Publications by authors named "Luojia Tang"

Introduction: Pulmonary embolism (PE) is among the most severe cardiovascular disorders worldwide. Timely and appropriate diagnosis of PE remains an important step in reducing PE related mortality and morbidity.

Methods: In this retrospective single-center cohort study, we comprehensively compared the screening performances of several clinical scoring systems (Wells score [WS], Revised Geneva score [RGS], WS + d-Dimer [D-D], RGS + D-D, WS + PE rule-out criteria [PERC] and RGS + PERC) among PE suspected patients.

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Background: Pulmonary embolism is a severe cardiovascular disease and can be life-threatening if left untreated. However, the detection rate of pulmonary embolism using existing pretest probability scores remained relatively low and clinical rule out often relied on excessive use of computed tomographic pulmonary angiography.

Methods: We retrospectively collected data from pulmonary embolism suspected patients in Zhongshan Hospital from July 2018 to October 2022.

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Lipopolysaccharide (LPS), one of the most prominent pathogen-associated molecular patterns (PAMPs), activates macrophages, causing release of toxic cytokines (i.e. tumor necrosis factor (TNF)-α) that may provoke inflammation and endotoxin shock.

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Introduction: Triple negative breast cancer (TNBC) is a heterogeneous collection of biologically diverse cancers, which contributes to variable clinical outcomes. Previously, we identified a TNBC subtype that has a luminal phenotype and expresses the androgen receptor (AR+). TNBC cells derived from these luminal AR + tumors have high frequency phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutations.

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Background: Autophagy is characterized by the sequestration of cytoplasm and organelles into multimembrane vesicles and subsequent degradation by the cell's lysosomal system. It is linked to many physiological functions in human cells including stress response, protein degradation, organelle turnover, caspase-independent cell death and tumor suppression. Malignant transformation is frequently associated with deregulation of autophagy and several tumor suppressors can modulate autophagic processes.

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The tumor suppressor p53 is commonly mutated in human cancers. However, two homologs of p53, p63 and p73, are frequently overexpressed in tumors and are associated with tumor subtypes, clinical outcomes, and responses to therapy. There are many isoforms of p53, p63 and p73 (the p53 family).

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In various human diseases, altered gene expression patterns are often the result of deregulated gene-specific transcription factor activity. To further understand disease on a molecular basis, the comprehensive analysis of transcription factor signaling networks is required. We developed an experimental approach, combining chromatin immunoprecipitation (ChIP) with a yeast-based assay, to screen the genome for transcription factor binding sites that link to transcriptionally regulated target genes.

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