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Author Heydari, N.; Larsen, D.A.; Neira, M.; Beltran Ayala, E.; Fernandez, P.; Adrian, J.; Rochford, R.; Stewart-Ibarra, A.M. url  doi
openurl 
  Title Household Dengue Prevention Interventions, Expenditures, and Barriers to Aedes aegypti Control in Machala, Ecuador Type Journal Article
  Year 2017 Publication International Journal of Environmental Research and Public Health Abbreviated Journal Int J Environ Res Public Health  
  Volume 14 Issue 2 Pages  
  Keywords Aedes/*growth & development; Animals; Dengue/epidemiology/*prevention & control; Ecuador/epidemiology; Housing; Humans; Insect Vectors/*virology; Insecticides/*economics; Mosquito Control/*economics/*methods; Mosquito Nets/*economics; Socioeconomic Factors; Aedes aegypti; Ecuador; Kap; dengue fever; economic cost; mosquito control  
  Abstract The Aedes aegypti mosquito is an efficient vector for the transmission of Zika, chikungunya, and dengue viruses, causing major epidemics and a significant social and economic burden throughout the tropics and subtropics. The primary means of preventing these diseases is household-level mosquito control. However, relatively little is known about the economic burden of Ae. aegypti control in resource-limited communities. We surveyed residents from 40 households in a high-risk community at the urban periphery in the city of Machala, Ecuador, on dengue perceptions, vector control interventions, household expenditures, and factors influencing purchasing decisions. The results of this study show that households spend a monthly median of US$2.00, or 1.90% (range: 0.00%, 9.21%) of their family income on Ae. aegypti control interventions. Households reported employing, on average, five different mosquito control and dengue prevention interventions, including aerosols, liquid sprays, repellents, mosquito coils, and unimpregnated bed nets. We found that effectiveness and cost were the most important factors that influence people's decisions to purchase a mosquito control product. Our findings will inform the development and deployment of new Ae. aegypti control interventions by the public health and private sectors, and add to prior studies that have focused on the economic burden of dengue-like illness.  
  Address Center for Global Health and Translational Science, State University of New York Upstate Medical University, Syracuse, NY 13210, USA. amstew01@gmail.com  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1660-4601 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28212349 Approved no  
  Call Number ref @ user @ Serial 97645  
Permanent link to this record
 

 
Author Alshehri, M.M.; Robbins, S.M.; Senger, D.L. url  doi
openurl 
  Title The Role of Neurotrophin Signaling in Gliomagenesis: A Focus on the p75 Neurotrophin Receptor (p75NTR/CD271) Type Journal Article
  Year 2017 Publication Vitamins and Hormones Abbreviated Journal Vitam Horm  
  Volume 104 Issue Pages 367-404  
  Keywords Brain tumor; Cd271; Cancer stem cells; Glioblastoma; Glioma invasion; Nerve growth factor; Neurotrophin; p75(NTR)  
  Abstract The p75 neurotrophin receptor (p75NTR, a.k.a. CD271), a transmembrane glycoprotein and a member of the tumor necrosis family (TNF) of receptors, was originally identified as a nerve growth factor receptor in the mid-1980s. While p75NTR is recognized to have important roles during neural development, its presence in both neural and nonneural tissues clearly supports the potential to mediate a broad range of functions depending on cellular context. Using an unbiased in vivo selection paradigm for genes underlying the invasive behavior of glioma, a critical characteristic that contributes to poor clinical outcome for glioma patients, we identified p75NTR as a central regulator of glioma invasion. Herein we review the expanding role that p75NTR plays in glioma progression with an emphasis on how p75NTR may contribute to the treatment refractory nature of glioma. Based on the observation that p75NTR is expressed and functional in two critical glioma disease reservoirs, namely, the highly infiltrative cells that evade surgical resection, and the radiation- and chemotherapy-resistant brain tumor-initiating cells (also referred to as brain tumor stem cells), we propose that p75NTR and its myriad of downstream signaling effectors represent rationale therapeutic targets for this devastating disease. Lastly, we provide the provocative hypothesis that, in addition to the well-documented cell autonomous signaling functions, the neurotrophins, and their respective receptors, contribute in a cell nonautonomous manner to drive the complex cellular and molecular composition of the brain tumor microenvironment, an environment that fuels tumorigenesis.  
  Address Arnie Charbonneau Cancer Centre, University of Calgary, Calgary, AB, Canada. Electronic address: senger@ucalgary.ca  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0083-6729 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28215302 Approved no  
  Call Number ref @ user @ Serial 96606  
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Author Ludwig, K.; Kornblum, H.I. url  doi
openurl 
  Title Molecular markers in glioma Type Journal Article
  Year 2017 Publication Journal of Neuro-Oncology Abbreviated Journal J Neurooncol  
  Volume Issue Pages  
  Keywords Glioblastoma; Glioma stem cell; Molecular markers; Mutations; Pathways  
  Abstract Gliomas are the most malignant and aggressive form of brain tumors, and account for the majority of brain cancer related deaths. Malignant gliomas, including glioblastoma are treated with radiation and temozolomide, with only a minor benefit in survival time. A number of advances have been made in understanding glioma biology, including the discovery of cancer stem cells, termed glioma stem cells (GSC). Some of these advances include the delineation of molecular heterogeneity both between tumors from different patients as well as within tumors from the same patient. Such research highlights the importance of identifying and validating molecular markers in glioma. This review, intended as a practical resource for both clinical and basic investigators, summarizes some of the more well-known molecular markers (MGMT, 1p/19q, IDH, EGFR, p53, PI3K, Rb, and RAF), discusses how they are identified, and what, if any, clinical relevance they may have, in addition to discussing some of the specific biology for these markers. Additionally, we discuss identification methods for studying putative GSC's (CD133, CD15, A2B5, nestin, ALDH1, proteasome activity, ABC transporters, and label-retention). While much research has been done on these markers, there is still a significant amount that we do not yet understand, which may account for some conflicting reports in the literature. Furthermore, it is unlikely that the investigator will be able to utilize one single marker to prospectively identify and isolate GSC from all, or possibly, any gliomas.  
  Address Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Hkornblum@mednet.ucla.edu  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0167-594X ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28233083 Approved no  
  Call Number ref @ user @ Serial 96605  
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Author Brown, D.V.; Filiz, G.; Daniel, P.M.; Hollande, F.; Dworkin, S.; Amiridis, S.; Kountouri, N.; Ng, W.; Morokoff, A.P.; Mantamadiotis, T. url  doi
openurl 
  Title Expression of CD133 and CD44 in glioblastoma stem cells correlates with cell proliferation, phenotype stability and intra-tumor heterogeneity Type Journal Article
  Year 2017 Publication PloS one Abbreviated Journal PLoS One  
  Volume 12 Issue 2 Pages e0172791  
  Keywords AC133 Antigen/*metabolism; Animals; Antigens, CD44/*metabolism; Basic Helix-Loop-Helix Transcription Factors/metabolism; Biomarkers, Tumor/metabolism; Brain Neoplasms/*metabolism/pathology; Cell Proliferation; Female; Glioblastoma/*metabolism/pathology; Humans; Hypoxia; Mice; Mice, Inbred BALB C; Neoplasm Recurrence, Local; Neoplastic Stem Cells/*metabolism/pathology; Nerve Tissue Proteins/metabolism; Phenotype  
  Abstract Glioblastoma (GBM) is a heterogeneous tumor of the brain with a poor prognosis due to recurrence and drug resistance following therapy. Genome-wide profiling has revealed the existence of distinct GBM molecular subtypes that respond differently to aggressive therapies. Despite this, molecular subtype does not predict recurrence or drug resistance and overall survival is similar across subtypes. One of the key features contributing to tumor recurrence and resistance to therapy is proposed to be an underlying subpopulation of resistant glioma stem cells (GSC). CD133 expression has been used as a marker of GSCs, however recent evidence suggests the relationship between CD133 expression, GSCs and molecular subtype is more complex than initially proposed. The expression of CD133, Olig2 and CD44 was investigated using patient derived glioma stem-like cells (PDGCs) in vitro and in vivo. Different PDGCs exhibited a characteristic equilibrium of distinct CD133+ and CD44+ subpopulations and the influence of environmental factors on the intra-tumor equilibrium of CD133+ and CD44+ cells in PDGCs was also investigated, with hypoxia inducing a CD44+ to CD133+ shift and chemo-radiotherapy inducing a CD133+ to CD44+ shift. These data suggest that surveillance and modulation of intra-tumor heterogeneity using molecular markers at initial surgery and surgery for recurrent GBM may be important for more effective management of GBM.  
  Address Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28241049 Approved no  
  Call Number ref @ user @ Serial 96604  
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Author Roldos, M.I.; Hopenhayn, C.; Sacoto, F.; Bustamante, K. url  doi
openurl 
  Title Developing local health policy: Profiling needs and opportunities in the Municipality of Quito, Ecuador Type Journal Article
  Year 2017 Publication Journal of Public Health Policy Abbreviated Journal J Public Health Policy  
  Volume Issue Pages  
  Keywords Quito; local health policy; municipality; policy development; public health  
  Abstract We describe the steps taken and analysis applied in developing a local health policy agenda for the city of Quito, in Ecuador. In 2014, the Health Commissioner's Office of the Municipality of Quito analyzed the city's epidemiological health profiles, social determinants of health, the legal authority of the Municipality, and relevant literature to understand the city's health burden and develop a Ten-Year Health Plan (2015-2025). Results revealed that Quito's population suffered from noncommunicable chronic diseases (diabetes and hypertension) and identified the primary risk factors (poor nutrition, physical inactivity, and resulting overweight or obesity). Other common conditions included respiratory diseases, mental health conditions, deaths and injuries from motor vehicles, violence, and physical insecurity. The plan emphasized health promotion and disease prevention with the aim of transforming citizens' health perceptions with their active participation by fostering public and private intersectoral commitment to improve the quality of life of the population .  
  Address Epidemiology Surveillance, Health Commissioner's Office, Municipality of Quito, Ecuador  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0197-5897 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28242874 Approved no  
  Call Number ref @ user @ Serial 97335  
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