Malignant tumor is one of the important acquired risk factors of venous thromboembolism (VTE). As the transmembrane receptor of coagulation factor Ⅶ and activated coagulation factor Ⅶa
Humans ; Neoplasms/complications* ; Risk Factors ; Thromboplastin/metabolism* ; Thrombosis ; Venous Thromboembolism/physiopathology*

In addition to common clinical features, patients with coronavirus disease 2019 (COVID-19) have varying degree of coagulation dysfunction with the risk of thrombosis and/or bleeding. COVID-19 related coagulation dysfunction is a dynamic process, which may be accompanied by the formation of disseminated intravascular coagulation and is related to the severity of the disease. The imbalance of the body's immune and inflammatory response caused by coronavirus infection is an important cause of coagulation dysfunction. Dynamic monitoring as well as early prevention and treatment are of great significance for improving the prognosis of patients. This article reviews the research progress of COVID-19 related coagulation dysfunction, to provide reference for clinical research and management.
Betacoronavirus ; Blood Coagulation Disorders ; etiology ; Coronavirus Infections ; complications ; Humans ; Pandemics ; Pneumonia, Viral ; complications

Neutrophil extracellular traps(NET)is neutrophil-derived extracellular fiber web-like structure, composed of DNA scaffold studded with various active proteins. In addition to its bactericidal effect, NET is closely related to various diseases including immune disease, thrombosis and tumor. Recently, lots of researches have shown that NET is highly expressed in a variety of tumors, tumor cells and microenvironment can promote NET formation, whereas NET participates in tumor progression as well, and is closely related to tumor proliferation, metastasis and thrombosis, which provides new clinical thinking in tumor diagnosis as well as treatment indeed. This review will focus on the research progress of NET and tumor, meanwhile make a prospect for its clinical application value.
Extracellular Traps ; genetics ; Humans ; Neoplasms ; physiopathology ; Neutrophils ; pathology ; Tumor Microenvironment

Objective:To analyze the influence of CD19 isoforms to the efficacy of CD19/CD3 Bispecific T-cell Engager (BiTE) antibody, and explore the resistance mechanism of BiTE immunotherapy.Methods:Semi-quantitative RT-PCR (qRT-PCR) was used to detect the expression of CD19 mRNA isoforms before and after BiTE treatment in a patient with CD19 + B cell acute lymphoblastic leukemia (ALL) . CD19 isoforms were analyzed by Sanger sequencing. Flow cytometry and transcriptome sequencing were performed to analyze the expression of cell lineage specific molecules before and after BiTE treatment. Results:The expression of CD19 isoform with exon 2 deletion was identified at diagnosis. After relapsed and treatment of BiTE antibody, the patient did not achieve remission and CD19 antigen on leukemic cells turned negative detected by flow cytometry after BiTE treatment. However the expression ratio of CD19 isoform with exon 2 deletion was not increased. Flow cytometry phenotype and transcriptome sequencing confirmed that no linage switching developed, which suggested the expression of CD19 isoform caused by exon alternative splicing and lineage switching was not related to CD19 epitope loss in this patient. This patient achieved complete remission by sequential administration of self-developed CD22 CAR-T and CD19 CAR-T after disease progression.Conclusion:Targeting or combining an alternative antigen specific CAR-T may be a promising treatment option after losing CD19 expression in relapsed ALL.

Alzheimer's disease (AD) is a chronic central neurodegenerative disease. The pathological features of AD are the extracellular deposition of senile plaques formed by amyloid-β oligomers (AβOs) and the intracellular accumulation of neurofibrillary tangles formed by hyperphosphorylated tau protein. In this paper, an in vitro pathological model of AD based on neuronal network chip and its real-time dynamic analysis were presented. The hippocampal neuronal network was cultured on the microelectrode array (MEA) chip and induced by AβOs as an AD model to simultaneously record two firing patterns from the interneurons and pyramidal neurons. The spatial firing patterns mapping and cross-correlation between channels were performed to validate the degeneration of neuronal network connectivity. This biosensor enabled the detection of the AβOs toxicity responses, and the identification of connectivity and interactions between neuronal networks, which can be a novel technique in the research of AD pathological model .
Alzheimer Disease ; Amyloid beta-Peptides ; Humans ; Neurofibrillary Tangles ; tau Proteins

Alzheimer's disease (AD) is a chronic central neurodegenerative disease. The pathological features of AD are the extracellular deposition of senile plaques formed by amyloid-β oligomers (AβOs) and the intracellular accumulation of neurofibrillary tangles formed by hyperphosphorylated tau protein. In this paper, an in vitro pathological model of AD based on neuronal network chip and its real-time dynamic analysis were presented. The hippocampal neuronal network was cultured on the microelectrode array (MEA) chip and induced by AβOs as an AD model in vitro to simultaneously record two firing patterns from the interneurons and pyramidal neurons. The spatial firing patterns mapping and cross-correlation between channels were performed to validate the degeneration of neuronal network connectivity. This biosensor enabled the detection of the AβOs toxicity responses, and the identification of connectivity and interactions between neuronal networks, which can be a novel technique in the research of AD pathological model in vitro.
Alzheimer Disease ; Amyloid beta-Peptides ; Humans ; Neurofibrillary Tangles ; tau Proteins

Objective To investigate the application value of contrast-enhanced transrectal ultrasound (CE-TRUS) in differential diagnosis of prostate benign and malignant lesions. Methods A retrospective analysis of patients with prostate lesions detected by CE-TRUS from January 2014 to December 2016 in Southwest Hospital of Third Military Medical University was performed. Seventy-two cases of prostate disease with 88 lesions were confirmed by transrectal prostate biopsy under ultrasound guidance. The age of patients with benign and malignant lesions, serum prostate specific antigen (PSA), and the size of prostate and prostate inner gland were compared by independent sample t test. Pathologic results of transrectal prostate biopsy under ultrasound guidance were used as diagnostic gold standard, and the sensitivity, specificity and accuracy of CE-TRUS in diagnosis of benign and malignant prostate lesions were calculated. Results Sixty- seven lesions in 52 patients were benign prostatic diseases, and 21 lesions in 20 patients were prostate cancer in this study. The size of prostate and prostate inner gland were not different between patients with prostate cancer and benign prostatic diseases [(58.33±34.99) cm3vs (57.14±24.42) cm3, t=0.185, P=0.854; (34.98±19.96) cm3vs (33.89±17.65) cm3, t=0.213, P=0.832]. Most of prostate cancer lesions were in prostate outer gland area (15/21), and contrast-enhanced ultrasound imaging showed contrast enhancement increased mostly in arterial phase and faded faster than the surrounding tissues (16/21). However, most of prostate benign lesions were in prostate inner gland (47/67), and contrast-enhanced ultrasound imaging showed contrast enhancement was mostly equal with the surrounding tissue in arterial phase and faded the same as the surrounding tissues in venous phase (47/67). Pathologic results of transrectal prostate biopsy under ultrasound guidance were used as diagnostic gold standard, the sensitivity of CE-TRUS in diagnosis of benign and malignant prostate lesions was 85.71%, the specificity was 91.04%, and the accuracy was 89.77%. Two lesions were in prostate inner and outer gland border areas in the three missed prostate cancer lesions, and Gleason scores were all medium and high differentiated group. Six prostate benign lesions were diagnosed as malignant lesions, five lesions were confirmed prostate hyperplasia with chronic prostatitis and one was confirmed granulomatous inflammation with coagulation necrosis by transrectal prostate biopsy under ultrasound guidance. Conclusion CE-TRUS can effectively identify prostate benign and malignant lesions, and provides reliable information for accurate diagnosis of prostate cancer.

Pulmonary arterial hypertension (PAH) is a multi-etiological chronic disease characterized by a progressive elevation in pulmonary resistance and vascular remodeling. Its pathogenesis is complicated. Recently, emerging researches suggest that autophagy, as a self-protection mechanism maintaining the intracellular environment homeostasis in eukaryotes, participate in the occurrence and development of various types of PAH. Autophagy can regulate the survival, apoptosis of pulmonary vascular wall cells and secretion of vasoactive substances and inflammatory cytokines, thus influencing pulmonary vascular homeostasis. Some drugs based on regulating autophagy activity can effectively improve the prognosis of PAH. In this article, the regulatory role of autophagy on the development of pulmonary hypertension is reviewed to provide insight into PAH and its treatment.
Autophagy ; Humans ; Hypertension, Pulmonary ; Lung ; Pulmonary Artery

Diazepam ; poisoning ; Humans ; Paraquat ; poisoning ; Pulmonary Embolism ; chemically induced

Female ; Heart Arrest ; drug therapy ; etiology ; Humans ; Pulmonary Embolism ; complications ; Thrombolytic Therapy ; methods ; Young Adult