Chitin-based barrier immunity and its loss predated mucus-colonization by indigenous gut microbiota

Mammalian gut microbiota are integral to host health. However, how this association began remains unclear. We show that in basal chordates the gut space is radially compartmentalized into a luminal part where food microbes pass and an almost axenic peripheral part, defined by membranous delamination of the gut epithelium. While this membrane, framed with chitin nanofibers, structurally resembles invertebrate peritrophic membranes, proteome supports its affinity to mammalian mucus layers, where gut microbiota colonize. In ray-finned fish, intestines harbor indigenous microbes, but chitinous membranes segregate these luminal microbes from the surrounding mucus layer. These data suggest that chitin-based barrier immunity is an ancient system, the loss of which, at least in mammals, provided mucus layers as a novel niche for microbial colonization. These findings provide a missing link for intestinal immune systems in animals, revealing disparate mucosal environment in model organisms and highlighting the loss of a proven system as innovation

ネンチョウ ダウンショウジ ニ オケル ヒマン ヨウイン ノ ケントウ : カツドウ リョウ ト アンセイジ サンソ セッシュ リョウ ノ カンレン

The purpose of this study is to explore causes of obesity in Adolescents with Down’s syndrome. Five adolescents with Down’s syndrome and 5 undergraduate students participated in this study. It is measured that participant’s active mass in dairy life and Oxygen Uptake at Rest. There is no difference active mass between both group of Down’s sydrome and controls. However, the Oxygen Uptake at Rest of particpants with Down’s syndrome was less than the controls’. In conclusion, it was suggested that causes of obesity in Down’s syndrome was low Resting Energy Expenditure （REE)

Synergistic roles of the proteasome and autophagy for mitochondrial maintenance and chronological lifespan in fission yeast

Regulations of proliferation and quiescence in response to nutritional cues are important for medicine and basic biology. The fission yeast Schizosaccharomyces pombe serves as a model, owing to the shift of proliferating cells to the metabolically active quiescence (designate G0 phase hereafter) by responding to low nitrogen source. S. pombe G0 phase cells keep alive for months without growth and division. Nitrogen replenishment reinstates vegetative proliferation phase (designate VEG). Some 40 genes required for G0 maintenance were identified, but many more remain to be identified. We here show, using mutants, that the proteasome is required for maintaining G0 quiescence. Functional outcomes of proteasome in G0 and VEG phases appear to be distinct. Upon proteasome dysfunction, a number of antioxidant proteins and compounds responsive to ROS (reactive oxygen species) are produced. In addition, autophagy-mediated destruction of mitochondria occurs, which suppresses the loss of viability by eliminating ROS-generating mitochondria. These defensive responses are found in G0 but not in VEG, suggesting that the main function of proteasome in G0 phase homeostasis is to minimize ROS. Proteasome and autophagy are thus collaborative to support the lifespan of S. pombe G0 phase

Signal transduction: regulation of insulin secretion by changes in Ca2+ concentration and action in pancreatic B-cells

Defects in the regulation of insulin secretion from pancreatic β-cells largely contribute to the perturbations of glucose homeostasis in noninsulin-dependent diabetes (Type 2 diabetes). Under physiological conditions, the rate of insulin release is controlled by variations in the concentration of circulating nutrients and by various hormonal and neural signals. Hormones and neurotransmitters modulate β-cell function by binding to membrane receptors and activating transduction pathways essentially similar to those existing in other cell types. In contrast, glucose, the major physiological stimulus, does not bind to a receptor but must be metabolized to induce insulin secretion. The acceleration of β-cell metabolism results in the production of a number of potential second messengers that might trigger or modulate exocytosis of storage granules containing insulin. Another peculiarity of β-cells is not so much that they are electrically excitable, but that their membrane potential is controlled by metabolism. The electrical activity induced by glucose involves marked changes in the flux of many ions across the plasma membrane. One of these ions, Ca2+, plays a pre-eminent role in the regulation of insulin secretion. The first indication that Ca2+ ions are essential players in stimulus-secretion coupling in β-cells dates back to the observation that the stimulation of insulin secretion by glucose and other agents was abrogated by omission of extracellular Ca2+