bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determinants of breakfast consumption among adolescent girls: Application of the Health Promotion Model using Structural Equation Modeling
Authors: Imani-Nasab Mohammad-Hassan , ardalan Arash , Cheraghi Nasim , Piri Zahra Asadi , Ebrahimzadeh Farzad , bastami fatemeh 
Published: July 2020

Abstract
Background: Breakfast is an important sign of healthy nutrition for normal growth and development. Breakfast is considered as the most important meal of the day which is ignored by many adolescents. The purpose of this study was to predict breakfast behavior based on Pender Health Promotion Model(HPM) constructs using structural equation model(SEM).Methods: A descriptive-analytical study was performed on 450 high school female students in west of Iran in 2019. Sampling was done through a multi-stage method.The questionnaire contained two parts. The first part of which was about demographic and behavior of breakfast consumption; and the second part was a questionnaire based on Health Promotion Model. Data were analyzed by means of SPSS and AMOS both version of 20 software and using Chi-square test as well as regression correlation model.Results: The constructs of behavioral perceptions, commitment to action plan and behavioral effects explained 47% of the variance of breakfast intake behavior. In the structural equation model, the value of the chi-square statistic test came up to 429.2429 which was divided by resulted degree of freedom (1785), 2.405 and 5%, respectively (P<0.001). Fit indexes were either acceptable or good.Conclusion: The HPM is a suitable theory for predicting the commitment to action plan and behavior of breakfast consumption in Iran.The structural equation model was evaluated as a comprehensive model through both direct and indirect approaches to predict the relationship between breakfast consumption and the predictive factors. This model showed a multi-factorial nature of the predictive factors.
Changes in Lipid Composition associated with Electronic Cigarette Use
Authors: Middlekauff Holly , Williams Kevin , Su Baolong , Haptonstall Kacey , Araujo Jesus , Wu Xiaohui , Kim Jason , Sallam Tamer 
Published: July 2020

Abstract
Background- Electronic cigarette use is on the rise despite a number of reports linking electronic cigarettes with adverse health outcomes. Recent studies have suggested that alterations in lipid signaling may be one mechanism by which electronic cigarettes contribute to lung pulmonary function. Vitamin E acetate, for example, is synthetic form of Vitamin E transported via lipids, found to be associated with electronic cigarette associated lung injury. Lipids are absolutely critical for normal lung physiology and perturbations in a number of lipid pathways have been associated with respiratory illness. Is it conceivable that electronic cigarette use even in seemingly healthy cohorts are associated with alterations in lipid pathways? Methods- To investigate quantitative alterations in the plasma lipidome associated with electronic cigarette use in healthy we obtained plasma samples from 119 male and female participants with who were either: 1) chronic tobacco cigarette (TC) smokers (>12 months of self-reported TC use), 2) chronic Electronic cigarette (EC) users (>12 months of self-reported EC use), or 3) non-users. We measured quantitative lipid species across different lipid sub-classes from plasma samples using the Sciex Lipidyzer. Results- We found that male and female tobacco and electronic cigarette users had distinct lipidome signatures across a number of lipid species although the vast majority of lipids were unchanged when compared to non-users. Intriguingly, we found that female but not male electronic cigarette users had lower levels of plasmalogens, critical glycerophospholipids secreted by alveoli and required for normal surfactant function. Conclusions- In summary, our study does not reveal striking global changes in the lipidome associated with electronic cigarette use but we observed sex-specific changes in phospholipids known to be critical for lung function.
Long non-coding RNA H19 deficiency ameliorates bleomycin-induced pulmonary inflammation and fibrosis
Authors: Wan Xiaoyu , Tian Xinbei , Du Jun , Lu Ying , Xiao Yongtao 
Published: July 2020

Abstract
Background: The limited understanding of pathogenesis in idiopathic pulmonary fibrosis (IPF) impaired development of effective therapeutic strategies.The aim of this study was to investigate the role of long non-coding RNA H19 (lncRNA H19) in the progression of IPF. Methods: Bleomycin was used to induce pulmonary fibrosis in mice. The mRNAs and proteins expression in lung tissues with bleomycin-induced pulmonary fibrosis was determined by quantitative real-time polymerase chain reaction and western blot. H19 deficiency (H19-/-) were generated by CRISPR/Cas9 and were used to investigate the roles of H19 in the pulmonary inflammation and fibrosis in vivo.Results: The expression of H19 was up-regulated in fibrotic lungs patients with IPF and mouse lungs obtained from bleomycin-treated mice. H19 deficiency reduced bleomycin-induced pulmonary inflammation and inhibited the activation of Il6/Stat3 signaling. H19 deficiency ameliorated bleomycin-induced pulmonary fibrosis and repressed the activation of TGFβ-Smad and S1pr2/Sphk2 in the lungs of bleomycin-treated mice. H19 depletion attenuated the lung regeneration and reduced expression of activated Egfr. Conclusions: Our data suggest that H19 is a profibrotic lncRNA and a potential therapeutic target for pulmonary fibrosis.
The efficacy of combination therapies including antiviral drugs, methylprednisolone and daily proning in 20 patients with COVID-19 requiring invasive mechanical ventilation—Case series in a single critical care center in Osaka, Japan
Authors: Shimazu Haruka , Yoshiya Kazuhisa , Tamagaki Keisuke , Okamoto Yasutaka , Nakano Hitoshi , Okubata Hiroto , Miyano Yumiko , Matsunami Shuhei , Maruyama Shuhei , Kanayama Shuji , Iwamura Hiromu , Wada Daiki , Yoshihara Tomoyuki , Saito Fukuki , Nakamori Yasushi , Kuwagata Yasuyuki 
Published: July 2020

Abstract
Background: Since December 2019, the COVID-19 infection has drastically spread across China and the world, including Japan. Few reports so far have clarified the prognosis and treatment of critically ill patients managed with invasive mechanical ventilation. This study aimed to present the clinical courses of 20 critically ill patients with invasive mechanical ventilation, which may be valuable for determining future therapies and intensive care of critically ill patients with COVID-19.Methods: In this observational, single-center, cohort study, we included 20 critically ill patients with laboratory-confirmed SARS-CoV-2 infection who were admitted to our hospital ICU and required invasive mechanical ventilation. The patients’ general characteristics, laboratory data, treatments, and outcomes were assessed between survivors and non-survivors.Results: Among these 20 patients, 14 patients survived and 6 patients died. The lowest lymphocyte count (93 vs 279/μL, p<0.01) and the lowest platelet count (12 vs 152×103/μL, p<0.01) were significantly lower, and the highest KL-6 value (1584 vs 546 U/mL, p=0.02) was significantly higher, in the non-survivor group versus the survivor group during the patients’ ICU stay. In addition to antiviral treatments and daily proning of the patients, methylprednisolone was administered to all patients to control cytokine storm syndrome following the virus infection. Six patients died from complications such as fungal infection, but no patients died of respiratory failure. As a result, none of the patients required ECMO.Conclusion: This report described the prognosis of COVID-19 patients required invasive mechanical ventilation in a single Japanese critical care center. Multidisciplinary treatments using a single protocol, including antiviral therapies, anti-inflammatory therapies, and respiratory physiotherapies, were effective for critically ill COVID-19 patients who required invasive mechanical ventilation.
GLUT5 (SLC2A5) enables fructose-mediated proliferation independent of ketohexokinase
Authors: Liang Roger Jie , Taylor Samuel , Nahiyaan Navid , Song Junho , Murphy Charles J , Dantas Ezequiel , Cheng Shuyuan , Hsu Ting-Wei , Ramsamooj Shakti , Grover Rahul , Hwang Seo-Kyoung , Ngo Bryan , Cantley Lewis C , Rhee Kyu Y , Goncalves Marcus DaSilva 
Published: July 2020

Abstract

Background: Fructose is an abundant source of carbon and energy for cells to use for metabolism, but only certain cell types use fructose to proliferate. Tumor cells that can metabolize fructose have a fitness advantage over their neighboring cells, but the proteins that mediate fructose metabolism in this context are unknown. Here, we investigated the determinants of fructose-mediated cell proliferation.Methods: We quantified the ability of 14 cell lines to proliferate in fructose-containing media (i.e. the fructolytic ability) using live cell imaging and crystal violet assays. The expression and abundance of proteins related to fructose metabolism were assessed using RT-qPCR and western blot, respectively, for each cell line. Using a positive selection approach, we “trained” the non-fructolytic PC3 cell line to utilize fructose for proliferation. RNA-seq was then performed to identify key transcriptional changes associated with fructolytic ability. We overexpressed and deleted proteins associated with fructose metabolism, and performed metabolic profiling using the Seahorse Bioanalyzer and LC/MS-based metabolomics.Results: We found that neither the tissue of origin nor expression level of any single gene related to fructose catabolism determine a cell’s fructolytic ability. Cells cultured chronically in fructose can develop fructolytic ability if SLC2A5, encoding the fructose transporter, GLUT5, gets upregulated. Overexpression of GLUT5 in non-fructolytic cells enables growth in fructose-containing media across cells of different origins. GLUT5 permitted fructose to flux through glycolysis using hexokinase (HK) and not ketohexokinase (KHK).Conclusions: We show that GLUT5 is a robust and generalizable driver of fructose-dependent cell proliferation. This indicates that fructose uptake is a limiting factor for fructose-mediated cell proliferation. We further demonstrate that cancer cell proliferation with fructose is independent of KHK.
Significance of Druggable Targets (PD-L1, KRAS, BRAF, PIK3CA, MSI, and HPV) on Curatively Resected Esophageal Squamous Cell Carcinoma
Authors: Lee Hong Kyu , Kwon Mi Jung , Ra Yong Joon , Lee Hee Sung , Kim Hyoung Soo , Nam Eun Sook , Cho Seong Jin , Park Hye-Rim , Min Soo Kee , Seo Jinwon , Choe Ji-Young , Min Kyueng-Whan , Kang So Young 
Published: July 2020

Abstract
Background: Esophageal squamous cell carcinoma (ESCC) still remains intractable disease with few therapeutic options. Programmed death-ligand 1 (PD-L1), which is essential for immune evasion, is involved in the pathogenesis of ESCC and thus is a potential therapeutic target. PIK3CA, KRAS, and BRAF mutations, microsatellite instability (MSI) caused by deficient mismatch repair (dMMR), and human papillomavirus (HPV) can potentially upregulate PD-L1 expression, which might contribute to the clinical outcome of patients with ESCC. Methods: We investigated the significance of the present druggable markers [PD-L1, PIK3CA, KRAS, and BRAF mutations, MSI caused by deficient dMMR, and HPV] in 64 curatively resected ESCCs, using immunohistochemistry (PD-L1 and MMR protein expression), direct sequencing (KRAS, BRAF, and PIK3CA mutations), real-time PCR (HPV infection), and MSI using quasi-monomorphic markers. Results: PD-L1 expression, PIK3CA mutation, and MSI/dMMR were detected in 35.9%, 12.5%, and 17.2% of ESCCs, respectively. HPV was rarely detected (1.6%) (high-risk HPV68), whereas KRAS and BRAF mutations were not detected in ESCCs. PD-L1-positive tumors were not correlated with PIK3CA mutation or MSI/dMMR (all P>0.05). PD-L1, PIK3CA mutation, and MSI/dMMR characterized the patients associated with light smoking, female and younger age, and younger age and well-differentiated tumors, respectively (all P<0.05). In multivariate analysis, only PD-L1-positivity was an independent favorable prognostic factor for overall survival (OS) and disease-free survival (DFS) (P=0.023, P=0.014). In the PD-L1-negative ESCCs, PIK3CA mutation had a poor prognostic impact on both OS and DFS (P=0.006, P=0.002). Conclusions: PIK3CA mutation may be an alternative prognostic biomarker in PD-L1-negative curatively resected ESCCs that can be optional to identify high-risk patients with worse clinical outcome who require more intensive therapy and follow-up.
Efficiency and productivity change of public hospitals in Panama: Do management schemes matter?
Authors: Cordero Jose M. , García-García Agustín , Lau-Cortés Enrique , Polo Cristina 
Published: July 2020

Abstract
Background
In Latin American and Caribbean countries the main concern of public health care managers has been traditionally placed on problems related to funding, payment mechanisms and equity of access. However, more recently, there is a growing interest in improving the levels of efficiency and reducing costs in the provision of health services. In this paper we focus on measuring the efficiency of public hospitals in Panama, where no such studies have been conducted so far. One of the most interesting features of the public hospital system in this country is that there are two different management schemes that coexist, thus we can make a distinction between hospitals operating under the Social Security Fund (SSF) and those belonging to the Ministry of Health (MoH).
Methods
Our dataset includes data about 22 public hospitals (11 for each model) during the period 2005–2015. We rely on the use of Data Envelopment Analysis and the Malmquist Productivity index to calculate technical efficiency and productivity change of hospitals. In addition, we also apply bootstrapping techniques to calculate confidence intervals for the obtained efficiency and productivity scores in order to obtain more robust results.
Results
We find that, until the period 2012–2013, the performance of hospitals belonging to different systems experienced a similar trend. However, during the last years of the evaluated period the hospitals operating under the Social Security Fund clearly outperformed Ministry´s hospitals. The main explanation for these divergences seems to be the growth of technological change. Nevertheless, the use of bootstrapping to make statistical inferences reveals that some differences detected may not be significant.
Conclusion
We demonstrate that the results of traditional DEA and Malmquist index analyses need to be tested for statistical significance. Otherwise, the conclusions reached could be wrong.
The effects of BMMSC treatment on lung degeneration in elderly macaques
Authors: Yang Yukun , Ruan Guangping , Li Ye , Wang Yanying , Tian Chuan , Wang Qiang , He Huanyu , Zhu Gaohong , Dong Fang , Wang Mao , ZHU Xiangqing , Pan Xinghua 
Published: July 2020

Abstract
Age-related degeneration of lung tissues increases the risk of lung injury and exacerbates lung disease. It is also the main risk factor for chronic lung diseases (such as COPD, idiopathic pulmonary fibrosis, cancer, etc.). Here, we performed systematic screening, evaluation of elderly macaque model. A senile multiple organ dysfunction model was used to explored whether BMMSC could improve degeneration of lung tissues in an elderly macaque model. Using model evaluation tests, we found that the average alveolar area, Mean linear intercept（MLI） and fibrosis area in the elderly macaque models were significantly larger than in young rhesus monkeys (P <0.05), and the capillary density around the alveoli was significantly lower than in young macaque models (P <0.05). Intraveous infusion of BMMSC reduced the degree of pulmonary fibrosis in elderly macaque, increased the density of capillaries around the alveoli (P <0.05), and the number of type Ⅱ alveolar epithelium in elderly macaque (P <0.05). BMMSC infusion reduced lung tissue ROS level, systemic and lung tissue inflammation level and Treg cell ratio in elderly macaque model（P＜0.05）. Indirect co-cultivation revealed that BMMSC reduced the expression of senescence-related genes, ROS levels, apoptosis rate of aging type Ⅱ alveolar epithelial cells (A549 cells) and promoted their proliferation (P＜0.05).
Clinical Outcomes and Prognosis of Small-Cell Lung Cancer(SCLC) Patients After Surgery: a Single-Centre Retrospective Cohort Study from Peking Union Medical College Hospital
Authors: Chen Yeye , Liu Lei , Huang Cheng , Tian Zhenhuan , Liu Hongsheng , LI Shanqing 
Published: July 2020

Abstract
Background: Small-cell lung cancer (SCLC) patients are generally not considered to be candidates for surgical intervention. The role of surgery in the multidisciplinary treatment of SCLC remains controversial. The study aims to summarize and analyse the clinical characteristics and prognosis of SCLC patients after surgical treatment and identify the related prognostic factors.Methods: The clinical data of 130 SCLC patients (99 males and 31 females) who were treated by surgery and confirmed by postoperative pathological examination in Peking Union Medical College Hospital from April 2004 to April 2019 were analysed retrospectively.Results: The median age was 60 years (30-83 years), and the median disease duration was 2 months (0.5-48 months). The patients did not have specific clinical or imaging manifestations. Postoperative pathological examination revealed that 36 patients had stage I, 22 patients had stage II, 65 patients had stage III, and seven patients had stage IV SCLC. The median overall survival time was 50 months (95% confidence interval, 10.8-89.2 months). The median survival time of stage I, II, III, and IV SCLC patients were 148 months, 42 months, 32 months, and 10 months, respectively. In patients who underwent surgical treatment, postoperative adjuvant therapy and tumour stage were two significant influencing factors of survival (Cox multivariate analysis P < 0.05).Conclusions: Surgical treatment combined with adjuvant therapy can achieve satisfactory outcomes in selected SCLC patients. Adjuvant therapy and tumour stage are independent risk factors. Surgical treatment is indicated in SCLC patients preoperatively staged as I-IIIa, and anatomical lobectomy and lymphadenectomy combined with postoperative adjuvant therapy are recommended.
A Glycolysis-Based Three-Gene Signature Predicts Survival in Patients with Lung Squamous Cell Carcinoma
Authors: Huang Guichuan , Zhang Jing , Gong Ling , Huang Yi , Liu Daishun 
Published: July 2020

Abstract
Purpose: Lung cancer is one of the most lethal and most prevalent malignant tumors worldwide, and lung squamous cell carcinoma (LUSC) is one of major histological subtypes. Although, numerous biomarkers were found to be associated with prognosis in LUSC, the prediction effect of a single gene biomarker is not sufficient, especially for glycolysis-related genes. Therefore, we aimed to develop a novel glycolysis-related gene signature to predict survival of patients with LUSC. Material and Methods: The mRNA expression files and clinical information of LUSC were obtained from The Cancer Genome Atlas (TCGA) dataset. Results: Based on Gene set enrichment analysis (GSEA), we found 5 glycolysis-related gene sets were significantly enriched in LUSC tissues. Univariate and multivariate Cox proportional regression models were conducted to choose prognostic-related gene signature. Based on Cox proportional regression model, a risk score of three-gene signature (including HKDC1, ALDH7A1, and MDH1) was established to divide patients into high-risk and low-risk subgroups. We found that a risk score of three-gene signature was an independent of prognostic indicator in LUSC using multivariate Cox regression analysis.Conclusion: In conclusion, a glycolysis-based three-gene signature could serve as a novel biomarker in predicting prognosis of patients with LUSC, which provided more gene targets to cure LUSC patients.
Comprehensive Analysis of Immune Prognostic‐Related Genes in the Tumor Microenvironment of Hepatocellular Carcinoma
Authors: Gao Weike , Li Luan , Li Chengzhen , Yu Guanying , Zhang Lei , Zhang Dongsheng , Liu Caiyun , Hong Shuai , Wang Dongliang , Guo Peiming , Shi Guangjun 
Published: July 2020

Abstract
Background: The percentage of death resulted from hepatocellular carcinoma (HCC) remains high worldwide, despite surgical and chemotherapy treatment. Immunotherapy offers great promise in the treatment of a rapidly expanding spectrum of HCC. Therefore, further exploration of the immune-related signatures in the tumor microenvironment, which plays a vital role in tumor initiation and progression for immunotherapy is currently needed. Methods: In this present research, 866 immune-related difference expression genes (DEGs) were identified by integrating the DEGs between TCGA HCC and normal tissue and the immune genes from databases (Innate DB; Imm Port), and 144 candidate prognostic genes were defined through weighted gene co-expression network analysis (WGCNA). Results: Seven prognostic immune-related DEGs were determined with LASSO Cox PH model, which was followed by constructing the ImmuneRiskScore model based on the prognostic immune-related DEGs. The prognostic index of the ImmuneRiskScore was validated then in the dependent dataset. Patients were divided into high- and low-risk groups according to ImmuneRiskScore. The difference in ImmuneRiskScore and infiltration of immune cells between groups was detected and the correlation analysis for immunotherapy biomarkers was further explored. Conclusion:The ImmuneRiskScore of HCC could provide a prognostic signature and reflect immune characteristics within tumor microenvironment. Furthermore, it also may provide novel immunotherapy predictive biomarker for HCC patients in the near future.
Undirected graphs: is the shift-enabled condition trivial or necessary?
Authors: Chen Liyan , Cheng Samuel , He Kanghang , Stankovic Vlandimir , Stankovic Lina 
Published: July 2020

Abstract
It has recently been shown that, contrary to the wide belief that a shift-enabled condition (necessary for any shift-invariant filter to be representable by a graph shift matrix) can be ignored because any non-shift-enabled matrix can be converted to a shift-enabled matrix, such a conversion in general may not hold for a directed graph with non-symmetric shift matrix. This paper extends this prior work, focusing on undirected graphs where the shift matrix is generally symmetric. We show that while, in this case, the shift matrix can be converted to satisfy the original shift-enabled condition, the converted matrix is not associated with the original graph, that is, it does not capture anymore the structure of the graph signal. We show via a counterexample, that a non-shift-enabled matrix cannot be converted to a shift-enabled one and still maintain the topological structure of the underlying graph, which is necessary to facilitate localized signal processing.