Association between life's essential 8 and overactive bladder.

Limited research has explored the relationship between overactive bladder (OAB) and cardiovascular health (CVH). We aim to examine the correlation between OAB and CVH in American adults, utilizing the Life's Essential 8 (LE8). We included 70,190 individuals from the National Health and Nutrition Examination Survey spanning from 2005 to 2018. In our study, the independent variable is LE8 score, where higher scores denote better CVH. The dependent variable is the presence of OAB. We employed multivariable logistic regression along with restricted cubic splines to evaluate the association between LE8 and OAB. Additionally, we performed interaction analyzes on subgroups to validate the findings. There is a significant negative correlation between LE8 scores and OAB. Upon adjusting for all covariates, a 10-point increase in LE8 total score correlated with a 17% decrease in the odds of OAB [0.83 (95% CI 0.78, 0.89)]. Compared to participants with lower LE8 scores, those with higher LE8 scores had a 46% lower probability of developing OAB. Consistent results were also observed in the association between scores of four health behaviors and four health factors and OAB. Furthermore, a notable interaction was observed between LE8 scores and smoking status. This study showed a significant negative correlation between LE8 scores and OAB prevalence.

Bisphenol S impairs mitochondrial function by targeting Myo19/oxidative phosphorylation pathway contributing to axonal and dendritic injury.

Exposure to bisphenol S (BPS) is known to adversely affect neuronal development. As pivotal components of neuronal polarization, axons and dendrites are indispensable structures within neurons, crucial for the maintenance of nervous system function. Here, we investigated the impact of BPS exposure on axonal and dendritic development both in vivo and in vitro. Our results revealed that exposure to BPS during pregnancy and lactation led to a reduction in the complexity, density, and length of axons and dendrites in the prefrontal cortex (PFC) of offspring. Employing RNA sequencing technology to elucidate the underlying mechanisms of axonal and dendritic damage induced by BPS, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis highlighted a significant alteration in the oxidative phosphorylation (OXPHOS) pathway, essential for mitochondrial function. Subsequent experiments demonstrate BPS-induced impairment in mitochondrial function, including damaged morphology, decreased adenosine triphosphate (ATP) and superoxide dismutase (SOD) levels, and increased reactive oxygen species and malondialdehyde (MDA). These alterations coincided with the downregulated expression of OXPHOS pathway-related genes (ATP6V1B1, ATP5K, NDUFC1, NDUFC2, NDUFA3, COX6B1) and Myosin 19 (Myo19). Notably, Myo19 overexpression restored the BPS-induced mitochondrial dysfunction by alleviating the inhibition of OXPHOS pathway. Consequently, this amelioration was associated with a reduction in BPS-induced axonal and dendritic injury observed in cultured neurons of the PFC.

TDCPP and TiO2 NPs aggregates synergistically induce SH-SY5Y cell neurotoxicity by excessive mitochondrial fission and mitophagy inhibition.

Tris (1,3-dichloro-2-propyl) phosphate (TDCPP), a halogen-containing phosphorus flame retardant, is widely used and has been shown to possess health risks to humans. The sustained release of artificial nanomaterials into the environment increases the toxicological risks of their coexisting pollutants. Nanomaterials may seriously change the environmental behavior and fate of pollutants. In this study, we investigated this combined toxicity and the potential mechanisms of toxicity of TDCPP and titanium dioxide nanoparticles (TiO2 NPs) aggregates on human neuroblastoma SH-SY5Y cells. TDCPP and TiO2 NPs aggregates were exposed in various concentration combinations, revealing that TDCPP (25 µg/mL) reduced cell viability, while synergistic exposure to TiO2 NPs aggregates exacerbated cytotoxicity. This combined exposure also disrupted mitochondrial function, leading to dysregulation in the expression of mitochondrial fission proteins (DRP1 and FIS1) and fusion proteins (OPA1 and MFN1). Consequently, excessive mitochondrial fission occurred, facilitating the translocation of cytochrome C from mitochondria to activate apoptotic signaling pathways. Furthermore, exposure of the combination of TDCPP and TiO2 NPs aggregates activated upstream mitochondrial autophagy but disrupted downstream Parkin recruitment to damaged mitochondria, preventing autophagosome-lysosome fusion and thereby disrupting mitochondrial autophagy. Altogether, our findings suggest that TDCPP and TiO2 NPs aggregates may stimulate apoptosis in neuronal SH-SY5Y cells by inducing mitochondrial hyperfission and inhibiting mitochondrial autophagy.

Neurotoxicity of Titanium Dioxide Nanoparticles: A Comprehensive Review.

The increasing use of titanium dioxide nanoparticles (TiO2 NPs) across various fields has led to a growing concern regarding their environmental contamination and inevitable human exposure. Consequently, significant research efforts have been directed toward understanding the effects of TiO2 NPs on both humans and the environment. Notably, TiO2 NPs exposure has been associated with multiple impairments of the nervous system. This review aims to provide an overview of the documented neurotoxic effects of TiO2 NPs in different species and in vitro models. Following exposure, TiO2 NPs can reach the brain, although the specific mechanism and quantity of particles that cross the blood-brain barrier (BBB) remain unclear. Exposure to TiO2 NPs has been shown to induce oxidative stress, promote neuroinflammation, disrupt brain biochemistry, and ultimately impair neuronal function and structure. Subsequent neuronal damage may contribute to various behavioral disorders and play a significant role in the onset and progression of neurodevelopmental or neurodegenerative diseases. Moreover, the neurotoxic potential of TiO2 NPs can be influenced by various factors, including exposure characteristics and the physicochemical properties of the TiO2 NPs. However, a systematic comparison of the neurotoxic effects of TiO2 NPs with different characteristics under various exposure conditions is still lacking. Additionally, our understanding of the underlying neurotoxic mechanisms exerted by TiO2 NPs remains incomplete and fragmented. Given these knowledge gaps, it is imperative to further investigate the neurotoxic hazards and risks associated with exposure to TiO2 NPs.

Chronic exposure to titanium dioxide nanoparticles induces deficits of locomotor behavior by disrupting the development of NMJ in Drosophila.

Titanium dioxide nanoparticles (TiO2 NPs) are widely used in several consumer products. However, because of their neurotoxic nature, exposure to TiO2 NPs could impair locomotor behavior. Whether the impairment in locomotor behavior caused by TiO2 NPs exposure is sustained and the effects is gender-specific has remained elusive, warranting further studies to elucidate the underlying mechanisms. Thus, we established a Drosophila model to study the effects of chronic TiO2 NPs exposure on the locomotor behavior of Drosophila in different generations and explore the underlying mechanisms. Chronic TiO2 NPs exposure caused accumulation of Ti in the body and affected the life history traits of Drosophila. Furthermore, chronic exposure to TiO2 NPs decreased the total crawling distance of larvae and the total movement distance of adult males in the F3 generation, indicating the damage caused to the locomotor behavior of Drosophila. Impaired neuromuscular junction (NMJ) morphology was observed, manifested by the reduced number of boutons, size of boutons, and branch length of NMJ. In addition, several differentially expressed genes (DEGs) related to NMJ development were selected by RNA sequencing and their expression was confirmed by quantitative real-time-polymerase chain reaction (qRT-PCR). Compared with the control group, the gene expression of Cyp6a17, frac, and kek2 in the TiO2 NPs exposure group decreased, whereas that of Gba1a, Hll and List was elevated. These findings indicated that chronic TiO2 NPs exposure damage the morphology of NMJ by altering the expression of genes related to NMJ development, consequently causing locomotor behavior deficits in Drosophila.

Room Temperature Hydroxyl Group-Assisted Preparation of Hydrophobicity-Adjustable Metal-Organic Framework UiO-66 Composites: Towards Continuous Oil Collection and Emulsion Separation.

Developing a straightforward and effective hydrophobic modification for metal-organic frameworks (MOFs) under mild conditions is meaningful for MOF applications. Here, a post-synthetic modification approach assisted with metal hydroxyl groups at room temperature is reported to induce hydrophobicity in the hydrophilic UiO-66. The bonding between Zr-OH in UiO-66 and n-tetradecylphosphonic acid (TDPA) is the vital force for the modifier TDPA. Superhydrophobic and superoleophilic composites were constructed for efficient oil-water separation by coating TDPA-modified UiO-66 (P-UiO-66) on commercial melamine sponges (MS) and filter papers (FP) with water contact angles of 153.2° and 155.6°, respectively. The P-UiO-66/MS composite could quickly and selectively absorb oily liquids up to 43 times its weight from water. The P-UiO-66/MS achieved continuous oil collection with high separation efficiencies (≥99.4 %). In addition, P-UiO-66/FP and P-UiO-66/MS showed high separation efficiencies for water-in-oil emulsions (≥98.5 %) and oil-in-water emulsions, respectively, with high resistance to low/high temperatures and acid/base conditions. The metal hydroxyl group-assisted post-synthetic modification strategy offers a facile and broad way to prepare hydrophobic MOFs for promising applications in environmental fields.

Repair of a severe palm injury with anterolateral thigh and ilioinguinal flaps: A case report.

BACKGROUND: In daily life and work, there are more and more patients with trauma to the hand, which often results in skin and soft tissue defects. Although there are many repair methods, the function and appearance of the fingers will be adversely affected if the repair is inadequate. CASE SUMMARY: In the present report we describe an 18-year-old male patient whose right hand was mangled by a machine. X-ray imaging showed that a right hand bone (middle finger) was absent and the alignment was poor. After hospitalization, he was diagnosed with a severe right hand injury, skin and soft tissue defects, partial finger defects, and a skin degloving injury. He underwent reconstructive surgery with anterolateral thigh and ilioinguinal flaps. After two repair operations, satisfactory results were obtained, including good fracture healing, good skin flap shape, and good wrist joint function. CONCLUSION: This case highlights the good effect of anterolateral thigh and ilioinguinal flaps repair technique on severe palm injury.