Background: Pleural effusion is a common pulmonary embolism (PE) complication, which has been documented to increase the risk of death in PE and relate to disease progression. However, the incidence of pleural effusion varies among studies and its association with PE outcome is still unclear. This study sought to determine the pooled incidence and prognostic value of pleural effusion events in patients with PE. Methods: We systematically searched the PubMed, EMBASE, SCOPE, Web of Science, Cochrane, LILACS, CINAHL, EBSCO, AMED, and OVID databases from the inception of each database to 7 September 2022 with a restriction on human studies, to identify studies assessing the association between pleural effusion and PE including all prospective and retrospective clinical studies. An exploratory meta-analysis was performed using a random-effects model. We evaluated the heterogeneity and performed subgroup analyses. Results: The final meta-analysis included 29 studies involving 13,430 PE patients. The pooled incidence of pleural effusion in PE patients was 41.2% (95% CI: 35.7–46.6%), which tended to be unilateral (pooled incidence: 60.8%, 95% CI: 45.7–75.8%) and small (pooled incidence: 85.9%, 95% CI: 82.6–89.1%). Pooled analysis using a random-effects model (I2 = 53.2%) showed that pleural effusion was associated with an increased risk of 30-day mortality (RR 2.19, 95% CI: 1.53–3.15, p < 0.001, I2 = 67.1%) and in-hospital mortality (RR 2.39, 95% CI: 1.85–3.09, p < 0.001, I2 = 37.1%) in patients with PE. Conclusions: Our meta-analysis found that PE patients had a high incidence of pleural effusion, which was usually unilateral and small. Pleural effusion generally increases 30-day and in-hospital mortality in patients with PE, and it is recommended that physicians be aware of the risk of death from PE, especially when patients have pleural effusion. Further investigations focusing on PE with pleural effusion are warranted.
<div>Abstract<p>Nasopharyngeal carcinoma is an Epstein–Barr virus (EBV)-related malignancy. Recently, we found that the EBV-encoded miRNA <i>BART2-5p</i> was increased in the serum of patients with preclinical nasopharyngeal carcinoma and that the copy number positively correlated with disease progression. In this study, we established its role in nasopharyngeal carcinoma progression and explored underlying mechanisms and clinical significance. <i>BART2-5p</i> was an independent unfavorable prognostic factor for progression-free survival and its circulating abundance positively associated with distant metastasis. Ectopic expression of <i>BART2-5p</i> promoted migration and invasion of EBV-negative nasopharyngeal carcinoma cells, whereas genetic downregulation of <i>BART2-5p</i> in EBV-positive nasopharyngeal carcinoma cells decreased aggressiveness. Mechanistically, <i>BART2-5p</i> targeted <i>RND3</i>, a negative regulator of Rho signaling. Downregulation of <i>RND3</i> phenocopied the effect of <i>BART2-5p</i> and reconstitution of <i>RND3</i> rescued the phenotype. By suppressing <i>RND3, BART2-5p</i> activated Rho signaling to enhance cell motility. These findings suggest a novel role for EBV miRNA <i>BART2-5p</i> in promoting nasopharyngeal carcinoma metastasis and its potential value as a prognostic indicator or therapeutic target.</p>Significance:<p>This study shows that EBV-encoded BART2-5p miRNA suppresses expression of the RND3 Rho family GTPase, consequently promoting ROCK signaling, cell motility, and metastatic behavior of NPC cells.</p></div>
High‐grade tumors with poor differentiation usually show phenotypic resemblance to their developmental ancestral cells. Cancer cells that gain lineage precursor cell properties usually hijack developmental signaling pathways to promote tumor malignant progression. However, the molecular mechanisms underlying this process remain unclear. In this study, the chromatin remodeler chromodomain‐helicase‐DNA‐binding‐protein 1‐like (CHD1L) was found closely associated with liver development and hepatocellular carcinoma (HCC) tumor differentiation. Expression of CHD1L decreased during hepatocyte maturation and increased progressively from well‐differentiated HCCs to poorly differentiated HCCs. Chromatin immunoprecipitation followed by high‐throughput deep sequencing found that CHD1L could bind to the genomic sequences of genes related to development. Bioinformatics‐aided network analysis indicated that CHD1L‐binding targets might form networks associated with developmental transcription factor activation and histone modification. Overexpression of CHD1L conferred ancestral precursor‐like properties of HCC cells both in vitro and in vivo . Inhibition of CHD1L reversed tumor differentiation and sensitized HCC cells to sorafenib treatment. Mechanism studies revealed that overexpression of CHD1L could maintain an active “open chromatin” configuration at promoter regions of estrogen‐related receptor‐beta and transcription factor 4, both of which are important regulators of HCC self‐renewal and differentiation. In addition, we found a significant correlation of CHD1L with developmental transcriptional factors and lineage differentiation markers in clinical HCC patients. Conclusion: Genomic amplification of chromatin remodeler CHD1L might drive dedifferentiation of HCC toward an ancestral lineage through opening chromatin for key developmental transcriptional factors; further inhibition of CHD1L might “downgrade” poorly differentiated HCCs and provide novel therapeutic strategies. (H epatology 2016;63:1544‐1559)
To evaluate the application of various obstructive sleep apnea (OSA) screening scales in patients with acute ischemic stroke.One hundred and two patients with acute ischemic stroke were enrolled continuously during July 2016 and March 2017 from Sir Run Run Shaw Hospital, Zhejiang University School of Medicine. All patients were assessed by the same physician with various OSA screening scales, including Epworth scale, Berlin questionnaire, STOP-Bang questionnaire, SOS scale, four-variable scale and its modified version. Polysomnography was performed in Sleeping Disorder Center on each patient. According to the apnea-hypopnea index (AHI) acquired from polysomnography, patients were divided into moderate-severe OSA group (AHI ≥ 15, n=58) and normal-mild OSA group (AHI<15, n=44). The efficiencies of the scales in identification of patients with moderate or severe OSA were analyzed and compared.The ROC curves showed that the four-variable scale and its modified version had higher area under curve (0.806 and 0.807, both P<0.01) for diagnosis of moderate-severe OSA, and the cut-off values for Epworth scale, Berlin questionnaire, STOP-Bang questionnaire, SOS scale, four-variable scale and its modified version were 9, 2, 4, 15, 11, 10, respectively. The sensitivities, specificities, positive and negative predictive values of four-variable scale and its modified version in diagnosis of moderate-severe OSA were higher than those of other scales.Compared with Epworth scale, Berlin questionnaire, STOP-Bang questionnaire and SOS scale, the four-variable scale and its modified version are more effective in screening of OSA for patients with acute ischemic stroke.
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