[Research progress on long non-coding RNA (lncRNA) in osteoarthritis].

Osteoarthritis(OA) is a common clinical disease. The incidence of OA increases significantly with age, and the quality of life of patients is seriously affected. In the pathogenesis of OA, cartilage degeneration is the main cause. There are many long non-coding RNA (lncRNA) specifically expressed in osteoarthritis, which is closely related to the occurrence and development of osteoarthritis. Based on the latest research from 2014 to 2019, this paper summarizes the differential expression of lncRNA in osteoarthritis, the mechanism of lncRNA regulating chondrocyte function, and the mechanism of lncRNA regulating cartilage matrix metabolism. The fact that the expression of lncRNA is altered at different stages of OA development indicates that lncRNA can be developed forlife. The biomarkers and therapeutic targets can provide reference for the prevention, treatment and research of osteoarthritis.

[Distal Chevron osteotomy of the first metatarsal and soft-tissue release for hallux valgus].

OBJECTIVE: To explore distal Chevron osteotomy of the first metatarsal and soft-tissue release for the treatment of mild and moderate hallux valgus. METHODS: From June 2015 to June 2017, 32 patients(40 feet) with mild and moderate hallux valgus were treated with distal Chevron osteotomy with soft tissue release. including 3 males(3 feet) and 29 females (37 feet), aged from 22 to 80 years old with an average of 57.57 years old. The courses of disease ranged from 2 to 32 years with an average of 14 years. Among them, 9 feet were mild, 31 feet were moderate. Patients were combined with bunion, pain around the first metatarsal joint, and pain increased during weight-bearing walking before opertaion. AP and lateral X-rays on weight-bearing were performed, hallux valgus angle(HVA) and intermetatarsal angle(IMA) between the first and the second metatarsal were examined before and after operation. AOFAS score was applied to evaluate clinical effects. RESULTS: All patients were followed up from 12 to 24 months with an average of 15.2 months.Fracture wounds were healed well without infection and metatarsal head necrosis occurred. Preoperative HVA (32.08±5.59)° and IMA (11.63±2.24)° decreased to (10.31±4.36)° and (5.02°±2.34)°after operation at 12 months, and had statistical difference before and after operation (P<0.05). AOFAS score increased from 56.75±6.42 before operation to 88.80±3.99 after operation at 12 months(P<0.05). CONCLUSIONS: Distal Chevron osteotomy of the first metatarsal and soft-tissue release for the treatment of mild and moderate hallux valgus could obtain good effects and provide more options for hallux valgus treatment.

Meta-analysis of the association of IL1-RN variable number of tandem repeats polymorphism with osteoarthritis risk.

OBJECTIVE: The aim of this meta-analysis was to clarify the role of Interleukin-1 receptor antagonist gene (IL1-RN) Variable Number of Tandem Repeats (VNTR) polymorphism on the risk of OA by means of meta-analysis. METHODS: Eligible articles were retrieved from PubMed, Web of science and Google scholar with a total of 1187 OA cases and 2659 controls. The strength of the association between the IL1-RN VNTR polymorphism and the risk of OA was assessed by odds ratios (ORs) with the corresponding 95% confidence interval (CI) for each study. RESULTS: The meta-analysis of seven published studies retrieved from the literature search showed a significantly increased OA risk in the recessive model analysis (22 vs 2L + LL: Pb = 0.18, I2 = 32.8, OR(95% CI) = 1.50(1.12, 2.02), P = 0.007), the additive model analysis (22 vs LL: Pb = 0.08, I2 = 46.8, OR(95% CI) = 1.56(1.15, 2.12), P = 0.004) and in the allele contrast model (2 vs L: Pb = 0.02, I2 = 58.8, OR(95% CI) = 1.20(1.05, 1.36), P = 0.007). By subgroup analysis, the IL1-RN VNTR polymorphism was found to be significantly associated with OA susceptibility in Caucasian and Hospital based case-control study (HCC) groups. CONCLUSION: This meta-analysis showed that IL1-RN VNTR polymorphism may increase the susceptibility to OA. More studies with detailed information are needed to validate our conclusion. LEVEL OF EVIDENCE: Level III, diagnostic study.

Cloning, characterization and phylogenetic relationships of stxI, a endoxylanase-encoding gene from Streptomyces thermonitrificans NTU-88.

A thermostable xylanase gene (stxI) obtained from Streptomyces thermonitrificans NTU-88 on domain analysis revealed an N-terminal catalytic domain featuring homology to a known xylanase within the glycoside hydrolase family 11. Recombinant STXI retained more than 60% of its activity following its incubation for at 60 degrees C for 24h. These characteristics were close to thermophile and mesophile Streptomyces strains. The main hydrolysis products of xylan degraded by STXI included large xylooligosaccharide fragments. These results indicated that STXI was a typical endoxylanase. As regards the phylogenetic relationships of GH11, STXI and the other xylanase deriving from Streptomyces were included in a subgroup of the aerobic bacterial group. This result implied that the evolutionary relationships between the various xylanases deriving from Streptomyces strains were convergent.

NLRP1 and NLRP3 inflammasomes mediate LPS/ATP­induced pyroptosis in knee osteoarthritis.

Pyroptosis is triggered by inflammasomes after its activation by various inflammatory stimulations, including lipopolysaccharide (LPS) and improper pH. This may result in programmed death of the affected cell. It is well known that NLRP1 and NLRP3 inflammasomes mediate the production of various cytokines in inflammatory disorders; however, it is still unknown whether NLRP1 and NLRP3 inflammasomes can influence the LPS­induced pyroptosis in the progression of knee osteoarthritis (KOA). In the present study, the correlation between the NLRP inflammasomes and fibroblast­like synoviocytes (FLSs) pyroptosis was investigated in vivo and in vitro. Human synovial samples were collected from KOA patients and the expression of NLRP1 and NLRP3 inflammasomes was analyzed. Human FLS were isolated in vitro and stimulated with LPS. To determine whether NLRP1 and NLRP3 inflammasomes are involved in FLS pyroptosis, NLRP1 and NLRP3 small interfering RNAs (siRNAs) were used. The results showed that the expression of NLRPs and inflammasome­related proteins were upregulated and FLS stimulated with LPS+ATP resulted in cell pyroptosis. However, LPS+ATP­induced pyroptosis was attenuated by NLRP1 and NLRP3 siRNAs. The results of the present study indicate that LPS­induced FLS pyroptosis may be mediated by either NLRP1 or NLRP3 inflammsomes. Overall, based on the data obtained from patients and in vitro cells, the present finsings showed that NLRP1 and NLRP3 inflammasomes are highly involved in the FLS inflammation and pyroptosis. Furthermore, inhibition of NLRP1 and NLRP3 led to a remarkable reduction of pyroptosis­related cytokines. Thus, NLRP1 and NLRP3 inflammasomes may be important in the pathogenesis of OA and may represent a novel therapeutic target.

Association between high levels of Notch3 expression and high invasion and poor overall survival rates in pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is a commonly fatal tumour. It is characterized by early metastasis and high mortality. Many patients die as a result of PDAC tumour progression. However, the underlying mechanism of invasion and metastasis in PDAC is still not fully understood. Previous studies showed that the Notch signalling pathway may play an important role in the progression of tumour invasion and metastasis. However, it is not yet known whether the Notch signalling pathway participates in the progression of invasion in PDAC. In the present study, immunohistochemistry showed that a high expression of Notch3 was correlated with tumour grade, metastasis, venous invasion and American Joint Committee on Cancer (AJCC) tumor-node-metastasis (TNM) stage. Kaplan-Meier curves suggested that a high expression of Notch3 was a significant risk factor for shortened survival time. We also showed that inhibition of Notch3 had an anti­invasion role in PDAC cells. In vitro, the inhibition of Notch3 reduced the migration and invasion capabilities of PDAC cells by regulating the expressions of E-cadherin, CD44v6, MMP-2, MMP-9, VEGF and uPA via regulating the COX-2 and ERK1/2 pathways. These results indicated that downregulation of the Notch signalling pathway may be a novel and useful approach for preventing and treating PDAC invasion.