Objective To study the morphological characteristics of femurs of adult human and 11 kinds of adult animals fromcattle, horses, pigs, goats, sheep, dogs, cats, rabbits, geese, ducks, chickens, and to establish an effective species identification method among various species. Methods The 4 cmmid-dia-physeal segment of the femur fromadult human (older than 20 years old) at autopsy w as obtained. Addi-tionally, the 4 cmones from11 kinds of adult animals w ere obtained. After decalcification, all femurs w ere made into slices, and then w ere observed by optical microscope. The 25 indexes w ere selected and analyzed by step discriminant analysis according to differences betw een human and mammal, human and poultry, and human and 11 kinds of animals. Results The histological structure of bone mineral density of middle part of femur had obvious characteristics among the species. And the morphology and number of osteon show ed the trend of obvious biological evolution. There w ere 11 indexes w ith significant differ-ences betw een human and 11 kinds of animals to establish some mathematical models to discriminate all species. The correct discrimination rate w as 96.3% betw een human and mammal. The correct discrimina-tion rate w as up to 100% betw een human and poultry, and w as 89.4% among human, mammal and poultry. Conclusion The mathematical models have good correct discrimination rate among human and the other animals, w hich could be applied in the practical species identification cases.

Objective To explore the mechanism of action of curcumin in the treatment of silicosis by network pharmacology combined with molecular docking technology. Methods The targets prediction network of curcumin in treating silicosis was established based on the collection of targets of curcumin and silicosis in multiple databases, cross-targets were submitted to the STRING database, and their connectivity was analyzed by Cytoscape software. Gene ontology (GO) function analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on the top 20 genes. The molecular docking was performed on the key targets to study the mechanism of action of curcumin in treating silicosis. Results A total of 311 targets related to curcumin, 270 targets related to silicosis, and 74 cross-targets were obtained from the databases. GO function analysis revealed 2 665 related pathways, and KEGG pathway enrichment analysis revealed 188 related pathways. Molecular docking results showed that curcumin had good binding ability with the targets of mitogen-activated protein kinase 3 (MAPK3), interleukin (IL) 6, serine/threonine kinase 1 (AKT1), vascular endothelial growth factor A (VEGFA), signal transducer and activator of transcription 3, albumin, Jun proto-oncogene, tumor necrosis factor (TNF), IL1B, tumor protein p53, C-C motif chemokine ligand 2 and fibronectin 1. Conclusion The therapeutical effects of curcumin on silicosis were implemented through multi-targets and multi-pathways. Curcumin may play a role in the treatment of silicosis by binding to the core targets MAPK3, IL6, AKT1, VEGFA and TNF and regulating the MAPK, IL6, TNF, phosphatidylinositol 3-kinase/protein kinase B and VEGF signaling pathways.

Objective To detect and analyze the susceptibility genes of methyl acetate poisoning in patients by whole exome sequencing. Methods Two patients with occupational acute severe methyl acetate poisoning and their first-degree relatives who work in the same occupation and position with similar working hours were selected as the research subjects by judgment sampling method. Peripheral blood was collected for whole exome sequencing. The sequencing data was compared with the public genome database to screen the mutation sites and find out the gene sites related to methyl acetate poisoning. The suspected pathogenic mutation genes were annotated and interpreted. Results The results of whole exome sequencing showed that there were 40 differential genes between the patients with methyl acetate poisoning and their first-degree relatives, including 80 single nucleotide polymorphisms and eight Indel with specific marker sequence index. Among these, the genes with strong correlation were carboxyesterase 1 (CES1) and mucin (MUC) 5B. The CES1 gene loci c.248C>T (p.Ser83Leu) heterozygous mutations, MUC5B gene loci c.6635C>T (p.Thr2212Met) and c.7685C>T (p.Thr2562Met) heterozygous mutations in patients with methyl acetate poisoning were detected. They were missense mutations. By constructing a protein-protein interaction network, a total of 11 pairs of interactions with high levels of evidence were identified, involving genes such as lysine methyltransferase 2C, HECT and RLD domains containing E3 ubiquitin protein ligase 2, neutrophil cytoplasmic factor 1, nicotinamide adenine dinucleotide phosphate oxidase 3, C-terminal binding protein 2, zinc finger protein 717, FSHD region gene 2 family member C, FSHD region gene 1, MUC4, MUC6, MUC5B, and MUC12. Conclusion The polymorphism of CES1 and MUC5B genes may be related to the occurrence and development of methyl acetate poisoning in patients.

Objective To evaluate the effect of hydrogen on autophagy during inflammatory responses following lung injury in burned mice.Methods Ninety-six clean-grade healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups (n=24 each) using a random number table:sham operation group (SH group),H2 group (H2 group),burn group (B group) and burn plus H2 group (B+H2 group).Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a 92 ℃ scald device for 18 s in B and B+H2 groups.Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a scald device of skin temperature for 18 s in SH and H2 groups.Mice inhaled 2％ H2 for 1 h starting from 1 and 6 h after burn in H2 and B+H2 groups.The animals were sacrificed at 24 h after burn and lungs were removed for determination of wet/dry weight ratio (W/D rario),expression of autophagy-related microtubule-associated protein 1 light chain 3 (LC3) (by Western blot),activity of myeloperoxidase (MPO),and contents of interleukin-6 (IL-6) and high mobility group box 1 (HMGBI) (by enzyme-linked immunosorbent assay).The ratio of LC3-Ⅱ to LC3-Ⅰ expression (LC3-Ⅱ/LC3-Ⅰ) was calculated.The bronchoalveolar lavage fluid (BALF) was collected at 24 h after burn to detect the concentrations of IL-6 and HMGB1 and to count neutrophil.Results Compared with group SH,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGB1 in BALF and neutrophil count were significantly increased at 24 h after scald in B and B+H2 groups (P＜0.05).Compared with group B,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGBl in BALF and neutrophil count were significantly decreased at 24 h after scald in group B+H2 (P＜0.05).Conclusion Hydrogen can alleviate the lung injury in burned mice,and the mechanism is related to enhancing autophagy.

Lamin B1 (LMNB1) is highly expressed in liver cancer tissues, and its influence and mechanism on the proliferation of hepatocellular carcinoma cells were explored by knocking down the expression of the protein. In liver cancer cells, siRNAs were used to knock down LMNB1. Knockdown effects were detected by Western blotting. Changes in telomerase activity were detected by telomeric repeat amplification protocol assay (TRAP) experiments. Telomere length changes were detected by quantitative real-time polymerase chain reaction (qPCR). CCK8, cloning formation, transwell and wound healing were performed to detect changes in its growth, invasion and migration capabilities. The lentiviral system was used to construct HepG2 cells that steadily knocked down LMNB1. Then the changes of telomere length and telomerase activity were detected, and the cell aging status was detected by SA-β-gal senescence staining. The effects of tumorigenesis were detected by nude mouse subcutaneous tumorigenesis experiments, subsequent histification staining of tumors, SA-β-gal senescence staining, fluorescence in situ hybridization (FISH) for telomere analysis and other experiments. Finally, the method of biogenesis analysis was used to find the expression of LMNB1 in clinical liver cancer tissues, and its relationship with clinical stages and patient survival. Knockdown of LMNB1 in HepG2 and Hep3B cells significantly reduced telomerase activity, cell proliferation, migration and invasion abilities. Experiments in cells and tumor formation in nude mice had demonstrated that stable knockdown of LMNB1 reduced telomerase activity, shortened telomere length, senesced cells, reduced cell tumorigenicity and KI-67 expression. Bioinformatics analysis showed that LMNB1 was highly expressed in liver cancer tissues and correlated with tumor stage and patient survival. In conclusion, LMNB1 is overexpressed in liver cancer cells, and it is expected to become an indicator for evaluating the clinical prognosis of liver cancer patients and a target for precise treatment.
Animals ; Mice ; Telomerase/metabolism* ; Carcinoma, Hepatocellular/genetics* ; Liver Neoplasms/genetics* ; Telomere Shortening ; In Situ Hybridization, Fluorescence ; Mice, Nude ; Telomere/pathology* ; Carcinogenesis