Nivel de motivación en los estudiantes de licenciatura en enfermería. Primer año del nuevo modelo pedagógico. Curso 2006-2007 / Level of Motivation in Nursing Students. First Year of the New Pedagogical Model. Course 2006-2007

La enseñanza de la enfermería en Cuba se inicia antes de 1959. En aquella época se disponía de escasos recursos materiales y humanos, estando los existentes muy mal distribuidos y no eran accesibles a la mayoría de la población. Con el triunfo de la Revolución se crean nuevos programas y se da una mayor prioridad a la formación de recursos humanos en enfermería. Teniendo en cuenta que el trabajo pedagógico tiene entre sus objetivos brindar a los alumnos una adecuada formación y reafirmación vocacional, siendo la educación el proceso de modificación del comportamiento primario, es natural que constituya un punto de partida en la formación de estos profesionales. Por tal motivo en este trabajo pretendemos valorar el nivel de motivación de los estudiantes de primer año de Licenciatura en Enfermería por la carrera, para ello se realizó un estudio retrospectivo y longitudinal seleccionando al azar una muestra de 93 estudiantes de un universo de 156 a los cuales se les aplicó una encuesta. La información fue procesada a través del método porcentual aritmético y fue reflejada en tablas cuyos resultados fueron, la solicitud de la carrera en primera opción por la mayoría de los estudiantes y la expresión de que la solicitaron por vocación, siendo la asignatura Fundamentos de Enfermería lo que ha ayudado a fomentar esta vocación. Palabras clave: MOTIVACIÓN, Estudiantes de Enfermería, Educación Vocacional ABSTRACT Teaching in Nursing in Cuba starts before 1959, and at that time scarce material and human resources were available, these being wrongly distributed and were not accessible to most of the population. With the Triumph of the Revolution new programs are designed and the formation of human resources in Nursing are more prioritized. Considering that the pedagogical work has as one of its objectives providing the students with an appropriate formation and vocational reaffirmation, being education the process of modification and primary behavior, it's natural for it to be starting point in the formation of these professionals. That is why, in this paper we aim at assessing the level of motivation of first-year Nursing students for their major. To that end, a retrospective, longitudinal study was carried out, randomly choosing a 93-student small sample out of the whole sample of 156, who were surveyed. The information was processed through the arithmetic percentage method and tabled whose results were that most students applied for their major as a first choice and stated that they applied for it out of vocation, being the subject of Nursing Guidelines which most helped to encourage this vocation. Key words: Motivation, Nursing Students, Vocational Educatio

Nivel de motivación en los estudiantes de licenciatura en enfermería. Primer año del nuevo modelo pedagógico. Curso 2006-2007 / Level of Motivation in Nursing Students. First Year of the New Pedagogical Model. Course 2006-2007

La enseñanza de la enfermería en Cuba se inicia antes de 1959. En aquella época se disponía de escasos recursos materiales y humanos, estando los existentes muy mal distribuidos y no eran accesibles a la mayoría de la población. Con el triunfo de la Revolución se crean nuevos programas y se da una mayor prioridad a la formación de recursos humanos en enfermería. Teniendo en cuenta que el trabajo pedagógico tiene entre sus objetivos brindar a los alumnos una adecuada formación y reafirmación vocacional, siendo la educación el proceso de modificación del comportamiento primario, es natural que constituya un punto de partida en la formación de estos profesionales. Por tal motivo en este trabajo pretendemos valorar el nivel de motivación de los estudiantes de primer año de Licenciatura en Enfermería por la carrera, para ello se realizó un estudio retrospectivo y longitudinal seleccionando al azar una muestra de 93 estudiantes de un universo de 156 a los cuales se les aplicó una encuesta. La información fue procesada a través del método porcentual aritmético y fue reflejada en tablas cuyos resultados fueron, la solicitud de la carrera en primera opción por la mayoría de los estudiantes y la expresión de que la solicitaron por vocación, siendo la asignatura Fundamentos de Enfermería lo que ha ayudado a fomentar esta vocación. Palabras clave: MOTIVACIÓN, Estudiantes de Enfermería, Educación Vocacional ABSTRACT Teaching in Nursing in Cuba starts before 1959, and at that time scarce material and human resources were available, these being wrongly distributed and were not accessible to most of the population. With the Triumph of the Revolution new programs are designed and the formation of human resources in Nursing are more prioritized. Considering that the pedagogical work has as one of its objectives providing the students with an appropriate formation and vocational reaffirmation, being education the process of modification and primary behavior, it's natural for it to be starting point in the formation of these professionals. That is why, in this paper we aim at assessing the level of motivation of first-year Nursing students for their major. To that end, a retrospective, longitudinal study was carried out, randomly choosing a 93-student small sample out of the whole sample of 156, who were surveyed. The information was processed through the arithmetic percentage method and tabled whose results were that most students applied for their major as a first choice and stated that they applied for it out of vocation, being the subject of Nursing Guidelines which most helped to encourage this vocation. Key words: Motivation, Nursing Students, Vocational Educatio

Breakdown of Mucin as Barrier to Digestive Enzymes in the Ischemic Rat Small Intestine

Loss of integrity of the epithelial/mucosal barrier in the small intestine has been associated with different pathologies that originate and/or develop in the gastrointestinal tract. We showed recently that mucin, the main protein in the mucus layer, is disrupted during early periods of intestinal ischemia. This event is accompanied by entry of pancreatic digestive enzymes into the intestinal wall. We hypothesize that the mucin-containing mucus layer is the main barrier preventing digestive enzymes from contacting the epithelium. Mucin breakdown may render the epithelium accessible to pancreatic enzymes, causing its disruption and increased permeability. The objective of this study was to investigate the role of mucin as a protection for epithelial integrity and function. A rat model of 30 min splanchnic arterial occlusion (SAO) was used to study the degradation of two mucin isoforms (mucin 2 and 13) and two epithelial membrane proteins (E-cadherin and toll-like receptor 4, TLR4). In addition, the role of digestive enzymes in mucin breakdown was assessed in this model by luminal inhibition with acarbose, tranexamic acid, or nafamostat mesilate. Furthermore, the protective effect of the mucin layer against trypsin-mediated disruption of the intestinal epithelium was studied in vitro. Rats after SAO showed degradation of mucin 2 and fragmentation of mucin 13, which was not prevented by protease inhibition. Mucin breakdown was accompanied by increased intestinal permeability to FITC-dextran as well as degradation of E-cadherin and TLR4. Addition of mucin to intestinal epithelial cells in vitro protected against trypsin-mediated degradation of E-cadherin and TLR4 and reduced permeability of FITC-dextran across the monolayer. These results indicate that mucin plays an important role in the preservation of the mucosal barrier and that ischemia but not digestive enzymes disturbs mucin integrity, while digestive enzymes actively mediate epithelial cell disruption

A Critical Tryptophan and Ca2+ in Activation and Catalysis of TPPI, the Enzyme Deficient in Classic Late-Infantile Neuronal Ceroid Lipofuscinosis

Tripeptidyl aminopeptidase I (TPPI) is a crucial lysosomal enzyme that is deficient in the fatal neurodegenerative disorder called classic late-infantile neuronal ceroid lipofuscinosis (LINCL). It is involved in the catabolism of proteins in the lysosomes. Recent X-ray crystallographic studies have provided insights into the structural/functional aspects of TPPI catalysis, and indicated presence of an octahedrally coordinated Ca(2+).Purified precursor and mature TPPI were used to study inhibition by NBS and EDTA using biochemical and immunological approaches. Site-directed mutagenesis with confocal imaging technique identified a critical W residue in TPPI activity, and the processing of precursor into mature enzyme.NBS is a potent inhibitor of the purified TPPI. In mammalian TPPI, W542 is critical for tripeptidyl peptidase activity as well as autocatalysis. Transfection studies have indicated that mutants of the TPPI that harbor residues other than W at position 542 have delayed processing, and are retained in the ER rather than transported to lysosomes. EDTA inhibits the autocatalytic processing of the precursor TPPI.We propose that W542 and Ca(2+) are critical for maintaining the proper tertiary structure of the precursor proprotein as well as the mature TPPI. Additionally, Ca(2+) is necessary for the autocatalytic processing of the precursor protein into the mature TPPI. We have identified NBS as a potent TPPI inhibitor, which led in delineating a critical role for W542 residue. Studies with such compounds will prove valuable in identifying the critical residues in the TPPI catalysis and its structure-function analysis

AMPA Receptor Surface Expression Is Regulated by S-Nitrosylation of Thorase and Transnitrosylation of NSF

Umanah et al. show that the S-nitrosylation of Thorase and the transnitrosylation of NSF are responsible for NMDAR-activated trafficking of AMPARs underlying synaptic plasticity. © 2020 The Author(s) The regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) trafficking affects multiple brain functions, such as learning and memory. We have previously shown that Thorase plays an important role in the internalization of AMPARs from the synaptic membrane. Here, we show that N-methyl-D-aspartate receptor (NMDAR) activation leads to increased S-nitrosylation of Thorase and N-ethylmaleimide-sensitive factor (NSF). S-nitrosylation of Thorase stabilizes Thorase-AMPAR complexes and enhances the internalization of AMPAR and interaction with protein-interacting C kinase 1 (PICK1). S-nitrosylated NSF is dependent on the S-nitrosylation of Thorase via trans-nitrosylation, which modulates the surface insertion of AMPARs. In the presence of the S-nitrosylation-deficient C137L Thorase mutant, AMPAR trafficking, long-term potentiation, and long-term depression are impaired. Overall, our data suggest that both S-nitrosylation and interactions of Thorase and NSF/PICK1 are required to modulate AMPAR-mediated synaptic plasticity. This study provides critical information that elucidates the mechanism underlying Thorase and NSF-mediated trafficking of AMPAR complexes. © 2020 The Author(s)1

Pleiotropic Effects of Deubiquitinating Enzyme Ubp5 on Growth and Pathogenesis of Cryptococcus neoformans

Ubiquitination is a reversible protein modification that influences various cellular processes in eukaryotic cells. Deubiquitinating enzymes remove ubiquitin, maintain ubiquitin homeostasis and regulate protein degradation via the ubiquitination pathway. Cryptococcus neoformans is an important basidiomycete pathogen that causes life-threatening meningoencephalitis primarily in the immunocompromised population. In order to understand the possible influence deubiquitinases have on growth and virulence of the model pathogenic yeast Cryptococcus neoformans, we generated deletion mutants of seven putative deubiquitinase genes. Compared to other deubiquitinating enzyme mutants, a ubp5Δ mutant exhibited severely attenuated virulence and many distinct phenotypes, including decreased capsule formation, hypomelanization, defective sporulation, and elevated sensitivity to several external stressors (such as high temperature, oxidative and nitrosative stresses, high salts, and antifungal agents). Ubp5 is likely the major deubiquitinating enzyme for stress responses in C. neoformans, which further delineates the evolutionary divergence of Cryptococcus from the model yeast S. cerevisiae, and provides an important paradigm for understanding the potential role of deubiquitination in virulence by other pathogenic fungi. Other putative deubiquitinase mutants (doa4Δ and ubp13Δ) share some phenotypes with the ubp5Δ mutant, illustrating functional overlap among deubiquitinating enzymes in C. neoformans. Therefore, deubiquitinating enzymes (especially Ubp5) are essential for the virulence composite of C. neoformans and provide an additional yeast survival and propagation advantage in the host

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

The mucosal/epithelial barrier disruption and transport of pancreatic digestive enzymes in early stages of intestinal ischemia

Following reduced blood flow or trauma (e.g. in a car accident, explosion, burn, major surgery) a cascade of reactions leads to Shock and subsequently multi-organ failure (MOF) even if the organs were not affected by the initial trauma. Identifying the root cause of shock is of extraordinary importance and one of the greatest challenges for Bioengineering analysis. Shock is associated with one of the highest levels of mortality and no effective medical treatment exists. We have obtained evidence that pancreatic digestive enzymes are key players and we hypothesize that the intestinal mucosal/epithelial layer provides a physical barrier that prevents the entry of digestive enzymes, normally contained within the lumen of the intestine, and during ischemic states this layer becomes disrupted allowing access of these enzymes into the intestinal wall. The rationale for the proposed study is to provide an enhanced understanding of fundamental mechanisms in the degradation of the mucosal epithelial barrier and subsequent transport of digestive enzymes. In this study I propose to investigate during early stages of intestinal ischemia the transport and activity of digestive enzymes across the epithelial wall and determine changes in the mucosal epithelial barrier. I will investigate mechanisms leading to the disruption of the mucosal barrier using a rat model of splanchnic ischemia as well as non-ischemic models designed to understand whether events characteristic of ischemia, such hypoxia, ATP depletion or drop in pH, are responsible for the disruption of the mucosal/epithelial barrier. Furthermore, I will investigate alterations in intestinal permeability in order to understand the mechanism by which digestive enzymes or any other cytotoxic mediators are transported into the systemic circulation. The results of these studies will determine the role of the mucosal epithelial barrier in the transport of digestive enzymes into the intestinal wall and it will provide insight into the development of new treatments for shoc

The mucosal/epithelial barrier disruption and transport of pancreatic digestive enzymes in early stages of intestinal ischemia

Following reduced blood flow or trauma (e.g. in a car accident, explosion, burn, major surgery) a cascade of reactions leads to Shock and subsequently multi-organ failure (MOF) even if the organs were not affected by the initial trauma. Identifying the root cause of shock is of extraordinary importance and one of the greatest challenges for Bioengineering analysis. Shock is associated with one of the highest levels of mortality and no effective medical treatment exists. We have obtained evidence that pancreatic digestive enzymes are key players and we hypothesize that the intestinal mucosal/epithelial layer provides a physical barrier that prevents the entry of digestive enzymes, normally contained within the lumen of the intestine, and during ischemic states this layer becomes disrupted allowing access of these enzymes into the intestinal wall. The rationale for the proposed study is to provide an enhanced understanding of fundamental mechanisms in the degradation of the mucosal epithelial barrier and subsequent transport of digestive enzymes. In this study I propose to investigate during early stages of intestinal ischemia the transport and activity of digestive enzymes across the epithelial wall and determine changes in the mucosal epithelial barrier. I will investigate mechanisms leading to the disruption of the mucosal barrier using a rat model of splanchnic ischemia as well as non-ischemic models designed to understand whether events characteristic of ischemia, such hypoxia, ATP depletion or drop in pH, are responsible for the disruption of the mucosal/epithelial barrier. Furthermore, I will investigate alterations in intestinal permeability in order to understand the mechanism by which digestive enzymes or any other cytotoxic mediators are transported into the systemic circulation. The results of these studies will determine the role of the mucosal epithelial barrier in the transport of digestive enzymes into the intestinal wall and it will provide insight into the development of new treatments for shoc

The Autodigestion Hypothesis for Shock and Multi-organ Failure

An important medical problem with high mortality is shock, sepsis and multi-organ failure. They have currently no treatments other than alleviation of symptoms. Shock is accompanied by strong markers for inflammation and involves a cascade of events that leads to failure in organs even if they are not involved in the initial insult. Recent evidence indicates that pancreatic digestive enzymes carried in the small intestine after mixing with ingested food are a major cause for multi-organ failure. These concentrated and relatively non-specific enzymes are usually compartmentalized inside the intestinal lumen as requirement for normal digestion. But after breakdown of the mucosal barrier they leak into the wall of the intestine and start an autodigestion process that includes destruction of villi in the intestine. Digestive enzymes also generate cytotoxic mediators, which together are transported into the systemic circulation via the portal venous system, the intestinal lymphatics and via the peritoneum. They cause various degrees of cell and organ dysfunction that can reach the point of complete organ failure. Blockade of digestive enzymes in the lumen of the intestine in experimental forms of shock serves to reduce breakdown of the mucosal barrier and autodigestion of the intestine, organ dysfunctions and mortality