Comparison of Intravenous, Topical, or Combined Routes of Tranexamic Acid in Primary Total Knee Arthroplasty.

Introduction: The optimal route and dosing regimen of tranexamic acid (TXA) in primary total knee arthroplasty (TKA) remains unclear. This study aims to explore if there was a synergistic effect of intravenous (IV) and topical TXA on blood loss and risk of complications. Materials and methods: From Jan 2019 to June 2021, medical records of patients aged 65 years or older who underwent primary unilateral TKA for primary osteoarthritis were retrospectively reviewed. The included patients were divided into 3 groups according to the methods of TXA application: Intravenous (IV) group, topical group, or combined group. Propensity-score match was used to reduce the bias and imbalance of confounding variables. The primary outcome was total blood loss. Results: The total blood loss, hidden blood loss, and the reduction of Hb concentration in the combined group were significantly lower than in the IV group and topical group (all P < .01). There is no significant difference in the transfusion rate, length of hospital stay, and incidence of thromboembolic events (both P > .05). Conclusions: Combined administration of IV and topical TXA is the most effective approach to decrease blood loss and postoperative Hb drop in the treatment of TKA without increasing any risk of complications.

Correction to: LncRNA MIR497HG inhibits colorectal cancer progression by the miR-3918/ACTG2 axis.

This corrects the article DOI: 10.1007/s12041-022-01367-w.

LncRNA MIR497HG inhibits colorectal cancer progression by the miR-3918/ACTG2 axis.

The roles of long non-coding RNAs (lncRNAs) have been discussed and analysed in previous studies. The messenger RNAs (mRNAs) are frequently reported to be regulated by lncRNAsin colorectal cancer (CRC).Here,we elucidated the role of themRNAactin gamma 2 (ACTG2) in CRC progression using SW837 and LOVO cells. Gene expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR) and subcellular localization was assessed using subcellular fractionation assay. Cell counting kit-8 (CCK-8), colony formation, and Transwell assayswere performed to detectCRCcell phenotypes.RNApulldown, luciferase reporter, andRNAimmunoprecipitation (RIP) assays were conducted to reveal the interactionsamongmicroRNA-3918 (miR-3918), lncRNAmir-497-195 cluster host gene (MIR497HG) and ACTG2. The ACTG2 level was downregulated in CRC cells and samples. ACTG2 overexpression suppressed CRC cell proliferation, migration, and invasion. Additionally, miR-3918 inhibition increased the level of ACTG2 and the interaction between miR-3918 and ACTG2 was verified. MIR497HG was markedly downregulated in CRC cells and samples. Overexpression of MIR497HG decreased miR-3918 expression while increased ACTG2 expression. Further, the inhibitory effects exerted by MIR497HG overexpression on malignant phenotypes of CRC cells were reversed by ACTG2 knockdown.MIR497HGexerts inhibitory effects on CRC progression by the miR-3918/ACTG2 axis.Our study conducted a systematic analysis of the biological roles of ACTG2, miR-3918 and MIR497HG, and the relationship among them in CRC progression. ACTG2 and MIR497HG were found to be tumour suppressors in CRC cell growth. More importantly, a novel ceRNA network, with MIR497HG as a ceRNA to regulate the miR-3918/ACTG2 axis, was found to play a key role in CRC cell proliferation, migration and invasion.