Nuclear Magnetic Resonance in Dilute Ni-Base Alloys

The nuclear magnetic resonance (NMR) of impurity nuclei have been observed in Ni-base alloys using a steady state method and a spin echo method. Firstly, measurments of the NMR frequency of the Cuv s , Niv 1, Cou y , Feu w and Mnu u nuclei in Ni alloys was measured as a function of temperature in the range from 4.2°K to 550°K, respectively. The temperature dependences of the internal fields are not identical to that of the magnetization of Ni host. The discrepancy depends on the hyperfine constant. Furthermore, the pressure dependence of their fields at 273°K in the range 1 to 8000 kg/cm2 has been measured with the result that the dl_nH_i/dP of Cuv s , Nv 1, Cou y and Mnu u nuclei in Ni alloys are 1.66×10{ w (kg/c㎡){ 1, 1.20×10{ v (kg/c㎡){ 1, 1.74×10{ w (kg/c㎡){ 1 and -3.32×10{ w (kg/cm2){ 1, respectively. It is found that the resonance frequency of the impurity nuclei is not proportional to the bulk magnetization even at constant volume. A brief discussion on mechanisms possible as the source of the exchange interaction is given.Article信州大学理学部紀要 4(1): 25-37(1969)departmental bulletin pape

Genetic Variation in the Testis-Specific GSG3/CAPZA3 Gene Encoding for the Actin Regulatory Protein in Infertile Males

ｱｸﾁﾝｷｬｯﾋﾟﾝｸﾞ蛋白質 GSG3/CAPZA3 は､受精可能な精子の形態形成に重要な役割を担っている｡GSG3/CAPZA3 遺伝子は､ｲﾝﾄﾛﾝﾚｽ遺伝子として哺乳類に保存され､ﾏｳｽにおいてﾐｯｾﾝｽ変異が精子の減少と形態異常を誘導し､雄性不妊症の原因となることが知られている｡日本人において男性不妊症と GSG3/CAPZA3 遺伝子多型の関係を調べるため､261人の男性不妊症患者と139人の妊孕性が確認された男性ﾎﾞﾗﾝﾃｨｱの遺伝子多型を調べた｡その結果､妊孕性が確認された男性ﾎﾞﾗﾝﾃｨｱの一人にｱﾐﾉ酸置換を伴う一塩基多型がﾍﾃﾛ接合型として検出された｡このことから､GSG3/CAPZA3 遺伝子には､他の精子細胞特異的ｲﾝﾄﾛﾝﾚｽ遺伝子に比べて遺伝子多型が極めてわずかしか存在しないことが示唆された｡The actin capping protein GSG3/CAPZA3 plays a physiologically important role in maintaining sperm architecture for fertilization. The GSG3/CAPZA3 gene is conserved in mammals and lacks introns. A missense mutation in the CAPZA3 gene in mice causes male infertility by reducing the concentration and changing the shape of sperm. To investigate possible associations between GSG3/CAPZA3 gene variations and impaired spermatogenesis in Japanese males, we screened for mutations in GSG3/CAPZA3 using DNA from 261 sterile male patients and 139 male volunteers who were fertile. A single nucleotide polymorphism(SNP)was found in one sample in the heterozygous state in the fertile male volunteers. The results indicate that compared with other germ-cell-specific intronless genes the change was restricted in GSG3/CAPZA3 protein

A Review of ERCC1 Gene in Bladder Cancer: Implications for Carcinogenesis and Resistance to Chemoradiotherapy

The excision repair cross-complementing group 1 (ERCC1) gene performs a critical incision step in DNA repair and is reported to be correlated with carcinogenesis and resistance to drug or ionizing radiation therapy. We reviewed the correlation between ERCC1 and bladder cancer. In carcinogenesis, several reports discussed the relation between ERCC1 single nucleotide polymorphisms and carcinogenesis in bladder cancer only in case-control studies. Regarding the relation between ERCC1 and resistance to chemoradiotherapy, in vitro and clinical studies indicate that ERCC1 might be related to resistance to radiation therapy rather than cisplatin therapy. It is controversial whether ERCC1 predicts prognosis of bladder cancer treated with cisplatin-based chemotherapy. Tyrosine kinase receptors or endothelial-mesenchymal transition are reported to regulate the expression of ERCC1, and further study is needed to clarify the mechanism of ERCC1 expression and resistance to chemoradiotherapy in vitro and to discover novel therapies for advanced and metastatic bladder cancer

Discovery of a TEKTIN-t/TEKT2 Gene Variant Encoding Sperm Flagellar Protein in Japanese Males

ﾃｸﾁﾝは､ﾀﾞｲﾆﾝとともに精子の鞭毛や繊毛の形成に関与したﾀﾝﾊﾟｸ質である｡ﾃｸﾁﾝには､ﾋﾄにおいて少なくとも6種類の遺伝子の存在が報告されている｡ﾃｸﾁﾝ遺伝子のうち､Tektin-t/Tekt2､Tekt3､もしくは Tekt4 が欠失することによって､精子の鞭毛が機能不全を起こし､なかでも Tektin-t/Tekt2 遺伝子の欠失は､雄性不妊症になることがﾏｳｽで示されている｡男性不妊症の原因にﾃｸﾁﾝ遺伝子の機能不全が関与することが予想される｡私たちは､ﾋﾄ TETIN-t/TEKT2 遺伝子の遺伝子多型と男性不妊症との関係について調べるため､282人の原因不明の男性不妊症患者と89人の妊孕性が確認された男性ﾎﾞﾗﾝﾃｨｱの遺伝子の解析を行った｡その結果､日本人男性不妊症患者に有意に検出される TETIN-t/TEKT2 遺伝子の変化は見られなかった｡これらの結果は､TETIN-t/TEKT2 は､日本人男性不妊症の原因遺伝子となる割合は非常に低くいことを示すとともに､今後の大規模な男性不妊症の原因となる遺伝子の解析に役に立つものと考えられる｡TEKTIN proteins contribute to the formation of cilia and flagella together with dynein. At least six types of TEKTIN genes have been reported in humans. The disruption of Tektin-t/Tekt2, Tekt3, or Tekt4 in mice causes sperm flagellar dysfunction, and Tektin-t/Tekt2 null male mice are infertile. To investigate the possible association between variations in TEKTIN-t/TEKT2 and impaired spermatogenesis in Japanese males, we screened for mutations in TEKTIN-t/TEKT2 using DNA from 282 sterile male patients and 89 proven-fertile male volunteers. Six polymorphisms were found in the open reading frame of TEKTIN-t/TEKT2, but no significant differences in genotype frequency were identified in the infertile subjects(P>0.05). We also did not detect a previously reported TEKTIN-t/TEKT2 gene variant in our subjects. These data may be applied to future large-scale genetic analyses of the association between genetic background and male infertility

Nuclear Magnetic Relaxation Times of Mn⁵⁵ in Dilute MnFe Alloys

Nuclear magnetic relaxation times (T₁ and T₂) were measured in dilute MnFe alloys. The relaxation processes are effected by the Mn-impurity and related by the functions with impurity concentrations.Article信州大学理学部紀要 10(2): 81-84(1976)departmental bulletin pape

Alterations in the steroid hormone receptor co-chaperone FKBPL are associated with male infertility: a case-control study

RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.Abstract Background Male infertility is a common cause of reproductive failure in humans. In mice, targeted deletions of the genes coding for FKBP6 or FKBP52, members of the FK506 binding protein family, can result in male infertility. In the case of FKBP52, this reflects an important role in potentiating Androgen Receptor (AR) signalling in the prostate and accessory glands, but not the testis. In infertile men, no mutations of FKBP52 or FKBP6 have been found so far, but the gene for FKBP-like (FKBPL) maps to chromosome 6p21.3, an area linked to azoospermia in a group of Japanese patients. Methods To determine whether mutations in FKBPL could contribute to the azoospermic phenotype, we examined expression in mouse and human tissues by RNA array blot, RT-PCR and immunohistochemistry and sequenced the complete gene from two azoospermic patient cohorts and matching control groups. FKBPL-AR interaction was assayed using reporter constructs in vitro. Results FKBPL is strongly expressed in mouse testis, with expression upregulated at puberty. The protein is expressed in human testis in a pattern similar to FKBP52 and also enhanced AR transcriptional activity in reporter assays. We examined sixty patients from the Japanese patient group and found one inactivating mutation and one coding change, as well as a number of non-coding changes, all absent in fifty-six controls. A second, Irish patient cohort of thirty showed another two coding changes not present in thirty proven fertile controls. Conclusions Our results describe the first alterations in the gene for FKBPL in azoospermic patients and indicate a potential role in AR-mediated signalling in the testis.Published versio

Male Infertility and Its Causes in Human

Infertility is one of the most serious social problems facing advanced nations. In general, approximate half of all cases of infertility are caused by factors related to the male partner. To date, various treatments have been developed for male infertility and are steadily producing results. However, there is no effective treatment for patients with nonobstructive azoospermia, in which there is an absence of mature sperm in the testes. Although evidence suggests that many patients with male infertility have a genetic predisposition to the condition, the cause has not been elucidated in the vast majority of cases. This paper discusses the environmental factors considered likely to be involved in male infertility and the genes that have been clearly shown to be involved in male infertility in humans, including our recent findings

SNPs within the Intron-less TAF7 Gene Encoding a General Transcription Factor in Japanese Males

TAF7 は転写開始と伸長に必須な転写開始前複合体に含まれる｡精巣において､TAF7 は細胞の増殖を伴う精原細胞と第一精母細胞の核に局在し､また､TAF7 の精巣特異的ｱｲｿｻﾞｲﾑである TAF7L は､精子細胞分化過程で核に局在する｡このことから､雄性生殖細胞では､細胞増殖を伴う精原細胞では TAF7 が､その後の精子分化過程では TAF7L が転写調節に機能していることが考えられる｡今回私たちは､細胞増殖をともなう精原細胞で発現する TAF7 ｲﾝﾄﾛﾝﾚｽ遺伝子について､男性不妊症と TAF7 の遺伝子多型の関係を調べるため､282人の日本人男性不妊症患者と96人の妊孕性が確認された日本人男性ﾎﾞﾗﾝﾃｨｱの遺伝子多型を調べた｡その結果､男性不妊症性患者において､5\u27 非翻訳領域に CTC の3塩基欠失と､ｱﾐﾉ酸置換を伴う一塩基多型がそれぞれﾍﾃﾛ接合型として各々一人づつ検出された｡ The National Center for Biotechnology Information には TAF7 に関して多くの一塩基多型が登録されているが､日本人男性に関してそれらの遺伝子多型はほとんどが検出されなかった｡新たに同定されたこれらの遺伝子多型は､体質と遺伝子多型の大規模な解析に役立つものと考えられる｡TAF7 is a part of the protein complex that is indispensable for the start of transcription. In the testis, TAF7 localizes on nuclei in spermatogonia and primary spermatocytes during proliferation. To examine whether genetic polymorphisms of the intron-less TAF7 gene are associated with male infertility, we screened TAF7 for genetic polymorphisms using DNA from 282 sterile and 96 fertile male volunteers. We identified 11 genetic polymorphisms in the TAF7 region. Although many single nucleotide polymorphisms (SNPs) have been reported in the SNP database of the National Center for Biotechnology Information, we found a novel CTC deletion and one SNP with an amino acid substitution in the TAF7 genomic region in infertile patients. These genetic polymorphisms might be causes of male sterility. These results will be useful for analyzing the association of traits and genetic polymorphisms in further large-scale genetic analyses

Boosting charge separation in organic photovoltaics: unveiling dipole moment variations in excited non-fullerene acceptor layers

The power conversion efficiency (PCE) of organic photovoltaics (OPVs) has reached more than 19% due to the rapid development of non-fullerene acceptors (NFAs). To compete with the PCEs (26%) of commercialized silicon-based inorganic photovoltaics, the drawback of OPVs should be minimized. This drawback is the intrinsic large loss of open-circuit voltage; however, a general approach to this issue remains elusive. Here, we report a discovery regarding highly efficient NFAs, specifically ITIC. We found that charge-transfer (CT) and charge dissociation (CD) can occur even in a neat ITIC film without the donor layer. This is surprising, as these processes were previously believed to take place exclusively at donor/acceptor heterojunctions. Femtosecond time-resolved visible to mid-infrared measurements revealed that in the neat ITIC layers, the intermolecular CT immediately proceeds after photoirradiation (<0.1 ps) to form weakly-bound excitons with a binding energy of 0.3 eV, which are further dissociated into free electrons and holes with a time-constant of 56 ps. Theoretical calculations indicate that stacking faults in ITIC (i.e., V-type molecular stacking) induce instantaneous intermolecular CT and CD in the neat ITIC layer. In contrast, J-type stacking does not support such CT and CD. This previously unknown pathway is triggered by the larger dipole moment change on the excited state generated at the lower symmetric V-type molecular stacking of ITIC. This is in sharp contrast with the need of sufficient energy offset for CT and CD at the donor-acceptor heterojunction, leading to the significant voltage loss in conventional OPVs. These results demonstrate that the rational molecular design of NFAs can increase the local dipole moment change on the excited state within the NFA layer. This finding paves the way for a groundbreaking route toward the commercialization of OPVs