Physical and Chemical Factors Affecting the Adherence of Pseudomonas aeruginosa to a Rabbit Cornea Cell Line (SIRC) Cells

Adherence of Pseudomonas aeruginosa to SIRC cells was examined by the use of 14C-lysine labeled organisms. Pretreatment of P. aeruginosa with heating, 3% formaldehyde, or ultraviolet caused a significant decrease in adherence to SIRC cells, whereas that with lipase, hyaluronidase, trypsin or protease did not. Treatment of SIRC cells with trypsin, protease, lipase or neuraminidase did not influence the adherence of P. aeruginosa to the cell. Treatment of P. aeruginosa with mannose or galactose inhibited the adherence, while that with fructose, lactose or glucose did not. Treatment of SIRC cells with galactosidase or mannosidase reduced the adherence of the organism. No correlation was demonstrated between the adhering ability and hydrophobicity of P. aeruginosa. The results suggest that both the viability in bacterial site and mannose and/or galactose molecules in cellular site are closely connected with the adherence of P. aeruginosa to SIRC cells

Adherence of Protease-Deficient Mutants of Pseudomonas aeruginosa to a Rabbit Cornea Cell Line (SIRC) Cells

Seven protease-deficient mutants were isolated from Pseudomonas aeruginosa strain IFO 3455 which was mutagenized with nitrosoguanidine. Characterization of these mutants in vitro revealed that all mutants showed pleiotropic changes in the production of other extracellular substances. Among the mutants, two were chosen for a bacterial adherence test to Rabbit Cornea Cell Line (SIRC) cells. One mutant (IFO 3455-2) completely lost its protease activity. Another (IFO 3455-3) retained a low protease activity and was relatively similar to the parental strain with respect to extracellular products except for protease. Both mutants gave not a marked but a slight decrease of adherence as compared with the parental strain. This finding suggests that besides protease more factors are involved in the adhesion between P. aeruginosa and SIRC cells

Epitaxial growth of FeSe0.5_{0.5}Te0.5_{0.5} thin films on CaF2_2 substrates with high critical current density

In-situ epitaxial growth of FeSe$_{0.5}$Te$_{0.5}$ thin films is demonstrated on a non-oxide substrate CaF$_2$. Structural analysis reveals that compressive stress is moderately added to 36-nm thick FeSe$_{0.5}$Te$_{0.5}$, which pushes up the critical temperature above 15 K, showing higher values than that of bulk crystals. Critical current density at $T$ = 4.5 K reaches 5.9 x 10$^4$ Acm$^{-2}$ at $\mu_0H$ = 10 T, and 4.2 x 10$^4$ Acm$^{-2}$ at $\mu_0H$ = 14 T. These results indicate that fluoride substrates have high potential for the growth of iron-based superconductors in comparison with popular oxide substrates.Comment: 9 pages, 3 figures, to be published in Applied Physics Express 4, 053101 (2011

Molecular Transformation of 2-Methylazulenes: An Efficient and Practical Synthesis of 2-Formyl- and 2-Ethynylazulenes

First published: 09 Jan 20182-Formylazulene derivatives have been obtained in good yields by the reactions of 2-methylazulenes with N,N-dimethylformamide dimethyl acetal, followed by oxidative cleavage of the intermediately formed enamines with NaIO4. Vilsmeier formylation of 1-phenyl-3-methylazulenes also afforded the corresponding 2-formylazulenes in moderate yields. The treatment of a 2-methylazulene derivative bearing a formyl group at the 1-position with sodium methoxide led, through a self-condensation reaction, to a trans-1-(azulen-1-yl)-2-(azulen-2-yl)ethylene derivative, the structure of which was verified by single-crystal X-ray diffraction analysis. The 2-formylazulenes obtained were transformed into 2-ethynylazulenes in good yields by a modified Seyferth-Gilbert reaction. The reactivity of a 1-iodoazulene bearing a 2-formyl function in palladium-catalyzed cross-coupling reactions has also been examined.ArticleEUROPEAN JOURNAL OF ORGANIC CHEMISTRY. 2018(9):1145-1157 (2018)journal articl

Adult phenology of two species of tiger beetles (Carabidae, Cicindelinae) and estimates of population size of Cylindela elisae , in Tottori Sand Dunes, Honshu, Japan in 2016.

2015年の調査に引き続き，2016年の夏季にも鳥取砂丘オアシス周辺で標識再捕により，当地で絶滅が心配されるエリザハンミョウの生息数を推定した。マークできた個体はエリザハンミョウが270（昨年は304），カワラハンミョウが170（昨年は77），コハンミョウが4（昨年は1：昨年調査の報告書である鶴崎ら2016では「コニワハンミョウ」と誤記）であった。Jolly-Seber法によるエリザハンミョウの個体数推定値はもっとも多かった調査日（6月28日と7月16日）でともに約1,460で，2015年の2,300個体よりも少なかった。おそらく2016年の夏季の高気温のため，成虫の出現期は2015年よりも早く推移し，6 月中旬には成虫が出現し，8月下旬には終息した。エリザハンミョウの幼虫の営巣地はオアシス周辺の尻無川右岸の裸地であるが，成虫は左岸のコウボウシバ群落でも見つかった。カワラハンミョウの成虫は6月下旬から10月上旬まで見られ，170個体をマークしたが再捕獲できた個体は皆無であった。コハンミョウは尻無川の近くで4個体マークしたが本種も再捕獲にいたらなかった。昨年の2個体（マークしたのは1個体）に続けての確認で，細々ではあるが，本種は当地で世代を繰り返している可能性が高い。 / Following a survey of the population size of a tiger beetle species, Cylindera elisae(Motschulsky,1859) in the Tottori Sand Dunes, Tottori City, in 2015 (Tsurusaki et al.2016), we estimated population size of　the same population of the same species also in 2016 by using mark-recapture experiments. A total of　270 adults of Cy. elisae , 170 adults of Chaetodera laetescripta (Motschulsky, 1860) and 4 adults of Myriochila　speculifera (Chevrolat, 1865) (This species was　erroneously recorded as Cicindela　transbaicalica japanensis　Chaudoir, 1863 in Tsurusaki et al. 2016) were individually marked during the summer in 2016.　None of　those　adults marked were recaptured for the　two latter species. The highest number of　adults of Cy. elisae estimated　by the Jolly-Seber method was ca. 1,460 recorded on both　28 June and 16 July

Dysregulation of RNF213 promotes cerebral hypoperfusion

RNF213 is a susceptibility gene for moyamoya disease, yet its exact functions remain unclear. To evaluate the role of RNF213 in adaptation of cerebral blood flow (CBF) under cerebral hypoperfusion, we performed bilateral common carotid artery stenosis surgery using external microcoils on Rnf213 knockout (KO) and vascular endothelial cell-specific Rnf213 mutant (human p.R4810K orthologue) transgenic (EC-Tg) mice. Temporal CBF changes were measured by arterial spin-labelling magnetic resonance imaging. In the cortical area, no significant difference in CBF was found before surgery between the genotypes. Three of eight (37.5%) KO mice died after surgery but all wild-type and EC-Tg mice survived hypoperfusion. KO mice had a significantly more severe reduction in CBF on day 7 than wild-type mice (KO, 29.7% of baseline level; wild-type, 49.3%; p = 0.038), while CBF restoration on day 28 was significantly impaired in both KO (50.0%) and EC-Tg (56.1%) mice compared with wild-type mice (69.5%; p = 0.031 and 0.037, respectively). Changes in the subcortical area also showed the same tendency as the cortical area. Additionally, histological analysis demonstrated that angiogenesis was impaired in both EC-Tg and KO mice. These results are indicative of the essential role of RNF213 in the maintenance of CBF

Autosomal dominant pseudohypoaldosteronism type 1 with a novel splice site mutation in MR gene

<p>Abstract</p> <p>Background</p> <p>Autosomal dominant pseudohypoaldosteronism type 1 (PHA1) is a rare inherited condition that is characterized by renal resistance to aldosterone as well as salt wasting, hyperkalemia, and metabolic acidosis. Renal PHA1 is caused by mutations of the human mineralcorticoid receptor gene (<it>MR</it>), but it is a matter of debate whether <it>MR </it>mutations cause mineralcorticoid resistance via haploinsufficiency or dominant negative mechanism. It was previously reported that in a case with nonsense mutation the mutant mRNA was absent in lymphocytes because of nonsense mediated mRNA decay (NMD) and therefore postulated that haploinsufficiency alone can give rise to the PHA1 phenotype in patients with truncated mutations.</p> <p>Methods and Results</p> <p>We conducted genomic DNA analysis and mRNA analysis for familial PHA1 patients extracted from lymphocytes and urinary sediments and could detect one novel splice site mutation which leads to exon skipping and frame shift result in premature termination at the transcript level. The mRNA analysis showed evidence of wild type and exon-skipped RT-PCR products.</p> <p>Conclusion</p> <p>mRNA analysis have been rarely conducted for PHA1 because kidney tissues are unavailable for this disease. However, we conducted RT-PCR analysis using mRNA extracted from urinary sediments. We could demonstrate that NMD does not fully function in kidney cells and that haploinsufficiency due to NMD with premature termination is not sufficient to give rise to the PHA1 phenotype at least in this mutation of our patient. Additional studies including mRNA analysis will be needed to identify the exact mechanism of the phenotype of PHA.</p