Decreased APOC1 expression inhibited cancer progression and was associated with better prognosis and immune microenvironment in esophageal cancer.

Several studies have demonstrated the involvement of apolipoprotein C1 (APOC1) in multiple cancers. However, the role of APOC1 in esophageal cancer (ESCA) has not been elucidated. Hence, we examined the expression of APOC1 in ESCA tissues acquired from The Cancer Genome Atlas (TCGA) database and clinical samples from our hospital. An investigation of the association of APOC1 with the clinicopathological characteristics, prognosis, and diagnosis of ESCA was carried out on the basis of survival, receiver operating characteristics, and correlation analyses. Gene ontology, KEGG analysis, and protein-protein interaction network showed that co-expressed APOC1 genes were involved in the functions, mechanisms, and action network. The effects of APOC1 expression on ESCA cells were explored using CCK-8, migration and invasion assays. The relationship between APOC1 expression and ESCA immune-infiltrating cells and cell markers were examined using correlation analysis. We found that APOC1 was overexpressed in TCGA ESCA tissues and the same was validated in clinical ESCA tissues, with the area under the curve for APOC1 being 0.887. Overexpression of APOC1 was associated with short overall survival, disease-specific survival, progression-free interval, T stage, pathological stage, body mass index, and histological grade. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Furthermore, APOC1 expression positively correlated with the ESTIMATE, immune, and stromal scores in ESCA. Overexpression of APOC1 correlated with the tumor purity, B cells, T helper cells, natural killer cells, cytotoxic cells, and other immune cells. Moreover, APOC1 was involved in ESCA progression via T cell receptor, B cell receptor, and other immune signaling pathways. Thus, APOC1 overexpression is expected to be a biomarker for dismal prognosis and diagnosis of ESCA. Inhibition of APOC1 expression significantly reduced the proliferation, migration, and invasion of ESCA cells. Overexpression of APOC1 was associated with the immune microenvironment in ESCA. Thus, APOC1 may be an efficient biomarker for proper prognosis and diagnosis of ESCA.

Renal Parenchymal Thickness as a Predictor of Post Percutaneous Kidney Biopsy Complication.

OBJECTIVE: To investigate the relationship of renal parenchymal thickness and the risk of developing post-procedure hematoma. METHODS: Ultrasound-guided percutaneous renal biopsy was performed in 122 patients who underwent percutaneous kidney biopsy between January 2013 and -December 2013 at Tai-he hospital. Post-biopsy renal ultrasound was performed within 12 h after the biopsy to assess the presence of hematoma in biopsied kidney. Logistic regression analysis was used to determine the effect of parenchymal thickness on formation of hematoma adjusted for other nonstructural patient-related factors such as age, sex, systolic and diastolic blood pressure, serum creatinine, and urea. RESULTS: The incidence of complication was 19.4%, all of which were hematoma less than 5 cm. None of the patients went on to have severe complications that required clinical, surgical, or radiological intervention. Out of the collected clinical and anatomical parameters, renal parenchymal thickness of the biopsied kidney was found to be the only factor with strong association with complication risks. CONCLUSION: This is the first study investigating the impact of structural perimeters on complication risks of percutaneous renal biopsy. Renal parenchymal thickness is a significant predictor of presence of hematoma evident on post-biopsy ultrasound evaluation, which would be used in the early prevent the complications of percutaneous renal biopsy.