Objective To investigate the expression of malondialdehyde ( MDA) in esophageal mu-cosa of different types of gastroesophageal reflux disease ( GERD) patients and its role in the esophageal in-flammation. Methods According to the inclusion and exclusion criteria, 42 patients hospitalized in the the Xinjiang Uygur Autonomous Region People's Hospital from December 2017 to October 2018 were selected as the research group. 8 healthy subjects completed physical examination were set up as healthy control group. GERD completed GERDQ score, 24 h pH monitoring, and taken 3 cm on the dentate line of the esophagus as a specimen. The study group was divided into non-erosive reflux disease (NERD) group (17 cases) and Ero-sive reflux disease [erosive esophagitis (RE)] group (25 cases). Then hematoxylin-eosin (HE) staining, immunohistochemistry, real-time polymerase chain reaction ( qPCR ) , enzyme-linked immunosorbent assay (ELISA) methods were used to detect inflammation, oxidative stress (MDA), antioxidant enzyme [manga-nese superoxide dismutase (Mn SOD), glutathione (GSH), catalase (CAT)], and proinflammatory cyto-kines [monocyte chemotactic protein-1 (MCP-1), interlukin-8 (IL-8), tumor necrosis factorα(TNF-α)]. Results There was no significant difference in body mass index ( BMI ) between the three groups ( P >0. 05). 24 h pH monitoring of esophagus showed that the indexes of weak acid reflux (40. 05). In RE group , the infiltration of immune cells (neutrophils, eosinophils), nipple lengthening, edema and other inflammatory changes were found in the esophageal mucosa, and the inflammation score reached the peak, which was signif-icantly higher than that in NERD group, with statistical significant difference (P<0. 001). The positive ex-pression of MDA in the two groups ( NERD, RE) was higher than that in the control group, and the MDA ex-pression in the RE group was almost covered with the full layer esophagus. The serum MDA concentration in the NERD and RE groups was significantly higher than that in the control group (P<0. 001). Compared with the NERD group, the serum MDA in the RE group reached the peak (P<0. 01). The relative expression of mRNA ( Mn SOD, GSH and CAT) in NERD group and RE group was significantly decreased, and there was a significant difference between the three groups (P<0. 001). Compared with the NERD group, the mRNA expression level of Mn SOD and CAT in RE group was significantly decreased (P<0. 01). The relative ex-pression of mRNA (MCP-1, IL-8, TNF- α) increased significantly in the two groups (NERD, RE), and there was a statistically significant difference between the three groups ( P <0. 001 ) . Compared with the NERD group, the expression of its inflammatory factors in the RE group significantly increased (P<0. 01). Conclusions The expression level of MDA in different types of GERD is significantly higher, which may be closely related to esophageal inflammation induced by acid reflux.

BACKGROUND:Toll-like receptors are an important class of pattern recognition receptors that have important functions in pathogen immunity and cytokine synthesis by recognizing specific molecular patterns.Previous studies have found that different types of bone tissue cells also express Toll-like receptors.Activation or inhibition of Toll-like receptors can have significant effects on osteoblast and osteoclast function through multiple pathways. OBJECTIVE:To summarize the expression and action pathways of Toll-like receptors in osteoblasts and osteoclasts,in order to further elucidate the biological mechanisms involved in the regulation of Toll-like receptors under physiological and pathological conditions. METHODS:Relevant literature was retrieved from databases such as PubMed and CNKI as of December 2022.The Chinese and English search terms included"Toll-like receptor,osteoblast,osteoclast,mesenchymal stem cells,macrophage,cytokine,signaling pathway".According to the research needs,the corresponding criteria were established to screen the final literature. RESULTS AND CONCLUSION:(1)Toll-like receptors could directly regulate osteoblast and osteoclast differentiation through the activation of related signaling pathways.(2)Toll-like receptor activation induces cytokine production and exerts regulatory effects.(3)Toll-like receptor activation can affect the survival and migration ability of osteoblasts and osteoclasts.(4)Toll-like receptors in osteoblasts and osteoclasts are activated in certain diseases and pathological settings and are involved in intercellular interactions.

BACKGROUND:Tumor necrosis factor-α is a broadly acting inflammatory cytokine that plays an important role in the immune inflammatory response of the body.The current study concluded that tumor necrosis factor-α has significant biological effects on a variety of bone tissue cells. OBJECTIVE:To summarize the expression and action pathways of tumor necrosis factor-α in osteoblastic and osteoclastic cells to further elucidate the regulatory role of tumor necrosis factor-α on bone tissue cells. METHODS:PubMed and CNKI were searched until March 2023,and the Chinese search terms included"tumor necrosis factor α,osteoblast,osteoclast,osteoclast,osteoprogenitor";the English search terms included"TNF-α,osteoblast,osteoclast,osteocyte,osteoprogenitor cell".The corresponding criteria were established according to the research needs,and the final literature was screened.Finally,77 articles were included for review. RESULTS AND CONCLUSION:(1)Tumor necrosis factor-α is participating in regulating the recruitment,appreciation,and differentiation of osteoprogenitor cells,but leads to osteoprogenitor cell stripping and death under specific environments.It also participates in bone resorption directly or indirectly through secreted enzymes.(2)Tumor necrosis factor-α can increase the level of inflammatory factors in the environment by activating relevant signaling pathways in osteoclast lineage cells or directly induce the generation of osteoclasts in specific environments.(3)Tumor necrosis factor-α can inhibit osteogenic differentiation by activating nuclear factor-κB signaling pathway,inhibiting the expression of transcription factors such as RUNX2 and Osterix,and inducing apoptosis and necrotizing apoptosis in osteoblasts.(4)Tumor necrosis factor-α inhibits osteogenesis and promotes osteoclastogenesis by activating the nuclear factor-κB signaling pathway in osteocytes and inducing cytokines such as RANKL,SOST,and DKK1,while enhancing apoptosis of the osteocytes,as well as bone resorption around the apoptotic bone tissue.(5)Taken together,the effect of tumor necrosis factor-α in bone tissue is mainly to inhibit osteogenesis and promote osteoclastosis.The biological effect of tumor necrosis factor-α in bone tissue cells is usually dependent on the activation of tumor necrosis factor receptor and nuclear factor-κB signaling pathways.(6)The interaction of tumor necrosis factor-α with other tissue cell types surrounding bone tissue and its role in bone immune regulation still deserve attention in future studies.

Objective To analyze the differential expression of non-coding RNAs (ncRNAs) from liver tissues adjacent to hepatic cystic echinococcosis (CE) lesions and distant normal liver tissues using whole transcriptome sequencing, and perform functional annotations of differentially expressed ncRNAs, so as to explore the potential role of ncRNAs in the pathogenesis of CE. Methods Intraoperative liver tissue specimens adjacent to hepatic CE lesions and distant normal liver tissue specimen were sampled from patients with hepatic CE, and the expression profiles of microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs) were detected using whole transcriptome sequencing. Differentially expressed genes were identified, and functional annotations were performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. In addition, a circRNA/lncRNA-miRNA-messenger RNA (mRNA) competing endogenous RNA (ceRNA) network was constructed using the Cytoscape software, and the expression of hub miRNAs in the network was validated using real-time quantitative reverse transcription PCR (RT-qPCR) assay. Results A total of 41 differentially expressed miRNAs were identified between the adjacent and distal tissues of hepatic CE lesions, including 8 up-regulated and 33 down-regulated miR-NAs, which were significantly enriched in biological processes of Ras signaling and neutrophil activation. Five differentially expressed circRNAs were detected, including 3 up-regulated and 2 down-regulated circRNAs, which were significantly enriched in molecular functions of hormone signaling pathways and RNA transcription regulation. A total of 447 differentially expressed lncRNAs were identified, including 200 up-regulated and 247 down-regulated lncRNAs, which were involved in cell proliferation, immune regulation, and extracellular matrix remodeling pathways. MiRNA target analysis predicted hsa-miR-27a-5p, hsa-miR-21-3p, and hsa-miR-181b-2-3p as hub nodes in the ceRNA network. RT-qPCR assay detected that the relative expression levels of ENSG00000253736, HAS2-AS1, PCSK6, hsa-miR-21-3p, hsa-miR-27a-5p, MIR23AHG, VIPR1-AS1, LINC02910, and hsa-miR-181b-2-3p were 3.00 ± 0.25, 2.75 ± 0.33, 1.01 ± 0.51, 2.65 ± 0.41, 1.01 ± 0.29, 1.10 ± 0.31, 1.05 ± 0.27, 0.25 ± 0.49, and 2.56 ± 0.35 in adjacent tissues of hepatic CE lesions, normalized to that in distant tissues from hepatic CE lesions, respectively (t = 6.21, 5.83, 7.51, 7.46, 6.12, 6.65, 7.13, 1.87 and 7.81, all P values < 0.01), which was consistent with whole transcriptome sequencing results. Conclusions Differentially expressed ncRNAs from adjacent and distal liver tissues of hepatic CE lesions may contribute to the pathological mechanisms of CE through mediating cell proliferation, immune evasion, and inflammatory responses, in which hsa-miR-27a-5p and hsa-miR-21-3p may serve as hub miRNAs.