BackgroundFew studies have suggested a relationship between inflammation and cerebral venous thrombosis (CVT). This retrospective study aimed to explore the changes in inflammation in different CVT stages and the correlation between inflammation and severity and outcome of CVT.MethodsIn total, 95 suitable patients with CVT and 41 controls were compared. Patients with CVT were divided into three groups. The inflammatory factors studied included hypersensitive C-reactive protein (Hs-CRP), interleukin-6 (IL-6), and neutrophil-to-lymphocyte ratio (NLR) in the peripheral blood and immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) in the cerebrospinal fluid (CSF). The severity of CVT was evaluated with the modified Rankin Scale (mRS), the National Institutes of Health Stroke Scale (NIHSS), fundus condition, intracranial pressure (ICP), and complications on admission. The short-term outcome was evaluated with the mRS at discharge.ResultsThe following results were obtained: (1) Inflammatory factor levels in patients with CVT were higher than those in the controls. (2) Inflammatory factor levels in the acute and subacute stages were significantly higher than those in the chronic stage (all P < 0.05). (3) Serum NLR and CSF IgM levels were positively related to baseline degree of disability (odds ratio [OR], 1.279, 95% confidence interval [CI] 1.009–1.621, P = 0.042; OR 1.402, 95% CI 1.036–1.896, P = 0.028). The Hs-CRP level was positively correlated with the baseline occurrence of seizure (OR 1.040, 95% CI 1.001–1.080, P = 0.043). The baseline serum NLR (r = 0.244, P = 0.017), CSF IgA (r = 0.615, P < 0.001), CSF IgM (r = 0.752, P < 0.001), and CSF IgG (r = 0.248, P = 0.015) levels were positively associated with NIHSS. (4) The baseline NLR was significantly associated with high risk of poor outcome at discharge (OR 1.339, 95% CI 1.097–1.784, P = 0.007). Moreover, the ROC showed that NLR ≥ 4.205 could better predict the poor outcome at discharge. The data were analyzed using SPSS.ConclusionsInflammation may develop after CVT and gradually decrease during the course. Inflammation was significantly correlated with severity on admission and short-term poor outcome at discharge in CVT.
BackgroundPulmonary enteric adenocarcinoma (PEAC), a rare type of non-small cell lung cancer, has similar histological and immunohistochemical morphology to colorectal adenocarcinoma. Cadherin-17 (CDH17) and SATB homeobox 2 (SATB2) immunoexpression have recently been demonstrated in colorectal adenocarcinoma. In this study, we evaluated the value of CDH17 and SATB2 in the diagnosis of pulmonary enteric adenocarcinoma and metastatic colorectal adenocarcinoma.MethodsA total of 13 PEAC cases and 27 metastatic colorectal adenocarcinoma cases were enrolled in our cohort study. We analyzed the expressions of CK7, CK20, CDX-2, villin, cadherin-17 (CDH17), and SATB homeobox 2 (SATB2) using immunohistochemistry. Staining intensity and percentage of positive-staining cells were recorded. Sensitivity and specificity values for immunostains, individually and in combination, were computed and compared.ResultsCombining CDH17 and SATB2 resulted in high sensitivity (76.92%) and specificity (100%). In our study, the use of CK7+, napsin A+, TTF-1+, napsin A+TTF-1+ in combination with CDH17-/SATB2- had a higher area under the curve compared to the combination CDH17-/SATB2-. However, no significant differences were observed between the combination CDH17-/SATB2- and other combinations (P>0.05).ConclusionsIn combination, CDH17 and SATB2 serve as potential optimal markers for the differential diagnosis of PEAC and metastatic colorectal adenocarcinoma.
Accumulating evidence has suggested that the dysregulation of miRNA is an important factor in the pathogenesis of lung cancer. Here, we demonstrate that miR‐335 expression is reduced in non‐small cell lung cancer (NSCLC) tumors relative to non‐cancerous adjacent tissues, while the expression of Tra2β is increased. In addition, clinical data revealed that the increased Tra2β and decreased miR‐335 expression observed in NSCLC cells was associated with poor patient survival rates. In vitro experimentation showed that the overexpression of miR‐335 inhibited the growth, invasion and migration capabilities of A459 lung cancer cells, by targeting Tra2β. In contrast, inhibition of miR‐335 or overexpression of the Tra2β target gene stimulated the growth, invasion and migratory capabilities of A459 lung cancer cells in vitro. Furthermore, overexpression of miR‐335 or inhibition of Tra2β decreased the phosphorylation of Rb‐S780 and Rb‐AKT. Overall, these findings suggest that the downregulation of miR‐335 in A459 lung cancer cells promoted cell proliferation through upregulation of Tra2β, mediated via activation of the AKT/mTOR signaling pathway, and suggest that miR‐335 may have potential as a novel therapeutic target for NSCLC.
Background TUBA1C is a microtubule component that is involved in a variety of cancers. Our main objective was to investigate TUBA1C expression, its prognostic value, its potential biological functions, and its impact on the immune system of patients with lung adenocarcinoma (LUAD). Methods The Cancer Genome Atlas (TCGA), Gene Expression Profiling Interactive Analysis (GEPIA) and Immunohistochemistry Analysis were used to analyze TUBA1C expression, its clinicopathology, overall survival (OS), and disease-free survival (DFS) in LUAD patients. We also determined the correlation between TUBA1C and tumor-infiltrating immune cells (TIICs) by using CIBERSORT and GEPIA databases. To determine the expression of TUBA1C in LUAD, we analyzed a collection of immune infiltration levels and cumulative survival of LUAD tissues in TIMER database. By using UALCAN, STRING, and GeneMANIA databases, we investigated the protein-coding genes related to TUBA1C and its co-expression genes in LUAD tissues. Gene set enrichment analysis (GSEA) was performed by using the TCGA dataset. Results The mRNA and the protein expression of TUBA1C were found to be up-regulated in LUAD tissues. The univariate analysis indicated that an increased expression of TUBA1C was significantly correlated to the following parameters: age, stage, and lymph node metastasis. An over-expression of TUBA1C was associated with a poor prognosis of LUAD. In TIMER and CIBERSORT databases, we found that TUBA1C is correlated with 13 types of TIICs: activated B cell, activated CD4 T cell, central memory CD4 T cell, effector memory CD8 T cell, eosinophils, immature B cell, gamma-delta T cell, immature dendritic cell, mast cell, memory B cell, natural killer T cell, regulatory T cell, and type 2T helper cell. By performing GSEA, we found that TUBA1C is closely correlated to cell cycle, p53 signaling pathway, glycolysis, and gluconeogenesis. Conclusions Our findings indicate that TUBA1C is associated with TIICs in tumor microenvironment. Therefore, it serves as a novel prognostic biomarker and a target for future treatment methods of LUAD.
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