Gut microbiota profiling in obese children from Southeastern China.

Childhood obesity not only has a negative impact on a child's health but is also a significant risk factor for adult obesity and related metabolic disorders, making it a major global public health concern. Recent studies have revealed the crucial role of gut microbiota in the occurrence and development of obesity, in addition to genetic and lifestyle factors. In this study, we recruited 19 normal-weight children and 47 children with varying degrees of obesity. A questionnaire survey was conducted to inquire about the family background, lifestyle habits and dietary composition of the 66 children. Findings indicate that fathers of obese children tend to be obese themselves, while children with highly educated mothers are more likely to maintain a normal weight. Furthermore, overweight children tend to spend more time on electronic devices and less time on physical activities compared to their normal-weight counterparts. Obese children exhibit significant differences in breakfast and dinner dietary composition when compared to children with normal weight. Additionally, the gut microbiota of these 66 children was analyzed using 16S rRNA sequencing. Analysis of gut microbiota composition showed similar compositions among children with varying degrees of obesity, but significant differences were observed in comparison to normal-weight children. Obese children exhibited a reduced proportion of Bacteroidota and an increased proportion of Firmicutes, resulting in an elevated Firmicutes/Bacteroidota ratio. Moreover, Actinobacteriota were found to be increased in the gut microbiota of children with varying degrees of obesity. PICRUSt analysis indicated significant metabolic differences in the microbiota functions between obese and normal-weight children, suggesting the composition of gut microbiota could be a crucial factor contributing to obesity. These findings provide valuable insights for the treatment of childhood obesity.

Effects of Through-Bond and Through-Space Conjugations on the Photoluminescence of Small Aromatic and Aliphatic Aldimines.

Through-bond conjugation (TBC) and/or through-space conjugation (TSC) determine the photophysical properties of organic luminescent compounds. No systematic studies have been carried out to understand the transition from aromatic TBC to non-aromatic TSC on the photoluminescence of organic luminescent compounds. In this work, a series of small aromatic and aliphatic aldimines were synthesized. For the aromatic imines, surprisingly, N,1-diphenylmethanimine with the highest TBC is non-emissive, while N-benzyl-1-phenylmethanimine and N-cyclohexyl-1-phenylmethanimine emit bright fluorescence in aggregate states. The aliphatic imines are all emissive, and their maximum emission wavelength decreases while the quantum yield increases with a decrease in steric hindrance. The imines show concentration-dependent and excitation-dependent emissions. Theoretical calculations show that the TBC extents in the aromatic imines are not strong enough to induce photoluminescence in a single molecule state, while the intermolecular TSC becomes dominant for the fluorescence emissions of both aromatic and aliphatic imines in aggregate states, and the configurations and spatial conformations of the molecules in aggregate states play a key role in the formation of effective TSC. This study provides an understanding of how chemical and spatial structures affect the formation of TBC and TSC and their functions on the photoluminescence of organic luminescent materials.

Cotransplantation with RADA16-PRG-Self-Assembled Nanopeptide Scaffolds, Bone Mesenchymal Stem Cells and Brain-Derived Neurotrophic Factor-Adeno-Associated Virus Promote Functional Repair After Acute Spinal Cord Injury in Rats.

We transplanted RADA16-PRG self-assembled nanopeptide scaffolds (SAPNSs), bone mesenchymal stem cells (BMSCs), and a brain-derived neurotrophic factor (BDNF)-expressing adeno-associated virus (AAV) into rats subjected to acute spinal cord injury (SCI) to investigate the effects of these transplantations on acute SCI repair and explore their mechanisms. Forty-eight SCI rats were randomly divided into four groups: BBR, BR, B, and NC groups. Seven and 28 days after SCI, evoked potentials (EPs) and BBB scores were assessed to evaluate the recovery of rats' motor behavior and sensory function after injury. HE and toluidine blue staining were performed to investigate the histological structure of the spinal cord tissue of rats from each group, and immunofluorescence staining was used to observe the red fluorescent protein (RFP) intensity of BMSCs and glial fibrillary acidic protein (GFAP) and neurofilament (NF) in the damaged area in each group. RT-PCR was utilized to detect the expression levels of the BDNF, GFAP, and neuron-specific enolase (NSE) genes in the injured area in each group. The results showed that cotransplantation of RADA16-PRG-SAPNs, BMSCs, and BDNF-AVV promoted the spinal cord's motor and sensory function of SCI rats; increased levels of BMSCs, inhabited glial cells proliferation, and promoted neurons proliferations in the injured area; and increased NF, BDNF, and NSE levels and decreased its GFAP in the injured area. Thus, cotransplantation of RADA16-PRG-SAPNS, BMSCs, and BDNF-AAV can prolong the survival time of BMSCs in rats, reduce the postoperative scarring caused by glial proliferation, and promote the migration and proliferation of neurons in the injured area, resulting in the promotion of functional repair after acute SCI.