Purpose: Neoadjuvant chemotherapy (NACT) is increasingly adopted in the therapy of breast cancer (BC) patients with positive axillary nodes (cNþ), but the reliability and feasibility of sentinel lymph node biopsy (SLNB) following NACT are still controversial. The objective of the present study is to conduct an updated meta-analysis on this issue. Methods: A literature search was performed using PubMed, Cochrane, Embase, and Web of Science to identify papers published from January 1, 2000 to October 22, 2020 to research SLNB after NACT in BC patients. Studies that met the quality standard were enrolled for this meta-analysis. Results: A total of 3578 participants from 27 trials were included in this meta-analysis. The pooled estimate of the identification rate (IR) for SLNB was 91 %, and the false negative rate (FNR) was 15 %. The pooled negative prediction value (NPV), accuracy, specificity, and sensitivity were 82 %, 89 %, 97 %, and 85 %, respectively. In subgroup analysis, the application of dual mapping could clearly decrease the FNR. The FNR was significantly high in the luminal types, and it declined as more sentinel lymph nodes (SLNs) were removed. Conclusion: SLNB following NACT is now technically feasible for BC with cNþ. However, it must be emphasized that the FNR is unacceptable high.

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In recent years, an increasing number of studies have reported that long non-coding RNAs (lncRNAs) play essential regulatory roles in myogenic differentiation. In this study, a specific LncRNA XLOC_015548 (Lnc000280) was identified. However, little research has explored its mechanism of action by constructing XLOC_015548 gene editing cell models. In this study, relevant sequences were obtained according to the RNA-seq results. Subsequently, XLOC_015548 knockdown and over-expression lentiviral vectors were constructed, and the C2C12 myoblast cell line was transfected to prepare the XLOC_015548 gene-edited myoblast model. The in vitro analysis revealed that over-expression of XLOC_015548 significantly promoted the proliferation and differentiation of myoblasts and the formation of myotubes, whereas the opposite result was obtained in the knockdown group. XLOC_015548 regulated myogenic differentiation and affected the expression of myogenic differentiation regulators such as Myod, myogenin, and MyHC. Regarding the signaling pathway, we found that XLOC_015548 correlated with the phosphorylation level of MAPK/MEK/ERK pathway proteins. And the degree of phosphorylation was positively correlated with the protein expression of myogenic differentiation regulators. In conclusion, a new gene-edited myoblast model was constructed based on the lncRNA regulator XLOC_015548. The in vitro cell experiments verified that XLOC_015548 had regulatory effects on muscle growth and myoblast differentiation. These findings provide a laboratory foundation for the clinical application of lncRNAs as regulatory factors in the treatment of disuse muscle atrophy.

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Review question / Objective: For the sake of better apprehending the nexus between ferroptosis and chondrocytes in osteoarthritis (OA), proffering novel insights and opening-up new orientation for in-depth research in both pre-clinical and clinical settings, it is warranted to initiate one rigorous and robust systematic review (SR) based upon up-to-date in-vivo and in-vitro research advances on this topic. To the best our knowledge, no SRs concerning ferroptosis and chondrocytes in OA have been published thus far. Condition being studied: Osteoarthritis (OA) is the most common form of arthritis, which menaces 7% of the human population globally. With the aged tendency of population and higher rates of obesity, the incidence of OA is anticipated to proliferate, which will entail a mounting impact and major challenges for global health care and each country’s public health systems unavoidably. In virtue of the onset of OA is mighty knotty, its etiology and underlying molecular mechanisms have not been expressly expounded. However, the salient role that cartilage degeneration acts in the progression of OA has been widely acknowledged. Chondrocytes are consequential for the safeguard of cartilage homeostasis and the functional integrity of the articular cartilage. Once the homeostatic equilibrium of the extracellular matrix (ECM) synthesis and degradation is smashed, OA comes up.