Publications by authors named "Marin-Garcia J"

Traumatic abdominal wall hernia (TAWH) is a protrusion of contents through a defect in the abdominal wall as a consequence of a blunt injury. The objective of this review was to describe demographic and clinical aspects of this rare pathology, identifying the optimal moment for surgical intervention, evaluating the need to use mesh, and analyzing the effectiveness of surgical treatment. Thus, a systematic review using PubMed, Embase, and Scopus databases was carried out between January 2004 and March 2024.

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COVID-19 pandemic has sent millions of people to hospitals worldwide, exhausting on many occasions the capacity of healthcare systems to provide care patients required to survive. Although several epidemiological research works have contributed a variety of models and approaches to anticipate the pandemic spread, very few have tried to translate the output of these models into hospital service requirements, particularly in terms of bed occupancy, a key question for hospital managers. This paper proposes a tool for predicting the current and future occupancy associated with COVID-19 patients of a hospital to help managers make informed decisions to maximize the availability of hospitalization and intensive care unit (ICU) beds and ensure adequate access to services for confirmed COVID-19 patients.

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Improving the delivery of patient care is an ongoing challenge in the National Health Service (NHS). This challenge is not insignificant in the process of chemotherapy administration for oncology patients. The present research is motivated by a public Spanish hospital in which oncology patients receive medical care in the Oncology Day Hospital (ODH).

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This study examines the relationship between structural and psychological empowerment and its effects on employees' psychological, physical, and social well-being. Despite the quantity of previously published works, empirical evidence about these relationships in the workplace is scarce. We developed a mediation model in which structural empowerment predicts employee well-being via psychological empowerment.

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Lean healthcare aims to manage and improve the processes in the healthcare sector by eliminating everything that adds no value by improving quality of services, ensuring patient safety and facilitating health professionals' work to achieve a flexible and reliable organization. Value Stream Mapping (VSM) is considered the starting point of any lean implementation. Some papers report applications of VSM in healthcare services, but there has been less attention paid to their contribution on sustainability indicators.

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Given the importance that environmental management is acquiring, the main aim of this work is to know what the state of the field kaizen and green practices is at present. A systematic narrative review is conducted in accordance with the PRISMA Statement. Two databases (Web of Science and Scopus) were searched.

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The aim of this paper is to study whether there is a change in the association between employment conditions and European employees' well-being at three different time points (the years 2005, 2010 and 2015), characterized by different socio-economic contexts. We based our study on the European Working Conditions Survey. Logistic regressions were performed by adjusting for gender, age, level of education, seniority, occupation, establishment size, activity sector and economic activity.

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The concept of empowering leadership (EL) has attracted widespread academic and practical interest and different questionnaires have been developed to measure it. However, there are no instruments to measure EL in the Spanish language. This article presents the translation, adaptation, and validation of a scale to measure this construct.

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Objectives: The aim of this study was to assess the agreement and compare the performance of three different instruments in assessing risk of bias (RoB) of comparative cohort studies included in a health psychology meta-analysis.

Study Design And Setting: Three tools were applied to 28 primary studies included in the selected meta-analysis: the Newcastle-Ottawa Scale, quality of cohort studies (Q-Coh), and risk of bias in nonrandomized studies of interventions (ROBINS-I).

Results: Interrater agreement varied greatly from tool to tool.

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Mitochondria play a crucial role in a variety of cellular processes ranging from energy metabolism, generation of reactive oxygen species (ROS) and Ca(2+) handling to stress responses, cell survival and death. Malfunction of the organelle may contribute to the pathogenesis of neuromuscular, cancer, premature aging and cardiovascular diseases (CVD), including myocardial ischemia, cardiomyopathy and heart failure (HF). Mitochondria contain their own genome organized into DNA-protein complexes, called "mitochondrial nucleoids," along with multiprotein machineries, which promote mitochondrial DNA (mtDNA) replication, transcription and repair.

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All multicellular organisms develop during evolution the highly regulated and interconnected pathways of cell death. This complex network contributes to the pathogenesis of various cardiovascular disorders including ischemia/reperfusion injury, myocardial infarction, heart failure, dysrhythmias and atherosclerosis. Chronic cardiac remodeling response and transition to overt HF have been associated with modestly increased apoptosis, although the actual burden of chronic cell loss attributable to apoptosis is not clear.

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The highly regulated processes of mitochondrial fusion (joining), fission (division) and trafficking, collectively called mitochondrial dynamics, determine cell-type specific morphology, intracellular distribution and activity of these critical organelles. Mitochondria are critical for cardiac function, while their structural and functional abnormalities contribute to several common cardiovascular diseases, including heart failure (HF). The tightly balanced mitochondrial fusion and fission determine number, morphology and activity of these multifunctional organelles.

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Mitochondria play a crucial role in a variety of cellular processes ranging from energy metabolism, generation of reactive oxygen species (ROS), and Ca(2+) handling to stress responses, cell survival, and death. Malfunction of the organelle may contribute to the pathogenesis of neuromuscular disorders, cancer, premature aging, and cardiovascular diseases, including myocardial ischemia, cardiomyopathy, and heart failure. Mitochondria are unique as they contain their own genome organized into DNA-protein complexes, so-called mitochondrial nucleoids, along with multiprotein machineries, which promote mitochondrial DNA (mtDNA) replication, transcription, and repair.

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With the impressive advancement in high-throughput 'omics' technologies over the past two decades, epigenetic mechanisms have emerged as the regulatory interface between the genome and environmental factors. These mechanisms include DNA methylation, histone modifications, ATP-dependent chromatin remodeling and RNA-based mechanisms. Their highly interdependent and coordinated action modulates the chromatin structure controlling access of the transcription machinery and thereby regulating expression of target genes.

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Despite significant progress in cardiovascular medicine, myocardial ischemia and infarction, progressing eventually to the final end point heart failure (HF), remain the leading cause of morbidity and mortality in the USA. HF is a complex syndrome that results from any structural or functional impairment in ventricular filling or blood ejection. Ultimately, the heart's inability to supply the body's tissues with enough blood may lead to death.

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Human heart failure (HF) is one of the leading causes of morbidity and mortality worldwide. Currently, heart transplantation and implantation of mechanical devices represent the only available treatments for advanced HF. Two alternative strategies have emerged to treat patients with HF.

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Over the past decade, mitochondria have emerged as critical integrators of energy production, generation of reactive oxygen species (ROS), multiple cell death, and signaling pathways in the constantly beating heart. Clarification of the molecular mechanisms, underlying mitochondrial ROS generation and ROS-induced cell death pathways, associated with cardiovascular diseases, by itself remains an important aim; more recently, mitochondrial dynamics has emerged as an important active mechanism to maintain normal mitochondria number and morphology, both are necessary to preserve cardiomyocytes integrity. The two opposing processes, division (fission) and fusion, determine the cell type-specific mitochondrial morphology, the intracellular distribution and activity.

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Myocardial ischemia results in early and progressive damage to mitochondrial structure and function, but the molecular events leading to these changes have not been clearly established. We hypothesized that mitochondrial dysfunction and a coordinated expression of nuclear and mitochondrial genes occur in a time-dependent manner by relating the time courses of changes in parameters of mitochondrial bioenergetics after ischemia-reperfusion. Using a Langendorff rat heart model, mitochondrial bioenergetics and protein levels were assessed at different times of ischemia and ischemia/reperfusion.

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Ageing reduces the ability of cardiac myocytes to respond to inotropic agents. We hypothesized that hypoxia-inducible factor-1 (HIF-1) would improve the functional and Ca(2+) transient responses of ageing myocytes to the inotropic agents and this would act, in part, through altered mitochondrial activity. Young (3-4 months) and older Fischer 344 rats (18-20 months) were used.

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Mitochondria have been central in the development of some of the most important ideas in modern biology. Since the discovery that mitochondria have its own DNA and specific mutations and deletions were found in association with neuromuscular and heart diseases, as well as in aging, an extraordinary number of publications have followed, and the term mitochondrial medicine was coined. Recently, it has been found that thyroid hormone (TH) stimulates cardiac mitochondrial biogenesis increasing myocardial mitochondrial mass, mitochondrial respiration, oxidative phosphorylation (OXPHOS), enzyme activities, mitochondrial protein synthesis (by stimulation in a T3-dependent manner), cytochrome, phospholipid and mtDNA content.

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Background: Specific myocardial mitochondrial enzymatic dysfunction and apoptotic remodeling occur in pacing-induced heart failure. We sought to define their regional distribution and molecular basis in the failing heart.

Methods And Results: Enzyme dysfunction was assessed in mitochondrial subpopulations and immunoblot analysis was performed using homogenate proteins from the left atria (LA) and left ventricle (LV) of paced and control mongrel dogs.

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Heart disease including myocardial infarction and ischemia is associated with the irreversible loss of cardiomyocytes and vasculature, both via apoptosis or necrosis. However, the native capacity for the renewal and repair of myocardial tissue is inadequate as have been current therapeutic measures to prevent left ventricular remodeling. Cell transplantation has emerged as a potentially viable therapeutic approach to directly repopulate and repair the damaged myocardium.

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