Preparation of Aerogel-like Silica Foam with the Hollow-Sphere-Based 3D Network Skeleton by the Cast-in Situ Method and Ambient Pressure Drying

Silica aerogels have incomparable advantages among thermal insulation materials because of their ultralow density and thermal conductivity, but cumbersome production processes, high cost, and low mechanical stability limit their practical application. In this study, a novel aqueous process to prepare lightweight aerogel-like silica foams (ASFoams) through the cast-in situ method and ambient pressure drying was proposed with multiblock polyurethane surfactant as the vesicle template. ASFoams possess a unique loose stacking morphology of the silica hollow sphere with a 3D network structure as the skeleton, which endues ASFoams with a low density of 0.059 g/cm3, low thermal conductivity of 36.1 mW·k–1·m–1, and pretty good mechanical properties. These properties make ASFoams a promising option for thermal insulation in industrial, aerospace, and other extreme environmental conditions. In addition, the micromorphology of ASFoams can be adjusted by changing the reaction conditions, which may provide a facile method for the preparation of a silica aerogel-like foam with adjustable microstructure

Insights into the Acceleration Mechanism of Intracellular N and Fe Co-doped Carbon Dots on Anaerobic Denitrification Using Proteomics and Metabolomics Techniques

Bulk carbon-based materials can enhance anaerobic biodenitrification when they are present in extracellular matrices. However, little information is available on the effect of nitrogen and iron co-doped carbon dots (N, Fe-CDs) with sizes below 10 nm on this process. This work demonstrated that Fe–NX formed in N, Fe-CDs and their low surface potentials facilitated electron transfer. N, Fe-CDs exhibited good biocompatibility and were effectively absorbed by Pseudomonas stutzeri ATCC 17588. Intracellular N, Fe-CDs played a dominant role in enhancing anaerobic denitrification. During this process, the nitrate removal rate was significantly increased by 40.60% at 11 h with little nitrite and N2O accumulation, which was attributed to the enhanced activities of the electron transport system and various denitrifying reductases. Based on proteomics and metabolomic analysis, N, Fe-CDs effectively regulated carbon/nitrogen/sulfur metabolism to induce more electron generation, less nitrite/N2O accumulation, and higher levels of nitrogen removal. This work reveals the mechanism by which N, Fe-CDs enhance anaerobic denitrification and broaden their potential application in nitrogen removal

M-CSFr inhibitor suppressed mechanical allodynia in early phase of neuropathic pain and microglial proliferation of spinal dorsal horn after peripheral nerve injury.

<p>(left in A) In early phase, the GW2580 (100 nmol, i.t.) was given 3 times at same time, 25 and 40 hours after SNI as arrows shown in bottom. Whereas GW2580 had no effect on mechanical allodynia at 1 day after SNI, mechanical allodynia from 2 to 3 days after SNI was partially but significantly blocked by the repetitive administration of GW2580. (right in A) In late phase, the GW2580 (100 nmol, i.t.) was given 3 times at 12 and 13 and 13 2/3 days after SNI as arrows shown in bottom. Repetitive injection of GW2580 had no effect on the late phase of neuropathic pain after peripheral nerve injury. Open circles indicate vehicle treated animals, solid circles indicate GW2580 treated animals. Data represent as mean ± SEM; <i>n</i> = 4–6 per group; #, <i>p</i> <0.05 compared with pretreatment; §, <i>p</i> < 0.05 compared with vehicle animals at 2 days after SNI. (B) Iba1 (upper lane), ki67 (middle lane) and p-p38 (bottom lane) immunostaining in dorsal horn (lamina I-III) in the contralateral and ipsilateral side of vehicle treated animals and ipsilateral side of GW2580 treated animals at day 2 after SNI. (C) Graphs show quantification of the number of iba1, ki67 and p-p38 positive cells. (D, E) Double immunofluorescence shows that ki67 (green in D) and p-p38 (green in E) are predominantly colocalized with Iba1 (red in D, E) positive cells in spinal dorsal horn of vehicle treated animals at day 2. <i>n</i> = 4 per group; #, <i>p</i> <0.05; ctr, contra; Scale bar: 100 μm in B; 25 μm in D, E.</p

MS/MS spectra of compounds 37 (a) and 41 (b) and proposed fragmentation pathways of compound 37.

<p>MS/MS spectra of compounds 37 (a) and 41 (b) and proposed fragmentation pathways of compound 37.</p

MS/MS spectra of compound 35 and proposed fragmentation pathways of compound 35.

<p>MS/MS spectra of compound 35 and proposed fragmentation pathways of compound 35.</p

M-CSF receptor mRNA robustly induced in spinal microglia after peripheral nerve injury.

<p>PCR products from the spinal cord (L4-5) taken from 0 (naive), 0.5, 1, 2, 3, 7, and 14 days after SNI. Representative gel panels are shown in A. M-CSFr mRNA levels was normalized against GAPDH (<i>n</i> = 4, mean ± SEM; #, <i>p</i> < 0.05 compared with naive). Darkfield ISHH-images show the expression of M-CSFr mRNA (B, D) in spinal cord of naive (B) and 3 days after nerve injury (D). (C, E) Higher magnification brightfield images of dorsal horn of the left-hand photographs. Sections were counterstained by H-E. (F-H) Double labeling analysis of M-CSFr mRNA at 3 days after SNI. Photographs show combined ISHH for M-CSFr with NeuN (F), GFAP (G) and Iba1 (H) of the spinal dorsal horn at 3 days after SNI. Arrowheads indicate single-labeled cells by ISHH (aggregation of grains), and open arrowheads indicate single immunostained cells (brown staining). Sections were counterstained by hematoxylin. Arrows indicate double-labeled cells. Scale bar = 500 μm in B, D; 25 μm in C, E-H. contra, contralateral; ipsi, ipsilateral.</p

Expression of mRNA for a series of CSFs and IL-34 in DRG after peripheral nerve injury.

<p>PCR products from the L4-5 DRG taken from 0 (naive), 0.5, 1, 2, 3, 7, and 14 days after SNI. Representative gel panels are shown in A. (B) Electrophoresis image shows positive control bands for each primer set in thymus. Use of each gene primers result in PCR products of 474 bp (M-CSF), 524 bp (IL-34), 384 bp (GM-CSF), 531bp (G-CSF), and 270 bp (GAPDH), respectively. (C) Graphs show Quantification of the relative mRNA levels of M-CSF (left), IL-34 (right) in DRG after SNI and M-CSF (middle) in DRG after intraplantar injection of CFA. M-CSF and IL-34 mRNA levels were normalized against GAPDH (<i>n</i> = 4; mean ± SEM; #, <i>p</i> < 0.05 compared with naive). (D-M) Expression pattern of M-CSF and IL-34 mRNAs in DRG after peripheral nerve injury. Darkfield ISHH-images show the expression of M-CSF (D, F) and IL-34 (J, L) mRNAs in DRG of naive (D, J) and 2 days after nerve injury (F, L), respectively. (E, G, K, M) Higher magnification brightfield images of the left-hand photographs. The solid arrowheads indicate samples of the positively labeled cells. Sections were counterstained by H-E. (H) Scatterplot diagrams showing the distribution of M-CSF mRNA in DRGs of naive (left) and 2 days after nerve injury (right). Individual cell profiles are plotted according to the cross-sectional area (um²; along the x-axis) and signal intensity (S/N ratio, along the y-axis). The red dashed lines indicate the borderline between the negatively and positively labeled cells (S/N ratio = 5). (I) Photograph shows the double labeling study of ISHH for M-CSF mRNA with immunostaining of ATF3 in DRG at 2 days after nerve injury. Sections were counterstained by hematoxylin. Open arrowheads indicate single immunostained cells (brown staining). Arrows indicate double-labeled cells. Scale bar = 500 μm in D, F, J, L; 25 μm in E, G, I; 12.5 μm in K, M.</p

Repetitive intrathecal administration of M-CSF induced mechanical hypersensitivity and microglial proliferation of spinal dorsal horn.

<p>(A) The recombinant M-CSF (10 μg, i.t.) was given twice at a 24 h interval, and the behavioral testing was performed 24 h after the each injection. The arrows shown in bottom are time point of injections. Open circles indicate vehicle treated animals (<i>n</i> = 5), solid circles indicate recombinant M-CSF treated animals (<i>n</i> = 5). #, <i>p</i> < 0.05 compared with pretreatment; †, <i>p</i> < 0.05 compared with vehicle animals at 1 day after injection, §, <i>p</i> < 0.05 compared with vehicle animals at 2 days after injection. Data represent as mean ± SEM; <i>n</i> = 5 per group. (B) Iba1 (upper lane), ki67 (middle lane) and p-p38 (bottom lane) immunostaining in dorsal horn (lamina I-III) vehicle and recombinant M-CSF treated animals. (C) Graphs show quantification of the number of iba1, ki67 and p-p38 positive cells. (D, E) Double immunofluorescence shows that ki67 (green in D) and p-p38 (green in E) are predominantly colocalized with Iba1 (red in D, E) positive cells in spinal dorsal horn of M-CSF treated animals at day 2. Data represent as mean ± SEM; <i>n</i> = 4 per group. #, <i>p</i> < 0.05 compared with vehicle;Scale bar: 100 μm in B; 25 μm in D, E.</p

MS/MS spectra and proposed fragmentation pathways of compounds 39, 40, 42 and 45.

<p>MS/MS spectra and proposed fragmentation pathways of compounds 39, 40, 42 and 45.</p

EIC-MS peaks of all possible caffeoylquinic acids in Re-Du-Ning injection.

<p>EIC-MS peaks of all possible caffeoylquinic acids in Re-Du-Ning injection.</p