Association of Proton Pump Inhibitor and Infection and Major Adverse Clinical Events in Patients With ST-Elevation Myocardial Infarction: A Propensity Score Matching Analysis.

Background: Infections are not common but important in patients with acute myocardial infarction, and are associated with worse outcomes. Infection was proved to be associated with the use of proton pump inhibitor (PPI) in several cohorts. It remains unclear whether PPI usage affects infection in patients with acute myocardial infarction. Methods: We consecutively enrolled patients with ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) from January 2010 to June 2018. All patients were divided into the PPI group and non-PPI group according to whether the PPI was used. The primary endpoint was the development of infection during hospitalization. Results: A total of 3027 patients were finally enrolled, with a mean age of 62.2 ± 12.6 years. 310 (10.2%) patients were developed infection during hospitalization. Baseline characteristics were similar between the PPI and non-PPI groups (n = 584 for each group) after propensity score analysis. PPI usage was significantly associated with infection based on the propensity score matching analysis (adjusted OR = 1.62, 95% CI = 1.02-2.57, P = 0.041). Comparing to patients with non-PPI usage, PPI administration was positively associated with higher risk of in-hospital all-cause mortality (adjusted OR = 3.25, 95% CI = 1.06-9.97, P = 0.039) and in-hospital major adverse clinical events (adjusted OR = 3.71, 95% CI = 1.61-8.56, P = 0.002). Subgroup analysis demonstrated that the impact of PPI on infection was not significantly different among patients with or without diabetes and patients with age ≥65 years or age <65 years. Conclusion: PPI usage was related to a higher incidence of infection during hospitalization, in-hospital all-cause mortality, and in-hospital major adverse clinical events (MACE) in STEMI patients.

Are Routine Postoperative Laboratory Tests Really Necessary After Lumbar Spinal Surgery?

BACKGROUND: For patients undergoing lumbar spinal surgery, many surgeons routinely perform laboratory tests within 3 days after surgery. However, few studies have reported the necessity for routine laboratory tests for patients with uncomplicated cases within 3 days after surgery. METHODS: We performed a retrospective study of patients with lumbar degenerative disease who had undergone lumbar spinal surgery from May 2014 to May 2017. The perioperative patient information was recorded. The abnormal postoperative laboratory tests were recorded. Finally, the incidence and risk factors for patients requiring postoperative clinical treatment were analyzed. RESULTS: A total of 1915 patients were included in the present study. Postoperative laboratory tests had been ordered for 870 patients (45.43%). Of these patients, only a small proportion had required postoperative clinical intervention to treat abnormal serum hemoglobin (2.53%), albumin (1.95%), serum potassium (0.92%), or serum calcium (6.55%) levels. Multivariate logistic regression analysis showed that female gender and operative time were risk factors for the need for blood transfusion after lumbar spinal surgery. Age and operative time were risk factors for patients requiring albumin supplementation after lumbar spinal surgery. Finally, intraoperative blood loss and operative time were independent risk factors for patients requiring calcium supplementation after surgery. CONCLUSIONS: Owing to the small number of postoperative clinical interventions for abnormal laboratory test results, we believe that the use of routine laboratory tests within 3 days after lumbar spinal surgery for patients with uncomplicated cases are unnecessary. Our results showed that operative time is a potential risk factor for the necessity for clinical treatment after lumbar spinal surgery.

Let-7a inhibits osteosarcoma cell growth and lung metastasis by targeting Aurora-B.

PURPOSE: Accumulating studies showed that the expression of microRNAs (miRNAs) was dysregulated in osteosarcoma (OS). In this study, we sought to investigate the effect of let-7a on OS progression and its potential molecular mechanism. PATIENTS AND METHODS: Quantitative real-time PCR (qRT-PCR) was performed to evaluate the expression level of let-7a and Aurora-B (AURKB) in OS tissues and cells. The OS cells were treated with let-7a mimic, let7a inhibitor, negative mimic and Lv-AURKB combined with let-7a. The ability of cell proliferation, migration and invasion was measured using Cell Counting Kit-8 (CCK-8) and wound-healing and transwell invasion assays. The protein of AURKB, NF-κßp65, MMP2 and MMP9 was measured by Western blot analysis. Xenograft model was performed to investigate the effects of let-7a on tumor growth and metastasis. The lung metastasis was measured by counting the metastatic node using H&E staining. RESULTS: Let-7a expression was significantly underexpressed in OS cell lines and tissues compared with human osteoblast cell lines, hFOB1.19, and adjacent normal bone tissues. Exogenous let-7a inhibited the viability, migratory and invasive ability of OS cells in vitro. In addition, the overexpression of AURKB in OS cells could partly rescue let-7a-mediated tumor inhibition. Also, the overexpression of let-7a inhibited OS cell growth and lung metastasis in vivo. Furthermore, the results showed that let-7a could decrease the expression of NF-κßp65, MMP2 and MMP9 proteins by targeting AURKB in OS cells. CONCLUSION: Let-7a inhibits the malignant phenotype of OS cells by targeting AURKB at least partially. Targeting let-7a and AURKB/NF-κß may be a novel therapeutic strategy for the treatment of OS.

The risk factors for bone metastases in patients with colorectal cancer.

This retrospective analysis aim to evaluate the potential risk factors for bone metastases (BM) in patients who were diagnosed with colorectal cancer (CRC).A total of 2790 patients diagnosed with CRC between January 2006 and December 2016 were collected in this study. All patients were divided into 2 groups, BM and no BM. The associations between biomarkers (including age, gender, histopathological types, alkaline phosphatase (ALP), carcinoembryonic antigen (CEA), cancer antigen 125, and so on), and BM in patients with CRC were analyzed. All the analyses were conducted by SPSS software (version 22.0, SPSS, Chicago, IL).Of all patients, 74 (2.7%) were identified with BM. The level of serum ALP, CEA, and cancer antigen 125 in patients with BM were obviously higher than those without BM (P < .001, P = .005, and P < .001). And the cut-off values of ALP, CEA, and cancer antigen 125 were 85.5 U/L, 6.9 mmol/L, and 16.8 mmol/L, respectively.ALP, CEA, and cancer antigen 125 were identified as the independent risk factors for BM in patients with CRC.

Extracellular vesicles-mediated signaling in the osteosarcoma microenvironment: Roles and potential therapeutic targets.

Osteosarcoma (OS) is the most common non-hematologic malignant tumor of bone in children. It is usually characterized by a high risk of developing lung metastasis and poor prognosis. Extracellular vesicles (EVs) are cell-derived nanoparticles with a small size of 50-200 nm in diameter. As a communicator, the contents of the EVs secreted via either fusing with lysosomes for degradation and recycling or fusing with the cell plasma membrane into the extracellular environment, which play an important role in regulating the tumor microenvironment of OS and mediating the Wnt/ß-catenin and TGF-ß signalings. Increasing evidences suggest that EVs have significant role in OS growth, progression, metastasis and drug resistance. In this study, the roles of EVs in the physiology and pathogenesis of OS and the potential attractive therapeutic target for the treatment of OS were reviewed.

Potential Molecular Mechanisms of AURKB in the Oncogenesis and Progression of Osteosarcoma Cells: A Label-Free Quantitative Proteomics Analysis.

Our previous study indicated that knockdown of Aurora-B inhibit the proliferation of osteosarcoma cells. But the function and molecular mechanisms of Aurora-B in osteosarcoma cells growth and metastasis remains unclear. The aim of this study was to investigate the molecular mechanisms of Aurora-B in the progression of osteosarcoma. Osteosarcoma cells (U2-OS and 143B) were treated with specific Lentivirus-Vectors (up or downregulation Aurora-B). The ability of cells proliferation, migration, and invasion was measured using Cell-Counting Kit-8, wound healing and transwell invasion assays. Furthermore, based on label-free quantitative proteomic analysis of potential molecular mechanisms of Aurora-B in human 143B cells. A total of 25 downregulated and 76 upregulated differentially expressed proteins were screened in terms of the change in their expression abundance. We performed functional annotation and functional enrichment analyses. Gene ontology enrichment, KEGG analysis, and protein-protein interaction networks were constructed and analyzed. We found that the PTK2 may play an important role in the progression of osteosarcoma cells. Finally, Western blot revealed that expression of PTK2, AKT, PI3K, and nuclear factor-kappaB increased after over expression of Aurora-B. Overall, these data highlight that Aurora-B may promote the malignant phenotype of osteosarcoma cells by activating the PTK2/PI3K/AKt/nuclear factor-KappaB pathway.