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Currently, it is still a great challenge in clinical practice to accurately diagnose autism spectrum disorder (ASD). To address this challenge, in this study we propose a method for automatic diagnosis of ASD based on multi-atlas graph convolutional networks and ensemble learning. Firstly, we extract multiple feature representations based on functional connectivity (FC) of different brain atlases from fMRI data of each subject. Then, to obtain the features that are more helpful for ASD automatic diagnosis, we propose a multi-atlas graph convolutional network method (MAGCN). Finally, to combine different feature representations, we propose a stacking ensemble learning method to perform the final ASD automatic diagnostic task. Our proposed method is evaluated on 949 subjects (including 419 subjects with ASD and 530 subjects with typical control (TC)) from the Autism Brain Imaging Data Exchange (ABIDE). Experimental results show that our proposed method achieves an accuracy of 75.86% and an area under the receiver operating characteristic curve (AUC) of 0.8314 for automatic diagnosis of ASD. In addition, compared with some methods published in recent years, our proposed method obtains the best performance of ASD diagnosis. Overall, our proposed method is effective and promising for automatic diagnosis of ASD in clinical practice.

Objective To explore the protective function of vitamin D (VD)/vitamin D receptor (VDR) on the development of oral lichen planus (OLP) and elaborate the underling mechanism of it. Methods H&E staining, myeloid Peroxidase (MPO) assays, quantitative PCR (qPCR), western blotting and Elisa were used to test the human biopsies and serum. QPCR, western blotting, Elisa and siRNA transfection were also performed in LPS-induced keratinocytes to observe the functions of vitamin D and VDR. Results The lack of VDR in the diseased biopsies from OLP patients was associated with activated helper T-cell type 1 (Th1)-driven inflammatory response. Importantly, the status of serum 25-hydroxyvitamin D of OLP patients was reduced consistently. In a cultured cell model, 1,25(OH)2D3 could downregulate excessive production of pro-inflammatory factors induced by lipopolysaccharide (LPS) in keratinocyte HaCat cells. Mechanistically, even though LPS-induced cytokines in keratinocytes were inhibited both by nuclear factor-κB (NF-κB) inhibitor and by activator protein 1 (AP-1) inhibitor, VDR-dependent 1,25(OH)2D3 blocked the activation of phosphorylated-NF-κB p65 rather than c-Jun/c-Fos in the presence of LPS stimulation. Conclusion These results suggest that 1,25(OH)2D3 plays an anti-inflammatory role in OLP by mediating NF-κB signaling pathway but not AP-1 signaling pathway with a VDR-dependent manner, predicting vitamin D supplement may be a potential strategy for the OLP management. This article is protected by copyright. All rights reserved.

Background: Diabetes Mellitus (DM) accelerates progress of lung cancer. Hyperglycemia, a critical feature of DM, promotes lung cancer metastasis. Mogroside V is a triterpenoid glycoside from Siraitia grosvenorii. Interestingly, mogroside V not only plays an anti-diabetic role, but also has anti-tumor effects. Objective: In this study, we investigated the metastatic efficiency of mogroside V in lung cancer cells cultured in hyperglycemia. Methods: Two lung cancer cell lines-A549 and H1299 were cultured in normoglycemia (5.5mM glucose) and hyperglycemia (25mM glucose). Cellular proliferation was tested by MTT, invasion was examined by transwell assay, migration was measured by wound healing assay, cytoskeleton was stained by Phalloidin-TRITC and the expressions of EMT markers and Rho-GTPase family protein were detected by western blot. Results: Hyperglycemia promoted the invasion and migration of A549 and H1299 cells compared with normoglycemia. Mogroside V inhibited the hyperglycemia-induced invasion and migration. Hyperglycemia promoted epithelial-mesenchymal transition (EMT), while mogroside V could reverse this process through up-regulating E-Cadherin expression and down-regulating N-Cadherin, Vimentin, Snail expressions. Furthermore, mogroside V fractured microfilaments and reduced Rho A, Rac1, Cdc42 and p-PAK1 expressions under hyperglycemic conditions. Conclusion: These results suggest that mogroside V inhibits hyperglycemia-induced lung cancer cells migration and invasion through reversing EMT and damaging cytoskeleton.

Apolipoprotein B plays a central role in lipoprotein metabolism. Many studies have evaluated the association between Apolipoprotein B gene polymorphisms (XbaI, EcoRI, SpIns/Del, MspI) and the risk for coronary artery disease and myocardial infarction. However, the results remain inconsistent, particularly among different populations. To more precisely determine the association between Apolipoprotein B gene polymorphisms and coronary artery disease/myocardial infarction risk, we performed a meta-analysis via a comprehensive search of electronic databases (up to February 1st, 2015), odds ratios (OR) and 95 % confidence intervals were calculated using a fixed or random effect model. A total of 47 studies, with 9411 coronary artery disease/myocardial infarction cases and 9082 controls, were included in this meta-analysis. The combined results revealed significant associations between an increased risk of coronary artery disease/myocardial infarction and EcoRI (AA vs GG: OR 1.511, 95 % confidence interval (CI) 1.098, 2.078) and SpIns/Del (DD vs II: OR 1.331, 95 % CI 1.064, 1.665) alleles in the general population. In a subgroup analysis stratified by ethnicity, the T allele of the XbaI variant was associated with a decreased risk in Caucasians, whereas it was associated with an increased risk among the East Asian population. No significant correlation was detected between the A allele of the MspI variant and the coronary artery disease/myocardial infarction risk in either the general population or any ethnic subgroup. The results of our study suggest that Apolipoprotein B gene polymorphisms may affect the coronary artery disease/myocardial infarction susceptibility and these effects may display notable discrepancies among different populations.

Objective We performed a prospective observational study to explore the prognostic value of plasma galectin-3, a biomarker for fibrosis and inflammation, in Chinese patients with heart failure (HF). Methods and results Galectin-3, N-terminal pro B-type natriuretic peptide (NT-proBNP) and other clinically related variables were measured in consecutive HF patients in Beijing Hospital. Specifically, galectin-3 was detected by an enzyme-linked immunosorbent assay. The primary end point was major adverse cardiac events (MACE), including all-cause mortality or readmission at the end of follow-up. The secondary end point was all-cause mortality. The adjusted hazard ratio (HR) was determined by COX regression model. In total, 272 patients were included in this study with a median age of 77 years, of whom 55.9% were male. During a median follow-up of 584 (415-813) days, 53 patients (19.5%) died and 103 patients (37.9%) died and/or required readmission. Plasma galectin-3 levels by tertiles were associated with an increased risk for the primary end point (P 0.001). Kaplan-Meier survival curves showed that the third tertile of galectin-3 was associated with an increased rate of MACE, compared with the first and second tertiles, with the log rank P 0.001 and P = 0.001, respectively. In addition, the multivariate COX regression model showed that the highest tertile of galectin-3 was associated with an increased risk for MACE (HR =2.13, 95% confidence interval: 1.24-3.68, P = 0.006), compared with the lowest tertile after adjustment for age, NT-proBNP, creatinine, uric acid, albumin, haemoglobin, and estimated glomerular filtration rate (eGFR). Conclusion Plasma galectin-3 is an independent predictor of all-cause mortality and/or readmission in Chinese patients with HF.

To explore the correlation between the clinical indicators of patients with advanced lung cancer and lung infectious agent, 370 cases (including 222 patients with Candida, 148 patients with Klebsiella) which have 21 clinical indicators was subjected to data mining in this paper. We used random forest-recursive feature selection (RF-RFE) algorithm to select features, and Random Forest (RF), Support Vector Machine (SVM) and Decision Tree (DT) were used to classify the two infections respectively, and the corresponding classification error was estimated by 10 times 10 fold cross-validation. The result of the experiment shows that the classification model has high specificity with Klebsiella and RF has a better performance on classification classifying Candida and Klebsiella.

The present study aimed to determine the levels of cathepsin B (cath B), cathepsin L (cath L), cystatin C, urokinase plasminogen activator (u-PA) and urokinase plasminogen activator receptor (u-PAR) in the sera of patients with lung cancer compared to healthy controls using ELISA. Concomitantly, the relationship between the components and clinicopathological prognosis was analyzed. The study included 30 healthy volunteers and 105 lung cancer patients. Blood samples were collected and cath B, cath L, cystatin C, u-PA and u-PAR measurements were made using ELISA. Results showed that the levels of cath B, cath L, cystatin C, u-PA and u-PAR were significantly higher in the patient group compared to the healthy controls. The significance was marked for cath B and mild for u-PAR in correlation with lymph node metastasis. There was no significance for other parameters. Notably, patients with a combination of high cystatin C and high cath B levels had significantly lower survival probability as compared to those with cystatin C(+)/cath B(-) or with cystatin C(-)/cath B(-). Similarly, patients with a combination of high u-PA and u-PAR experienced significantly shorter survival. Furthermore, the univariate analysis revealed that cath B, u-PAR, lymph node metastases, stage and grade were related to survival. However, findings of the multivariate Cox analysis indicated that the sera levels of cath B, u-PAR and lymph node metastases may serve as independent prognostic variables in patients with lung cancer.

Rationale: About 50% of patients with a diagnosis of nonsmall cell lung carcinoma exhibit metastatic disease at the time of diagnosis. The preferential sites of extrapulmonary spread are the lymph nodes, liver, brain, adrenal glands, and bones; gastrointestinal tract perforation secondary to metastatic lung cancer is extremely rare. Patient concerns: A 60-year-old male nonsmoker patient presented with a 20-day history of facial, neck, and right upper limb edema. Physical examination revealed a 3.5 cm mass in his right chest. Computed tomography (CT) revealed a 4 cm mass near the right lung hilum. Diagnosis: Biopsy of the right chest wall mass revealed low differentiated lung adenocarcinoma. Additionally, retroperitoneal lymphadenopathy, pericardial effusion, metastases in the mediastinum, bilateral adrenal gland, and right thoracic wall nodule, as well as multiple bone metastases were also found. Interventions: Since the patient was diagnosed with multiple metastatic lung cancer, chemotherapy was started. One week after chemotherapy, he experienced a sudden acute abdominal pain. Abdominal CT examination indicated the possibility of intestinal perforation. Hence, the patient underwent an emergency operation. During the surgical procedure, 2 perforations of size 1×1 cm2 were discovered at 110 cm and 140 cm of the jejunum from Treitz's ligament. Then, an intestinal resection and end-to-end anastomosis were performed. The pathological diagnosis of the resected specimen revealed that it was a metastatic lung adenocarcinoma of small intestine. Outcomes: The patient died 10 days after operation and 19 days following the cancer diagnosis due to septic shock. Lessons: Gastrointestinal tract metastasis from the lung is uncommon, but the survival rate is extremely low; therefore, it should be considered as a possibility in patients who present with any of the gastrointestinal symptoms.

Lung cancer is the most common malignancy worldwide. This study aimed to identify miRNA biomarkers of lung adenocarcinoma and to investigate their molecular mechanisms. miRNA expression profiling of tumor tissues and adjacent normal tissues from 10 patients were detected using microarray. Differentially expressed miRNAs (DEMs) were identified, and were verified using quantitative reverse transcription-PCR. Thereafter, correlations between DEM expression and clinicopathological features were determined in 49 patients. Furthermore, Targetscan was utilized to predict target genes, among which transcription factors (TFs) were identified. The interactions among miRNAs, TFs and target genes were used to construct an miRNA-TF-target network. Totally, 11 DEMs were identified, among which two downregulated miRNAs (miR-126-3p and miR-451a) were validated. Low levels of miR-126-3p and miR-451a were associated with poor pathological stage, large tumor diameter and lymph node metastasis (P0.05). Receiver operating characteristic analysis showed that both miRNAs could predict pathological stage, tumor diameter and lymph node metastasis of lung adenocarcinoma (AUC0.65, P0.05). For miR-126-3p, 154 target genes were predicted (e.g., PLXNB2), which were enriched in 29 pathways mainly concerning apoptosis and cancer. For miR‑451a, 397 target genes were predicted, which were enriched in 5 pathways including 'PPAR signaling pathway'. Ten genes were co-regulated by miR-126-3p and miR-451a, e.g., TSC1. Furthermore, an miRNA-TF-target network was constructed, and a sub-network was identified, including 2 miRNAs, 15 targets, and 7 TFs. In conclusion, miR-126-3p and miR-451a predicted the severity of lung adenocarcinoma. However, the possible mechanisms explored by bioinformatics need to be further validated.

The present study reports the case of a 77-year-old female that was asymptomatic at presentation and was found to possess a lesion that was incidentally identified on a computed tomography (CT) scan. The CT scan revealed a non-homogeneous, hypodense, non-lobulated solid mass, ~1.2 cm in diameter, in the left upper lobe of the lung that demonstrated minimal contrast enhancement. The following CT scan was performed only two years later. This scan revealed that the non-homogeneous round mass had increased in size to ~1.7 cm in diameter, and possessed an irregular margin, in addition to being slightly lobulated with no calcification or fat. Combined positron emission tomography and CT revealed a lobulated mass that was ~1.9 cm in diameter, demonstrating an irregular margin with involvement of the mediastinal pleura. Slight uptake of 18F-fluorodeoxyglucose was also detected. The final histological diagnosis was pulmonary hamartoma.

BACKGROUND: Atrial fibrillation (AF) is one of the most common types of arrhythmia in humans. Recently, many studies have investigated the relationship between human atrial fibrillation and the single nucleotide polymorphism (SNP) of rs1805127 (A>G) in KCNE1 gene, but the results were still inconsistent and inconclusive. METHOD: Electronic databases and bibliographies of retrieved studies were searched. We performed a meta-analysis of ten case-control studies, including 2099 cases and 2252 controls, to evaluate the association of rs1805127 polymorphism (A>G) with the risk of AF. Random-effects model was used when the heterogeneity was obvious; otherwise, fixed-effects model was applied. Meta-regression was performed to examine potential source of heterogeneity. Egger's test and Begg's test were used to detect publication biases. RESULTS: The results showed a significantly increased risk of AF in homozygote comparison (GG vs. AA:OR = 1.899, 95%CI: 1.568, 2.300; Pheterogeneity = 0.217), heterozygote comparison (GA vs. AA:OR = 1.436, 95% CI:1.190, 1.732; Pheterogeneity = 0.739), dominant model(GA /GG vs. AA: OR = 1.624, 95%CI: 1.361, 1.938; Pheterogeneity = 0.778) and recessive model (GG vs. GA/AA: OR = 1.394, 95%CI:1.152, 1.686; Pheterogeneity = 0.03). Meta-regression revealed that the sample size and the types of AF were the source of the heterogeneity. CONCLUSION: The rs1805127 polymorphism (A>G) of KCNE1 is associated with an increased risk of AF, which suggests the rs1805217 polymorphism of KCNE1 gene may play an important role in the pathogenesis of AF.

Curcumin, a natural and crystalline compound isolated from the plant Curcuma longa with low toxicity in normal cells, has been shown to protect against carcinogenesis and prevent tumor development. However, little is known about antimetastasis effects and mechanism of curcumin in lung cancer. Rac1 is an important small Rho GTPases family protein and has been widely implicated in cytoskeleton rearrangements and cancer cell migration, invasion and metastasis. In this study, we examined the influence of curcumin on in vitro invasiveness of human lung cancer cells and the expressions of Rac1. The results indicate that curcumin at 10 μM slightly reduced the proliferation of 801D lung cancer cells but showed an obvious inhibitory effect on epidermal growth factor or transforming growth factor β1-induced lung cancer cell migration and invasion. Meanwhile, we demonstrated that the suppression of invasiveness correlated with inhibition of Rac1/PAK1 signaling pathways and matrix metalloproteinase (MMP) 2 and 9 protein expression by combining curcumin treatment with the methods of Rac1 gene silence and overexpression in lung cancer cells. Laser confocal microscope also showed that Rac1-regulated actin cytoskeleton rearrangement may be involved in anti-invasion effect of curcumin on lung cancer cell. At last, through xenograft experiments, we confirmed the connection between Rac1 and the growth and metastasis inhibitory effect of curcumin in vivo. In summary, these data demonstrated that low-toxic levels of curcumin could efficiently inhibit migration and invasion of lung cancer cells through inhibition of Rac1/PAK1 signaling pathway and MMP-2 and MMP-9 expression, which provided a novel insight into the molecular mechanism of curcumin against lung cancer.

Pulmonary sclerosing hemangioma (PSH) is a relatively rare benign neoplasm, often asymptomatic and presenting as a solitary pulmonary nodule on radiological imaging studies. In the present case report, we examined a case of PSH in a young adult female, and reviewed the literature pertaining to PSH with an emphasis on (18)F-fluorodeoxyglucose positron emission tomography/computed tomography ((18)FDG PET/CT) and pathology. Immunohistochemical staining was also performed to confirm the diagnosis of sclerosing hemangioma. The results revealed that the tumor cells were immunopositive for epithelial membrane antigen, thyroid transcription factor-1 and vimentin and cytoskeleton 7. The patient recovered and was discharged. Thus, (18)FDG PET/CT may be used in the diagnosis of a solitary benign pulmonary nodule.