ゲラチンスポンジ塞栓下での血管再疎通時におけるフィブロネクチンの局在

血管再疎通時におけるフィブロネクチンの局在について検討した.家兎耳介動脈にゲラチンスポンジを塞栓させ,塞栓部位を経時的に生検し,ヘマトキシリン・エオジン染色と,抗フィブロネクチン抗体による蛍光抗体間接法を施行した.ヘマトキシリン・エオジン標本ではいまだ内皮細胞が障害脱落している動注1週間後,蛍光抗体間接法では,動注直後より消失していた弾性板内側のフィブロネクチンが再び陽性となった.内皮細胞損傷後の血管修復のごく初期の段階では,まずフィブロネクチンなどが,動脈壁に接着し透過性亢進の阻止などの役割を負うと思われる.This paper demonstrates the localization of fibronectin (FN) at injury and repair of blood vessels. Rabbits caudal auricular arteries were embolized with gelatin sponge powder. Biopsy specimens were taken from the embolic lesions. These were stai ned with hematoxyline-eosin solution and anti-FN antibody employing indirect immunofluorescence method. FN was found to localize along the inner side of elastic membrane at one week after embolization, although the endothelial cells of most lesions had disappeared. From these observations, it seems that FN would appear initially at the time of regeneration of the inner coat and inhibit the increased vascular permeability

A Light-microscopic Observation of Rabbit Auricular Artery Embolization with Gelatin Sponge Powder

Rabbit auricular arteries were embolized with gelatin sponge powder. A suspension of less than 0.5 ml was required when injection into the auricular artery. Embolic lesions were distinguishable by palpation and inspection. Gelatin sponge was seen in arterial lumina of 500-1000 μm in diameter, and was absorbed in about one month mainly by phagocytosis of histiocytes. The inner coat of the artery disappeared just after embolization. Endothelial cells proliferated into the thrombus from the 7th day, and then formed a new vascular canal in one to two months, accompanied by a thick inner coat mainly composed of smooth muscle cells. Ischemic necrosis did not occur

Design of peptide-containing N5-unmodified neutral flavins that catalyze aerobic oxygenations

Simulation of the monooxygenation function of flavoenzyme (Fl-Enz) has been long-studied with N5-modified cationic flavins (FlEt+), but never with N5-unmodified neutral flavins (Fl) despite the fact that Fl is genuinely equal to the active center of Fl-Enz. This is because of the greater lability of 4a-hydroperoxy adduct of Fl, FlOOH, compared to those of FlEt+, FlEtOOH, and Fl-Enz, FlOOH-Enz. In this study, Fl incorporated into a short peptide, flavopeptide (Fl-Pep), was designed by a rational top-down approach using a computational method, which could stabilize the corresponding 4a-hydroperoxy adduct (FlOOH-Pep) through intramolecular hydrogen bonds. We report catalytic chemoselective sulfoxidation as well as Baeyer–Villiger oxidation by means of Fl-Pep under light-shielding and aerobic conditions, which are the first Fl-Enz-mimetic aerobic oxygenation reactions catalyzed by Fl under non-enzymatic conditions

Fatal bacteremia due to immotile Vibrio cholerae serogroup O21 in Vientiane, Laos – a case report

<p>Abstract</p> <p>Background</p> <p>Human infections with non-O1, non-O139 <it>V. cholerae </it>have been described from Laos. Elsewhere, non cholera-toxin producing, non-O1, non-O139 <it>V. cholerae </it>have been described from blood cultures and ascitic fluid, although they are exceedingly rare isolates.</p> <p>Case presentation</p> <p>We describe a farmer who died with <it>Vibrio cholerae </it>O21 bacteremia and peritonitis in Vientiane, Laos, after eating partially cooked apple snails (<it>Pomacea canaliculata</it>) and mussels (<it>Ligumia </it>species). The cultured <it>V. cholerae </it>were non-motile. PCR detected <it>ompW </it>and <it>toxR </it>gene regions but not the <it>ctxA, ompU, omp K </it>and <it>TCP </it>gene regions. Although the organisms lacked flagellae on scanning electron microscopy, they possessed the <it>Vibrio </it>flagellin <it>flaA </it>gene.</p> <p>Conclusion</p> <p>Severe bacteremic non-O1, non-O139 <it>V. cholerae </it>is reported from Laos. The organisms were unusual in being non-motile. They possessed the <it>Vibrio </it>flagellin <it>flaA </it>gene. Further research to determine the reasons for the non-motility and virulence is required.</p

Interplay between DNA polymerases β and λ in repair of oxidation DNA damage in chicken DT40 cells

DNA polymerase λ (Pol λ) is a DNA polymerase β (Pol β)-like enzyme with both DNA synthetic and 5'-deoxyribose-5'-phosphate lyase domains. Resent biochemical studies implicated Pol λ as a backup enzyme to Pol ß in the mammalian base excision repair (BER) pathway. To examine the interrelationship between Pol λ and Pol ß in BER of DNA damage in living cells, we disrupted the genes for both enzymes either singly or in combination in the chicken DT40 cell line and then characterized BER phenotypes. Disruption of the genes for both polymerases caused hypersensitivity to H2O2-induced cytotoxicity, whereas the effect of disruption of either polymerase alone was only modest. Similarly, BER capacity in cells after H2O2 exposure was lower in Pol β−/−/Pol λ−/− cells than in Pol β−/−, wild-type and Pol λ−/− cells, which were equivalent. These results suggest that these polymerases can complement for one another in counteracting oxidative DNA damage. Similar results were obtained in assays for in vitro BER capacity using cell extracts. With MMS-induced cytotoxicity, there was no significant effect on either survival or BER capacity from Pol λ gene disruption. A strong hypersensitivity and reduction in BER capacity was observed for Pol β−/−/Pol λ−/− and Pol β−/− cells, suggesting that Pol β had a dominant role in counteracting alkylation DNA damage in this cell system

DNA polymerases ν and θ are required for efficient immunoglobulin V gene diversification in chicken

Polν and Polθ have specialized functions in immunoglobulin gene rearrangements and only contribute to DNA repair when other homologous recombination–related DNA polymerases are absent