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Biology subjects

Kido, T.

Publications and source records attributed to Kido, T..

3 recordsLinked to original sources

Deep Microbial Colonization in 2-Billion-Year-Old Ultramafic Rock from the Bushveld Complex

Archean cratons may provide stable microbial habitats in the deep subsurface, as evidenced by the discovery of billion-year-old crustal fluids1,2. However, the long-term habitability of these cratonic environments is uncertain, as polymetamorphic evolution in most cratons typically destroys microbial habitats through mineral reactions and porosity loss3,4. Preservation of deep microbial habitats is more likely where mantle-derived magma intruded the craton after metamorphic overprinting4. Here we report the discovery of dense microbial colonization at 814 m depth within the 2.05-billion-year-old, unmetamorphosed Bushveld Igneous Complex intrusion, South Africa5. Using advanced contamination-control protocols6,7 and synchrotron-based X-ray spectroscopy, we identified indigenous microbial cells localized at the rims of phlogopite, a hydrous phyllosilicate mineral. Our study reveals that microbial colonization is associated with Fe(III) derived from the structure of phlogopite, where the dehydrogenation likely oxidizes Fe(II) to Fe(III) coupled to H2 generation8. Despite the absence of fracture-driven fluid ingress in the unfractured rock matrix, aqueous alteration evidenced at the rims by potassium removal indicates a self-sustaining habitat driven by an internal redox gradient9. These findings demonstrate that aqueous alteration of ultramafic rocks can sustain isolated microbial life over geological timescales, significantly expanding the potential for long-term habitability on both Earth and Mars4,10.

microbiology↗

Development of a high throughput system to screen compounds that revert the activated hepatic stellate cells to a quiescent-like state

Chronic liver injury induces fibrosis that often proceeds to cirrhosis and hepatocellular carcinoma, indicating that prevention and/or resolution of fibrosis is a promising therapeutic target. Hepatic stellate cells (HSCs) are the major driver of fibrosis by expressing extracellular matrices (ECM). HSCs, in the normal liver, are quiescent and activated by liver injury to become myofibroblasts that proliferate and produce ECM. It has been shown that activated HSCs (aHSCs) become a "quiescent-like" state by removal of liver insults. Therefore, deactivation agents can be a therapeutic drug for advanced liver fibrosis. Using aHSCs prepared from human induced pluripotent stem cells, we found that aHSCs were reverted to a quiescent-like state by a combination of chemical compounds that either inhibit or activate a signaling pathway, Lanifibranor, SB431542, Dorsomorphin, retinoic acid, palmitic acid and Y27632, in vitro. Based on these results, we established a high throughput system to screen agents that induce deactivation and demonstrate that a single chemical compound can induce deactivation.

cell biology↗

The administration of high-mobility group box 1 fragment prevents deterioration of cardiac performance by enhancement of bone marrow mesenchymal stem cell homing in the delta-sarcoglycan-deficient hamster

ObjectivesWe hypothesized that systemic administration of high-mobility group box 1 fragment attenuates the progression of myocardial fibrosis and cardiac dysfunction in a hamster model of dilated cardiomyopathy by recruiting bone marrow mesenchymal stem cells thus causing enhancement of a self-regeneration system.\n\nMethodsTwenty-week-old J2N-k hamsters, which are {delta}-sarcoglycan-deficient, were treated with systemic injection of high-mobility group box 1 fragment (HMGB1, n=15) or phosphate buffered saline (control, n=11). Echocardiography for left ventricular function, cardiac histology, and molecular biology were analyzed. The life-prolonging effect was assessed separately using the HMGB1 and control groups, in addition to a monthly HMGB1 group which received monthly systemic injections of high-mobility group box 1 fragment, 3 times (HMGB1, n=11, control, n=9, monthly HMGB1, n=9).\n\nResultsThe HMGB1 group showed improved left ventricular ejection fraction, reduced myocardial fibrosis, and increased capillary density. The number of platelet-derived growth factor receptor-alpha and CD106 positive mesenchymal stem cells detected in the myocardium was significantly increased, and intra-myocardial expression of tumor necrosis factor stimulating gene 6, hepatic growth factor, and vascular endothelial growth factor were significantly upregulated after high-mobility group box 1 fragment administration. Improved survival was observed in the monthly HMGB1 group compared with the control group.\n\nConclusionsSystemic high-mobility group box 1 fragment administration attenuates the progression of left ventricular remodeling in a hamster model of dilated cardiomyopathy by enhanced homing of bone marrow mesenchymal stem cells into damaged myocardium, suggesting that high-mobility group box 1 fragment could be a new treatment for dilated cardiomyopathy.

molecular biology↗