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MUSCLE PROTEIN SYNTHESIS IN VITRO IN CHICKS FED A LOW-PROTEIN DIET
Kita, K.,Kuzuya, Y.,Matsunami, S.,Okumura, J. Asian Australasian Association of Animal Productio 1996 Animal Bioscience Vol.9 No.2
Muscle protein synthesis in vitro was measured in chicks fed low-protein(10% CP) and control(20% CP) diets. Right leg muscles (M. gastrocnemius) were mounted on a support made of stainless steel to stretch in constant tension, whereas left leg muscles were unmounted. Both leg muscles were incubated in Dulbecco's modified Eagle's medium including L-[$4-^3H$] phenylalanine for 60 min to measure in vitro protein synthesis. There was no significant difference in fractional synthesis rate(FSR) of muscle protein between both dietary protein levels, whereas FSR with stretch in constant tension was significantly higher than that without constant tension due to an increase in the absolute synthesis rate(ASR) per unit RNA(the efficiency of RNA to synthesize protein). The ASR of muscle protein in chicks fed the control diet was significantly higher than that in the low-protein diet group.
Identification of a New Race and Development of DNA Markers Associated with Powdery Mildew in Melon
( Hoy Taek Kim ),( Jong In Park ),( Arif Hasan Khan Robin ),( Tomoko Ishikawa ),( Maki Kuzuya ),( Manabu Horii ),( Katsutoshi Yashiro ),( Ill Sup Nou ) 한국육종학회 2016 Plant Breeding and Biotechnology Vol.4 No.2
Powdery mildew disease caused by an obligatory parasitic fungus Podosphaera xanthii is a serious problem of melon (Cucumis melo L.) production worldwide. Severity of problem is further associated with emergence of new races over the years. In this study a new race of powdery mildew fungus was discovered from Ibaraki, Japan. The race was different from all other existing races of P. xanthii occurring in Japan. Phenotypic and genetic analysis established the new fungus type as a new race, N5. Ten melon lines were infected with a total of eight fungal races including the new N5 race and it was found that all melon lines had different disease reactions against the new race compared to other seven races. Only four melon genotypes were found resistant out of 42 commercial cultivars and lines were tested. Disease reactions of two sets of F2 populations and one set of backcross population revealed that two separate epistatic gene loci located in two different linkage groups (LG), LG II and LG XII, interact together for the resistant or susceptible reaction of melon lines. A total of six simple sequence repeat (SSR) markers were found polymorphic in melon lines out of 16 tested in response to N5 race. Two different sets of F2 populations between resistant and susceptible melon lines were assessed with two polymorphic SSR markers located in two different groups, LG II and LG XII. SSR genotyping yielded 78% and 94% expected polymerase chain reaction fragments in favor of resistance or susceptibility of F2 populations of CM17187×PMR5 and PMR45×PMR5 of melon lines, respectively.
Cathepsin K Activity Controls Injury-Related Vascular Repair in Mice
Hu, Lina,Cheng, Xian Wu,Song, Haizhen,Inoue, Aiko,Jiang, Haiying,Li, Xiang,Shi, Guo-Ping,Kozawa, Eiji,Okumura, Kenji,Kuzuya, Masafumi American Heart Association, Inc. 2014 Hypertension Vol.63 No.3
<P>Cathepsin K (CatK) is one of the most potent mammalian collagenases. We showed previously the increased expression of CatK in human and animal atherosclerotic lesions. Here, we hypothesized that ablation of CatK mitigates injury-induced neointimal hyperplasia. Male wild-type (CatK<SUP>+/+</SUP>) and CatK-deficient (CatK<SUP>−/−</SUP>) mice underwent ligation or a combination of ligation and polyethylene cuff-replacement injuries to the right common carotid artery just proximal to its bifurcation, and they were then processed for morphological and biochemical studies at specific time points. On operative day 28, CatK<SUP>−/−</SUP> significantly reduced neointimal formation and neovessel formation in both single- and combination-injured arteries compared with the Cat K<SUP>+/+</SUP> mice. At early time points, CatK<SUP>−/−</SUP> reduced the lesion macrophage contents and medial smooth muscle cell proliferation, the mRNA levels of monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, chemokine ligand-12, and the gelatinolytic activity related to matrix metalloproteinase-2/-9. An aorta-explant assay revealed that smooth muscle cell movement was impaired in the CatK<SUP>−/−</SUP> mice compared with the CatK<SUP>+/+</SUP> mice. In addition, the smooth muscle cells and macrophages from CatK<SUP>−/−</SUP> mice had less invasive ability through a reconstituted basement membrane barrier. This vasculoprotective effect was mimicked by Cat inhibition with <I>trans</I>-epoxysuccinyl-L-leucylamido-{4-guanidino} butane (E64<I>d</I>). These results demonstrate an essential role of CatK in neointimal lesion formation in response to injury, possibly via the reduction of toll-like receptor-2/-4–mediated inflammation and smooth muscle cell proliferation, suggesting a novel therapeutic strategy for the control of endovascular treatment–related restenosis by regulating CatK activity.</P>