bluuebunny/crossref_metadata_2025_split huggingface dataset:
The joint impact of prediagnostic inflammatory markers and cardiorespiratory fitness on the risk of cancer mortality
Authors: Pletnikoff P. P. , Laukkanen J. A. , Tuomainen T. P. , Kurl S. 
Published: July 2017

Independently, cardiorespiratory fitness (CRF), C‐reactive protein (CRP), and leukocyte count have been shown to predict cancer death. Little is known about the joint impact of CRF and prediagnostic markers of inflammation, particularly leukocyte count and CRP, and their prognostic value with cancer death. The aim of this study was to explore the association between prediagnostic inflammatory markers and CRF with cancer mortality. A population‐based cohort of 2270 men from Eastern Finland with no cancer history at baseline participated in the study. CRP, leukocyte count, and CRF data were among the measures collected at baseline. Blood leukocyte count was measured with a cell counter, and serum CRP concentrations were measured using an immunometric assay. The highest value or plateau of directly measured oxygen consumption by a respiratory gas analyzer during an incremental exercise test to exhaustion was used to describe CRF. Over an average follow‐up of 22 years, 272 cases of cancer mortality occurred. In a multivariate model, the joint impact of high leukocyte count (>5.40 × 109/L) and low CRF (VO2max < 30.08 mL kg−1 min−1) had a 1.85‐fold (95% CI 1.30‐2.63, P < .01) increased risk for cancer death compared to men with low leukocyte count (<5.40 × 109/L) and high CRF (VO2max > 30.08 mL kg−1 min−1). The joint impact of CRP and CRF shared no association with cancer mortality in a multivariate model. The joint impact of high leukocyte count and low CRF increases risk for cancer death, suggesting it is a better predictor of cancer death compared to the joint impact of CRP and CRF.
Case study on the use of a combined system as an intermediate solution in Brazil: cost estimate
Authors: Goncalves Mariana L. R. , Kleidorfer Manfred , Rauch Wolfgang 
Published: July 2017

AbstractAs a developing country, Brazil has to deal with a lack of basic sanitation. One of the major challenges is the treatment of wastewater. While 94% of Brazilian municipalities have stormwater systems, only 55% are connected to a wastewater system. To help improve the current situation, this study estimates the costs for implementing an intermediate solution, which is designed to ease the transition towards a separate wastewater treatment system. This solution utilizes a combined sewer system approach in areas where stormwater systems have already been implemented. A case study was carried out assessing two possible alternatives for a wastewater treatment system with data from the city of Joinville. Both alternatives are separate systems but one has a combined system as an intermediate solution. The results show that the alternative with an intermediate combined system will reduce the short‐term financial burden on governments in comparison to the separate sewer system approach.
THE EFFECT OF ALKALINE TREATMENT AND FIBER LENGTH ON PINEAPPLE LEAF FIBER REINFORCED POLY LACTIC ACID BIOCOMPOSITES
Authors: Ramli Siti Nur Rabiatutadawiah , Md. Fadzullah Siti Hajar Sheikh , Mustafa Zaleha 
Published: July 2017

The awareness of natural fibers as alternative materials to synthetic fibers in composite applications have increased briskly due to lightweight, non-toxic, low cost and abundantly available. To-date, there are still limited works on fully biodegradable composites also known as biocomposites, especially using long pineapple leaf fiber (PALF) reinforced poly lactic acid biocomposites. Thus, this study presents an investigation of the effects of alkaline treatment and use of different fiber length on the mechanical performance of pineapple leaf fibers reinforced poly lactic acid, biocomposites. Flexural testing was conducted via ASTM D790. The results showed enhancement in flexural properties of the biocomposites when the PALF fibers were treated with alkaline treatment, suggesting an effect of improving mechanical interlocking between matrix and reinforcement due to rougher fiber surface. The flexural strength and modulus of long treated fibers increased from 56.47 MPa and 4.24 GPa to 114.03 MPa and 5.70 GPa respectively compared to long untreated fibers. Â In addition, the effect of fiber length is also proven to affect the overall performance of the biocomposites, in which the long PALF fiber composites exhibit superior flexural properties to those of the short fiber reinforced PLA biocomposites, i.e. flexural modulus of 5.7 GPa and 0.22 GPa for the long fiber composites and short fiber composites respectively. The existence of sodium hydroxide, (NaOH) on PALF fibers were confirmed by FTIR analysis. Surface morphology of both untreated and treated samples was studied by using a scanning electron microscope (SEM). Results from both analyses suggest removal of lignin and hemicellulose on the alkaline-treated PALF fiber reinforced composites led to a rougher fibers surface and formed a better fiber-matrix adhesion, as reflected in the flexural properties of the biocomposites as reported above.
Reviewer Acknowledgements
Authors: Walter Andrew 
Published: July 2017

Studies in Engineering and Technology (SET) would like to acknowledge the following reviewers for their assistance with peer review of manuscripts for this issue. Many authors, regardless of whether SET publishes their work, appreciate the helpful feedback provided by the reviewers. Their comments and suggestions were of great help to the authors in improving the quality of their papers. Each of the reviewers listed below returned at least one review for this issue.Reviewers for Volume 4, Number 1António Calha, Polytechnic Institute of Portalegre, PortugalCarmen Pérez-Sabater, Universitat Poltècnica de València, SpainCélio Gonçalo Marques, Polytechnic Institute of Tomar, PortugalDeborah Christine Robinson, University of Derby, UKElena Jerves, University of Cuenca, EcuadorEnisa Mede, Bahcesehir University, TurkeyEsra DERELİ-Eskişehir Osmangazi University, TurkeyEsra DERELİ-Eskişehir Osmangazi University, TurkeyIntakhab Khan, King Abdulaziz University, Saudi ArabiaJohn Cowan, Edinburgh Napier University, UKLisa Marie Portugal, Grand Canyon University, USALorna T. Enerva, Polytechnic University of the Philippines, PhilippinesM. Emin Türkoğlu, Afyon Kocatepe University, TurkeyMarcie Zaharee, The MITRE Corporation, USAMeral Seker, Alanya Alaaddin Keykubat University, TurkeyMustafa Çakır, Marmara Üniversity, TurkeyNerina Fernanda Sarthou, Univ. Nacional del Centro de la Provincia de Buenos Aires, ArgentinaNicole Celestine, The University of Western Australia, AustraliaNiveen M. Zayed, MENA College of Management, JordanPirkko Siklander, University of Lapland, FinlandRichard Penny, University of Washington Bothell, USARui Manuel Carreteiro, National Institute of Psychology and Neurosciences, PortugalSamad Mirza Suzani, Islamic Azad University, IranYalçın Dilekli, Aksaray University, Turkey Andrew WalterEditorial AssistantStudies in Engineering and Technology-------------------------------------------Redfame Publishing9450 SW Gemini Dr. #99416Beaverton, OR 97008, USATel: 1-503-828-0536 ext. 504Fax: 1-503-828-0537E-mail: set@redfame.comURL: http://set.redfame.com
Differential effects of late gestation maternal overnutrition on the regulation of surfactant maturation in fetal and postnatal life
Authors: Lock Mitchell C. , McGillick Erin V. , Orgeig Sandra , McMillen I. Caroline , Mühlhäusler Beverly S. , Zhang Song , Morrison Janna L. 
Published: July 2017

Key points
Offspring of overweight and obese women are at greater risk for respiratory complications at birth.
We determined the effect of late gestation maternal overnutrition (LGON) in sheep on surfactant maturation, glucose transport and fatty acid metabolism in the lung in fetal and postnatal life.
There were significant decreases in surfactant components and numerical density of surfactant producing cells in the alveolar epithelium due to LGON in the fetal lung. However, there were no differences in the levels of these surfactant components between control and LGON lambs at 30 days of age.
The reduced capacity for surfactant production in fetuses as a result of LGON may affect the transition to air breathing at birth.
There was altered glucose transport and fatty acid metabolism in the lung as a result of LGON in postnatal life. However, there is a normalisation of surfactant components that suggests accelerated maturation in the lungs after birth.
AbstractWith the increasing incidence of obesity worldwide, the proportion of women entering pregnancy overweight or obese has increased dramatically. The fetus of an overnourished mother experiences numerous metabolic changes that may modulate lung development and hence successful transition to air breathing at birth. We used a sheep model of maternal late gestation overnutrition (LGON; from 115 days’ gestation, term 147 ± 3 days) to determine the effect of exposure to an increased plane of nutrition in late gestation on lung development in the fetus (at 141 days’ gestation) and the lamb (30 days after birth). We found a decrease in the numerical density of surfactant protein positive cells, as well as a reduction in mRNA expression of surfactant proteins (SFTP‐A, ‐B and ‐C), a rate limiting enzyme in surfactant phospholipid synthesis (phosphate cytidylyltransferase 1, choline, α; PCYT1A), and glucose transporters (SLC2A1 and SLC2A4) in the fetal lung. In lambs at 30 days after birth, there were no differences between Control and LGON groups in the surfactant components that were downregulated in the LGON fetuses. However, mRNA expression of SFTP‐A, PCYT1A, peroxisome proliferator activated receptor‐γ, fatty acid synthase and fatty acid transport protein were increased in LGON lambs compared to controls. These results indicate a reduced capacity for surfactant production in late gestation. While these deficits are normalised by 30 days after birth, the lungs of LGON lambs exhibited altered glucose transport and fatty acid metabolism, which is consistent with an enhanced capacity for surfactant synthesis and restoration of surfactant maturity in these animals.
Abstract 1: Galectins in glioblastoma: opportunities for combined therapy
Authors: Cachia David , Chatterjee Arindam Rano , Vandergrift William Alexander , Patel Sunil J. , Rabinovich Gabriel A. , Das Arabinda 
Published: July 2017

Abstract
Background: Despite aggressive treatment, including surgical resection, radiation and chemotherapy, over 90% of glioblastoma (GB) patients experience tumor recurrence. This may be due to high migratory potential, angiogenesis, molecular heterogeneity and a strong immunosuppressive environment. GB expresses high levels of carbohydrate-binding galectin proteins and histone deacetylase (HDAC) activity. The aim of this study was: 1) identify the differential expressions of galectin 1-15 protein levels in human GB patient samples as compared to normal tissue (obtained from Institutional Tissue Bank) and (2) modulate the galectin functions with and without a HDAC inhibitor (DATS: Dially Triisulfide and SAHA: Suberoylanilide Hydroxamic Acid ) or bevacizumab in in vitro GB models.
Methods: The effects of TMZ, ionizing radiation, or combined chemoradiation on galectin protein secretion and expression were assessed in human GB cells and human umbilical vein endothelial cells (HUVECs).
Results: We found increased galectin-1 protein expression in human GB tissue. We also observed that HUVEC co-culture with GB cells increased galectin-1 protein expression by 14 - 20% following bevacizumab, and conferred a bevacizumab protective benefit to GB cells. Our in vitro models promisingly demonstrated that 72 hr treatments with 25 µM of galectin 1 inhibitor + HDAC inhibitor induce antitumor activity in GB cells. Western blot and activities assay results also demonstrated that combination blockade of HDAC activity and galectin-1 augmented apoptosis in GB cells, which mechanistically involves activation of caspase-3 and inhibition of anti-apoptotic protein (survivin, p-Akt, and Mcl-1 expression).
Conclusion: Our in vitro culture results suggest possible benefit in combining a galectin inhibitor with an HDAC inhibitor in GB. Further studies in different animal models are warranted.
Citation Format: David Cachia, Arindam Rano Chatterjee, William Alexander Vandergrift, Sunil J. Patel, Gabriel A. Rabinovich, Arabinda Das. Galectins in glioblastoma: opportunities for combined therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1. doi:10.1158/1538-7445.AM2017-1
Abstract 108: In vitro and in vivo characterization of novel scorpion venom-based peptides for the treatment of colon cancer
Authors: Li Bin , KWOK Hang Fai 
Published: July 2017

Abstract
In the last decade, many of the venom-based bioactive peptides demonstrated with a broad and diverse spectrum of pharmacological activities, which help to enlarging the current drug-screening library for searching of new specific biomarkers and novel prototype drugs for diagnosis of diseases such as cancer. Moreover, it paved a new insight to overcome the current drug discovery problems, which including drug resistance problem, side effect and so on.
Here we report the discovery of a panel of novel venom-based peptides, which can significantly inhibit the growth of human colon cancer cells. Through our in-house developed high throughput screening techniques and bioinformatics analysis, we successfully isolated eight novel peptides from scorpion venoms with anticancer activities. We performed a series of anti-proliferative assays to demonstrate that these peptides could inhibit the growth of a broad spectrum of tumor cells, especially in human colon cancer cell line; while almost have no effect on normal human epithelial cells. Haemolysis assay was also performed to show our peptides do not cause any harm on normal human red blood cells, which point to the direction of bringing those peptides into the preclinic trial studies. Before the in vivo studies, we are currently investigating the anticancer mechanisms and involved signal pathways of these peptides. LDH assay and real-time live cell analysis were performed, and from those data it indicates that the peptides might actually work by inhibiting the cancer cell growth instead of disrupt their cell membrane directly. Flow cytometry and western bolt results also showed that the peptides have a significant G1 phase cell cycle arrest effect through inhibiting cyclin dependent kinases CDK4 and up-regulating the expression of cell cycle protein regulator Cyclin D3, p27, p21. Moreover, from our current data, it demonstrated that our peptides wouldn’t induce any apoptosis during the cell cycle process. With the solid anticancer mechanism/pathway data, the potential anticancer peptides to target in vivo malignant tumor will be evaluated in cancer xenograft animal model to demonstrate the growth inhibitor activity of our lead peptides.
In summary, our study demonstrate that our peptides can inhibit tumor cell growth via cell-cycle arrest, and almost have no cytotoxicity on human epithelial cells, which could lead our lead peptides to further clinical investigation for the new strategy of peptide mono-/combination therapy.
Citation Format: Bin Li, Hang Fai KWOK. In vitro and in vivo characterization of novel scorpion venom-based peptides for the treatment of colon cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 108. doi:10.1158/1538-7445.AM2017-108
Abstract 124: Imipridone ONC201 promotes intra-tumoral accumulation of CD3+/NK+ cells that contribute to its anti-tumor efficacy
Authors: Wagner Jessica , Kline C. Leah , Zhou Lanlan , Zloza Andrew , Chesson Charles , Newman Jenna , Kaufman Howard , Bertino Joseph , Stein Mark , El-Deiry Wafik 
Published: July 2017

Abstract
ONC201, a first-in-class oral anti-tumor agent, upregulates the pro-apoptotic immune cytokine TRAIL and activates the integrated stress response leading to upregulation of death receptor 5 in bulk tumor and cancer stem cells. We previously demonstrated that ONC201 exerts a dose- and schedule-dependent effect on tumor progression in vivo while suppressing Akt/ERK signaling in tumors in a dose/frequency-dependent manner (Wagner et al., AACR, 2016). We also provided evidence that ONC201 exhibits a potent anti-metastatic effect (Wagner et al., AACR, 2016). We observe accumulation and activation of TRAIL-secreting NK+ cells within ONC201-treated tumors in C57/BL6, Balb/c, and athymic nude tumor-bearing mice. Importantly, ONC201 exerts in vivo anti-tumor efficacy on tumor cell lines that are ONC201-resistant in vitro, including acquired stable resistance. Using the NK-depleting antibody GM1, we demonstrate that the activation and TRAIL secretion of NK cells by ONC201 significantly contributes to in vivo anti-tumor efficacy, including TRAIL/ONC201-resistant tumors. We are currently investigating how ONC201 recruits NK cells to the tumor by examining NK-recruiting chemokine factors within the tumor site. We have also demonstrated upregulation of CD3+ T cells by ONC201 in syngeneic mice. Finally, we observed an increase in activated TRAIL-secreting NK cells in the peripheral blood of patients upon ONC201 administration in the clinic. Our results demonstrate novel and potentially significant increases in cytotoxic NK cell recruitment to tumors. The results offer a unique pathway of immune stimulation for cancer therapy that may be combined with immune checkpoint or targeted cancer therapy strategies. We are currently investigating the role of NK cells and CD3+ cells in ONC201’s ability to inhibit metastasis by using a metastatic model that involves surgically removing the primary tumor and allowing metastases to grow in vivo before treatment. These findings indicate that ONC201 possess immunomodulatory activity and provide a rationale for combining ONC201 with PD-1/PDL-1 inhibitors, a combination we are currently testing in syngeneic immunocompetent mouse models.
Citation Format: Jessica Wagner, C. Leah Kline, Lanlan Zhou, Andrew Zloza, Charles Chesson, Jenna Newman, Howard Kaufman, Joseph Bertino, Mark Stein, Wafik El-Deiry. Imipridone ONC201 promotes intra-tumoral accumulation of CD3+/NK+ cells that contribute to its anti-tumor efficacy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 124. doi:10.1158/1538-7445.AM2017-124
Abstract 1275: Genetic variations in cancer-related significantly mutated genes and lung cancer susceptibility
Authors: Zhang Liren , Zhang Yanwei , Li Rong , Chang David W. , Ye Yuanqing , Minna John D. , Roth Jack A. , Han Baohui , Wu Xifeng 
Published: July 2017

Abstract
Cancer initiation and development are driven by key mutations in driver genes. Applying high-throughput sequencing technologies and bioinformatics analyses, The Cancer Genome Atlas (TCGA) project has recently identified panels of genetic mutations that contributed to or associated with the etiology of various cancers. However, there are few studies investigating the germline genetic variations in these highly mutated genes and lung cancer susceptibility. In this multi-phase study, we aimed to comprehensively evaluate the 1655 tagSNPs located in the 127 significantly mutated genes (SMGs) identified by TCGA, and test their association with risk of lung cancer in a total of 7355 patients and 7301 healthy controls. We found that 11 SNPs in 8 genes showed consistent association (P&lt;0.1) and 8 SNPs significantly associated with lung cancer risk (P&lt;0.05) in both discovery and validation phases. The most significant SNP A was associated with a decreased risk of lung cancer (OR=0.91, 95%CI: 0.87-0.96, P=2.3×10-4). Cumulative analysis of the 11 SNPs showed consistently elevated risk with increasing number of unfavorable genotypes (P for trend=1.2×10-10). In stratified analyses, the association of SNP A and lung cancer risk appeared stronger among population of younger age at diagnosis and never smokers. The eQTL-analysis indicated that genotypes of four SNPs significantly correlated with the expression of their genes respectively. From TCGA data, expression of the identified genes were significantly different in lung tumors compared with normal tissues, and the genes’ highest mutation frequency was found in lung cancers. Integrative pathway analysis (IPA) indicated the identified genes were mainly involved in major cell cycle regulatory pathway suggesting the underlying biological processes. In summary, this study revealed novel genetic variants in SMGs associated with lung cancer risk, which might contribute to elucidating the biological network involved in lung cancer development.
Citation Format: Liren Zhang, Yanwei Zhang, Rong Li, David W. Chang, Yuanqing Ye, John D. Minna, Jack A. Roth, Baohui Han, Xifeng Wu. Genetic variations in cancer-related significantly mutated genes and lung cancer susceptibility [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1275. doi:10.1158/1538-7445.AM2017-1275