Castillodolan8152
-fatal GSWs have a large economic and societal impact that warrants further research and consideration by the public and policy makers.
Loss of the Y-chromosome is a common event in different tumor types but its prevalence and clinical relevance in renal cell tumors is still not understood.
It was the aim of this study to estimate the frequency and clinical relevance of Y-loss in kidney neoplasms. A cohort of 1,252 male renal tumors was analyzed in a tissue microarray format by fluorescence in-situ hybridization (FISH).
Y-loss was found in 47% of tumors. The frequency of this alteration varied markedly between kidney tumor subtypes. Y-loss was most prevalent in papillary renal cell carcinoma (RCC) (77%) followed by chromophobe RCC (60%), oncocytoma (51%), clear cell RCC (39%) and clear cell (tubulo)papillary RCC (19%). Y-loss was linked to higher patient age and smaller tumor size at diagnosis. Mean age (95% CI) was 65 (64-66) years in patients with Y-loss in their tumor compared to 60 (58-61) years in patients without Y-loss (P<0.0001). Significant correlations between Y-loss and tumor phenotype were found only for papillary carcinomas (P=0.002), especially for type 1 (P=0.03).
Y-loss is present in different histologic subtypes of renal neoplasm. The highest frequency is in papillary RCC, where it may represent a potentially relevant prognostic biomarker suggesting favorable disease outcome.
Y-loss is present in different histologic subtypes of renal neoplasm. The highest frequency is in papillary RCC, where it may represent a potentially relevant prognostic biomarker suggesting favorable disease outcome.
Severe fever with thrombocytopenia syndrome is caused by infection with the severe fever with thrombocytopenia syndrome virus.
Between April 2011 and December 2019, data on consecutive patients who were diagnosed with severe fever with thrombocytopenia syndrome were prospectively collected from five medical centers in China. The score of the death risk model was correlated with the platelet-to-lymphocyte ratio and the neutrophil-to-lymphocyte ratio. Multivariable Cox analyses were used to identify the independent factors associated with mortality.
During the study period, 763 patients were diagnosed with severe fever with thrombocytopenia syndrome; 415 of these patients were enrolled in our study. We found that the neutrophil-to-lymphocyte ratio of the group that died was significantly higher on admission (P=0.007) than that of the group that survived, and the neutrophil-to-lymphocyte ratio showed a positive correlation with the score of the death risk model. Multivariate Cox regression suggested that a neutrophil-to-lymphocyte ratio greater than 5.4 was an independent risk factor for survival time (HR=6.767, P=0.011). Platelet-to-lymphocyte ratio did not show a special role in this study.
A neutrophil-to-lymphocyte ratio greater than 5.4 can increase the risk of death and decrease the survival time of patients. In summary, the neutrophil-to-lymphocyte ratio provides a supplementary means for effectively managing severe fever with thrombocytopenia syndrome (SFTS).
A neutrophil-to-lymphocyte ratio greater than 5.4 can increase the risk of death and decrease the survival time of patients. In summary, the neutrophil-to-lymphocyte ratio provides a supplementary means for effectively managing severe fever with thrombocytopenia syndrome (SFTS).
The use of angiotensin II inhibitors is associated with a low risk of recurrence and metastasis in hepatocellular carcinoma (HCC) patients. Vascular cell adhesion molecule-1 (VCAM-1) is a key factor in tumor metastasis.
The effects of angiotensin II and irbesartan (an angiotensin II inhibitor) on HCC were explored with a xenograft model, microarray analysis and cell adhesion experiments. The relationship between the expression of VCAM-1 in HCC tissues and prognosis was analyzed with public and our institutional clinical databases. Asunaprevir The effects of angiotensin II, irbesartan and VCAM-1 on adhesion and metastasis in HCC were explored with a xenograft model and cell adhesion experiments. The regulatory mechanisms were analyzed by Western blot analysis.
Angiotensin II type 1 receptor and VCAM-1 were expressed in HCC tissues. Irbesartan inhibited HCC growth and metastasis in vivo and weakened the adhesion of HCC cells to endothelial cells, an effect that was enhanced by angiotensin II. VCAM-1 was found to be an independent risk factor for recurrence and survival in HCC patients with microvascular invasion. Angiotensin II upregulated VCAM-1 expression, and this upregulation was inhibited by irbesartan. Angiotensin II enhanced adhesion mainly by promoting the expression of VCAM-1 in HCC cells. Irbesartan inhibited the expression of VCAM-1 by reducing p38/MAPK phosphorylation activated by angiotensin II in HCC cells.
Irbesartan attenuates metastasis by inhibiting angiotensin II-activated VCAM-1 via the p38/MAPK pathway in HCC.
Irbesartan attenuates metastasis by inhibiting angiotensin II-activated VCAM-1 via the p38/MAPK pathway in HCC.
Most lung cancer patients are diagnosed at an advanced stage with metastases. link2 There was no population-based data on metastases in non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (
) mutation. This study focused on the metastases in NSCLC patients with
mutation.
In our research, we retrospectively studied 365 NSCLC patients with
mutation (
positive-mutant group) were not resistant to first-generation
TKIs and 316 NSCLC patients with T790M mutation (T790M-mutant group) who were resistant to first-generation
TKIs. In the study, we also investigated sex, smoking status, age at diagnosis, histology, T, N, and M stage, and mutation status. In addition, we analyzed metastatic sites in stage IV patients.
Among the
positive-mutant group, 248 (67.95%) patients were stage IV disease. Among them, 41 patients had brain metastases, 86 patients had bone metastases, 16 patients had liver metastases, 168 patients had intrapulmonary metastases, and 39 patients had metas diagnosis, which indicated that metastases related to driving mutations, such as EGFR positive mutation or T790M mutation, but not to the survival time. Lung cancer patients with T790M mutation were more likely to metastasize before the diagnosis.
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with high rates of metastasis and recurrence. link3 Conventional clinical treatments are ineffective for it as it lacks therapeutic biomarkers. Figuring out the biomarkers related to TNBC will be beneficial for its clinical treatment and prognosis.
Five independent datasets downloaded from the Gene Expression Omnibus database were merged to identify differentially expressed genes between TNBC and non-TNBC samples by using the MetaDE.ES method followed by mapping the differentially expressed genes into a protein-protein interaction network. Meanwhile, the weighted gene co-expressed network analysis (WGCNA) of The Cancer Genome Atlas data was performed to screen the hub genes. The gene functional analyses were conducted by Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The correlation between gene expression level and patient overall survival was evaluated by survival analysis.
A total of 11 differentially expressed genes (
,
,
,
,
,
,
,
,
,
,
) were obtained from the protein-protein interaction network with degree >10. WGCNA revealed 5 hub genes (
,
,
,
,
) that were significantly associated with TNBC. Cell cycle, oocyte meiosis, spliceosome were the pathways significantly enriched in these genes according to GO functionally annotated terms and KEGG pathways analysis. The Kaplan-Meier curves showed that the expression levels of
,
,
were significantly associated with the survival time of TNBC patients (P<0.05).
A total of 16 genes significantly associated with TNBC were identified by bioinformatic analyses. Among these 16 genes,
,
,
might be able to be used as biomarkers of TNBC.
A total of 16 genes significantly associated with TNBC were identified by bioinformatic analyses. Among these 16 genes, HSPB1, IFI16, TPX2 might be able to be used as biomarkers of TNBC.
The clinical outcome of mitral valve repair (MVP) is considerably more favorable than that of mitral valve replacement (MVR) in patients with degenerative mitral disease. However, rheumatic heart disease (RHD) is still the predominant cause of mitral valve surgery in developing countries and the advantages of MVP in RHD have still not been definitely proven. The aim of this meta-analysis was thus to evaluate the suitability of MVP in patients with RHD. Considering the difference between mechanical and biological valves, we distinguished them from each other and compared them with MVP individually.
A comparison of clinical outcomes of MVP and MVR in patients with RHD was performed based on clinical trial data. Relevant articles published from January 1, 1990 until March 1, 2020 were identified in Pubmed, Cochrane Library, and China National Knowledge Infrastructure database (CNKI). Studies that lacked direct comparisons between MVP and MVR were excluded.
A total of 16 studies with 8659 patients were inclsurgeons, MVP can be performed for some suitable patients with RHD and is preferred for elderly patients or patients with contraindications of anticoagulation. However, MVR is more appropriate when concomitant AVR is needed.
Musclin is involved in the regulation of natriuretic peptide (NP) clearance and may affect the concentration of atrial natriuretic peptide (ANP). It has also been found to play an important role in several diseases, such as diabetes mellitus and hypertension. Both abnormalities in ANP and associated medical history are involved in the pathogenesis of atrial fibrillation (AF). However, plasma concentration of musclin as a biomarker for risk stratification in patients with AF has not been fully investigated.
Plasma musclin levels were measured in 290 patients with AF (including 199 paroxysmal AF patients and 91 persistent AF patients) and 120 control subjects. The association between plasma musclin levels and AF onset, as well as its predictive effects on clinical outcomes after cryoballoon ablation were analyzed.
AF patients were found to have a lower concentration of plasma musclin than healthy controls. Moreover, in the non-diabetic group and normal N-terminal pro-brain natriuretic peptide (NT-proBNP) ies suggest that musclin could be a predictive factor for the onset of AF.
Many studies have shown an elevated level of cholesterol in colon tumors as compared to normal tissue. Obesity and high low-density lipoprotein cholesterol (LDL-C) are known risk factors for colon cancer. However, the role of LDL-C in colon cancer patients with normal body mass index (BMI) remains elusive.
Levels of serum cholesterol and oxysterols were quantified by ultra-performance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS) from 129 individuals with normal BMI, including 32 with solitary polyp, 36 with multiple polyps, and 31 with adenocarcinoma as well as 32 healthy controls. In vitro, colon cancer cells were treated with LDL-C and assayed for chemokines via RNA-Seq and mitochondrial morphology via transmission electron microscopy and immunofluorescence. Additionally, correlation analysis was performed between LDL-C-induced chemokines and the overall survival of colon cancer patients from the Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx), and the Human Protein Atlas (HPA) database.
