Laminin γ1 C-terminal Glu to Gln mutation induces early postimplantation lethality

Daiji Kiyozumi, Yukimasa Taniguchi, Itsuko Nakano, Junko Toga, Emiko Yagi, Hidetoshi Hasuwa, Masahito Ikawa, and Kiyotoshi Sekiguchi, "Laminin γ1 C-terminal Glu to Gln mutation induces early postimplantation lethality", Life Science Alliance, Vol.1, No.5, e201800064, Life Science Alliance, 201

Factors influencing acute high-grade restenosis in emergency percutaneous transluminal coronary angioplasty for acute myocardial infarction.

We studied the factors which may induce acute high grade restenosis in emergency percutaneous transluminal coronary angioplasty (PTCA). PTCA was attempted in 50 patients with acute myocardial infarction, and the balloon catheter passed successfully across the occlusion site in 47 (94%) of the patients. These 47 patients were analyzed. &#34;Acute restenosis&#34; was defined as a lesion which was revascularized to less than 50% luminal reduction narrowed again to more than 75% luminal reduction 5 min after the balloon inflation. Univariate and multivariate analyses were used for determining factors which significantly influenced acute restenosis. The incidence of at least one restenosis episode was 45%. Multiple regression analysis selected 5 factors associated significantly with an increased rate of acute restenosis: 1) angiographic evidence of dissection, 2) lesion in the right coronary artery (RCA), 3) lack of or insufficient administration of thrombolytic agent preceding PTCA, 4) curved lesion and 5) relatively small balloon/artery diameter ratio. Acute restenosis correlated significantly with late reocclusion. This study indicates that it is important to administer a thrombolytic agent prior to emergency PTCA, and to use an adequately sized balloon to the artery when the acute restenosis occurs by using relatively smaller sized balloon. The present data also demonstrated that patients with RCA and a curved lesion have a relatively high risk of acute restenosis. This study indicates how patients with relatively high risk of acute restenosis may be identified.</p

Studies on the Prevention of Casting Defects (Ⅰ)

As the results of examination of the defective casting in the three foudrys in Tottori city, the author found the next facts. The rate of the formation of defective casting in two foundrys were several percents, but on one foudry it amounted to 20%. The rate of the formation of defective casting has been subjected to the greater influence of the kinds of casting and the founders than the seasons. The casting defects were caused mainly due to erosion scab, blow, cut, un-convincing missum, insffecient beeding, inclusion, crush, warped casting and broken casting. According to the above facts, the author considered that the subjects of inquiry about this problem are as follows : molding sand, molding method, molding box and the equipment, method of dissolusion, casting method, and method of pouring gate

Laminin γ1 C-terminal Glu to Gln mutation induces early postimplantation lethality

Daiji Kiyozumi, Yukimasa Taniguchi, Itsuko Nakano, Junko Toga, Emiko Yagi, Hidetoshi Hasuwa, Masahito Ikawa, and Kiyotoshi Sekiguchi, "Laminin γ1 C-terminal Glu to Gln mutation induces early postimplantation lethality", Life Science Alliance, Vol.1, No.5, e201800064, Life Science Alliance, 201

REST and its downstream molecule Mek5 regulate survival of primordial germ cells

AbstractIn mouse embryos, some primordial germ cells (PGCs) are eliminated by apoptosis, but the molecular pathways that lead to PGC survival versus apoptosis have not been fully characterized. Here, we found that REST (repressor element 1-silencing transcription factor), a transcription factor that binds a conserved regulatory element, NRSE/RE1, played a role in PGC survival. REST expression was higher in PGCs than in surrounding somatic cells. Moreover, in mouse embryos with a PGC-specific conditional REST mutation, the PGC population experienced more apoptosis and was significantly smaller than that in control embryos; these findings indicated that REST functioned in a cell-autonomous fashion that was critical for PGC survival. Several anti-apoptotic genes were among the previously identified REST-target gene candidates; moreover, some of these genes were downregulated in the REST-deficient PGCs. Mek5, which encodes a component in the a MAP kinase cascade, was one of these downregulated REST-target gene candidates, and a Mek5 mutation, like the REST mutation, caused an increase in PGC apoptosis; these finding suggested that REST promoted PGC survival via regulation of the Mek5 expression. Importantly, there were a normal number of PGCs in the REST mutants at birth, and both the male and female REST-mutant adults were fertile; these final observations revealed that the PGC population was very robust and could recover from a genetically induced reduction in cell number