12 research outputs found

    Proliferation following tetraploidization regulates the size and number of erythrocytes in the blood flow during medaka development, as revealed by the abnormal karyotype of erythrocytes in the medaka TFDP1 mutant

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    For the delivery of oxygen, the correct size/number of erythrocytes is required for proper blood flow. By combined analyses of wild-type (WT) medaka and the kyoho (kyo) mutant, we found proliferation-mediated adaptation of size/number in erythrocytes for blood flow under active angiogenesis during medaka development. Before the start of heart beating in the WT medaka, the karyotype of erythrocytes was 2N-4N. After the start of blood flow, the karyotype changed to 4N-8N with tetraploidization, and the cell size became larger. After the start of intersegmental and pharyngeal blood flow, the erythrocytes became smaller. The medaka mutant kyo showed erythrocytes of large size, and positional cloning of kyo demonstrated the candidate gene TFDP1, indicating higher polyploidization due to arrest in S phase in flowing erythrocytes of the kyo mutant. From our findings we uncovered a previously unrecognized system for the observed increase in flowing erythrocyte number: proliferation of erythrocytes following tetraploidization is regulated by the tight relationship between erythropoiesis and angiogenesis during embryonic development

    The Effects of Enteral Nutrition on the Intestinal Environment in Patients in a Persistent Vegetative State

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    Enteral nutrition (EN) is a rational approach to providing nutritional intake via the intestines in patients who are unable to tolerate parenteral nutrition. We conducted a preliminary study to investigate the effects of EN on the intestinal environment in 10 patients in a persistent vegetative state (PVS) (n = 5 each in the EN and EN with probiotics; Clostridium butyricum MIYAIRI 588) groups compared with 10 healthy controls. The results of 16S amplicon sequencing of the intestinal microbiota showed that EN led to dysbiosis with a decrease in α-diversity and an obvious change in β-diversity. A particularly significant decrease was seen in useful intestinal bacteria such as Bifidobacterium and butyrate-producing bacteria. Analysis of intestinal metabolites also supported these results, showing significant decreases in butyric and pyruvic acid after EN. Although C. butyricumMIYAIRI 588 improved some intestinal metabolites that were decreased after EN, it did not improve the dysbiosis of the intestinal microbiota. These findings indicate that EN causes dysbiosis of the intestinal microbiota and an imbalance in some intestinal metabolites in patients in a PVS. Moreover, although C. butyricumMIYAIRI 588 improved the imbalance of some intestinal metabolites after EN, it did not prevent dysbiosis of the intestinal microbiota

    TH1 cell-inducing Escherichia coli strain identified from the small intestinal mucosa of patients with Crohn’s disease

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    International audienceDysbiotic microbiota contributes to the pathogenesis of Crohn's disease (CD) by regulating the immune system. Although pro-inflammatory microbes are probably enriched in the small intestinal (SI) mucosa, most studies have focused on fecal microbiota. This study aimed to examine jejunal and ileal mucosal specimens from patients with CD via double-balloon enteroscopy. Comparative microbiome analysis revealed that the microbiota composition of CD SI mucosa differs from that of non-CD controls, with an increased population of several families, including Enterobacteriaceae, Ruminococcaceae, and Bacteroidaceae. Upon anaerobic culturing of the CD SI mucosa, 80 bacterial strains were isolated, from which 9 strains representing 9 distinct species (Escherichia coli, Ruminococcus gnavus, Klebsiella pneumoniae, Erysipelatoclostridium ramosum, Bacteroides dorei, B. fragilis, B. uniformis, Parabacteroides distasonis, andStreptococcus pasteurianus) were selected on the basis of their significant association with CD. The colonization of germ-free (GF) mice with the 9 strains enhanced the accumulation of T(H)1 cells and, to a lesser extent, T(H)17 cells in the intestine, among which anE. colistrain displayed high potential to induce T(H)1 cells and intestinal inflammation in a strain-specific manner. The present results indicate that the CD SI mucosa harbors unique pro-inflammatory microbiota, including T(H)1 cell-inducingE. coli, which could be a potential therapeutic target
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