Ultra-Stretchable Composite Organohydrogels Polymerized Based on MXene@Tannic Acid-Ag Autocatalytic System for Highly Sensitive Wearable Sensors.

Conductive hydrogels have attracted widespread attention in the fields of biomedicine and health monitoring. However, their practical application is severely hindered by the lengthy and energy-intensive polymerization process and weak mechanical properties. Here, a rapid polymerization method of polyacrylic acid/gelatin double-network organohydrogel is designed by integrating tannic acid (TA) and Ag nanoparticles on conductive MXene nanosheets as catalyst in a binary solvent of water and glycerol, requiring no external energy input. The synergistic effect of TA and Ag NPs maintains the dynamic redox activity of phenol and quinone within the system, enhancing the efficiency of ammonium persulfate to generate radicals, leading to polymerization within 10 min. Also, ternary composite MXene@TA-Ag can act as conductive agents, enhanced fillers, adhesion promoters, and antibacterial agents of organohydrogels, granting them excellent multi-functionality. The organohydrogels exhibit excellent stretchability (1740%) and high tensile strength (184 kPa). The strain sensors based on the organohydrogels exhibit ultrahigh sensitivity (GF = 3.86), low detection limit (0.1%), and excellent stability (>1000 cycles, >7 days). These sensors can monitor the human limb movements, respiratory and vocal cord vibration, as well as various levels of arteries. Therefore, this organohydrogel holds potential for applications in fields such as human health monitoring and speech recognition.

Moderate-intensity physical activity reduces the role of serum PFAS on COPD: A cross-sectional analysis with NHANES data.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has emerged as a leading cause of chronic disease morbidity and mortality globally, posing a substantial public health challenge. Perfluoroalkyl substances (PFAS) are synthetic chemicals known for their high stability and durability. Research has examined their potential link to decreased lung function. Physical activity (PA) has been identified as one of the primary modalities of the non-pharmacological treatment of COPD. METHODS: To investigate the relationship between PFAS and COPD, and whether physical activity could reduce the risk of COPD caused by PFAS exposure, we used data from the NHANES 2013-2018, a cross-sectional study. Logistic regression analysis was used to examine the associations between PFAS and COPD in adult populations, and their associations in different PA types. RESULTS: We finally included 4857 participants in the analysis, and found that Sm-PFOS (OR: 1.250), PFOA (OR: 1.398) and n-PFOA (OR: 1.354) were closely related to COPD; After stratified by gender, age and smoking, the results showed that Sm-PFOA (OR: 1.312) was related to COPD in female adult, and PFOA (OR: 1.398) and n-PFOA (OR: 1.354) were associated with COPD in male adults; The associations of Sm-PFOS (OR: 1.280), PFOA (OR: 1.481) and n-PFOA (OR: 1.424)with COPD tended to be stronger and more consistent in over 50 years old adults; Sm-PFOS was related to COPD in current smoker (OR: 1.408), and PFOA was related to COPD in former smoker (OR: 1.487); Besides, in moderate-intensity PA group, there were no associations of Sm-PFOS, PFOA and n-PFOA with COPD stratified by gender, age and smoking. CONCLUSION: PFAS exposure may increase the risk of developing COPD, but regular moderate-intensity physical activity can protect individuals from evolving to the disease. However, longitudinal studies are needed to support these preliminary findings.

Critical COVID-19, Victivallaceae abundance, and celiac disease: A mediation Mendelian randomization study.

Celiac disease exhibits a higher prevalence among patients with coronavirus disease 2019. However, the potential influence of COVID-19 on celiac disease remains uncertain. Considering the significant association between gut microbiota alterations, COVID-19 and celiac disease, the two-step Mendelian randomization method was employed to investigate the genetic causality between COVID-19 and celiac disease, with gut microbiota as the potential mediators. We employed the genome-wide association study to select genetic instrumental variables associated with the exposure. Subsequently, these variables were utilized to evaluate the impact of COVID-19 on the risk of celiac disease and its potential influence on gut microbiota. Employing a two-step Mendelian randomization approach enabled the examination of potential causal relationships, encompassing: 1) the effects of COVID-19 infection, hospitalized COVID-19 and critical COVID-19 on the risk of celiac disease; 2) the influence of gut microbiota on celiac disease; and 3) the mediating impact of the gut microbiota between COVID-19 and the risk of celiac disease. Our findings revealed a significant association between critical COVID-19 and an elevated risk of celiac disease (inverse variance weighted [IVW]: P = 0.035). Furthermore, we observed an inverse correlation between critical COVID-19 and the abundance of Victivallaceae (IVW: P = 0.045). Notably, an increased Victivallaceae abundance exhibits a protective effect against the risk of celiac disease (IVW: P = 0.016). In conclusion, our analysis provides genetic evidence supporting the causal connection between critical COVID-19 and lower Victivallaceae abundance, thereby increasing the risk of celiac disease.

Imbalance between hippocampal projection cell and parvalbumin interneuron architecture increases epileptic susceptibility in mouse model of methyl CpG binding protein 2 duplication syndrome.

OBJECTIVE: Methyl CpG-binding protein 2 (MECP2) duplication syndrome is a rare X-linked genomic disorder affecting predominantly males, which is usually manifested as epilepsy and autism spectrum disorder (ASD) comorbidity. The transgenic line MeCP2Tg1 was used for mimicking MECP2 duplication syndrome and showed autism-epilepsy co-occurrence. Previous works suggested that the excitatory/inhibitory (E/I) imbalance is a potential common mechanism for both epilepsy and ASD. The projection neurons and parvalbumin (PV) interneurons account for the majority of E/I balance in the hippocampus. Therefore, we explored how structural changes of projection and PV+ neurons occur in the hippocampus of MeCP2Tg1 mice and whether these morphological changes contribute to epilepsy susceptibility. METHODS: We used the interneuron Designer receptors exclusively activated by designer drugs mouse model to inhibit inhibitory neurons in the hippocampus to verify the epilepsy susceptibility of MeCP2Tg1 (FVB, an inbred strain named as sensitivity to Friend leukemia virus) mice. Electroencephalograms were recorded for the definition of seizure. We performed retro-orbital injection of virus in MeCP2Tg1 (FVB):CaMKIIα-Cre (C57BL/6) mice or MeCP2Tg1:PV-Cre (C57BL/6) mice and their littermate controls to specifically label projection and PV+ neurons for structural analysis. RESULTS: Epilepsy susceptibility was increased in MeCP2Tg1 mice. There was a reduced number of PV neurons and reduced dendritic complexity in the hippocampus of MeCP2Tg1 mice. The dendritic complexity in MeCP2Tg1 mice was increased compared to wild-type mice, and total dendritic spine density in dentate gyrus of MeCP2Tg1 mice was also increased. Total dendritic spine density was increased in CA1 of MeCP2Tg1 mice. SIGNIFICANCE: Overexpression of MeCP2 may disrupt crucial signaling pathways, resulting in decreased dendritic complexity of PV interneurons and increased dendritic spine density of projection neurons. This reciprocal modulation of excitatory and inhibitory neuronal structures associated with MeCP2 implies its significance as a potential target in the development of epilepsy and offers a novel perspective on the co-occurrence of autism and epilepsy.

Aberrant expression of thyroidal hormone receptor α exasperating mitochondrial dysfunction induced sarcopenia in aged mice.

Disrupted mitochondrial dynamics and mitophagy contribute to functional deterioration of skeletal muscle (SM) during aging, but the regulatory mechanisms are poorly understood. Our previous study demonstrated that the expression of thyroid hormone receptor α (TRα) decreased significantly in aged mice, suggesting that the alteration of thyroidal elements, especially the decreased TRα, might attenuate local THs action thus to cause the degeneration of SM with aging, while the underlying mechanism remains to be further explored. In this study, decreased expression of myogenic regulators Myf5, MyoD1, mitophagy markers Pink1, LC3II/I, p62, as well as mitochondrial dynamic factors Mfn1 and Opa1, accompanied by increased reactive oxygen species (ROS), showed concomitant changes with reduced TRα expression in aged mice. Further TRα loss- and gain-of-function studies in C2C12 revealed that silencing of TRα not only down-regulated the expression of above-mentioned myogenic regulators, mitophagy markers and mitochondrial dynamic factors, but also led to a significant decrease in mitochondrial activity and maximum respiratory capacity, as well as more mitochondrial ROS and damaged mitochondria. Notedly, overexpression of TRα could up-regulate the expression of those myogenic regulators, mitophagy markers and mitochondrial dynamic factors, meanwhile also led to an increase in mitochondrial activity and number. These results confirmed that TRα could concertedly regulate mitochondrial dynamics, autophagy, and activity, and myogenic regulators rhythmically altered with TRα expression. Summarily, these results suggested that the decline of TRα might cause the degeneration of SM with aging by regulating mitochondrial dynamics, mitophagy and myogenesis.