Effects of different types of flame-retardant treatment on the flame performance of polyurethane/wood-flour composites.

To improve the flammability of foamed polyurethane/wood-flour composites (FWPC), ammonium polyphosphate (APP) was used as a flame retardant to modified FWPC. The effects of different flame treatment processes on flame performance, smoke suppression, thermal property, and surface micrographs of flame retardant FWPC were investigated. The results showed that FWPC with the addition or impregnation process both improved the combustion behaviors. Compared with the addition process, FWPC-impregnation (FWPC-I) had a lower total heat release (THR), lower peak heat release rate (PHRR), prolonged time to ignition (TTI), more residues, and better combustion safety. FWPC-I had the highest residual carbon rate reaching 39.98%. A flame-retardant layer containing the P-O group was formed in the residual carbon of FWPC-I. Although APP had negative effects on the physical properties of FWPC, it was an effective flame-retardant ability for foamed polyurethane/wood-flour composites.

O-GlcNAcylation Is Required for the Survival of Cerebellar Purkinje Cells by Inhibiting ROS Generation.

Purkinje cells (PCs), as a unique type of neurons output from the cerebellar cortex, are essential for the development and physiological function of the cerebellum. However, the intricate mechanisms underlying the maintenance of Purkinje cells are unclear. The O-GlcNAcylation (O-GlcNAc) of proteins is an emerging regulator of brain function that maintains normal development and neuronal circuity. In this study, we demonstrate that the O-GlcNAc transferase (OGT) in PCs maintains the survival of PCs. Furthermore, a loss of OGT in PCs induces severe ataxia, extensor rigidity and posture abnormalities in mice. Mechanistically, OGT regulates the survival of PCs by inhibiting the generation of intracellular reactive oxygen species (ROS). These data reveal a critical role of O-GlcNAc signaling in the survival and maintenance of cerebellar PCs.

Fasting blood glucose-to-glycated hemoglobin ratio for evaluating clinical outcomes in patients with ischemic stroke.

Background: Stress hyperglycemia frequently occurs in patients with acute ischemic stroke (AIS). The influence of stress hyperglycemia on the outcomes of patients with AIS remains ambiguous. Methods: Data from our institution on patients with AIS between June 2020 and June 2021 were retrospectively analyzed. The severity of the stroke was assessed using the National Institutes of Health Stroke Scale (NIHSS) at admission, and the primary endpoint was functional outcomes. Stress hyperglycemia was measured by the glucose-to-HbA1c ratio. In the multivariable analysis, two models that retained or excluded the NIHSS were adopted to explore the relationship between stress hyperglycemia and outcomes. The receiver operating characteristic curve (ROC) was calculated to determine an optimized cutoff value. Results: The optimal cutoff value was 1.135. When all patients were included, model 1 did not find an association between the glucose-to-HbA1c ratio and functional outcomes. In model 2, the glucose-to-HbA1c ratio×10 (Glucose-to-HbA1c ratio ×10) was the independent predictor of functional outcomes (OR 1.19, 95% CI 1.07-1.33, p < 0.01). Separately, in patients without diabetes, the glucose-to-HbA1c ratio×10 was the independent predictor of functional outcomes in both model 1 (OR 1.37, 95% CI 1.08-1.73, p = 0.01) and model 2 (OR 1.48, 95% CI 1.22-1.79, p < 0.01), but not in patients with diabetes. In addition, the glucose-to-HbA1c ratio×10 was the independent predictor of stroke severity (OR 1.16, 95% CI 1.05-1.28, p < 0.01). Conclusion: The glucose-to-HbA1c ratio was associated with more severe AIS. Specifically, the glucose-to-HbA1c ratio was associated with the functional outcomes in patients without diabetes but not in patients with diabetes.

Spliceosomal GTPase Eftud2 regulates microglial activation and polarization.

Elongation factor Tu GTP binding domain protein 2 (Eftud2) is a spliceosomal GTPase that serves as an innate immune modulator restricting virus infection. Microglia are the resident innate immune cells and the key players of immune response in the central nervous system. However, the role of Eftud2 in microglia has not been reported. In this study, we performed immunofluorescent staining and western blot assay and found that Eftud2 was upregulated in microglia of a 5xFAD transgenic mouse model of Alzheimer's disease. Next, we generated an inducible microglia-specific Eftud2 conditional knockout mouse line (CX3CR1-CreER; Eftud2f/f cKO) via Cre/loxP recombination and found that Eftud2 deficiency resulted in abnormal proliferation and promoted anti-inflammatory phenotype activation of microglia. Furthermore, we knocked down Eftud2 in BV2 microglia with siRNA specifically targeting Eftud2 and found that Eftud2-mediated regulation of microglial proinflammatory/anti-inflammatory phenotype activation in response to inflammation might be dependent on the NF-κB signaling pathway. Our findings suggest that Eftud2 plays a key role in regulating microglial polarization and homeostasis possibly through the NF-κB signaling pathway.

In Situ Polymerization and Flame Retardant Mechanism of Bio-Based Nitrogen and Phosphorus Macromolecular Flame Retardant in Plywood.

To improve the flame retardant performance of plywood and reduce the reagent loss and moisture absorption of the flame retardant, a bio-based supramolecular flame retardant is prepared by vacuum-pressure impregnation and high-temperature in situ polymerization in plywood. The best value of bonding strength appears at 170 °C, and the limiting oxygen index (LOI) of 170BF-B plywood is 42.3%. After hot pressing, the moisture absorption rate of the 170BF-B veneer is only 18.51%, while the loss resistance rate achieves 83.45%. Its residue at 700 °C is 91.36% higher than that of poplar veneer. In the combustion process, the peak value of heat release rate (PHRR) and heat release rate (HRR) of 170BF-B plywood are only 10.69% and 37.11% of that of untreated plywood. After combustion, an intumescent flame retardant layer exhibits a graphitization trend. In the flame retardant layer, there are not only functional groups, such as P═O, PO4 3- , POC decomposed by flame retardant but also characteristic functional groups of wood fiber, like C═O, CH, etc. The prepolymer BF-B, which is composed of phytic acid, urea, and dicyandiamide polymerized with chitosan or lignocellulose to form a supramolecular flame retardant connected with POC and PON functional groups, thus improving the flame retardant and anti-loss property by in situ polymerization.

Disruption of rack1 suppresses SHH-type medulloblastoma formation in mice.

INTRODUCTION: Medulloblastoma (MB) is a malignant pediatric brain tumor that arises in the cerebellar granular neurons. Sonic Hedgehog subtype of MB (SHH-MB) is one of the major subtypes of MB in the clinic. However, the molecular mechanisms underlying MB tumorigenesis are still not fully understood. AIMS: Our previous work demonstrated that the receptor for activated C kinase 1 (Rack1) is essential for SHH signaling activation in granule neuron progenitors (GNPs) during cerebellar development. To investigate the potential role of Rack1 in MB development, human MB tissue array and SHH-MB genetic mouse model were used to study the expression of function of Rack1 in MB pathogenesis. RESULTS: We found that the expression of Rack1 was significantly upregulated in the majority of human cerebellar MB tumors. Genetic ablation of Rack1 expression in SHH-MB tumor mice could significantly inhibit MB proliferation, reduce the tumor size, and prolong the survival of tumor rescue mice. Interestingly, neither apoptosis nor autophagy levels were affected in Rack1-deletion rescue mice compared to WT mice, but the expression of Gli1 and HDAC2 was significantly decreased suggesting the inactivation of SHH signaling pathway in rescue mice. CONCLUSION: Our results demonstrated that Rack1 may serve as a potential candidate for the diagnostic marker and therapeutic target of MB, including SHH-MB.

VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer.

Voltage-dependent anion channels (VDACs) are situated in the outer membrane of the mitochondria and serve as gatekeepers that control metabolite and ion exchange between the cytosol and mitochondria. VDAC1 is one of the most studied members of the VDAC protein family and is overexpressed in multiple types of cancer. However, the specific biological function and regulatory mechanism of VDAC1 in breast cancer remains unclear. The present study investigated the biological role of VDAC1 in breast cancer cells using an MTS assay. The association of clinicopathological features with VDAC1 in breast cancer was analyzed by Gene Expression Profiling Interactive Analysis. The regulatory mechanism of VDAC1 was determined by cell transfection, western blot analysis, reverse transcription-quantitative (q)PCR analysis, chromatin immunoprecipitation (ChIP) and ChIP-qPCR analysis. The results of the present study demonstrated that VDAC1 promoted breast cancer proliferation and was associated with a poor prognosis in patients with breast cancer. Additionally, it was observed that the expression of VDAC1 could be decreased by the bromodomain inhibitor (JQ1), and bromodomain-containing protein 4 (BRD4) was indicated to be a regulator of VDAC1. Furthermore, results suggested that VDAC1 may be involved in the resistance of breast cancer to JQ1. Collectively, the present findings uncovered important aspects of the function of VDAC1 in the tumor progression of breast cancer, and may provide a basis for potential therapeutic strategies for the treatment of breast cancer.