Plataforma Moodle y su influencia en el aprendizaje virtual en los estudiantes de la Facultad de Filosofía, Guayaquil-Ecuador 2020

El trabajo de investigación “Plataforma Moodle y su influencia en el aprendizaje virtual”, se desarrolló con un diseño de tipo correlacional, transaccional cuasi experimental, enmarcado en el positivismo, por su naturaleza tiene enfoque Cuantitativo, que intenta limitar de forma intencional la información, por su finalidad, este tipo de investigación es básica, descriptiva, por su alcance temporal es transversal. El análisis del objetivo general: Determinar la influencia de la plataforma Moodle en el aprendizaje virtual en los estudiantes de la Facultad de Filosofía, Guayaquil – Ecuador 2020; aplicada la encuesta, a los 40 estudiantes de la Facultad de Filosofía, refleja que el 42.9% de los estudiantes poseen un nivel regular en el uso de la plataforma y el 42.1% es bueno en su uso, e indica que el nivel muy bueno es el 31.6% de estudiantes que utilizan bien la plataforma Moodle de acuerdo a la opinión del 31.6%. Con estos resultados se puede indicar que la investigación fue muy provechosa ayudó a valorar la jerarquía de Plataforma Moodle por consiguiente, los resultados consiguieron ser traídos para mejor progreso, permitiendo las trasmisiones de sensibilización que podrá ser utilizados con éxito para trabajos futuros de los estudiantes

Herramientas digitales para promover el trabajo colaborativo en docentes del área técnica de Guayaquil, Ecuador 2023

El objetivo principal de esta investigación es proponer un programa de herramientas digitales para fomentar el trabajo colaborativo entre los docentes del departamento de educación técnica de una institución educativa en Guayaquil, República del Ecuador, en el año 2023. La metodología empleada adopta un enfoque cuantitativo, de tipo básico, diseño no experimental, alcance explicativo y corte transversal. La población objetivo consta de 55 docentes, considerándose a todos los docentes como muestra mediante un muestreo censal. Se utiliza la técnica de encuesta, con el cuestionario como instrumento. Se llevó a cabo una prueba piloto con la participación de 20 personas para medir la confiabilidad de los instrumentos. Los resultados indicaron un coeficiente de 0.946 para la variable independiente y 0.966 para la variable dependiente, demostrando la confiabilidad de los instrumentos. Los resultados obtenidos revelaron una correlación significativa entre las variables con un nivel de significancia inferior a 0.001. En consecuencia, se acepta la hipótesis alterna, sugiriendo el uso de plataformas digitales que permitan la colaboración en tiempo real entre los miembros del equipo, facilitando el intercambio de documentos y comentarios

The autophagy protein ATG16L1 is required for Sindbis virus-induced eIF2α phosphorylation and stress granule formation

Sindbis virus (SINV) infection induces eIF2α phosphorylation, which leads to stress granule (SG) assembly. SINV infection also stimulates autophagy, which has an important role in controlling the innate immune response. The importance of autophagy to virus-induced translation arrest is not well understood. In this study, we show that the autophagy protein ATG16L1 not only regulates eIF2α phosphorylation and the translation of viral and antiviral proteins, but also controls SG assembly. Early in infection (2hpi), capsids were recruited by host factors Cytotoxic Granule-Associated RNA Binding Protein (TIA1), Y-box binding protein 1 (YBX1), and vasolin-containing protein 1 (VCP), to a single perinuclear body, which co-localized with the viral pattern recognition sensors, double stranded RNA-activated protein-kinase R (PKR) and RIG-I. By 6hpi, there was increased eIF2α phosphorylation and viral protein synthesis. However, in cells lacking the autophagy protein ATG16L1, SG assembly was inhibited and capsid remained in numerous small foci in the cytoplasm containing YBX1, TIA1 with RIG-I, and these persisted for over 8hpi. In the absence of ATG16L1, there was little phosphorylation of eIF2α and low levels of viral protein synthesis. Compared to wild type cells, there was potentiated interferon protein and interferon-stimulated gene (ISG) mRNA expression. These results show that ATG16L1 is required for maximum eIF2α phosphorylation, proper SG assembly into a single perinuclear focus, and for attenuating the innate immune response. Therefore, this study shows that, in the case of SINV, ATG16L1 is pro-viral, required for SG assembly and virus replication

The contribution of musculoskeletal disorders in multimorbidity: Implications for practice and policy

People frequently live for many years with multiple chronic conditions (multimorbidity) that impair health outcomes and are expensive to manage. Multimorbidity has been shown to reduce quality of life and increase mortality. People with multimorbidity also rely more heavily on health and care services and have poorer work outcomes. Musculoskeletal disorders (MSDs) are ubiquitous in multimorbidity because of their high prevalence, shared risk factors, and shared pathogenic processes amongst other long-term conditions. Additionally, these conditions significantly contribute to the total impact of multimorbidity, having been shown to reduce quality of life, increase work disability, and increase treatment burden and healthcare costs. For people living with multimorbidity, MSDs could impair the ability to cope and maintain health and independence, leading to precipitous physical and social decline. Recognition, by health professionals, policymakers, non-profit organisations, and research funders, of the impact of musculoskeletal health in multimorbidity is essential when planning support for people living with multimorbidity

Controlling embryonic stem cell proliferation and pluripotency: the role of PI3K-and GSK-3- dependent signalling

Abstract ESCs (embryonic stem cells) are derived from the inner cell mass of pre-implantation embryos and are pluripotent, meaning they can differentiate into all of the cells that make up the adult organism. This property of pluripotency makes ESCs attractive as a model system for studying early development and for the generation of specific cell types for use in regenerative medicine and drug screening. In order to harness their potential, the molecular mechanisms regulating ESC pluripotency, proliferation and differentiation (i.e. cell fate) need to be understood so that pluripotency can be maintained during expansion, while differentiation to specific lineages can be induced accurately when required. The present review focuses on the potential roles that PI3K (phosphoinositide 3-kinase) and GSK-3 (glycogen synthase kinase 3)-dependent signalling play in the co-ordination and integration of mouse ESC pluripotency and proliferation and contrast this with our understanding of their functions in human ESCs. Control of ESC (embryonic stem cell) fate: an overview ESCs are derived from early pre-implantation embryos and, when cultured appropriately, can be maintained in a proliferative, self-renewing and pluripotent state almost indefinitely. Pluripotency is the ability to differentiate into all of the cells found in an adult organism, while self-renewal describes the generation of a daughter stem cell from its mother. In the case of ESCs, self-renewal occurs symmetrically, such that when an undifferentiated ESC divides and pluripotency is maintained, both its progeny will be undifferentiated Over the last 5-10 years, our understanding of the molecular components involved in maintaining pluripotency of mESCs (mouse ESCs) has increased dramatically, from a simple 'prelude' where STAT3 (signal transducer and activator of transcription 3) activation by LIF (leukaemia Key words: cell cycle, embryonic stem cell, glycogen synthase kinase 3 (GSK-3), phosphoinositide 3-kinase (PI3K), pluripotency, proliferation, self-renewal. Abbreviations used: CDK, cyclin-dependent kinase; ESC, embryonic stem cell; Esrrb, oestrogenrelated receptor β; GSK-3, glycogen synthase kinase-3; hESC, human ESC; LIF, leukaemia inhibitory factor; MEK, mitogen-activated protein kinase/extracellular-signal-regulated kinase kinase; mESC, mouse ESC; miRNA, microRNA; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; siRNA, short interfering RNA. 1 To whom correspondence should be addressed (email [email protected]). inhibitory factor) was all that seemed necessary, to a complex 'symphony' where extrinsic factors, intracellular signals, transcription factors, epigenetic regulators and miRNAs (microRNAs) have all been implicated The ESC cell cycle mESCs proliferate rapidly in culture and display unique cell-cycle kinetics, distinct from those of somatic cells, dividing approximately every 11-16 h and exhibiting a shortened G 1 -phase INK4a [13] and neither do mESCs arrest following DNA damag

Case Reports1. A Late Presentation of Loeys-Dietz Syndrome: Beware of TGFβ Receptor Mutations in Benign Joint Hypermobility

Background: Thoracic aortic aneurysms (TAA) and dissections are not uncommon causes of sudden death in young adults. Loeys-Dietz syndrome (LDS) is a rare, recently described, autosomal dominant, connective tissue disease characterized by aggressive arterial aneurysms, resulting from mutations in the transforming growth factor beta (TGFβ) receptor genes TGFBR1 and TGFBR2. Mean age at death is 26.1 years, most often due to aortic dissection. We report an unusually late presentation of LDS, diagnosed following elective surgery in a female with a long history of joint hypermobility. Methods: A 51-year-old Caucasian lady complained of chest pain and headache following a dural leak from spinal anaesthesia for an elective ankle arthroscopy. CT scan and echocardiography demonstrated a dilated aortic root and significant aortic regurgitation. MRA demonstrated aortic tortuosity, an infrarenal aortic aneurysm and aneurysms in the left renal and right internal mammary arteries. She underwent aortic root repair and aortic valve replacement. She had a background of long-standing joint pains secondary to hypermobility, easy bruising, unusual fracture susceptibility and mild bronchiectasis. She had one healthy child age 32, after which she suffered a uterine prolapse. Examination revealed mild Marfanoid features. Uvula, skin and ophthalmological examination was normal. Results: Fibrillin-1 testing for Marfan syndrome (MFS) was negative. Detection of a c.1270G > C (p.Gly424Arg) TGFBR2 mutation confirmed the diagnosis of LDS. Losartan was started for vascular protection. Conclusions: LDS is a severe inherited vasculopathy that usually presents in childhood. It is characterized by aortic root dilatation and ascending aneurysms. There is a higher risk of aortic dissection compared with MFS. Clinical features overlap with MFS and Ehlers Danlos syndrome Type IV, but differentiating dysmorphogenic features include ocular hypertelorism, bifid uvula and cleft palate. Echocardiography and MRA or CT scanning from head to pelvis is recommended to establish the extent of vascular involvement. Management involves early surgical intervention, including early valve-sparing aortic root replacement, genetic counselling and close monitoring in pregnancy. Despite being caused by loss of function mutations in either TGFβ receptor, paradoxical activation of TGFβ signalling is seen, suggesting that TGFβ antagonism may confer disease modifying effects similar to those observed in MFS. TGFβ antagonism can be achieved with angiotensin antagonists, such as Losartan, which is able to delay aortic aneurysm development in preclinical models and in patients with MFS. Our case emphasizes the importance of timely recognition of vasculopathy syndromes in patients with hypermobility and the need for early surgical intervention. It also highlights their heterogeneity and the potential for late presentation. Disclosures: The authors have declared no conflicts of interes

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Stakeholder perceptions of supporting patients' return-to-work in primary care: a qualitative study

BACKGROUND: Over 2.6 million people in the UK are absent from work due to ill-health, yet, for many, accessing work-orientated vocational support to facilitate return-to-work (RTW) is challenging. The majority of fit notes are issued in primary care, making this an ideal setting to provide vocational support. AIM: As part of the Work And Vocational advicE (WAVE) randomised controlled trial (RCT; registry number NCT04543097), we explored the delivery of vocational support by trained Vocational Support Workers (VSWs), from the perspectives of patients, VSWs, employers and general practitioners. DESIGN & SETTING: In the WAVE RCT, patients from 10 UK general practices were randomised to the offer of usual care or usual care plus vocational support. This qualitative study explored stakeholder perspectives of the vocational support intervention. METHOD: Semi-structured interviews with participants in the intervention arm ( n=10), employers, VSWs and GPs ( n=5). Interviews were audio-recorded, transcribed and analysed using thematic analysis. Public and Patient Involvement was embedded throughout. RESULTS: Taking a person-centred, individualised approach to vocational support enabled VSWs to identify and mitigate RTW obstacles and support participants' self-efficacy to proactively negotiate RTW. The perceived independence of the VSWs from employers and healthcare was considered important and facilitated more open discussions about capabilities and RTW planning. CONCLUSION: Findings indicate that individualised and independent vocational support offered to patients referred from primary care was perceived by all stakeholders to be valuable to patients absent from work due to illness and supported their RTW planning. These insights can inform future models of vocational support