Comparison of the early clinical efficacy of the SuperPath approach versus the modified Hardinge approach in total hip arthroplasty for femoral neck fractures in elderly patients: a randomized controlled trial.

Purpose: To investigate the clinical efficacy and advantages of the SuperPath approach for total hip arthroplasty in the treatment of femoral neck fractures in the elderly population.

Methods: From February 2018 to March 2019, 120 patients were randomly divided into two groups with 60 patients each: the SuperPath group and the conventional group. The results evaluated included the general operation situation, serum markers, blood loss, pain score, hip function and prosthesis location analysis.

Erratum: H3K27 acetylation activated-COL6A1 promotes osteosarcoma lung metastasis by repressing STAT1 and activating pulmonary cancer-associated fibroblasts: Erratum.

[This corrects the article DOI: 10.7150/thno.51245.

The miR-19b-3p-MAP2K3-STAT3 feedback loop regulates cell proliferation and invasion in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is one of the most refractory malignancies worldwide. Mitogen-activated protein kinase 3 (MAP2K3) has a contradictory role in tumor progression, and the function and expression patterns of MAP2K3 in ESCC remain to be determined. We found that MAP2K3 expression to be downregulated in ESCC, and MAP2K3 downregulation correlated with clinically poor survival.

H3K27 acetylation activated-COL6A1 promotes osteosarcoma lung metastasis by repressing STAT1 and activating pulmonary cancer-associated fibroblasts.

Collagen type VI alpha 1 (COL6A1) has been found to be dysregulated in several human malignancies. However, the role of COL6A1 in osteosarcoma (OS) progression remains largely unclear. Here, we aimed to explore the clinical significance and biological involvement of COL6A1 in the OS cell migration and invasion.

Promoter methylation and clinical significance of GPX3 in esophageal squamous cell carcinoma.

Background: Glutathione peroxidase 3 (GPX3) provides critical protection against reactive oxygen species (ROS) in cells. Downregulation of GPX3 may contribute to carcinogenesis of esophageal squamous cell carcinoma (ESCC), but the mechanisms are not clear.

Materials And Methods: We examined the differences in gene expression between ESCC and normal esophageal epithelial, by using GEO datasets, and collected 136 ESCC tumors and adjacent normal tissues to confirm our findings.

Room Temperature Versus Warm Irrigation Fluid Used for Patients Undergoing Arthroscopic Shoulder Surgery: A Systematic Review and Meta Analysis.

Purpose: The aim of this study was to analyze whether warm irrigation fluid could reduce postoperative adverse effects in patients undergoing arthroscopic shoulder surgery compared with room temperature irrigation fluid.

Design: A systematic review and meta-analysis of clinical trials was performed.

Methods: A computerized search of electronic databases was performed.

STAT1 inhibits STAT3 activation in esophageal squamous cell carcinoma.

Background: Signal transducer and activator of transcription (STAT) 1 is an important transcription factor and has been reported to be a tumor suppressor in many types of cancer. However, another STAT family member, STAT3, is considered to be an oncogene. The cross-talk between STAT1 and STAT3 in cancer has not been fully demonstrated.

PRL-3 activates mTORC1 in Cancer Progression.

PRL-3, a metastasis-associated phosphatase, is known to exert its oncogenic functions through activation of PI3K/Akt, which is a key regulator of the rapamycin-sensitive mTOR complex 1 (mTORC1), but a coherent link between PRL-3 and activation of mTOR has not yet been formally demonstrated. We report a positive correlation between PRL-3 expression and mTOR phospho-activation in clinical tumour samples and mouse models of cancer and demonstrate that PRL-3 increased downstream signalling to the mTOR substrates, p70S6K and 4E-BP1, by increasing PI3K/Akt-mediated activation of Rheb-GTP via TSC2 suppression. We also show that PRL-3 increases mTOR translocation to lysosomes via increased mTOR binding affinity to Rag GTPases in an Akt-independent manner, demonstrating a previously undescribed mechanism of action for PRL-3.