bluuebunny/crossref_metadata_2025_split huggingface dataset:
Application of a new river classification scheme to Australia's tropical rivers
Authors: Erskine Wayne , Saynor Mike , Lowry John 
Published: May 2017

A revised typology of Australian tropical rivers was applied to the complete channel network (named and major rivers) shown on 1:250 000 topographic maps for three large drainage basins in northern Australia (Daly River, NT; Fitzroy River, WA; Flinders River, Qld). Reach mapping and classification were conducted using the revised typology. The 12 major river types proposed were: (1) bedrock rivers; (2) bedrock‐confined and ‐constrained rivers; (3) low sinuosity (straight) rivers; (4) meandering rivers; (5) wandering rivers; (6) anabranching rivers; (7) chains of ponds; (8) gullies; (9) floodouts; (10) lakes, swamps, billabongs and wetlands; (11) non‐channelized valley floors; and (12) estuarine rivers. The 12 major river types were developed based on river reach mapping for more than 264 000 km2 of tropical Australian catchments. At scales larger than 1:250 000, subdivision of each major river type is recommended. In the Daly and Fitzroy catchments, confined and constrained rivers dominate, whereas in the Flinders and Fitzroy catchments, anabranching rivers dominate. The dominant river types need benchmarking with adequate numbers of control reaches so that channel changes induced by human and natural impacts can be measured by reference to the stability of these controls. Wandering rivers, floodouts and non‐channelized valley floors were rare for the 1:250 000 channel network in northern Australia but need inclusion in national parks.
Playing the Vertical Power Game: The Impact of Local Authorities in Cantonal Parliaments on the Financing of Special Schools
Authors: Arnold Tobias 
Published: May 2017

AbstractThis study analyses the effect of local authorities in the Swiss cantonal parliaments on the allocation of special school costs. The empirical findings show that a higher share of local authorities in the cantonal legislature leads to a higher share of special school costs borne by the cantonal authorities. The effect is stronger for mayors compared to all members of local governments. Hence, mayors have a strong connection with their home municipality and use the political power of the accumulation of mandates for shifting undesirable costs from the local up to the cantonal level. This specific finding does not depend on the overall national constitutional framework, as the introduction of theNFA(Neuer Finanzausgleich) –in the course of which the federal state fully withdrew from financing special schools ‐ has not changed the magnitude of this effect.
Intratumoral injection of radioactive holmium (166Ho) microspheres for treatment of oral squamous cell carcinoma in cats
Authors: van Nimwegen S. A. , Bakker R. C. , Kirpensteijn J. , van Es R. J. J. , Koole R. , Lam M. G. E. H. , Hesselink J. W. , Nijsen J. F. W. 
Published: May 2017

Background & AimsA “microbrachytherapy” was developed as treatment option for inoperable tumours by direct intratumoral injection of radioactive holmium‐166 (
166Ho) microspheres (MS). 166Ho emits β‐radiation which potentially enables a high, ablative, radioactive‐absorbed dose on the tumour tissue while sparing surrounding tissues.Materials & MethodsSafety and efficacy of 166Ho microbrachytherapy were evaluated in a prospective cohort study of 13 cats with inoperable oral squamous cell carcinoma without evidence of distant metastasis.ResultsLocal response rate was 55%, including complete response or partial response (downstaging) enabling subsequent marginal resection. Median survival time was 113 days overall, and 296 days for patients with local response. Side effects were minimal. Tumour volume was a significant predictor of response.DiscussionResponse rate may be further improved by optimizing the intratumoral spatial distribution of 166Ho MS.Conclusion166Ho microbrachytherapy has potential as a minimally invasive, single procedure radio‐ablation treatment of unresectable tumours with minimal morbidity.
Treatment of meloxicam overdose in a dog via therapeutic plasma exchange
Authors: Walton Stuart , Ryan Kirk A. , Davis Jennifer L. , Acierno Mark 
Published: May 2017

AbstractObjectiveTo describe the treatment of a meloxicam overdose in a dog with therapeutic plasma exchange (TPE).Case SummaryA 6‐month‐old female Bulldog, presented for routine laparoscopic ovariectomy. Postoperatively the dog received an accidental overdose of meloxicam (1 mg/kg IV [intravenously]). The patient was treated with supportive medical therapy and TPE over 210 minutes achieving 1.2 plasma volume exchanges. During therapy, heparinized blood and effluent samples were collected. Meloxicam concentrations were determined in the samples by high pressure liquid chromatography. Post TPE, the dog continued to receive supportive medical therapy and was discharged 48 hours after the overdose. The dog remained asymptomatic for meloxicam intoxication. Follow‐up rechecks at 1 and 6 weeks were unremarkable with no further treatment required.New or Unique InformationThis report describes the successful use of TPE adjunctively following an acute meloxicam overdose. An 82% reduction of plasma meloxicam concentration was achieved over 210 minutes. Twenty‐four hours after therapy, a 47% sustained reduction of plasma meloxicam was measured after redistribution of drug between body compartments.
Detection of angiospastic disorders in the microcirculatory bed using laser diagnostics technologies
Authors: Makovik Irina N. , Dunaev Andrey V. , Dremin Victor V. , Krupatkin Alexander I. , Sidorov Viktor V. , Khakhicheva Lyudmila S. , Muradyan Vadim F. , Pilipenko Olga V. , Rafailov Ilya E. , Litvinova Karina S. 
Published: May 2017

The evaluation of the microcirculatory bed functional state and the identification of angiospastic disorders with related complications, when the pathological changes are reversible, have an important role in medical practice. The aim of this study was to evaluate the possibility of using optical noninvasive methods and the cold pressor test to solve this problem.A total of 33 patients with rheumatological diseases and 32 healthy volunteers were included in the study. Laser Doppler flowmetry, tissue reflectance oximetry and pulse oximetry were used as optical noninvasive methods. The parameters were recorded before, immediately after and 20[Formula: see text]min after the cold pressor test. Based on the measured parameters, the complex parameters of the microcirculatory bed were calculated.A detailed statistical analysis of the parameter changes for each individual in the two groups displayed diverse microcirculatory bed parameter responses upon cold exposure, with differing recovery of parameters after CPT. New diagnostic criteria were proposed for the identification of angiospastic disorders. According to the proposed criteria, 27 people of the volunteers group were confirmed to not display any disorders. In the patient group, however, 18 people were observed to have a relatively normal functional state of the microcirculatory bed, while 15 people were observed to have a possible tendency to angiospasm. To highlight the differences between a relatively normal state and presence of angiospastic disorders, statistical analysis of experimental data was carried out, which revealed significant differences. Further analysis of data with angiospastic disorders identified a relationship between their diagnoses and the results of laboratory studies.Thus, the evaluation of combined noninvasive optical diagnostic method use, the cold pressor test and proposed diagnostic criteria showed a positive result. This approach can be used to detect the presence of possible angiospastic disorders and related complications, as well as microcirculatory bed disorders against the background of other diseases.
2016 International Teletraffic Congress (ITC 28) Report
Authors: Hossfeld Tobias 
Published: May 2017

The 28th International Teletraffic Congress (ITC 28) was held on 12--16 September 2016 at the University of W\"urzburg, Germany. The conference was technically cosponsored by the IEEE Communications Society and the Information Technology Society within VDE, and in cooperation with ACM SIGCOMM. ITC 28 provided a forum for leading researchers from academia and industry to present and discuss the latest advances and developments in design, modelling, measurement, and performance evaluation of communication systems, networks, and services. The main theme of ITC 28, \emph{Digital Connected World}, reflects the evolution of communications and networking, which is continually changing the world we are living in. The technical program was composed of 37 contributed full papers, 6 short demo papers and three keynote addresses. Three workshops dedicated to timely topics were sponsored: Programmability for Cloud Networks and Applications, Quality of Experience Centric Management, Quality Engineering for a Reliable Internet of Services.
See ITC 28 Homepage: \url{https://itc28.org/}
Abstract A02: pRb-loss causes widespread changes to the transcriptome and proteome of cells
Authors: Miles Wayne O. 
Published: May 2017

Abstract
Loss of the Retinoblastoma 1, pRb, tumor-suppressor gene is widespread in tumor cells and causes de-regulation of the E2F transcription factors. Aberrant E2F activity results in the over expression of genes required for proliferation. To determine how pRb-loss changes cells, we depleted pRb from RPE cells using shRNAs and measured the effect on the transcriptome and proteome using RNA-sequencing and quantitative Mass Spectrometry. These approaches produced a number of unexpected findings including; (A) many E2F target genes are transcribed but poorly translated, (B) pRb-loss induces a strong interferon response, and (C) pRb-deficiency increases the protein levels of the extracellular matrix components. In addition, our results support previous reports linking pRb to mitochondrial activity and metabolic reprogramming. The changes to the transcriptome and proteome are extensive and complex and we are currently conducting an in-depth analysis of these results however our preliminary analysis suggests that loss of the pRb tumor-suppressor gene causes widespread and previously unappreciated changes in the transcriptome and proteome of cells. To begin to understand the mechanisms regulating these changes in translation potential, we have begun assessing the post-transcriptional mechanisms controlling the levels of the E2F-target genes. This group of genes is induced upon pRb-loss however no associated increase in protein levels is detected. To identify the mechanisms controlling the translation potential of this collection of genes, we search for enriched motifs of post-transcriptional regulators in these mRNAs. This analysis found a strong enrichment for the Pumilio (PUM) RNA-binding protein. RNA-immunoprecipitation experiments confirm that the levels of E2F target genes bound by PUM increase upon pRb-loss. To assay how PUM levels regulate the protein levels of the E2F target genes, we depleted PUM1 or PUM2 using siRNAs and conducted quantitative Mass Spectrometry. From this analysis, we find a strong increase in the levels of some E2F target genes upon PUM and pRb-loss. Collectively, these results are providing new insights into the proteomic changes induced after pRb-loss and is highlighting some of the post-transcriptional mechanisms buffering these effects.
Citation Format: Wayne O. Miles. pRb-loss causes widespread changes to the transcriptome and proteome of cells. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A02.
Abstract A03: FGF-WNT cooperativity and the role of lncRNAs in translational regulation in breast cancer
Authors: Nguyen Tuan M. , Kabotyanski Elena B. , Reineke Lucas C. , Mo Qianxing , Zhang Peng , Zhang Xiang , Chen Yiwen , Neilson Joel , Lloyd Richard E. , Rosen Jeffrey M. 
Published: May 2017

Abstract
The purpose of this study is to understand translational mechanisms underlying the cooperativity between FGF and WNT signaling in cancer progression. FGF and WNT signaling, crucial pathways in mammary stem cell self-renewal, are frequently deregulated in human cancer. We previously showed that acute activation of FGF signaling in the mammary gland of pubertal mice with WNT hyperactivation dramatically accelerates cancer progression. FGF-WNT-hyperactive tumor cells exhibit enhanced activation of translational machinery. Given the potential involvement of translational regulation in FGF-WNT induced tumorigenesis, we employed ribosome profiling to identify selectively translated and ribosome associated RNAs induced by acute FGF activation in vivo. Many genes associated with RNA processing and transport were translationally upregulated. Interestingly, the most translationally upregulated transcript was Malat1, originally thought to be a nuclear-restricted long noncoding RNA (lncRNA) that regulates transcription of cancer-associated genes. Along with Malat1, many lncRNAs were associated with ribosomes in FGF-WNT tumors. Malat1's association with polysomes upon acute FGF activation was confirmed by direct polysome analysis. We also demonstrated that Malat1 transcripts are transported to the cytoplasm during G2/M transition, implicating that Malat1 may be translated into small novel peptides or involved in translation regulation during this particular phase of cell cycle. Additionally, there is evidence that Malat1 is a direct downstream target of WNT signaling. Our findings indicate that FGF activation potentially increases the translation efficiency of WNT-target oncogenes including lncRNAs like Malat1, unraveling a novel mechanism of crosstalk between lncRNAs and translational regulation in cancer progression.
Citation Format: Tuan M. Nguyen, Elena B. Kabotyanski, Lucas C. Reineke, Qianxing Mo, Peng Zhang, Xiang Zhang, Yiwen Chen, Joel Neilson, Richard E. Lloyd, Jeffrey M. Rosen. FGF-WNT cooperativity and the role of lncRNAs in translational regulation in breast cancer. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A03.
Abstract A14: Proteomic analysis of paired malignant and non-malignant tissues from patients with NSCLC adenocarcinoma identified changes in translation initiation factors potentially important in oncogenesis
Authors: Miyamoto Suzanne , Fahrmann Johannes F. , Grapov Dmitry , Phinney Brett , Pass Harvey 
Published: May 2017

Abstract
An important aspect of the control of mRNA translation into protein in mammalian cells is the initiation process, which involves the activities of multiple eukaryotic translation initiation factors or eIFs. Genetic analyses of eIFs in yeast (S. cerevisiae) have defined the eIFs necessary for the basic translation of mRNAs into proteins, but additional subunits found in mammalian cells have not been as well defined in normal cells so how the activities and functions of eIFs may be dysregulated in cancers such as lung cancer are still being determined. Lung cancer causes the highest cancer mortality in men and women in the United States. Lung cancer, mostly non-small cell (NSCLC) adenocarcinoma is responsible for about 13% of all new cancer cases and 26% of all cancer deaths. We undertook a proteomic analysis of lung cancer by analyzing 39 pairs of malignant and non-malignant lung tissues obtained from patients with early stage NSCLC adenocarcinoma using trypsin digestion and tandem MS/MS. Examination of eIFs in these tissues showed significant proteomic differences with significant increases in eIFs, especially in eIF2A, eIF2B, 1 alpha, and eIF2B, 5 episilon (p-values &lt; 0.05). Smaller, but significant increased fold changes were also observed in eIF3B, eIF3G, eIF3J, eIF4G1, eIF4E eIF4A1 and eIF4H. Increased protein levels of EIF2AK2, the interferon induced eIF2A protein kinase was also detected. The eIF2alpha exchange rate may be an important aspect of tumorigenesis in lung cancer tissues with the increased exchange of GTP for GDP in eIF2A, hence the large increases in eIF2B subunits. Increases in eIF3 subunits, especially eIF3j, as well as increases in eIF4E and eIF4G1 correspond to increased protein synthesis rates and cellular proliferation. These early results need further investigation and related functional analysis to determine if the changes in eIFs correspond to important activities in the tumor cells or surrounding microenvironment and have mechanistic consequences in the growth and progression of lung cancer tumors.
Citation Format: Suzanne Miyamoto, Johannes F. Fahrmann, Dmitry Grapov, Brett Phinney, Harvey Pass. Proteomic analysis of paired malignant and non-malignant tissues from patients with NSCLC adenocarcinoma identified changes in translation initiation factors potentially important in oncogenesis. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A14.
Abstract A24: Translation control of tumor metastasis via FSTL1 binding with SPP1/OPN to modulated cytoskeleton remodeling
Authors: Chiou Jean , Lin Yuan-Feng , Hsiao Michael 
Published: May 2017

Abstract
Follistatin-like protein 1 (FSTL1) plays a critical role in lung organogenesis. However, the prognostic significance and functional consequence of FSTL1 downregulation remains unclear in lung cancer. Here we show that the reduced levels of FSTL1 are widely detected in tumors compared to normal tissues and reflect a poor clinical outcome in non-small cell lung cancer, especially lung adenocarcinoma. Moreover, we found that FSTL1 expression negatively correlates with the metastatic potential of lung cancer cells in vitro and in vivo. Whereas the antibody-based neutralization of extracellular FSTL1 enhances the cellular migration/invasion ability, the inclusion of recombinant FSTL1 protein diminishes the metastatic capacity of lung cancer cells in vitro and in vivo. Notably, the administration of FSTL1 was capable of effectively preventing the metastatic progression of lung cancer cells in an orthotropic animal model. The in vitro protein-protein interaction (PPI) assay demonstrated that FSTL1 directly binds to the pro-form of secreted phosphoprotein 1 (SPP1), also named osteopontin (OPN), and thereby restrains the proteolytic activation of SPP1/OPN, which leads to the inactivation of integrin/CD44-associated signaling cascades and actin cytoskeleton. Runx2 and osterix transcription factors are required for the expression of SPP1/OPN. Thus, FSTL1 compromised the SPP1/OPN related translation control activity through PPI mechanism to reverse the phenotype in lung cancer. The signature of combining low-level FSTL1 with high-level SPP1 predicts a worse prognosis in lung cancer patients. This study is the first to document the PPI between FSTL1 and SPP1/OPN and our findings provide a novel and effective strategy to combat SPP1/OPN-driven metastatic cancers with FSTL1 downregulation.
Citation Format: Jean Chiou, Yuan-Feng Lin, Michael Hsiao. Translation control of tumor metastasis via FSTL1 binding with SPP1/OPN to modulated cytoskeleton remodeling. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A24.
Abstract A28: Oxygen-dependent translatome remodeling is controlled by eIF2α dephosphorylation
Authors: Ho J.J. David , Balukoff Nathan C. , Cervantes Grissel , Rosa Ayalivis De La , Lee Stephen 
Published: May 2017

Abstract
Introduction: Eukaryotic translation initiation factor 2α (eIF2α) is a core component of the cellular translation machinery. Alterations in eIF2α phosphorylation constitute a key adaptation during a variety of physiological stresses, including oxygen deprivation (hypoxia). We recently found that cancer cells respond to hypoxia through the systemic reprogramming of cap-dependent mRNA translation efficiencies by switching to the hypoxic eIF4F, eIF4FH. In the present study, we sought to elucidate the role(s) of eIF2α phosphorylation and dephosphorylation in this translatome remodeling process. In particular, the growth arrest and DNA damage-inducible protein GADD34 has been reported as an adaptive, stress-activated mediator of eIF2α dephosphorylation. We aimed to determine the role of GADD34 in the cellular hypoxic response.
Findings: Our results indicate that hypoxia-induced eIF2α phosphorylation is a transient response with corresponding effects on translation efficiencies. Using next-generation mRNA sequencing (mRNA-seq), we reveal the dynamic profile of the translatome remodeling process during acute and chronic hypoxia. Our findings demonstrate that GADD34-mediated eIF2α dephosphorylation is required for hypoxic protein synthesis. GADD34 silencing results in high levels of eIF2α phosphorylation and severe global translational inhibition. Notably, GADD34 regulates the translation of hypoxia-inducible proteins in a hypoxia-inducible factor 2α (HIF-2α)-dependent manner. Finally, high throughput mass spectrometry (MS) analysis reveals several potential hypoxia-regulated GADD34 post-translational modifications (PTMs). Efforts are underway to validate and determine the effect(s) of these PTMs on GADD34 protein stability and/or activity.
Conclusion: We demonstrate that GADD34-mediated eIF2α dephosphorylation regulates oxygen-dependent translatome reprogramming in cancer cells. This pathway represents an exciting potential target for cancer therapeutics.
Citation Format: J.J. David Ho, Nathan C. Balukoff, Grissel Cervantes, Ayalivis De La Rosa, Stephen Lee. Oxygen-dependent translatome remodeling is controlled by eIF2α dephosphorylation. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A28.