OBJECTIVETo find an inhibitor to reduce the volatilization of formalin.

METHODThe saturated solution of sodium hydrosulphite (SHS) was sprayed on the surface of the anatomy specimens, then the concentration of formaldehyde in the air was tested.

RESULTSThe concentration of formaldehyde in the air of SHS sprayed group [(3.10 +/- 1.22) mg/m3] was significantly lower than that of the control group [(8.36 +/- 4.11) mg/m3, P < 0.01].

CONCLUSIONSHS may be a volatilization inhibitor for formalin, which could reduce the concentration of formaldehyde in the air.

Air Pollution, Indoor ; prevention & control ; Anatomy ; Formaldehyde ; analysis ; chemistry ; Sulfites ; chemistry ; Volatilization

Objective To investigate the expression and immune function of NOD2 signal in MyD88-/- mice. Methods MyD88-/- mice and wild-type C57 BL/6 mice were characterized by PCR. Mice model of pulmonary infection was constructed by tracheal instillation of BCG vaccine strain(attenuated strain of Mycobacterium). PBS tracheal instillation was used as negative control.Peripheral blood sample and lung tissue were collected aseptically 24 h after Mycobacterium challenge. Real-time PCR and Western blot were used to detect the expression of NOD2 gene and protein. IL-6 level in the peripheral blood was determined by enzymelinked immunosorbent assay. Results The expression of NOD2 protein in BCG infected mice was significantly higher than PBS negative control group. NOD2 protein expression in MyD88-/- mice was higher than in wild-type mice. BCG infection was associated with higher NOD2 protein expression than infection-free PBS control in both groups of animals. The IL-6 level in peripheral blood was significantly higher after BCG infection than PBS group in both MyD88-/- mice and wild type mice. Conclusions BCG can activate the NOD2 signaling pathway when MyD88-dependent pathway is deficient.

OBJECTIVE：To explo re the potential molecular mechanism of ursolic acid in the treatment of osteoporosis （OP）. METHODS：TCMSP，PubMed database and UniProt database were used to screen potential targets of monomer compound ursolic acid. OP related target genes were searched with GeneCards database. The common target genes of component-disease were obtained by Venny 2.1 online mapping tool. The protein-protein interaction （PPI）network of component-disease common target genes was constructed by using STRING database ，and topological analysis was carried out ；the core target genes ，whose degree value was greater than the average degree value ，were screened. GO functional annotation and KEGG pathway enrichment analysis of component-disease common target genes were carried out by DAVID database. AutoDock Vina 1.1.2 software was used for molecular docking ，using protein encoded by the core target gene as receptor and ursolic acid as ligand. RESULTS ：A total of 55 ursolic acid related target genes and 4 273 OP related target genes were excavated ，with a total of 44 common target genes. PPI network with above common target genes included 44 nodes and 513 edges，with an average node degree of 23.3. There were 24 core target genes ，including VEGFA，TP53，IL6，CASP3. There were 340 GO functional items were enriched （corrected P＜ 0.05），including 263 biological processes （negative regulation of apoptosis ，etc.），25 molecular functions （protein binding ，etc.） and 52 cell components （cytosol，etc.）. There were 90 KEGG signaling pathways （corrected P＜0.05），such as tumor pathway ， hepatitis B pathway ，TNF signaling pathway ，viral carcinogenesis and phosphatidylinositol 3 kinase/protein kinase B （PI3K-Akt） signaling pathway. The binding energy between ursolic acid and 6 proteins encoded by core target genes such as TP53 was lower than －5 kcal/mol，which had strong binding activity. CONCLUSIONS ：The therapeutic effect of ursolic acid on OP may be achieved by regulating VEGFA，TP53，IL6，CASP3，JUN and other core target genes and acting on multiple key pathways such as cancer pathway ， hepatitis B and TNF signaling