Notes

[Quantitative evaluation strategies to whitened matter microstructure based on diffusion tensor imaging and its program in long-term soreness research].
The ic-ELISA and colloidal gold immunochromatographic strip assay using the prepared monoclonal antibody against COT have been proved to be reliable for the rapid detection of COT in human urines, which may be used for monitoring of environmental tobacco smoke.
The ic-ELISA and colloidal gold immunochromatographic strip assay using the prepared monoclonal antibody against COT have been proved to be reliable for the rapid detection of COT in human urines, which may be used for monitoring of environmental tobacco smoke.
To investigate the role of IL-17A in promoting the activation of lung fibroblasts and the secretion of chemokine CXCL12, and to explore the possible mechanism.

Lung tissues of BALB/c mice were collected after intraperitoneal injection of recombinant mouse IL-17A (rmIL-17A). Real-time RT-PCR and Western blotting were used to detect the expression levels of α-smooth muscle actin (α-SMA) and collagen I in lung tissues, and immunohistochemical staining and real-time RT-PCR were used to determine the expression of CXCL12. Normal mouse primary lung fibroblasts were isolated and cultured, and identified by immunofluorescence staining with optical microscopy. Cells and supernatant of culture medium were collected after stimulation with rmIL-17A at different concentrations. mRNA levels of α-SMA, collagen I, and CXCL12 in the cells were determined by real-time RT-PCR, and the levels of collagen I and CXCL12 in the supernatant of culture medium were determined by ELISA.

The mRNA and protein levels of α-SMA and colnt of lung fibrosis. CXCL12, a chemokine secreted by activated fibroblasts, may be involved in this process.
To investigate the protective effect of
gene knockout on Alzheimer's disease (AD) in mice.

The animal model of AD was established by intraperitoneal injection of D-galactose and brain-localized injection of amyloid β-protein (Aβ)
in wild type C57BL/6 mice and
gene knockout mice. Morris water maze, Y maze and tail suspension test were used to assess the cognitive function and anxiety-like behaviors in mice. Aβ deposition in the hippocampus was detected by immunofluorescent staining. Western blotting analysis was conducted to detect the expression of related proteins in the brain. Mouse cortical primary neurons were cultured and AD cell model was established. MTT assay was used to detect cell viability after modeling.

Behavioral results showed that cognitive deficits were found in wide type mice after induction of AD as its prolonged escape latency (
<0.05) and decreased crossing number of platform and target zone duration (all
<0.05); while the knockout of
alleviated cognitive deficit induced by AD (all
<0.05). Aβ immunofluorescence staining showed that the deposition of Aβ in the hippocampal region and expression of cleaved caspase 3 in the brain in
knockout mice was reduced compared with that of wild type mice (all
<0.05). The expression of LC3-Ⅱ and P62 increased after AD was induced in wild type mice, while the autophagy in
knockout mice was activated as the increase expression of LC3-Ⅱ and decrease expression of P62 (all
<0.05). In the AD cell model, the results of MTT assay were consistent with the animal experiments, and the protective effect of
knockdown was eliminated after the treatment of the autophagy inhibitor chloroquine (all
<0.05).

The knockdown of
shows a protective effect on AD induced by D-galactose and Aβ
in mice, which may be related to its function of activating autophagy.
The knockdown of Sirt3 shows a protective effect on AD induced by D-galactose and Aβ1-40 in mice, which may be related to its function of activating autophagy.
To detect the differentially expressed inflammatory proteins in acute gouty arthritis (AGA) with protein chip.

The Raybiotech cytokine antibody chip was used to screen the proteomic expression in serum samples of 10 AGA patients and 10 healthy individuals. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were applied to determine the biological function annotation of differentially expressed proteins and the enrichment of signal pathways. ELISA method was used to verify the differential protein expression in 60 AGA patients and 60 healthy subjects. The ROC curve was employed to evaluate the diagnostic value of differential proteins in AGA patients.

According to|log
FC|>log
1.2 and corrected
<0.01, 4 most differentially expressed proteins in AGA patients were identified, including tumor necrosis factor receptor super family members Ⅱ (TNF RⅡ), macrophage inflammatory protein 1β (MIP-1β), interleukin-8 (IL-8), and granulocyte-macrophage colony stimulating factor (GM-CSF). GO and KEGG enrichment analysis showed that the differentially expressed proteins were related to inflammation, metabolism and cytokine pathways. find more The ELISA results showed that serum levels of differentially expressed proteins were significantly different between AGA patients and healthy subjects(all
<0.01). ROC curve analysis showed that the areas under the curve (AUCs) of GM-CSF, IL-8, MIP-1β and TNF RⅡ for predicting AGA were 0.657 (95%
0.560-0.760, sensitivity 68.33%, specificity 50.00%), 0.994 (95%
0.980-1.000, sensitivity 100.00%, specificity 61.67%), 0.980 (95%
0.712-0.985, sensitivity 95.00%, specificity 98.33%) and 0.965 (95%
0.928-1.000, sensitivity 100.00%, specificity 10.00%), respectively.

Proteomics can be applied to identify the biomarkers of AGA, which may be used for risk prediction and diagnosis of AGA patients.
Proteomics can be applied to identify the biomarkers of AGA, which may be used for risk prediction and diagnosis of AGA patients.
To investigate the functional pathways enriched and differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) of patients with gram-positive and gram-negative sepsis.

Dataset GSE9960 obtained from NCBI GEO database containing PBMC samples from 16 non-infectious systematic inflammatory response syndrome (SIRS) patients, 17 gram-positive septic patients and 18 gram-negative septic patients were included in the study. Functional pathway annotations were conducted by gene set enrichment analysis and weighted gene co-expression network analysis. DEGs were filtered and master DEGs were then validated in PBMCs of gram-positive septic, gram-negative septic and non-infectious SIRS patients.

The enriched gene sets in gram-positive sepsis and gram-negative sepsis were significantly different. The results indicated the opposite co-expression networks in SIRS and gram-negative sepsis, and the entirely different co-expression networks in gram-positive and gram-negative sepsis. Furthermore, we validated that
was up-regulated in gram-positive sepsis (
<0.
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