Chronic disease diagnosis model based on convolutional neural network and ensemble learning method.

Introduction: Chronic diseases have become one of the main causes of premature death all around the world in recent years. The diagnosis of chronic diseases is time-consuming and costly. Therefore, timely diagnosis and prediction of chronic diseases are very necessary. Methods: In this paper, a new method for chronic disease diagnosis is proposed by combining convolutional neural network (CNN) and ensemble learning. This method utilizes random forest (RF) as the base classifier to improve classification performance and diagnostic accuracy, and then combines AdaBoost to successfully replace the Softmax layer of CNN to generate multiple accurate base classifiers while determining their optimal attributes, achieving high-quality classification and prediction of chronic diseases. Results: To verify the effectiveness of the proposed method, real-world Electronic Medical Records dataset (C-EMRs) was used for experimental analysis. The results show that compared with other traditional machine learning methods such as CNN, K-Nearest Neighbor, and RF, the proposed method can effectively improve the accuracy of diagnosis and reduce the occurrence of missed diagnosis and misdiagnosis. Conclusions: This study will provide effective information for the diagnosis of chronic diseases, assist doctors in making clinical decisions, develop targeted intervention measures, and reduce the probability of misdiagnosis.

Genetics and epigenetics of melanoma.

[This retracts the article DOI: 10.3892/ol.2016.5093.].

Recent perspectives of epithelial ovarian carcinoma.

[This retracts the article DOI: 10.3892/ol.2016.5107.].

Nanotechnology for multimodality treatment of cancer.

[This retracts the article DOI: 10.3892/ol.2016.5322.].

Mitochondria targeting nano agents in cancer therapeutics.

[This retracts the article DOI: 10.3892/ol.2016.5302.].

Combinations in multimodality treatments and clinical outcomes during cancer.

[This retracts the article DOI: 10.3892/ol.2016.5242.].

Stem cell transplantation during cancer.

[This retracts the article DOI: 10.3892/ol.2016.5260.].

Hospital information technology in home care (Review).

[This retracts the article DOI: 10.3892/etm.2016.3664.].

Receptor tyrosine kinases in carcinogenesis.

[This retracts the article DOI: 10.3892/ol.2016.5200.].

Scorpion venoms in gastric cancer.

[This retracts the article DOI: 10.3892/ol.2016.5134.].

Risk of Active Pulmonary Tuberculosis among Patients with Coal Workers'Pneumoconiosis: A Case-control Study in China.

The aim of this study was to estimate the association between occupational, environmental, behavioral risk factors, and active pulmonary tuberculosis (PTB) among coal workers' pneumoconiosis (CWP) patients. A matched case-control study was conducted in 86 CWP patients with active PTB and 86 CWP controls without TB. A standardized questionnaire was used for risk factors assessment. Conditioned logistic regression analysis was used to identify associations between the risk factors and active PTB among CWP patients. The results showed that the stage of CWP, poor workplace ventilation, family history of TB, and exposure to TB were independent risk factors for active PTB in patients with CWP with which recommendations for improving work environments, and for case finding activities in patients with CWP could be made.

Zinc alpha2 glycoprotein protects against obesity-induced hepatic steatosis.

BACKGROUND/AIM: Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, impaired insulin sensitivity, and chronic low-grade inflammation. Our previous studies indicated that zinc alpha2 glycoprotein (ZAG) alleviates palmitate (PA)-induced intracellular lipid accumulation in hepatocytes. This study is to further characterize the roles of ZAG on the development of hepatic steatosis, insulin resistance (IR), and inflammation. METHODS: ZAG protein levels in the livers of NAFLD patients, high-fat diet (HFD)-induced or genetically (ob/ob) induced obese mice, and in PA-treated hepatocytes were determined by western blotting. C57BL/6J mice injected with an adenovirus expressing ZAG were fed HFD for indicated time to induce hepatic steatosis, IR, and inflammation, and then biomedical, histological, and metabolic analyses were conducted to identify pathologic alterations in these mice. The molecular mechanisms underlying ZAG-regulated hepatic steatosis were further explored and verified in mice and hepatocytes. RESULTS: ZAG expression was decreased in NAFLD patient liver biopsy samples, obese mice livers, and PA-treated hepatocytes. Simultaneously, ZAG overexpression alleviated intracellular lipid accumulation via upregulating adiponectin and lipolytic genes (FXR, PPARα, etc.) while downregulating lipogenic genes (SREBP-1c, LXR, etc.) in obese mice as well as in cultured hepatocytes. ZAG improved insulin sensitivity and glucose tolerance via activation of IRS/AKT signaling. Moreover, ZAG significantly inhibited NF-ĸB/JNK signaling and thus resulting in suppression of obesity-associated inflammatory response in hepatocytes. CONCLUSIONS: Our results revealed that ZAG could protect against NAFLD by ameliorating hepatic steatosis, IR, and inflammation.

Metal-Organic Framework-Derived Metal Oxide Embedded in Nitrogen-Doped Graphene Network for High-Performance Lithium-Ion Batteries.

Metal-organic frameworks (MOFs) are hybrid inorganic-organic materials that can be used as effective precursors to prepare various functional nanomaterials for energy-related applications. Nevertheless, most MOF-derived metal oxides exhibit low electrical conductivity and mechanical strain. These characteristics limit their electrochemical performance and hamper their practical application. Herein, we report a rational strategy for enhancing the lithium storage performance of MOF-derived metal oxide. The hierarchically porous Co3O4@NGN is successfully prepared by embedding ZIF-67-derived Co3O4 particles in a nitrogen-doped graphene network (NGN). The high electrical conductivity and porous structure of the NGN accelerates the diffusion of electrolyte ions and buffers stress resulting from the volume changes of Co3O4. As an anode material, the Co3O4@NGN shows high capacity (1030 mA h g-1 at 100 mA g-1), outstanding rate performance (681 mA h g-1 at 1000 mA g-1), and good cycling stability (676 mA h g-1 at 1000 mA g-1 after 400 cycles).

Dicer regulates non-homologous end joining and is associated with chemosensitivity in colon cancer patients.

DNA double-strand break (DSB) repair is an important mechanism underlying chemotherapy resistance in human cancers. Dicer participates in DSB repair by facilitating homologous recombination. However, whether Dicer is involved in non-homologous end joining (NHEJ) remains unknown. Here, we addressed whether Dicer regulates NHEJ and chemosensitivity in colon cancer cells. Using our recently developed NHEJ assay, we found that DSB introduction by I-SceI cleavage leads to Dicer upregulation. Dicer knockdown increased SIRT7 binding and decreased the level of H3K18Ac (acetylated lysine 18 of histone H3) at DSB sites, thereby repressing the recruitment of NHEJ factors to DSB sites and inhibiting NHEJ. Dicer overexpression reduced SIRT7 binding and increased the level of H3K18Ac at DSB sites, promoting the recruitment of NHEJ factors to DSBs and moderately enhancing NHEJ. Dicer knockdown and overexpression increased and decreased, respectively, the chemosensitivity of colon cancer cells. Dicer protein expression in colon cancer tissues of patients was directly correlated with chemoresistance. Our findings revealed a function of Dicer in NHEJ-mediated DSB repair and the association of Dicer expression with chemoresistance in colon cancer patients.

Prognostic role of ABO blood type in patients with extranodal natural killer/T cell lymphoma, nasal type: a triple-center study.

BACKGROUND: The prognostic significance of ABO blood type for lymphoma is largely unknown. We evaluated the prognostic role of ABO blood type in patients with extranodal natural killer (NK)/T-cell lymphoma (ENKTL). METHODS: We retrospectively analyzed clinical data of 697 patients with newly diagnosed ENKTL from three cancer centers. The prognostic value of ABO blood type was evaluated using Kaplan-Meier curves and Cox proportional hazard models. The prognostic values of the International Prognostic Index (IPI) and the Korean Prognostic Index (KPI) were also evaluated. RESULTS: Compared with patients with blood type O, those with blood type non-O tended to display elevated baseline serum C-reactive protein levels (P = 0.038), lower rate of complete remission (P = 0.005), shorter progression-free survival (PFS, P < 0.001), and shorter overall survival (OS, P = 0.001). Patients with blood type O/AB had longer PFS (P < 0.001) and OS (P = 0.001) compared with those with blood type A/B. Multivariate analysis demonstrated that age >60 years (P < 0.001), mass ≥5 cm (P = 0.001), stage III/IV (P < 0.001), elevated serum lactate dehydrogenase (LDH) levels (P = 0.001), and blood type non-O were independent adverse predictors of OS (P = 0.001). ABO blood type was found to be superior to both the IPI in discriminating patients with different outcomes in the IPI low-risk group and the KPI in distinguishing between the intermediate-to-low- and high-to-intermediate-risk groups. CONCLUSIONS: ABO blood type was an independent predictor of clinical outcome for patients with ENKTL.

miRNAs in vascular integrity.

Endothelial cells (ECs) are confirmed as important regulators of vascular integrity, particularly in relation to angiogenesis, wound repair post-injury, and during embryogenesis. Futher, miRNAs have been implicated in EC function and proliferation. Moreover, knockdown of these miRNAs resulted in altered expressions of several important regulators of endothelial biology and angiogenesis including vascular endothelial growth factor receptor 2, endothelial nitric oxide synthase and tubule formation capacity. Several miRNAs have been identified to play a role in the regulation of function, proliferation and growth of vascular ECs. These miRNAs may be important therapeutic targets in the treatment of a range of ischemic diseases, as well as in the regulation of angiogenesis during cancer and tumour progression. The present review discuss some of the important miRNAs having confirmed regulatory role in EC in connection espically with cardiovascular disease.

Transforming growth factor ß and its role in heart disease.

Myocardial infarction (MI) is a major form of heart disease that leads to immediate cardiomyocyte death due to ischemia and eventually fibrosis and scar formation and further dysfunction of myocardium and heart failure. Extracellular matrix (ECM) production and tissue repair is conducted by myofibroblasts, which are formed from the normal quiescent cardiac fibroblasts following transformational changes, through the active participation of transforming growth factor ß (TGFß) and its signaling pathways. TGFß appears to be a 'Master of all trades', with respect to cardiac fibrosis, as it can promote cardiomyocyte apoptosis and cardiac hypertrophy. TGFß signaling involves its binding to TGFß receptor type II (TGFßRII), which recruits TGFß receptor type I (TGFßRI), which are also known as activin receptor-like kinase (ALK) in five different isoforms. In canonical signaling pathways, ALK5 activates Smads 2 and 3, and ALK1 activates Smads 1 and 5. These pairs of Smads form a corresponding complex and then bind to Smad 4, to translocate into the nucleus, where transcriptional reprogramming is carried out to promote myofibroblast formation and ECM production, eventually leading to cardiac fibrosis. TGFß levels are elevated in MI, thereby aggravating the myocardial injury further. Several microRNAs are involved in the regulation of TGFß signaling at different steps, affecting different components. Therapeutic targeting of TGFß signaling at ALK1-5 receptor activity level has met with limited success and extensive research is needed to develop therapies based on the components of TGFß signaling pathway, for instance cardiac dysfunction and heart failure.

Tumor necrosis factor-related apoptosis-inducing ligand inhibits proliferation and induces apoptosis of prostate and bladder cancer cells.

The effect of recombinant and purified tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on the proliferation and apoptosis of PC-3 prostate cancer cells and the 5637 bladder cancer cells were investigated. We used a cell proliferation assay and flow cytometry to measure the proliferation and apoptosis of cancer cells after 24-h incubation of PC-3 and 5637 cells with different concentrations of TRAIL. PC-3 cell proliferation rate significantly decreased when TRAIL was used at concentrations of 20, 40, 80 and 160 ng/ml compared with the untreated group. In the 5637 cells, the proliferation rate significantly decreased when TRAIL was used at concentrations of 5, 10, 20 and 40 ng/ml compared with the untreated group. The flow cytometry results also confirmed that the apoptosis rate of both cancer cell lines increased with TRAIL protein concentration. In conclusion, recombinant and purified TRAIL has anticancer activity by inhibiting proliferation and promoting apoptosis of prostate and bladder cancer cells.

PCSK9 as a therapeutic target for cardiovascular disease.

It is well recognized that the elevated plasma level of low-density lipoprotein-cholesterol (LDL-C) is a major risk factor for atherosclerosis and cardiovascular disease (CVD). Deposition of pro-atherogenic LDL-C, on the intima of arterial wall, contributes to plaque formation and atherosclerosis, which further leads to lowered blood flow to vital organs and increased risk of CVD. The most commonly used statin therapy is effective in reducing dyslipidemia and preventing cardiovascular events only in about half of the patient population. However, in patients with familial hypercholesterolemia, these drugs were not effective to meet the required goals of lower LDL-C, and to reduce the CVD risk. Furthermore, many patients even develop intolerability to statins and resistance. The identification of pro-protein convertase subtilisin/kexin type 9 (PCSK9) and the association of PCSK9 mutations with familial hypercholesterolemia led to the identification of PCSK9 as a new therapeutic target for lowering LDL-C and dyslipidemia-associated CVD. PCSK9 is found to promote the degradation of LDL-receptor (LDLR), thus rendering it unavailable for recycling to hepatocyte plasma membrane, leading to elevated levels of circulating LDL-C, as it cannot be taken up into cells. While gain-of-function mutations aggravate the degradation of LDLR as in familial hypercholesterolemia whereas loss of function mutations reduce the ability of PCSK9 to promote the degradation of LDLR and thus lower the plasma level of LDL-C and dyslipidemia. Monoclonal antibodies against PCSK9 are currently being tested in clinical trials and are found to be efficacious in countering the activity of PCSK9 and thus control the plasma LDL-C and triglycerides even in statin non-responsive patients and protect against dyslipidemia-related CVD.

From inflammation to gastric cancer: Role of Helicobacter pylori.

Gastric cancer is a multifactorial disease and a leading cause of mortality and the risk factors for this include environmental factors and factors that influence host-pathogen interaction and complex interplay between these factors. Gastric adenocarcinomas are of two types, namely intestinal and diffuse type, and Helicobacter pylori (H. pylori) infection has been suspected of being causally linked to the initiation of chronic active gastritis, which leads to adenocarcinoma of the intestinal type. Even though most individuals with H. pylori infection do not show any clinical symptoms, long-term infection leads to inflammation of gastric epithelium and approximately 10% of infected patients develop peptic ulcers and 1-3% of patients develop gastric adenocarcinoma. Among the several mechanisms involved in tumorigenesis, CagA and peptidoglycan of H. pylori, which enter the infected gastric epithelial cells play an important role by triggering oncogenic pathways. Inflammation induced by H. pylori in gastric epithelium, which involves the cyclooxygenase-2/prostaglandin E2 pathway and IL-1ß, is also an important factor that triggers chronic active gastritis and adenocarcinoma. H. pylori infection induced oxidative stress and dysregulated E-cadherin/ß-catenin/p120 interactions and function also play a critical role in tumorigenesis. Environmental and dietary factors, in particular salt intake, are known to modify the pathogenesis induced by H. pylori. Gastric cancer induced by H. pylori appears to involve several mechanisms, making this mode of tumorigenesis a highly complicated process. Nevertheless, there are many events in this tumorigenesis that remain to be clarified and investigated.