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Copyright of Brazilian Journal of Management / Revista de Administração da UFSM is the property of Brazilian Journal of Management / Revista de Administracao da UFSM and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista de Comunicación 'Vivat Academia' is the property of Facultad de Ciencias de las Informacion de la Universidad Complutense (Espana) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Brazilian Journalism Research is the property of Sur le journalisme, About journalism, Sobre jornalismo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Mediterranean Journal of Communication / Revista Mediterránea de Comunicación is the property of Revista Mediterranea de Comunicacion / Mediterranean Journal of Communication and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The ectoparasite V. destructor is one of the major threats to Western honeybees' production (A. mellifera) worldwide, causing colony losses and reducing bees' productivity and pollinating capacity. Since parasitism produces high energy consumption in hosts, the aim of this study was to compare the effects of this ectoparasite on energy expenditure and survival rate in honeybees. Newborn bees were kept in chambers at 32 °C and 55% humidity with food ad libitum. Individual bees were taken at random and grouped into three treatments: T0 (no mites), T1 (one mite), and T2 (two mites). After the mites had fed on the bees, the metabolic rate (CO2 production = VCO2) was individually measured at 32 °C for 3 h. We also measured survival rate, using the same groups for 8 days. A significant effect of the number of mites on VCO2 was found (T0 = 3.14 μLCO2 min−1, T1 = 4.03 μLCO2 min−1 and T2 = 6.44 μLCO2 min−1, F(2) = 25.81, p < 0.001). The treatments did not affect significantly the bees' survival (p = 0.283), despite the survival rates recorded were 57.5% in T0, 42.5% in T1, and 40.0% in T2. V. destructor clearly increases the energetic cost of living in bees and provoking a reduction of the survival rate even when this value was not significant statistically. [ABSTRACT FROM AUTHOR]

Copyright of Palabra Clave is the property of Universidad de la Sabana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Estudios sobre el Mensaje Periodistico is the property of Universidad Complutense de Madrid and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The objective of this study was to make a quantitative comparison of flortaucipir PET retention with pathological tau and β-amyloid across a range of brain regions at autopsy. Methods: Patients with dementia (two with clinical diagnosis of AD, one undetermined), nearing the end of life, underwent 20-min PET, beginning 80 min after an injection of ~370 mBq flortaucipir [18F]. Neocortical, basal ganglia, and limbic tissue samples were obtained bilaterally from 19 regions at autopsy and subject-specific PET regions of interest corresponding to the 19 sampled target tissue regions in each hemisphere were hand drawn on the PET images. SUVr values were calculated for each region using a cerebellar reference region. Abnormally phosphorylated tau (Ptau) and amyloid-β (Aβ) tissue concentrations were measured for each tissue region with an antibody capture assay (Histelide) using AT8 and H31L21 antibodies respectively. Results: The imaging-to-autopsy interval ranged from 4–29 days. All three subjects had intermediate to high levels of AD neuropathologic change at autopsy. Mean cortical SUVr averaged across all three subjects correlated significantly with the Ptau immunoassay (Pearson r = 0.81; p < 0.0001). When Ptau and Aβ1-42 were both included in the model, the Ptau correlation with flortaucipir SUVr was preserved but there was no correlation of Aβ1-42 with flortaucipir. There was also a modest correlation between limbic (hippocampal/entorhinal and amygdala) flortaucipir SUVr and Ptau (Pearson r = 0.52; p < 0.080). There was no significant correlation between SUVr and Ptau in basal ganglia. Conclusions: The results of this pilot study support a quantitative relationship between cortical flortaucipir SUVr values and quantitative measures of Ptau at autopsy. Additional research including more cases is needed to confirm the generalizability of these results. Trial registration, NIH Clinicaltrials.gov NCT # 02516046. Registered August 27, 2015. https://clinicaltrials.gov/ct2/show/NCT02516046?term=02516046&draw=2&rank=1 [ABSTRACT FROM AUTHOR]

Deformed wing virus (DWV) is one of the most common viruses in apiaries worldwide, and its presence in Chilean apiaries is no exception. There are three well-defined master variants described as DWV-A, DWV-B (or VDV-1) and DWV-C. We studied the prevalence, load and recombinant genotypes among DWV variants in honey bees from Chilean apiaries. We also compared the viral load in each region in colonies that were treated or untreated against Varroa destructor. Using real-time PCR with specific primers enabled us to determine that DWV-A was the most prevalent (71%) throughout Chile, with a higher level than DWV-B (circa 3% prevalence), and almost 60-times more load, especially in northern Chile. The viral load was lower only in treated colonies located in the Metropolitana, Biobío/Ñuble and Los Ríos regions. The DWV-C genotype and recombinants were not detected. This suggests that viral recombinant events are limited since DWV-B is still uncommon in honey bee hives at present. This is the first study involving DWV-B in Chile. [ABSTRACT FROM AUTHOR]

Copyright of Mediterranean Journal of Communication / Revista Mediterránea de Comunicación is the property of Revista Mediterranea de Comunicacion / Mediterranean Journal of Communication and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Doxa Comunicación is the property of Fundacion Universitaria San Pablo - CEU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Honeybees are essential components to modern agriculture and economy. However, a continuous increase in cases of colony losses and colony depopulation are being reported worldwide. This critical situation has put the fragile equilibrium between bees and plants on the edge. As a consequence, several scientists have begun to focus their lines of research on this issue. Most researchers agree that there is no single explanation for the observed colony losses. Instead, these losses result from a synergistic interaction between different stressors. South America is not the exception; several cases of colony losses and colony depopulation were reported by beekeepers throughout the continent, yet no accurate data has been published to date. Therefore, this article attempts to analyze the past and present situation of honeybee health in South America, specifically in Argentina, Chile, Uruguay, Brazil, and Venezuela. Furthermore, it is intended to serve as a comparison to future colony losses, as well as to provide guidance for future hypothesis-driven research on the causes of colony mortality. We evaluate the impact of the main parasites and pathogens affecting honeybee colonies and discuss the role of each with respect to reported honeybee losses. We also contemplate the main challenges that each nation must confront with regards to honeybee health. [ABSTRACT FROM AUTHOR]

The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. Investigations into these pathologies have been restricted to cerebrospinal fluid assays, and positron emission tomography tracers that can image amyloid-β plaques. Tau tracers have recently been introduced into the field, although the utility of the tracer and its relationship to other Alzheimer biomarkers are still unknown. Here we examined tau deposition in 41 cognitively normal and 11 cognitively impaired older adults using the radioactive tau ligand (18)F-AV-1451 (previously known as T807) who also underwent a lumbar puncture to assess cerebrospinal fluid levels of total tau (t-tau), phosphorylated tau181 (p-tau181) and amyloid-β42 Voxel-wise statistical analyses examined spatial patterns of tau deposition associated with cognitive impairment. We then related the amount of tau tracer uptake to levels of cerebrospinal fluid biomarkers. All analyses controlled for age and gender and, when appropriate, the time between imaging and lumbar puncture assessments. Symptomatic individuals (Clinical Dementia Rating > 0) demonstrated markedly increased levels of tau tracer uptake. This elevation was most prominent in the temporal lobe and temporoparietal junction, but extended more broadly into parietal and frontal cortices. In the entire cohort, there were significant relationships among all cerebrospinal fluid biomarkers and tracer uptake, notably for tau-related cerebrospinal fluid markers. After controlling for levels of amyloid-β42, the correlations with tau uptake were r = 0.490 (P < 0.001) for t-tau and r = 0.492 (P < 0.001) for p-tau181 Within the cognitively normal cohort, levels of amyloid-β42, but not t-tau or p-tau181, were associated with elevated tracer binding that was confined primarily to the medial temporal lobe and adjacent neocortical regions. AV-1451 tau binding in the medial temporal, parietal, and frontal cortices is correlated with tau-related cerebrospinal fluid measures. In preclinical Alzheimer's disease, there is focal tauopathy in the medial temporal lobes and adjacent cortices. [ABSTRACT FROM AUTHOR]

The article presents a report of the positron emission tomography (PET) imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild Alzheimer's disease (AD). The identification of unique disease-related stereotypical spatial patterns for deposition of tau and Aβ using multivariate analysis is explored. The support models of AD used where tau pathology tracked changes in brain function responsible for the symptoms in AD are also tackled.

Amyloid PET imaging is an indispensable tool widely used in the investigation, diagnosis and monitoring of Alzheimer’s disease (AD). Currently, a reference region based approach is used as the mainstream quantification technique for amyloid imaging. This approach assumes the reference region is amyloid free and has the same tracer influx and washout kinetics as the regions of interest. However, this assumption may not always be valid. The goal of this work is to evaluate an amyloid imaging quantification technique that uses arterial region of interest as the reference to avoid potential bias caused by specific binding in the reference region. 21 participants, age 58 and up, underwent Pittsburgh compound B (PiB) PET imaging and MR imaging including a time-of-flight (TOF) MR angiography (MRA) scan and a structural scan. FreeSurfer based regional analysis was performed to quantify PiB PET data. Arterial input function was estimated based on coregistered TOF MRA using a modeling based technique. Regional distribution volume (VT) was calculated using Logan graphical analysis with estimated arterial input function. Kinetic modeling was also performed using the estimated arterial input function as a way to evaluate PiB binding (DVRkinetic) without a reference region. As a comparison, Logan graphical analysis was also performed with cerebellar cortex as reference to obtain DVRREF. Excellent agreement was observed between the two distribution volume ratio measurements (r>0.89, ICC>0.80). The estimated cerebellum VT was in line with literature reported values and the variability of cerebellum VT in the control group was comparable to reported variability using arterial sampling data. This study suggests that image-based arterial input function is a viable approach to quantify amyloid imaging data, without the need of arterial sampling or a reference region. This technique can be a valuable tool for amyloid imaging, particularly in population where reference normalization may not be accurate. [ABSTRACT FROM AUTHOR]

The development of new technologies is changing the habits of television consumption among young people. The multiplication of channels has intensified the fragmentation of the market and its audiences and the individualist atomization in the media preferences and consumption. This article is part of a research project aiming to establish television consumption preferences, opinions and habits of Spanish young people, aged between 14 and 25 years, and the differences between the two groups into which the respondents were divided (14-17 and 18-25). The article shows the extent to which Spanish youngsters have turned to new media as a source of entertainment.Indeed, one of the most groundbreaking results that should be highlighted is the difference between the two groups in their approach to the Internet as a source of entertainment.The article shows how the digital generation demands the adaptation of television content to the new platforms - such as the Internet or mobile phone - and the renewal of television formats. The findings of this study also point to trend indicators and guidelines that advertisers and media companies might be interested in when designing new creative and innovative television content. [ABSTRACT FROM AUTHOR]

Objective: To evaluate whether the amyloid-binding agent carbon 11-labeled Pittsburgh Compound B (11C-PiB) could differentiate Alzheimer disease (AD) from human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) in middle-aged HIV positive participants. Design: 11C-PiB scanning, clinical assessment, and cerebrospinal fluid (CSF) analysis were performed. Both χ2 and t tests assessed differences in clinical and demographic variables between HIV-positive participants and community-living individuals observed at the Knight Alzheimer's Disease Research Center (ADRC). Analysis of variance assessed for regional differences in amyloid-β protein 1-42 (Aβ42) using 11C-PiB. Setting: An ADRC and HIV clinic. Participants: Sixteen HIV-positive participants (11 cognitively normal and 5 with HAND) and 19 ADRC participants (8 cognitively normal and 11 with symptomatic AD). Main Outcome Measures: Mean and regional 11C-PiB binding potentials. Results: Participants with symptomatic AD were older (P<.001), had lower CSF Aβ42 levels (P<.001), and had higher CSF tau levels (P<.001) than other groups. Regardless of degree of impairment, HIV-positive participants did not have increased 11C-PiB levels. Mean and regional binding potentials were elevated for symptomatic AD participants (P<.001). Conclusions: Middle-aged HIV-positive participants, even with HAND, do not exhibit increased 11C-PiB levels, whereas symptomatic AD individuals have increased fibrillar Aβ42 deposition in cortical and subcortical regions. Observed dissimilarities between HAND and AD may reflect differences in Aβ42 metabolism. 11C-PiB may provide a diagnostic biomarker for distinguishing symptomatic AD from HAND in middle-aged HIV-positive participants. Future cross-sectional and longitudinal studies are required to assess the utility of 11C-PiB in older individuals with HAND. [ABSTRACT FROM AUTHOR]

Copyright of Zer: Journal of Communication Studies / Revista de Estudios de Comunicacion / Komunikazio Ikasketen Aldizkaria is the property of Universidad del Pais Vasco and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Alzheimer's disease (AD) pathology is estimated to develop many years before detectable cognitive decline. Fluid and imaging biomarkers may identify people in early symptomatic and even preclinical stages, possibly when potential treatments can best preserve cognitive function. We previously reported that cerebrospinal fluid (CSF) levels of amyloid-β42 (Aβ42) serve as an excellent marker for brain amyloid as detected by the amyloid tracer, Pittsburgh compound B (PIB). Using data from 189 cognitively normal participants, we now report a positive linear relationship between CSF tau/ptau181 (primary constituents of neurofibrillary tangles) with the amount of cortical amyloid. We observe a strong inverse relationship of cortical PIB binding with CSF Aβ42 but not for plasma Aβ species. Some individuals have low CSF Aβ42 but no cortical PIB binding. Together, these data suggest that changes in brain Aβ42 metabolism and amyloid formation are early pathogenic events in AD, and that significant disruptions in CSF tau metabolism likely occur after Aβ42 initially aggregates and increases as amyloid accumulates. These findings have important implications for preclinical AD diagnosis and treatment. [ABSTRACT FROM AUTHOR]