Influencia cultural en las estrategias creativas: análisis comparativo de campañas publicitarias entre España e Inglaterra

En el presente trabajo, mediante un análisis de contenido, profundizaremos en la comunicación publicitaria de España e Inglaterra. Partiendo de un análisis de las dos culturas, estableceremos una serie de variables con su correspondiente puntuación para así situar en un mapa cultural ambos países; una vez identificadas las diferencias, extrapolaremos dichas variables culturales a un análisis de comunicación publicitaria en pro de dilucidar la relación entre cultura y publicidad en ambas culturasGrado en Publicidad y Relaciones Pública

DEVELOPMENT AND VALIDATION OF A RAPID AND SIMPLE REVERSED-PHASE HPLC METHOD FOR THE DETERMINATION OF GEMCITABINE IN HUMAN PLASMA

Objective: In order to investigate the human plasma pharmacokinetics of dFdC, the objective of this work was to optimize and validate a rapid reversed-phase (RP) high-performance liquid chromatography (HPLC) method according to the guidelines of the international regulatory institutions: European Medicines Agency (EMA), Food and Drug Administration (FDA) and International Conference on Harmonization (ICH). Methods: Chromatographic runs were performed on a RP-ACE-C18 column. Mobile phase was constituted of sodium acetate buffer (pH 5) and acetonitrile, in gradient mode, at a flow rate of 1 mL/min. Gemcitabine and cytarabine (internal standard) were detected at 290 nm. Results: The method was shown to be selective, linear in the range of 0.25–10 mg/L (R2=0.9998), accurate and precise within-run and between-run as reflected by the coefficient of variation values (<15%) and the relative errors values (<15%), stable and robust to changes in the column temperature and detection UV wavelength. Detection limit and lower limit of quantification were 0.22 and 0.25 mg/L respectively. Conclusion: The developed method is useful to measuring gemcitabine plasmatic concentrations in pharmacokinetics studies and in therapeutic drug monitoring

β-Adrenoceptor Activation in Breast MCF-10A Cells Induces a Pattern of Catecholamine Production Similar to that of Tumorigenic MCF-7 Cells

Adrenaline, which participates in the neuroendocrine response that occurs during stress and perimenopause, may be tumorigenic. This exploratory study aimed at investigating whether non-tumorigenic and tumorigenic human breast epithelial cell lines are able to synthesize adrenaline. The study was carried out in non-tumorigenic (MCF-10A) and tumorigenic (MCF-7) human breast cell lines. Expression of enzymes involved in adrenaline synthesis was characterized by RT-qPCR, immunocytochemistry and western blot. Catecholamines and analogue compounds were quantified by HPLC-ECD. Functional assessment of the impact of drugs on cells' tumorigenic potential was assessed by determination of cell viability and clonogenic ability. Both MCF-10A and MCF-7 cells produce catecholamines, but the capacity to produce adrenaline is lower in MCF-10A cells. β-adrenoceptor activation increases the capacity of MCF-10A cells to produce adrenaline and favor both cell viability and colony formation. It is concluded that exposure of human breast epithelial cells to β-adrenoceptor agonists increases cell proliferation and the capacity to produce adrenaline, creating an autocrine potential to spread these adrenergic effects in a feed-forward loop. It is conceivable that these effects are related to tumorigenesis, bringing a new perspective to understand the claimed anticancer effects of propranolol and the increase in breast cancer incidence caused by stress or during perimenopause.info:eu-repo/semantics/publishedVersio

Endoperiodontal lesions: diagnosis first, then treatment and not always tooth extraction: a cross-sectional survey in Spain and a proposal of a clinical treatment protocol

Background: Endoperiodontal lesion (EPL) is defined as a pathological communication between pulpal and periodontal tissues. Currently, accurate diagnosis and treatment of this pathology are challenging. This study aims to identify the different endoperiodontal therapies to propose a clinical protocol to simplify and unify the criteria for EPL treatment. Material and Methods: Observational cross-sectional study through an electronic survey. This study matches STROBE guidelines. The anonymous questionnaire contained open-ended and close-ended questions and was distributed to dentistry professors of the UPV/EHU and different professionals from Spanish associations and scientific societies. The data collected were analyzed using descriptive and analytical statistics. Results: A total of 128 responses were obtained, of which 120 were active professionals or had not been so for less than 5 years. The majority of professionals were women (65.6%) and from the Basque Country (63.9%). A total of 86.6% reported having complementary studies to a degree or a bachelor’s degree. The treatments performed by these professionals were similar to those reported in the literature, which started with root canal treatment when there was an endodontic origin (91.5%), and with basic periodontal treatment when periodontal (51.3%). Conclusions: Considering the current scientific evidence and the clinical practice of professionals in the treatment of EPL, we designed a clinical protocol. This protocol needs validation in larger populations and with longer follow-ups

Brain stem adenosine receptors modulate centrally mediated hypotensive responses in conscious rats: A review

Abbreviations: A2A, adenosine subtype A2A receptor; A1, adenosine subtype A1 receptor; ABC, avidin biotin complex; ABD rat, aortic barodenervated rat; α2 AR, alpha 2 adrenergic receptor; αMNE, alpha methyl norepinephrine; ATP, adenosine triphosphate; BP, blood pressure; cAMP, cyclic adenosine monophosphate; CGS21680, 2-[4-[(2-carboxyethyl)phenyl]ethylaminophenyl]ethylamino]-5′-N-ethylcarboxamidoadenosine. Selective A2A receptor agonist; CNS, central nervous system; CPA, N6-cyclopentyladenosine. Selective A1 receptor agonist; DAG, diacylglycerol; DPCPX, 8-cyclopentyl-1,3-dipropylxanthine. Selective A1 receptor antagonist; I1, imidazoline subtype 1 receptor; I.C., intracisternal; IP3, Inositol Triphosphate; I.V., intravenous; JNK, C-Jun N-terminal kinase; L-NAME, Nω-nitro-l-arginine methyl ester hydrochloride. Non-selective nitric oxide synthase inhibitor; NOS, nitric oxide synthase; NO, nitric oxide; NTS, nucleus tractus solitarius; PC-PLC, phosphatidyl choline-selective phospholipase C; PC12 cells, pheochromocytoma cells; PD98059, selective extracellular signal regulated kinase inhibitor; ERK1/2, extracellular signal regulated kinase; PDE, phosphodiesterase; PKA, protein kinase A; RVLM, rostral ventrolateral medulla; SAPK, stress activated protein kinase; SCH58261, 5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-∈]-1,2,4-triazolo[1,5-c]pyrimidine. Selective adenosine A2A antagonist; SHR, spontaneously hypertensive rat; SND, sympathetic neuronal discharge; SO, sham operated = conscious normotensive rats; 8-SPT, 8-(p-sulfophenyl)-theophylline. Non-selective adenosine receptor blocker; WKY, Wistar Kyoto ra

Medication Adherence Measures: An Overview

WHO reported that adherence among patients with chronic diseases averages only 50% in developed countries. This is recognized as a significant public health issue, since medication nonadherence leads to poor health outcomes and increased healthcare costs. Improving medication adherence is, therefore, crucial and revealed on many studies, suggesting interventions can improve medication adherence. One significant aspect of the strategies to improve medication adherence is to understand its magnitude. However, there is a lack of general guidance for researchers and healthcare professionals to choose the appropriate tools that can explore the extent of medication adherence and the reasons behind this problem in order to orchestrate subsequent interventions. This paper reviews both subjective and objective medication adherence measures, including direct measures, those involving secondary database analysis, electronic medication packaging (EMP) devices, pill count, and clinician assessments and self-report. Subjective measures generally provide explanations for patient’s nonadherence whereas objective measures contribute to a more precise record of patient’s medication-taking behavior. While choosing a suitable approach, researchers and healthcare professionals should balance the reliability and practicality, especially cost effectiveness, for their purpose. Meanwhile, because a perfect measure does not exist, a multimeasure approach seems to be the best solution currently

Medication Adherence Measures: An Overview

WHO reported that adherence among patients with chronic diseases averages only 50% in developed countries. This is recognized as a significant public health issue, since medication nonadherence leads to poor health outcomes and increased healthcare costs. Improving medication adherence is, therefore, crucial and revealed on many studies, suggesting interventions can improve medication adherence. One significant aspect of the strategies to improve medication adherence is to understand its magnitude. However, there is a lack of general guidance for researchers and healthcare professionals to choose the appropriate tools that can explore the extent of medication adherence and the reasons behind this problem in order to orchestrate subsequent interventions. This paper reviews both subjective and objective medication adherence measures, including direct measures, those involving secondary database analysis, electronic medication packaging (EMP) devices, pill count, and clinician assessments and self-report. Subjective measures generally provide explanations for patient's nonadherence whereas objective measures contribute to a more precise record of patient's medication-taking behavior. While choosing a suitable approach, researchers and healthcare professionals should balance the reliability and practicality, especially cost effectiveness, for their purpose. Meanwhile, because a perfect measure does not exist, a multimeasure approach seems to be the best solution currently

The role of ascorbate in the activation of chromium(V) to its ultimate carcinogenic form

Chromium(V) compounds are established human carcinogens. It is now well accepted that chromium(V) is activated by a number of intracellular reducing agents to its ultimate carcinogenic form. However, despite intensive research efforts during the last ten years, both the nature of the ultimate DNA damaging species and the relative contribution of the various possible reductive pathways for the activation of chromium(V) remain obscure. Prompted by recent reports on the role of ascorbate as an important reductant of chromium(V) in vivo this study has investigated the potential of ascorbate to activate chromium(V) to DNA damaging species. Single-strand breaks (SSB) and apurinic/apyrimidinic sites (AP-sites) were readily observed in isolated DNA of the bacteriophage PM2 which was treated with chromate in the presence of ascorbate levels similar to those observed in mammalian cells. The number of both SSB and AP-sites rose with increasing concentrations of chromate. An as yet unidentified intermediate formed during the reduction of chromate by ascorbate was found to be responsible for the DNA damage. Molecular oxygen was essential for the process leading to SSB and AP-sites. Both these lesions occurred with equal probability and their formation followed a very similar time course. Attempts were made to probe the nature of the DNA damaging species arising from chromate/ascorbate. Modified DNA bases resulting from attack by hydroxyl radicals were not observed using Gas Chromatography-Mass Spectrometry in selective ion monitoring mode, ruling out hydroxyl radicals as the species causing SSB and AP-sites. Finally, the potential of the DNA lesions formed by chromium(V)/ascorbate to cause mutations was assessed. Treatment of plasmid DNA (pUC19) with chromate and ascorbate gave rise to elevated mutation frequencies in the lacZ' gene, detected after transformation of E. coli TG1, indicating that the reductive conversion of chromium(V) by ascorbate may be an important pathway in the causation of mutations

Trials, tricks and transparency: how disclosure rules affect clinical knowledge

Scandals of selective reporting of clinical trial results by pharmaceutical firms have underlined the need for more transparency in clinical trials. We provide a theoretical framework which reproduces incentives for selective reporting and yields three key implications concerning regulation. First, a compulsory clinical trial registry complemented through a voluntary clinical trial results database can implement full transparency (the existence of all trials as well as their results is known). Second, full transparency comes at a price. It has a deterrence effect on the incentives to conduct clinical trials, as it reduces the firms'gains from trials. Third, in principle, a voluntary clinical trial results database without a compulsory registry is a superior regulatory tool; but we provide some qualified support for additional compulsory registries when medical decision-makers cannot anticipate correctly the drug companies' decisions whether to conduct trials. Keywords: pharmaceutical firms, strategic information transmission, clinical trials, registries, results databases, scientific knowledge JEL classification: D72, I18, L1

Activation of β-Adrenoceptors Promotes Lipid Droplet Accumulation in MCF-7 Breast Cancer Cells via cAMP/PKA/EPAC Pathways

Physiologically, β-adrenoceptors are major regulators of lipid metabolism, which may be reflected in alterations in lipid droplet dynamics. β-adrenoceptors have also been shown to participate in breast cancer carcinogenesis. Since lipid droplets may be seen as a hallmark of cancer, the present study aimed to investigate the role of β-adrenoceptors in the regulation of lipid droplet dynamics in MCF-7 breast cancer cells. Cells were treated for up to 72 h with adrenaline (an endogenous adrenoceptor agonist), isoprenaline (a non-selective β-adrenoceptor agonist) and salbutamol (a selective β2-selective agonist), and their effects on lipid droplets were evaluated using Nile Red staining. Adrenaline or isoprenaline, but not salbutamol, caused a lipid-accumulating phenotype in the MCF-7 cells. These effects were significantly reduced by selective β1- and β3-antagonists (10 nM atenolol and 100 nM L-748,337, respectively), indicating a dependence on both β1- and β3-adrenoceptors. These effects were dependent on the cAMP signalling pathway, involving both protein kinase A (PKA) and cAMP-dependent guanine-nucleotide-exchange (EPAC) proteins: treatment with cAMP-elevating agents (forskolin or 8-Br-cAMP) induced lipid droplet accumulation, whereas either 1 µM H-89 or 1 µM ESI-09 (PKA or EPAC inhibitors, respectively) abrogated this effect. Taken together, the present results demonstrate the existence of a β-adrenoceptor-mediated regulation of lipid droplet dynamics in breast cancer cells, likely involving β1- and β3-adrenoceptors, revealing a new mechanism by which adrenergic stimulation may influence cancer cell metabolism