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61.
Yasushi Nakayama Junji Saito Hideki Bando Terunori Fujita 《Macromolecular chemistry and physics.》2005,206(18):1847-1852
Summary: Fluorinated bis(phenoxy‐imine)Ti complexes 1 – 3 combined with MgCl2/i‐BunAl(OR)3−n (MgCl2‐supported catalysts) were able to polymerize propylene in a living fashion at room temperature to provide slightly to highly syndiotactic poly(propylenes) (PPs) with extremely narrow distributions of molecular weight. These represent the first examples of MAO‐ and borate‐free group 4 metal‐based living catalysts. The supported complexes 2 and 3 formed PPs with higher syndiotacticity and Tm's than the corresponding homogeneous MAO‐activation systems (e.g., 3 : rr 97%, Tm 155 °C; MAO activation: rr 93%, Tm 152 °C). The measured Tm of 155 °C represents the highest known Tm for syndiotactic PPs synthesized at room temperature.
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63.
H. Yamada Y.-M. Jiang S. Oshima K. Wada F. Goshima T. Daikoku Y. Nishiyama 《Archives of virology》1998,143(6):1199-1207
Summary. We have identified the herpes simplex virus type 2 (HSV-2) UL4 gene product using a rabbit polyclonal antiserum raised against
a recombinant 6xHis-UL4 fusion protein expressed in Escherichia coli. The antiserum reacted specifically with a 27-kDa protein in HSV-2 186-infected cell lysates. The protein was not detectable
in the presence of the viral DNA synthesis inhibitor, suggesting that the UL4 gene was expressed as a γ2 gene. Indirect immunofluorescence studies localized the UL4 protein within the nucleus as discrete punctate forms at late
times postinfection. However, when expressed in the absence of other viral proteins, the UL4 protein was limited to the cytoplasm,
indicating that an interaction with one or more other virus-induced proteins was responsible for the nuclear localization
during infection. Subnuclear fractionation studies showed that the protein was released from the nuclear structure of infected
cells by high salt treatment. Moreover, the UL4 protein was detected in purified virions and light particles.
Received December 24, 1997 Accepted February 4, 1998 相似文献
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66.
Natsuo Yasui Keiichi Ozono Masayo Yamagata Hidehiko Kawabata Hideki Yoshikawa 《American journal of medical genetics. Part A》2001,99(4):328-330
A 23‐year‐old man was diagnosed as having X‐linked spondyloepiphyseal dysplasia tarda (SEDT; MIM 313400) based on his disproportionately short trunk, short stature, characteristic radiological features of the spine (posterior hump, end plate sclerosis, and disc space narrowing) and the hips (short and thick femoral necks), and positive family history. This Japanese family was found to have an intragenic deletion flanking intron 2 and exon 3 of the SEDL gene that not only included the 5′ untranslated region but also the coding sequence for the first methionine through the 25th alanine. This mutation was present in the proband and his unaffected mother (a heterozygote), but not in an unaffected sister and an unaffected uncle. The nature of the mutation predicted that the SEDL protein (Sedlin) was not produced in the proband, indicating that loss of Sedlin caused SEDT. © 2001 Wiley‐Liss, Inc. 相似文献
67.
Kazuko Sukegawa Shunji Tomatsu Toshiyuki Fukao Hideki Iwata Xiang-Qian Song Yukiji Yamada Seiji Fukuda Kouji Isogai Tadao Orii 《Human mutation》1995,6(2):136-143
Mucopolysaccharidosis type II (Hunter disease) is a lysosomal storage disorder caused by a deficiency of the enzyme iduronate-2-sulfatase. Varied clinical phenotypes of this disease have been described. To identify mutations in individual patients and to examine possible correlations between mutations and clinical phenotypes, we analyzed the iduronate-2-sulfatase gene in Japanese patients with different clinical phenotypes. Five missense mutations, S333L (severe), R468Q (severe), R468L (severe), W337R (intermediate), R48P (mild), and three nonsense mutations, W345X (severe), R443X (intermediate), Q531X (mild), were identified by the RT-PCR method. Transient expression in the enzyme-deficient fibroblasts revealed that all five missense mutant enzymes were synthesized as the normal-size precursor (73 kD), and the nonsense mutant enzymes were synthesized as truncated ones (W345X:54 kD, R443X:59 kD, and Q531X:69 kD), although stable mature enzymes (45–56 kD) were not detected by Western blot analysis. Further more, expression of the eight mutant cDNAs resulted in severe reductions of iduronate-2-sulfatase enzyme activity in comparison with a normal cDNA. © 1995 Wiley-Liss, Inc. 相似文献
68.
Hirokazu Taniguchi Kenjiro Hamamoto Takahiro Nagano Yuji Kishimoto Takashi Kimura Hideki Fujitake Kojiro Yasunaga 《Medical Electron Microscopy》1993,26(1):13-18
Ultrastructural myeloperoxidase (MPO) activity and myeloid-associated antigen (MyAg) expression were investigated in 12 adult
patients with acute lymphoblastic leukemia (ALL). Ultrastructural MPO was detected by 3 different methods. Immunophenotyping
was performed by flow cytometry, using a series of monoclonal antibodies. Ultrastructural MPO-positive blast cells were detected
in 6 patients (50%). In 5 of these 6 patients, the methods detecting both MPO and platelet peroxidase (PPO) activities found
MPO-positive blast cells more frequently than those detecting MPO activity alone. In 2 patients (17%), at least one kind of
MyAg was positive. Ultrastructural MPO activity was detected more frequently than MyAg expression in ALL patients. This method
of detecting PPO and MPO is recommended for detection of ultrastructural MPO-positive ALL. 相似文献
69.
Kiyohisa Sekizawa MDa Hideki Nakazawa MDa Masatoshi Morikawa MDa Kohei Yamauchi MDb Kazutaka Maeyama MDc Takehiko Watanabe MDc Hidetada Sasaki MDa 《The Journal of allergy and clinical immunology》1995,96(6)
Background: Histamine N-methyltransferase (HMT) modulates histamine- and antigen-induced bronchoconstriction. However, it is unclear whether vascular permeability evoked by an allergic reaction can be exaggerated by inhibition of HMT activity. Methods: We studied the effects of intravenously injected SKF 91488, a specific HMT inhibitor, on increases in plasma extravasation induced by intravenously injected histamine in unsensitized guinea pigs and by intravenously injected ovalbumin antigen in guinea pigs sensitized to ovalbumin in vivo with Evans blue dye as a marker. Results: Pretreatment with SKF 91488 shifted, in a dose-dependent fashion, the dose-response curves of the leakage of dye to histamine to lower concentrations in the trachea, main bronchi, and nasal mucosa. Likewise, pretreatment with SKF 91488 (20 mg/kg intravenously) significantly increased the leakage of dye induced by ovalbumin antigen (200 μg/kg intravenously) in three parts of the airway (p < 0.05). In contrast to SKF 91488, intravenously injected aminoguanidine, a specific inhibitor of diamine oxidase (16 mg/kg intravenously), did not alter the leakage of dye induced by histamine (from 0.001 μg/kg to 10 μg/kg intravenously) (p > 0.20). HMT activities were observed in the nasal mucosa, as well as in the trachea and main bronchi, as shown in a previous study. Conclusion: These findings suggest that HMT modulates the effects of exogenous histamine and endogenously released histamine induced by antigen challenge on plasma extravasation in the airway in guinea pigs in vivo. (J ALLERGY CLIN IMMUNOL 1995;96:910-6.) 相似文献
70.
Takusa Y Fukao T Kimura M Uchiyama A Abo W Tsuboi Y Hirose S Fujioka H Kondo N Yamaguchi S 《Molecular genetics and metabolism》2002,75(3):227-234
Very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is clinically classified into severe, intermediate, and myopathic forms. We identified mutations in three unrelated Japanese patients with VLCAD deficiency: two with the myopathic form and one with the intermediate form, all compound heterozygotes of K264E/M437V, A416T/1798delA, and P89S/IVS16-3delAA, respectively. We characterized four missense mutations, K264E, M437V, A416T, and P89S, by transisent expression analysis, using SV40-transformed fibroblasts derived from a VLCAD-null patient, as recipient cells. In transient expression of the wild-type VLCAD cDNA, VLCAD activity at 30 degrees C was higher than at 37 degrees C. Moreover, this temperature-sensitive character is more evident in all the mutant proteins tested than in wild type. Based on characterization of the five missense mutations identified in four Japanese patients, including data on one patient with the myopathic form previously reported, patients with the nonsevere forms (intermediate or myopathic forms) have missense mutations with residual activities in at least one allele. Expression analysis at 30 degrees C may be more useful for evaluating these missense mutations, compared with that at 37 degrees C. 相似文献