顎洞・鼻腔にかけて腫瘤性病変を認めた。生検による病理組織像は原発巣と同一の腺癌であった。初回入院時の頭部MRIをレトロスペクティブに検討したところ、左篩骨洞に腫瘤陰影があり、初診時にすでに副鼻腔転移を認めていたものと考えられた。[結論]副鼻腔転移は治療経過中に認められる報告が多いが、初診時にも無症状の副鼻腔転移を有する場合があり、慎重に診断して観察する必要がある。全文公開20101

MUTYH Gln324His gene polymorphism and genetic susceptibility for lung cancer in a Japanese population

<p>Abstract</p> <p>Background</p> <p>Genetic polymorphisms of DNA repair enzymes in the base excision repair (BER) pathway, may lead to genetic instability and lung cancer carcinogenesis. We investigated the interactions among the gene polymorphisms in DNA repair genes and lung cancer.</p> <p>Methods</p> <p>We analyzed associations among <it>OGG1 </it>Ser326Cys and <it>MUTYH </it>Gln324His gene polymorphisms in relation to lung cancer risk using PCR-RFLP. The study involved 108 lung cancer patients and 121 non-cancer controls divided into non-smokers, smokers according to pack-years smoked in Japanese.</p> <p>Results</p> <p>The results showed that the <it>MUTYH His/His </it>genotype compared with <it>Gln/Gln </it>genotype showed an increased risk for lung cancer (adjusted odds ratio [OR] 3.03, confidence interval [95%CI], 1.31–7.00, p = 0.010), whereas there was no significant increase for the <it>Gln/His </it>genotype (adjusted OR 1.35, 95%CI 0.70–2.61, p = 0.376). The <it>MUTYH His/His </it>genotype was at a borderline increased risk for both adenocarcinoma and squamous cell carcinoma (adjusted OR 2.50, 95%CI 0.95–6.62, p = 0.065 for adenocarcinoma; adjusted OR 3.20, 95%CI 0.89–11.49, p = 0.075 for squamous cell carcinoma, respectively). However, the <it>OGG1 Ser/Cys </it>or <it>Cys/Cys </it>genotypes compared with the <it>Ser/Ser </it>genotype did not have significantly increased risk for lung cancer, containing either adenocarcinoma or squamous cell carcinoma. The joint effect of tobacco exposure and the <it>MUTYH His/His </it>genotype compared with the <it>Gln/Gln </it>genotype showed a significant association with lung cancer risk in smokers, and there was not significantly increased in non-smokers (adjusted OR 3.82, 95%CI 1.22–12.00, p = 0.022 for smokers; adjusted OR 2.60, 95%CI 0.60–11.25, p = 0.200 for non-smokers, respectively). The effect of tobacco exposure and the <it>OGG1 </it>Ser326Cys showed also no significant risk for lung cancer.</p> <p>Conclusion</p> <p>Our findings suggest that the <it>MUTYH </it>Gln324His polymorphism appear to play an important role in modifying the risk for lung cancer in the Japanese population.</p