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The majority of human genes have multiple polyadenylation sites, which are differentially used through the process of alternative polyadenylation (APA). Dysregulation of APA contributes to numerous diseases, including cancer. However, specific genes subject to APA that impact oncogenesis have not been well characterized, and many cancer APA landscapes remain underexplored. Here, we used dynamic analyses of APA from RNA-seq (DaPars) to define both the 3′UTR APA profile in esophageal squamous cell carcinoma (ESCC) and to identify 3′UTR shortening events that may drive tumor progression. In four distinct squamous cell carcinoma datasets, BID 3′UTRs were recurrently shortened and BID mRNA levels were significantly upregulated. Moreover, system correlation analysis revealed that CstF64 is a candidate upstream regulator of BID 3′UTR length. Mechanistically, a shortened BID 3′UTR promoted proliferation of ESCC cells by disrupting competing endogenous RNA (ceRNA) cross-talk, resulting in downregulation of the tumor suppressor gene ZFP36L2. These in vitro and in vivo results were supported by human patient data whereby 3′UTR shortening of BID and low expression of ZFP36L2 are prognostic factors of survival in ESCC. Collectively, these findings demonstrate that a key ceRNA network is disrupted through APA and promotes ESCC tumor progression. Significance: High-throughput analysis of alternative polyadenylation in esophageal squamous cell carcinoma identifies recurrent shortening of the BID 3′UTR as a driver of disease progression.

Different clinicopathologic characteristics could contribute to inconsistent prognoses of small breast neoplasms (T1a/T1b). This study was done to conduct a retrospective analysis and establish a clinical prediction model to predict individual survival outcomes of patients with small carcinomas of the breast.Based on the Surveillance, Epidemiology, and End Results (SEER) database, eligible patients with small breast carcinomas were analyzed. Univariate analysis and multivariate analysis were performed to clarify the indicators of overall survival. Pooling risk factors enabled nomograms to be constructed and further predicted 3-year, 5-year, and 10-year survival of patients with small breast cancer. The model was internally validated for discrimination and calibration.A total of 17,543 patients with small breast neoplasms diagnosed between 2013 and 2016 were enrolled. Histologic grade, lymph node stage, estrogen receptor or progesterone receptor status, and molecular subtypes of breast cancer were regarded as the risk factors of prognosis in a Cox proportional hazards model (P .05). A nomogram was constructed to give predictive accuracy toward individual survival rate of patients with small breast neoplasms.This prognostic model provided a robust and effective method to predict the prognosis of patients with small breast cancer.

Lung cancer is the second most common form of cancer in both men and women. It is responsible for at least 25% of all cancer-related deaths in the United States alone. Accurate and early diagnosis of this form of cancer can increase the rate of survival. Computed tomography (CT) imaging is one of the most accurate techniques for diagnosing the disease. In order to improve the classification accuracy of pulmonary lesions indicating lung cancer, this paper presents an improved method for training a densely connected convolutional network (DenseNet). The optimized setting ensures that code prediction error and reconstruction error within hidden layers are simultaneously minimized. To achieve this and improve the classification accuracy of the DenseNet, we propose an improved predictive sparse decomposition (PSD) approach for extracting sparse features from the medical images. The sparse decomposition is achieved by using a linear combination of basis functions over the L2 norm. The effect of dropout and hidden layer expansion on the classification accuracy of the DenseNet is also investigated. CT scans of human lung samples are obtained from The Cancer Imaging Archive (TCIA) hosted by the University of Arkansas for Medical Sciences (UAMS). The proposed method outperforms seven other neural network architectures and machine learning algorithms with a classification accuracy of 95%.

Adenocarcinoma at the gastroesophageal junction (ACGEJ) has dismal clinical outcomes, and there are currently few specific effective therapies because of limited knowledge on its genomic and transcriptomic alterations. The present study investigates genomic and transcriptomic changes in ACGEJ from Chinese patients and analyzes their drug vulnerabilities and associations with the survival time. Here we show that the major genomic changes of Chinese ACGEJ patients are chromosome instability promoted tumorigenic focal copy-number variations and COSMIC Signature 17-featured single nucleotide variations. We provide a comprehensive profile of genetic changes that are potentially vulnerable to existing therapeutic agents and identify Signature 17-correlated IFN-α response pathway as a prognostic marker that might have practical value for clinical prognosis of ACGEJ. These findings further our understanding on the molecular biology of ACGEJ and may help develop more effective therapeutic strategies., Adenocarcinoma at the gastroesophageal junction has a dismal prognosis and few drug options. Here, the authors present genomic and transcriptomic features and potential therapeutic targets and prognostic biomarkers of Chinese and Caucasian tumours, and reveal the molecular similarities.

Ischemic stroke is a serious cardiovascular disease with high morbidity and mortality rates that affects millions of people worldwide.Currently, the only therapy with proven efficacy for acute ischemic stroke is alteplase, however, it still has many shortcomings and limitations. Therefore,we screen new compounds from traditional Chinese medicine to explore their efficacy against ischemic reperfusion injury. Procyanidins, a natural productextracted from grapes seed, which have been shown can ameliorate cerebral ischemic injury. However, the underlying mechanism is still not very clear. Theaim of this study was to investigate the effect of procyanidins on middle cerebral artery occlusion/reperfusion (MCAO/R)-mediated cerebral ischemic injuryand its underlying possible mechanisms. SD rats were used to evaluate the effect of procyanidins on MCAO/R induced cerebral ischemic injury in vivo. Histological analysis was used toassess neuronal apoptosis. Cell signaling was assayed by Western blot. In this study, we found that procyanidins can significantly ameliorate the middle cerebral artery occlusion/reperfusion (MCAO/R)-mediatedneurological deficits, and relieved brain edema, cerebral infarction volume, histopathological damage and apoptosis in rats. In addition, procyanidins canalso markedly inhibit MCAO/R and oxygen-glucose deprivation/reoxygenation (OGD/R)-mediated activation of TLR4-p38-NF-κB-NLRP3 signalingpathway in vitro and in vivo. Moreover, procyanidins can inhibit MCAO/R and OGD/R-induced the production of inflammatory cytokines such asinterleukin-1β (IL-1β) in vitro and in vivo. Besides, treatment with TLR4 inhibitor (Cli-095) in BV2 cell also shows the same effect. Altogether, these data suggested that procyanidins exerted a potential neuroprotective effect may by inhibit the TLR4-p38-NF-κB-NLRP3signaling pathway in the brain in MCAO/R rats.

Heart disease is the leading cause of death globally. The most common type of heart disease is coronary heart disease, which occurs when there is a build-up of plaque inside the arteries that supply blood to the heart, making blood circulation difficult. The prediction of heart disease is a challenge in clinical machine learning. Early detection of people at risk of the disease is vital in preventing its progression. This paper proposes a deep learning approach to achieve improved prediction of heart disease. An enhanced stacked sparse autoencoder network (SSAE) is developed to achieve efficient feature learning. The network consists of multiple sparse autoencoders and a softmax classifier. Additionally, in deep learning models, the algorithm’s parameters need to be optimized appropriately to obtain efficient performance. Hence, we propose a particle swarm optimization (PSO) based technique to tune the parameters of the stacked sparse autoencoder. The optimization by the PSO improves the feature learning and classification performance of the SSAE. Meanwhile, the multilayer architecture of autoencoders usually leads to internal covariate shift, a problem that affects the generalization ability of the network, hence, batch normalization is introduced to prevent this problem. The experimental results show that the proposed method effectively predicts heart disease by obtaining a classification accuracy of 0.973 and 0.961 on the Framingham and Cleveland heart disease datasets, respectively, thereby outperforming other machine learning methods and similar studies.

The problem posed by total blackout experienced in some parts of the globe due to power system (PS) voltage instability has been traced to continuous increase in power demand. Thus, it becomes imperative to assess voltage stability in a power grid. In this paper, a method which depends on the network characteristics of a power system is investigated. This method makes use of the admittance matrix between load to load nodes in an interconnected power system. Eigenvalue decomposition method is applied on the submatrix of the admittance matrix partitioned into generator and load nodes. A comparison of the suggested method with a load flow based voltage collapse proximity index (VCPI) is also carried out. The effectiveness of methods considered is tested on both the IEEE 30-bus and the Southern Indian 10-bus power networks. Results obtained shows that, the proposed method could assist and serve as a great tool in the investigation of voltage stability in a system as it decreases computational burdens.

Esophageal squamous-cell carcinoma (ESCC), one of the most prevalent and lethal malignant disease, has a complex but unknown tumor ecosystem. Here, we investigate the composition of ESCC tumors based on 208,659 single-cell transcriptomes derived from 60 individuals. We identify 8 common expression programs from malignant epithelial cells and discover 42 cell types, including 26 immune cell and 16 nonimmune stromal cell subtypes in the tumor microenvironment (TME), and analyse the interactions between cancer cells and other cells and the interactions among different cell types in the TME. Moreover, we link the cancer cell transcriptomes to the somatic mutations and identify several markers significantly associated with patients’ survival, which may be relevant to precision care of ESCC patients. These results reveal the immunosuppressive status in the ESCC TME and further our understanding of ESCC., Esophageal squamous-cell carcinomas (ESCC) have poor prognosis, and detailed molecular profiles are necessary to identify prognostic markers. Here the authors analyse 60 ESCC patient samples using scRNA-seq, TCR-seq and genomics; they find mucosal immunity markers associated with survival and immunosuppressive microenvironments.

Purpose. To identify the characteristics of the physical and mental health status of patients with pituitary adenomas, explore the postoperative reversibility of impaired health status, and assess the impact of clinical characteristics, hormone levels, anxiety, depression, and disease stigma on health status. Methods. We prospectively enrolled 147 and 138 patients with nonfunctioning and secretory pituitary adenomas, respectively. Health status was evaluated in 8 domains using the 36-item Short-Form Health Survey before and 3 months after transsphenoidal surgery. The Self-Rating Anxiety Scale, the Self-Rating Depression Scale, and the Stigma Scale for Chronic Illness were used to assess the psychological status. Results. Compared with the healthy population reference values, general physical and mental health, social functioning, and role limitations due to physical and psychological health problems were all found to be significantly impaired in the adenoma patients. Health status was worse in patients with adrenocorticotropic hormone- (ACTH-) secreting and growth hormone- (GH-) secreting adenomas than in patients with nonfunctioning adenomas. Among the patients, 11.6% had anxiety and 30.9% had depression. Higher scores for anxiety, depression, and disease stigma; older age; higher body mass index; and tumor recurrence were independent risk factors for health status impairment in at least one domain. Physical function impairment and role limitations caused by physical health problems became worse after surgery, whereas the mental component of health status remained the same. Conclusion. Health status was impaired in patients with pituitary adenomas, especially secretory adenomas. Physical function and role limitations were worse 3 months after surgery than before surgery. Mental problems, old age, obesity, and tumor recurrence reduced health status.

Esophageal squamous-cell carcinoma (ESCC), one of the most prevalent and lethal malignant disease, has a complex but unknown tumor ecosystem. Here, we decipher for the first time the full compositions of ESCC tumor based on analyzing 208,659 single-cell transcriptomes in ESCC derived from 60 individuals. We identify 8 essential expression programs from malignant epithelial cells and discovered 43 cell types including 26 immune cell and 17 nonimmune stromal cell subtypes in the tumor microenvironment (TME), and also explicate the interactions between cancer cells and other cells and the interactions among different cell types in the TME. Moreover, we have linked the cancer cell transcriptomes to the somatic mutations and identified several markers significantly associated with survival time in patients, which may be relevant to precision cares of ESCC patients. These results renew our understanding of ESCC and provide a valuable example and resource for investigating other types of solid tumor.

Investigating the biogeographical disjunction of East Asian and North American flora is key to understanding the formation and dynamics of biodiversity in the Northern Hemisphere. The small Cupressaceae genus Thuja, comprising five species, exhibits a typical disjunct distribution in East Asia and North America. Owing to obscure relationships, the biogeographical history of the genus remains controversial. Here, complete plastomes were employed to investigate the plastome evolution, phylogenetic relationships, and biogeographic history of Thuja. All plastomes of Thuja share the same gene content arranged in the same order. The loss of an IR was evident in all Thuja plastomes, and the B-arrangement as previously recognized was detected. Phylogenomic analyses resolved two sister pairs, T. standishii-T. koraiensis and T. occidentalis-T. sutchuenensis, with T. plicata sister to T. occidentalis-T. sutchuenensis. Molecular dating and biogeographic results suggest the diversification of Thuja occurred in the Middle Miocene, and the ancestral area of extant species was located in northern East Asia. Incorporating the fossil record, we inferred that Thuja likely originated from the high-latitude areas of North America in the Paleocene with a second diversification center in northern East Asia. The current geographical distribution of Thuja was likely shaped by dispersal events attributed to the Bering Land Bridge in the Miocene and subsequent vicariance events accompanying climate cooling. The potential effect of extinction may have profound influence on the biogeographical history of Thuja.

Esophageal squamous-cell carcinoma (ESCC) is one of the most lethal malignancies in the world and occurs at particularly higher frequency in China. While several genome-wide association studies (GWAS) of germline variants and whole-genome or whole-exome sequencing studies of somatic mutations in ESCC have been published, there is no comprehensive database publically available for this cancer. Here, we developed the Chinese Cancer Genomic Database-Esophageal Squamous Cell Carcinoma (CCGD-ESCC) database, which contains the associations of 69,593 single nucleotide polymorphisms (SNPs) with ESCC risk in 2022 cases and 2039 controls, survival time of 1006 ESCC patients (survival GWAS) and gene expression (expression quantitative trait loci, eQTL) in 94 ESCC patients. Moreover, this database also provides the associations between 8833 somatic mutations and survival time in 675 ESCC patients. Our user-friendly database is a resource useful for biologists and oncologists not only in identifying the associations of genetic variants or somatic mutations with the development and progression of ESCC but also in studying the underlying mechanisms for tumorigenesis of the cancer. CCGD-ESCC is freely accessible at http://db.cbi.pku.edu.cn/ccgd/ESCCdb. Keywords: Esophageal cancer, Germline variants, Somatic mutations, Association database, Chinese population

Background Goal-directed hemodynamic therapy (GDHT) has been used in the clinical setting for years. However, the evidence for the beneficial effect of GDHT on postoperative recovery remains inconsistent. The aim of this systematic review and meta-analysis was to evaluate the effect of perioperative GDHT in comparison with conventional fluid therapy on postoperative recovery in adults undergoing major abdominal surgery. Methods Randomized controlled trials (RCTs) in which researchers evaluated the effect of perioperative use of GDHT on postoperative recovery in comparison with conventional fluid therapy following abdominal surgery in adults (i.e., >16 years) were considered. The effect sizes with 95% CIs were calculated. Results Forty-five eligible RCTs were included. Perioperative GDHT was associated with a significant reduction in short-term mortality (risk ratio [RR] 0.75, 95% CI 0.61–0.91, p = 0.004, I 2 = 0), long-term mortality (RR 0.80, 95% CI 0.64–0.99, p = 0.04, I 2 = 4%), and overall complication rates (RR 0.76, 95% CI 0.68–0.85, p

SummaryWhole-genome sequencing has identified many amplified genes in esophageal squamous-cell carcinoma (ESCC); however, their roles and the clinical relevance have yet elucidated. Here we show TP53-induced glycolysis and apoptosis regulator (TIGAR) is a major player in ESCC progression and chemoresistance. TIGAR reprograms glucose metabolism from glycolysis to the glutamine pathway through AMP-activated kinase, and its overexpression is correlated with poor disease outcomes. Tigar knockout mice have reduced ESCC growth and tumor burden. Treatment of TIGAR-overexpressed ESCC cell xenografts and patient-derived tumor xenografts in mice with combination of glutaminase inhibitor and chemotherapeutic agents achieves significant more efficacy than chemotherapy alone. These findings shed light on an important role of TIGAR in ESCC and provide evidence for targeted treatment of TIGAR-overexpressed ESCC.SignificanceEffective and target therapies are required for ESCC, one of the most common types of digestive OR cancer. Little has been known about the biology of ESCC progression or potential molecular targets OR for treatment. Whole-genome sequencing and RNA sequencing studies in ESCC have identified OR many recurrent copy number gain genes; however, the roles and druggable relevance of these OR genes remains poorly understood. Herein we demonstrate that TIGAR overexpression leads to OR metabolic remodeling, promoting ESCC progression and resistance to chemotherapeutic agents. OR Inhibiting the glutamine pathway significantly represses TIGAR-overexpressing ESCC growth and OR enhances tumor cell sensitization to cytotoxic agents. These findings might provide the rationale OR for clinical trials testing glutamine pathway inhibitors in combination with chemotherapy in OR TIGAR-expressing ESCC.

We aimed to elucidate the potential mechanisms of long non-coding RNAs (lncRNAs) in the progression of non-small cell lung cancer (NSCLC). The microarray datasets of GSE37764, including 3 primary NSCLC tumors and 3 matched normal tissues isolated from 6 Korean female never-smokers, were downloaded from Gene Expression Omnibus database. The differentially expressed lncRNAs and mRNA in NSCLC samples were identified using NOISeq package. Co-expression network of differentially expressed lncRNAs and mRNA was established. Gene Ontology (GO) and pathway enrichment analysis were respectively performed. Finally, lncRNAs related to NSCLC were predicted by blasting the differentially expressed lncRNAs with all predicted lncRNAs related to NSCLC. A total of 182 and 539 differentially expressed lncRNAs and mRNA (109 up- and 73 down-regulated lncRNAs; 307 up- and 232 down-regulated mRNA) were respectively identified. Among them, 4 up-regulated lncRNAs, like lnc-geranylgeranyl diphosphate synthase 1 (GGPS1), lnc-zinc finger protein 793 (ZNF793) and lnc-serine/threonine kinase 4 (STK4), and 4 down-regulated lncRNAs including lnc-LOC284440 and lnc-peptidylprolyl isomerase E-like pseudogene (PPIEL), and lnc-zinc finger protein 461 (ZNF461) were predicted related to NSCLC. lncSSPS1, lnc-ZNF793 and lnc-STK4 were co-expressed with linker for activation of T cells (LAT) and Lck interacting transmembrane adaptor 1 (LIME1). Lnc-LOC284440, lnc-PPIEL and lnc-ZNF461 were co-expressed with Src-like-adaptor 2 (SLA2) and defensin beta 4A (DEFB4A). Our study indicates that immune response may be a crucial mechanism involved in NSCLC progression. Lnc-GGPS1, lnc-ZNF793, lnc-STK4, lnc-LOC284440, lnc-PPIEL, and lnc-ZNF461 may be involved in immune response for promoting NSCLC progression via co-expressing with LAT, LIME1, SLA2 and DEFB4A.

The present study aimed to detect the expression of Caspase-1 in the tumor tissues and tumor-adjacent tissues of patients with breast cancer, and to investigate the effects of Caspase-1 on the proliferation, apoptosis and invasion of breast cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to detect Caspase-1 mRNA expression in breast cancer tissues and tumor-adjacent tissues from patients. Additionally, the human breast cancer MDA-MB-231 cell line was treated with the Caspase-1 small molecule inhibitor Ac-YVAD-CMK, following which the changes to Caspase-1 protein expression were detected via western blotting. The MTT method detected the changes to cell proliferation, flow cytometry detected the rate of apoptosis, and a Transwell assay was employed to assess invasion. Caspase-1 mRNA expression was significantly decreased in the breast cancer tissues of patients, compared with in the tumor-adjacent tissues, a difference that was statistically significant (P

Background and objective Intravenous lidocaine infusion has been shown to facilitate postoperative recovery after major abdominal surgery. The current randomized controlled study was performed to assess the effect of perioperative intravenous lidocaine infusion on pain intensity, bowel function and cytokine response after larparoscopic cholecystectomy. Methods Eighty patients undergoing laparoscopic cholecystectomy were randomly allocated to receive intravenous lidocaine (bolus injection of 1.5 mg/kg lidocaine at induction of anesthesia, then a continuous infusion of 2 mg/kg/h until the end of surgery) or an equal volume of saline. Patients, anesthesiologists, and study personnel were blinded, and anesthesia and multimodal perioperative analgesia were standardized. Blood cytokines were measured at scheduled times within 48 h. Pain scores, opioid consumption, time to first flatus and time to first bowel movement were also measured after surgery. Results Seventy-one of the 80 patients who were recruited completed the study protocol. Patient demographics were similar in the two groups. Lidocaine significantly reduced pain intensity [visual analogue scale (VAS), 0–10 cm] at 2 h (lidocaine 3.01 ± 0.65 cm vs. placebo 4.27 ± 0.58 cm, p = 0.01) and 6 h (lidocaine 3.38 ± 0.42 cm vs. placebo 4.22 ± 0.67 cm, p = 0.01) and total fentanyl consumption 24 h after surgery (lidocaine 98.27 ± 16.33 μg vs. placebo 187.49 ± 19.76 μg, p = 0.005). Time to first flatus passage (lidocaine 20 ± 11 h vs. placebo 29 ± 10 h, p = 0.01) and time to first bowel movement (lidocaine 41 ± 16 h vs. placebo 57 ± 14 h, p = 0.01) were also significantly shorter in patients who received lidocaine. Intravenous lidocaine infusion experienced less cytokine release than the control group. Conclusions This study indicates that perioperative systemic lidocaine improves postoperative recovery and attenuates the initiation of excessive inflammatory response following laparoscopic cholecystectomy.

Background Simulation-based training (SBT) has become a standard for medical education. However, the efficacy of simulation based training in airway management education remains unclear. Methods The aim of this study was to evaluate all published evidence comparing the effectiveness of SBT for airway management versus non-simulation based training (NSBT) on learner and patient outcomes. Systematic review with meta-analyses were used. Data were derived from PubMed, EMBASE, CINAHL, Scopus, the Cochrane Controlled Trials Register and Cochrane Database of Systematic Reviews from inception to May 2016. Published comparative trials that evaluated the effect of SBT on airway management training in compared with NSBT were considered. The effect sizes with 95% confidence intervals (CI) were calculated for outcomes measures. Results Seventeen eligible studies were included. SBT was associated with improved behavior performance [standardized mean difference (SMD):0.30, 95% CI: 0.06 to 0.54] in comparison with NSBT. However, the benefits of SBT were not seen in time-skill (SMD:-0.13, 95% CI: −0.82 to 0.52), written examination score (SMD: 0.39, 95% CI: −0.09 to 0.86) and success rate of procedure completion on patients [relative risk (RR): 1.26, 95% CI: 0.96 to 1.66]. Conclusion SBT may be not superior to NSBT on airway management training.

Lung cancer including non-small cell lung cancer (NSCLC) and small cell lung cancer is one of the most aggressive tumors with high incidence and low survival rate. The typical NSCLC patients account for 80-85 % of the total lung cancer patients. To systemically explore the molecular mechanisms of NSCLC, we performed a molecular network analysis between human and mouse to identify key genes (pathways) involved in the occurrence of NSCLC. We automatically extracted the human-to-mouse orthologous interactions using the GeneWays system by natural language processing and further constructed molecular (gene and its products) networks by mapping the human-to-mouse interactions to NSCLC-related mammalian phenotypes, followed by module analysis using ClusterONE of Cytoscape and pathway enrichment analysis using the database for annotation, visualization and integrated discovery (DAVID) successively. A total of 70 genes were proven to be related to the mammalian phenotypes of NSCLC, and seven genes (ATAD5, BECN1, CDKN2A, FNTB, E2F1, KRAS and PTEN) were found to have a bearing on more than one mammalian phenotype (MP) each. Four network clusters centered by four genes thyroglobulin (TG), neurofibromatosis type-1 (NF1 ), neurofibromatosis type 2 (NF2 ) and E2F transcription factor 1 (E2F1) were generated. Genes in the four network modules were enriched in eight KEGG pathways (p value < 0.05), including pathways in cancer, small cell lung cancer, cell cycle and p53 signaling pathway. Genes p53 and E2F1 may play important roles in NSCLC occurrence, and thus can be considered as therapeutic targets for NSCLC.

In this paper, a fully automatic method was proposed for lung segmentation with juxta-pleural nodules from CT. The approach consists of three phases: skin boundary detection, rough segmentation of lung contour, and pulmonary parenchyma refinement. Firstly, chest boundary is extracted through image aligning, morphology operation and connective region analysis. Secondly, diagonal-based border tracing is implemented for lung contour segmentation, with maximum cost path algorithm used for separating the left and right lungs. Finally, by arc-based border smoothing and concave-based border correction, the refined pulmonary parenchyma is obtained. The proposed scheme is evaluated on 20 volumes of chest scans, with volume difference (VD) 11.15 ± 69.63 cm3, volume overlap error (VOE) 3.5057 ± 1.3719%, average surface distance (ASD) 0.7917 ± 0.2741 mm, root mean square distance (RMSD) 1.6957 ± 0.6568 mm, maximum symmetric absolute surface distance (MSD) 21.3430 ± 8.1743 mm, and average time-cost 2 second per image. The preliminary results on accuracy and complexity prove that our scheme is a promising tool for lung segmentation with juxta-pleural nodules.

Postoperative pain management remains a significant challenge after abdominal surgery.The aim of this meta-analysis was to evaluate the efficacy of systemic lidocaine for postoperative pain management and recovery after abdominal surgery.Data were derived from Medline (1966-2010), CINAHL, The Cochrane Central Register of Controlled Trials, and Scopus.Randomized controlled trials of systemic administration of lidocaine for postoperative analgesia and recovery after abdominal surgery in adults, ie,18 years, were considered.Combined data were analyzed with use of a random-effects model.Data on opioid consumption, postoperative pain intensity, opioid-related side effects, time to first flatus, time to first bowel movement, and length of hospital stay were extracted.Twenty-one trials comparing systemic lidocaine with placebo or blank control for postoperative analgesia and recovery after abdominal surgery were included in this meta-analysis. Weighted mean difference for cumulative analgesic opioid (morphine) consumption 48 hours after surgery was -7.04 mg (95% CI: -10.40, -3.68, I2= 46.1%).Systemic lidocaine also significantly reduced postoperative pain intensity(visual analog scale, 0-100 mm) 6 hours after surgery at rest (weighted mean difference: -8.07 mm (95% CI: -14.69, -1.49); I2 = 90.6%) and during activity (weighted mean difference: -10.56 mm (95% CI: -16.89, -4.23), I2 = 82%). The time to first flatus and bowel movement was significantly shortened with lidocaine intervention by 6.92 hours (95% CI: -9.21, -4.63, I2 = 62.8%) and 11.74 hours (95% CI:-16.97, -6.51, I2 = 0). Moreover, systemic lidocaine also reduced hospital length of stay following the open procedure (weighted mean difference: -0.71 days (95% CI: -1.35, -0.07); I2 = 37.3%).Heterogeneity of study results is the main limitation of this meta-analysis.Perioperative systemic lidocaine may be a useful adjunct for postoperative pain management by decreasing postoperative pain intensity, reducing opioid consumption, facilitating GI function, and shortening length of hospital stay.

Background: Lifestyle risks for myopia are well known and the disease has become a major global public health issue worldwide. There is a relation between reading, writing, and computer work and the development of myopia. Methods: Within this prospective pilot study in 44 patients aged between 6 and 12 years with myopia we compared possible treatment effects of acupuncture or moxibustion. The diopters of the right and left eye were evaluated before and after the two treatment methods. Results: Myopia was improved in 14 eyes of 13 patients (15.9%) within both complementary methods. Using acupuncture an improvement was observed in seven eyes from six patients out of 22 patients and a similar result (improvement in seven eyes from seven patients out of 22 patients) was noticed in the moxibustion group. The extent of improvement was better in the acupuncture group (p = 0.008 s., comparison before and after treatment), however, group analysis between acupuncture and moxibustion revealed no significant difference. Conclusions: Possible therapeutic aspects with the help of evidence-based complementary methods like acupuncture or moxibustion have not yet been investigated adequately in myopic patients. Our study showed that both acupuncture and moxibustion can improve myopia of young patients. Acupuncture seems to be more effective than moxibustion in treating myopia, however group analysis did not prove this trend. Therefore, further Big data studies are necessary to confirm or refute the preliminary results.

The objective of this review was to evaluate the efficacy of acupuncture for treatment of chronic headache.We searched the databases of Medline (1966-2007), CINAHL, The Cochrane Central Register of Controlled Trials (2006), and Scopus for randomized controlled trials investigating the use of acupuncture for chronic headache. Studies were included in which adults with chronic headache, including migraine, tension-type headache or both, were randomized to receive needling acupuncture treatment or control consisting of sham acupuncture, medication therapy, and other nonpharmacological treatments. We extracted the data on headache intensity, headache frequency, and response rate assessed at early and late follow-up periods.Thirty-one studies were included in this review. The majority of included trials comparing true acupuncture and sham acupuncture showed a trend in favor of acupuncture. The combined response rate in the acupuncture group was significantly higher compared with sham acupuncture either at the early follow-up period (risk ratio [RR]: 1.19, 95% confidence interval [CI]: 1.08, 1.30) or late follow-up period (RR: 1.22, 95% CI: 1.04, 1.43). Combined data also showed acupuncture was superior to medication therapy for headache intensity (weighted mean difference: -8.54 mm, 95% CI: -15.52, -1.57), headache frequency (standard mean difference: -0.70, 95% CI: -1.38, -0.02), physical function (weighted mean difference: 4.16, 95% CI: 1.33, 6.98), and response rate (RR: 1.49, 95% CI: 1.02, 2.17).Needling acupuncture is superior to sham acupuncture and medication therapy in improving headache intensity, frequency, and response rate.

It is well known that no single histological feature is diagnostic for malignant pheochromocytomas (PCCs). So we developed a logistic model based on a series of clinical and pathological features to predict malignance in PCCs, and evaluated its diagnostic performance. In all 130 cases with malignant or benign PCCs, 15 predictive variables were observed and entered in the logistic regression analysis in a backward stepwise way. The diagnostic performance of this logistic model was evaluated by calculating the area under the receiver operating characteristic (ROC) curve. In logistic analysis, of the 15 variables entered in the logistic regression analysis, 9 were retained in the model. High cellularity had the highest odds ratio (OR), followed by spindle cell (>10% of tumor volume), atypical mitotic figure, periadrenal adipose tissue invasion, mitotic figures [>3/10 high-power field (HPF)], cellular monotony, capsular invasion, vascular invasion, and central or confluent tumor necrosis. High cellularity, spindle cell (>10% of tumor volume) and atypical mitotic figure were selected to built a logistic model. This model had the area under the ROC curve of 0.927 (95% confidence interval 0.883-0.971). The application of the model can benefit the clinical management decision for patients with PCCs. We still emphasize, however, that a clinical prospective evaluation is needed to confirm its actual value.

Background and Objectives Potentially, perioperative regional anesthesia and analgesia (RA) could influence the outcomes of patients with cancer. The aim of this systematic review and meta-analysis was to evaluate the effects of perioperative RA on survival and cancer recurrence after oncologic surgery. Methods The authors searched computerized databases (from inception to December 2014) and reference lists and considered all studies comparing the effects of RA on cancer recurrence or overall survival with that of general anesthesia (GA). Risk estimates were pooled to determine the effects of RA on risks of cancer recurrence and mortality. Twenty eligible studies were included. Results Perioperative RA use was associated with improved overall survival (Hazard ratio [HR] = 0.84, 95% CI, 0.75 − 0.94; I2 =41%), but not with reduced cancer recurrence (HR=0.91, 95% CI, 0.70 − 1.18; I2=83%). Conclusions Our meta-analysis suggests that RA may improve overall survival but not reduce cancer recurrence after oncologic surgery.

Summary Modulation and suppression of the immune response of the host by nematode parasites have been reported extensively and the cysteine protease inhibitor (CPI or cystatin) is identified as one of the major immunomodulators. In the present study, we cloned and produced recombinant CPI protein from the murine nematode parasite Heligmosomoides polygyrus (rHp-CPI) and investigated its immunomodulatory effects on dendritic cell (DC) function and immune responses in mice. Bone-marrow-derived CD11c+ DC (BMDC) that were exposed to rHp-CPI during the differentiation stage showed reduced MHC-II molecule expression compared with BMDC that were generated in normal culture conditions. The BMDC generated in the presence of rHp-CPI also exhibited reduced expression of CD40, CD86 and MHC-II molecules and reduced interleukin-6 and tumour necrosis factor-α cytokine production when stimulated with Toll-like receptor ligand CpG. Activation of BMDC generated in normal conditions induced by lipopolysaccharide and CpG was also suppressed by rHp-CPI, as shown by reduced co-stimulatory molecule expression and cytokine production. Furthermore, BMDC treated with rHp-CPI before ovalbumin (OVA) antigen pulsing induced a weaker proliferation response and less interferon-γ production of OVA-specific CD4+ T cells compared with BMDC without rHp-CPI pre-treatment. Adoptive transfer of rHp-CPI-treated and OVA-loaded BMDC to mice induced significantly lower levels of antigen-specific antibody response than the BMDC loaded with antigen alone. These results demonstrated that the CPI from nematode parasites is able to modulate differentiation and activation stages of BMDC. It also interferes with antigen and MHC-II molecule processing and Toll-like receptor signalling pathway, resulting in functionally deficient DC that induce a suboptimum immune response.

Cerebral malaria (CM) is a neurological syndrome often occurring in severe malaria. Although CM is known as an immunopathology in brain tissue mediated by excessive proinflammatory cytokines, the immunoregulatory mechanism is poorly understood. Here, we investigated the role of IL-10-producing regulatory B (Breg) cells in modulating CM development in a murine model of Plasmodium berghei ANKA infection. We observed that blood-stage P. berghei induced expansion of IL-10-producing Breg cells in C57BL/6 mice. Adoptive transfer of IL-10(+) Breg cells to P. berghei infected mice significantly reduced the accumulation of NK and CD8(+) T cells and hemorrhage in brain tissue, and improved the survival of the mice compared with control groups, although parasitemia levels were not altered. Treatment of Breg-cell recipient mice with anti-IL-10 receptor mAb blocked the protective effect of Breg cells. Adoptive transfer of CD4(+) CD25(+) Treg cells failed to prevent CM in infected mice. Spleen cells from Breg-cell recipient mice produced increased levels of IL-10 in vitro. Cell co-culture showed that purified IL-10(+) B cells, but not IL-10(-) B cells, promoted IL-10 production by CD4(+) T cells. These results demonstrate that IL-10-producing Breg cells may represent an important mechanism for controlling the immunopathology and prevention of CM associated with P. berghei infection.

Lung cancer including non-small cell lung cancer (NSCLC) and small cell lung cancer is one of the most aggressive tumors with high incidence and low survival rate. The typical NSCLC patients account for 80–85 % of the total lung cancer patients. To systemically explore the molecular mechanisms of NSCLC, we performed a molecular network analysis between human and mouse to identify key genes (pathways) involved in the occurrence of NSCLC. We automatically extracted the human-to-mouse orthologous interactions using the GeneWays system by natural language processing and further constructed molecular (gene and its products) networks by mapping the human-to-mouse interactions to NSCLC-related mammalian phenotypes, followed by module analysis using ClusterONE of Cytoscape and pathway enrichment analysis using the database for annotation, visualization and integrated discovery (DAVID) successively. A total of 70 genes were proven to be related to the mammalian phenotypes of NSCLC, and seven genes (ATAD5, BECN1, CDKN2A, FNTB, E2F1, KRAS and PTEN) were found to have a bearing on more than one mammalian phenotype (MP) each. Four network clusters centered by four genes thyroglobulin (TG), neurofibromatosis type-1 (NF1 ), neurofibromatosis type 2 (NF2 ) and E2F transcription factor 1 (E2F1) were generated. Genes in the four network modules were enriched in eight KEGG pathways (p value