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SiO2/g-C3N4 composite aerogel material with high specific surface area and porous structure was prepared by direct ink writing 3D printing. The micro morphology and porous structure of the material were characterized，and its adsorption and catalytic degradation properties for high concentration Rhodamine B（RhB） in wastewater were tested. The research results showed that the 3D-printed SiO2 aerogel has a specific surface area of 482.1 m2/g，a nano porous structure with a pore volume of 1.195 cm3/g，and a good adsorption performance for RhB. The porous structure of SiO2/g-C3N4 composite aerogel prepared by modifying with g-C3N4 had little change and maintained high adsorption performance，and the removal rate of RhB（100 mg/L） by 3D-printed composite under UV could reach more than 99%. After five cycles of testing，the removal rate of RhB by SiO2/g-C3N4 composite aerogel was still 92.98%，compared with 55.75% for 3D-printed SiO2 aerogel. According to the mechanism analysis，g-C3N4 in the composite could absorb light energy and generate photogenerated electron-hole pairs ，the electron-hole pairs could react with H2O and O2 to produce oxidizing active substances superoxide radicals，and finally participated in the photocatalytic oxidation and reduction reaction to catalyze the degradation of RhB macromolecules. The high specific surface area of the 3D printing structure realized the large reaction contact area between the catalyst and RhB，and improved the photocatalytic degradation efficiency and cycle stability of the composite.

Traumatic brain injury (TBI), a risk factor for later-life dementia, leads to salient brain atrophy, particularly in the white matter. It is not clear how white matter atrophy progresses or why some brain regions are damaged while others are spared. We hypothesized that spatial variations of cell-specific gene expression contributed to the selective white matter loss vulnerability following mild TBI (mTBI). Gene expression data were sourced from the publicly available Allen Human Brain Atlas, which comprises microarray data spanning nearly the entire brain, derived from six neurologically normal adult donors. A total of 100 patients with acute stage (within 7 days post-injury) mTBI were enrolled. Of these, 60 patients were followed up at 3 months post-injury and 37 were followed up at 6–12 months post-injury. In addition, 59 healthy controls (HCs), matched for age, gender, and education, were included for comparative analysis. White matter volume changes were analyzed at both the acute stage, 3 months, and 6–12 months follow-up in mTBI patients compared with HCs. Patients with mTBI exhibited significant white matter atrophy in the frontal, parietal, and temporal cortices at 3 months post-injury, which even persisted at 6–12 months follow-up. In addition, mTBI patients with cognitive deficits showed more severe brain atrophy compared with those without cognitive deficits. Crucially, the gene expression marking endothelial cells and S1 pyramidal neurons were associated with increased brain atrophy, whereas the gene expression marking microglia and CA1 pyramidal neurons were associated with decreased brain atrophy in mTBI patients at 3 months post-injury. Microglia and endothelial cells can explain 23.6% of regional variations in the white matter atrophy. These findings suggested that modulating cellular activation, especially by promoting microglial activation at 3 months post-injury, might be a promising approach to prevent white matter atrophy, enhance cognitive outcomes, and reduce the risk of later-life dementia. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is considered to initiate cerebrovascular pathology, involving in the development of multiple forms of neurodegeneration. However, it is unknown the relationships between imaging marker of cerebrovascular injury (white matter hyperintensity, WMH), its load on white matter tract and disrupted brain dynamics with cognitive function in mild TBI (mTBI). MRI data and neuropsychological assessments were collected from 85 mTBI patients and 52 healthy controls. Between‐group difference was conducted for the tract‐specific WMH volumes, white matter integrity, and dynamic brain connectivity (i.e., fractional occupancies [%], dwell times [seconds], and state transitions). Regression analysis was used to examine associations between white matter damage, brain dynamics, and cognitive function. Increased WMH volumes induced by mTBI within the thalamic radiation and corpus callosum were highest among all tract fibers, and related with altered fractional anisotropy (FA) within the same tracts. Clustering identified two brain states, segregated state characterized by the sparse inter‐independent component connections, and default mode network (DMN)‐centered integrated state with strongly internetwork connections between DMN and other networks. In mTBI, higher WMH loads contributed to the longer dwell time and larger fractional occupancies in DMN‐centered integrated state. Every 1 mL increase in WMH volume within the left thalamic radiation was associated with a 47% increase fractional occupancies, and contributed to 65.6 s delay in completion of cognitive processing speed test. Our study provided the first evidence for the structural determinants (i.e., small vessel lesions) that mediate the spatiotemporal brain dynamics to cognitive impairments in mTBI. [ABSTRACT FROM AUTHOR]

To enhance the anesthetic efficacy and reduce toxic side effects, a strategy is proposed involving the utilization of general anesthetics of Propofol (Pro) and Etomidate (Eto) to synergistic inhibition GABA receptors simultaneously. Four‐in‐one molecular aggregates were prepared to implement this strategy, which comprised of Pro and Eto with the bridging molecule monoglyceride monooleate (GMO) and surfactant F127 through intermolecular forces. The blood‐brain barrier (BBB) targeted lactoferrin (LF) is affixed to their surface, obtaining the final molecular aggregates. By employing lactoferrin enrich aggregates to the BBB, followed by ultrasound combine microbubbles to open the BBB, a remarkable 4.5‐fold enhancement in brain drug delivery was achieved. The molecular aggregates group maintained stable parameters of heart rate, diastolic blood pressure, and systolic blood pressure. A notable increase of more than twice therapeutic index (TI) value was observed, implying their higher anesthesia efficiency and reduced toxicity. Electroencephalogram (EEG) experiments demonstrate a significant elevation in the proportion of δ waves from 28% to 80% for aggregates, accompanied by a nearly fivefold reduction in the proportion of θ waves, meaning a significant improvement in synergistic anesthesia effectiveness (interaction index 0.289) with lower drug dosage. Furthermore, mouse immunofluorescence brain slice experiments suggest Pro and Eto enter the GABA receptor simultaneously, resulting in synergistic inhibition of GABA receptors. [ABSTRACT FROM AUTHOR]

Al2O3-SiO2 aerogel (ASA) was prepared by convenient ambient pressure drying using inexpensive AlCl3·H2O as precursor, and silicon was deposited during the aging of aluminum gel. To explore the influence of Chloride ion on the property of ASA, ion exchange technology was used to remove the Chloride ion in the aluminum sol. ASA exhibits a low thermal conductivity of 0.029 W m−1 K−1 at room temperature, and the specific surface area of Cl-free ASA after heat-treated at 1200 °C is 95.2 m2/g, which is higher than that of the chlorine-containing aerogel (11.4 m2/g), showing enhanced thermal stability of ASA. Analysis of XRD and XPS indicate that the removal of chloride ions makes it more difficult for ASA to establish Al–O–Si groups during the aging process, so the γ-Al2O3 and cristobalite phase do not transform to mullite phase at 1200 °C. Due to the better thermal stability of ASA, it has great potential for high-temperature applications in the fields of insulation, thermal protection materials, and building external wall thermal insulation. [ABSTRACT FROM AUTHOR]

Recent evidence suggests that enhanced neutrophil extracellular trap (NET) formation activates plasmacytoid dendritic cells and serves as a source of autoantigens in SLE. We propose that aberrant NET formation is [...]

Hierarchical N-doped carbon nanotubes (NCTs) with controllable aspect ratios were developed for CO2 adsorption. In this work, NCTs were synthesized by coating different amounts of 3-aminophenol/formaldehyde resin (APF) on the outer layer of silica nanotubes, carbonizing in N2 at 700∘C and removing the silica and Ni template by hydrofluoric acid etching. The obtained NCTs were activated by K2CO3. After activation, micropores on the activated N-doped carbon nanotubes (ANCTs) were enriched, the micro-surface area and pore volume of ANCT-1.0 reached 1195 m2 g − 1 and 0.45 cm3 g − 1 , respectively, and the corresponding adsorption capacity increased by 50% (4.50 mmol g − 1 at 0∘C and 1 bar). Moreover, ANCT-1.0 maintained a high stability throughout consecutive adsorption–desorption cycles. The advantages of hierarchical N-doped carbon nanotubes, including their meso–microporous structures, high geometric aspect ratio and good stability, make them valuable and promising materials to capture carbon dioxide. N-doped carbon nanotubes (NCTs) were synthesized by coated different amounts of 3-aminophenol/formaldehyde resin on the outer layer of silica nanotubes, carbonized and acid etching. After activation by K2CO3, more micropores are generated on the surface of NCTs, which increased the surface areas and pore volumes of NCTs. The mesoporous in the adsorbent provides an ideal channel for the transmission of CO2. The van der Waals force between CO2 molecule and micropores in the wall effectively enhancing the adsorption capacity of NCTs. [ABSTRACT FROM AUTHOR]

Individuals with systemic lupus erythematosus (SLE) have a striking increase in the risk of premature atherosclerosis, a complication preceded by significant subclinical vascular damage. A proposed mechanism leading to accelerated vascular disease in SLE is an imbalance between vascular damage and repair, as patients with this disease display significant abnormalities in phenotype and function of endothelial progenitor cells. In addition, individuals with SLE have a higher incidence of insulin resistance which may further contribute to the increased cardiovascular risk. This study examined the role of the peroxisome proliferator activated receptor gamma agonist pioglitazone in improving endothelial function, endothelial progenitor cell numbers and functional capacity, metabolic parameters, and disease activity in the lupus-prone murine model New Zealand Black/New Zealand White (NZB x NZW)F(1). Ten-week-old prenephritic female NZB/NZW F(1) mice were exposed to 10 or 25 mg/kg/day of oral pioglitazone or vehicle for 15 or 24 wk. Mice exposed to pioglitazone exhibited pronounced enhancement in endothelial-dependent vasorelaxation of thoracic aortas and in endothelial progenitor cell function, as assessed by the capacity of bone marrow-derived endothelial progenitor cells to differentiate into mature endothelial cells. Pioglitazone-treated mice showed improvement in insulin resistance, adipokine, and lipid profile. Kidneys from pioglitazone-treated mice showed significant decreases in immune complex deposition, renal inflammation, T cell glomerular infiltration, and intrarenal synthesis of TNF-alpha, IL-1beta, and VCAM-1. These results indicate that peroxisome proliferator-activated receptor gamma agonists could serve as important tools in the prevention of premature cardiovascular disease and organ damage in SLE.