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Biology subjects

Ku, H.

Publications and source records attributed to Ku, H..

2 recordsLinked to original sources

Solid Foods Drive the Maturation of the Gut Microbiota During Infancy

The establishment of a healthy gut microbiota in early life is an important determinant of long-term health, yet how the introduction of solid foods as a key nutritional transition shapes the gut microbiota development remains understudied. We aimed to characterize the impact of solid food introduction (complementary feeding) on the compositional succession and functional maturation of the infant gut microbiota during weaning. Infant faecal samples and corresponding dietary data were collected at five time points: pre-weaning (PREW, 4-6 months of age) 4, 8, and 12 weeks after first solid food introduction (WK4, WK8, WK12), and the late weaning stage (LATW, ~12 months) when infants were transitioning to a family diet. Faecal microbiota composition was profiled using full-length 16S rRNA gene sequencing. Solid food introduction induced marked restructuring of the gut microbiota, characterized by significant increases in richness, evenness, and phylogenetic diversity (p < 0.01), together with the emergence of adult-associated taxa, including Faecalibacterium, Ruminococcus, and members of the Lachnospiraceae. These changes were most pronounced at late weaning and were strongly associated with increased intakes of plant-derived complex carbohydrates and dietary protein (Spearman correlation r > 0.30, FDR < 0.001). Butyrate-producing capability, a functional feature of gut microbiota maturation, was correlated with the establishment of key adult-like species, including Ruminococcus bromii and Faecalibacterium prausnitzii (Spearman correlation, r > 0.30, FDR < 0.001). Additionally, the reshaping of the gut microbiota by complementary feeding also attenuated microbial diversity associated with early-life factors, including delivery mode and household pet exposure. Together, these findings suggest that nutrient transitions during complementary feeding are key drivers of infant gut microbiota development and maturation, highlighting weaning as a critical window for shaping the gut microbiota and a potential target for early-life nutritional interventions to promote gut health and associated wellbeing.

microbiology↗

Time dependent response of daunorubicin on cytotoxicity, cell cycle and DNA repair in acute lymphoblastic leukaemia

Daunorubicin is commonly used in the treatment of acute lymphoblastic leukaemia (ALL). Various mechanisms of action for daunorubicin have been proposed and its action is likely to be multi-modal. The aim of this study was to explore the kinetics of double strand break (DSB) formation of three ALL cell lines following exposure to daunorubicin and to investigate the effects of daunorubicin on the cell cycle and the protein kinases involved in specific checkpoints following DNA damage and recovery periods. Three ALL cell lines CCRF-CEM and MOLT-4 derived from T lymphocytes and SUP-B15 derived from B lymphocytes were examined following 4 hours treatment with daunorubicin chemotherapy and varying recovery periods. Daunorubicin induced different degrees of toxicity in all cell lines and consistently generated reactive oxygen species. Daunorubicin was more potent at inducing DSB in MOLT-4 and CCRF-CEM cell lines while SUP-B15 cells showed delays in DSB repair and significantly more resistance to daunorubicin compared to the other cell lines as measured by {gamma}H2AX assay. Daunorubicin also causes cell cycle arrest in all three cell lines at different checkpoints at different times. These effects were not due to mutations in Ataxia-telangiectasia mutated (ATM) as sequencing revealed none in any of the three cell lines. However, p53 was phosphorylated at serine 15 only in CCRF-CEM and MOLT-4 but not in SUP-B15 cells. The lack of active p53 may be correlated to the increase of SOD2 in SUP-B15 cells. The delay in DSB repair and lower sensitivity to daunorubicin seen in the B lymphocyte derived SUP-B15 cells could be due to loss of function of p53 thus causing variations in the DNA repair pathways.

cancer biology↗