La autoevaluación basada en criterios como elemento de evaluación en asignaturas de carga cognitiva elevada / Self-assessment based on criteria as an evaluation element in subjects with a high cognitive load

Introducción: La autoevaluación se ha definido como el proceso mediante el cual los alumnos deciden si han alcanzado o no los estándares definidos. La autoevaluación es una herramienta valiosa para identificar debilidades y fortalezas en los estudiantes de Medicina. Objetivo: Comparar los resultados de una prueba de autoevaluación basada en criterios con los resultados de un examen estandarizado para evaluar conocimientos disciplinares en Fisiología. Sujetos y métodos: En este trabajo desarrollamos y aplicamos una herramienta de autoevaluación a estudiantes de segundo año de la carrera de Medicina en la asignatura de Fisiología de la Facultad de Medicina de la Universidad Nacional Autónoma de México. Luego recopilamos comentarios y los dividimos en calificaciones clasificadas como ‘calificaciones altas’ y ‘calificaciones bajas’. Finalmente, comparamos los resultados de la autoevaluación con los de una prueba objetiva (prueba estandarizada) que evalúa los conocimientos disciplinares de fisiología. Resultados: Los alumnos que consideran que han realizado un esfuerzo y trabajo constante durante el curso se valoran mejor que los alumnos que no lo hacen. Por otro lado, encontramos diferencias significativas entre la prueba objetiva y la autoevaluación. Conclusiones: La autoevaluación basada en criterios puede ayudar a evaluar cualidades más allá del conocimiento disciplinario.(AU)

Introduction: Self-assessment has been defined as the process by which students decide whether or not they haveachieved the defined standards. Self-assessment is a valuable tool to identify weaknesses and strengths in medical students. Objective: To compare the results of a self-assessment test based on criteria with the results of a standardized exam to assess disciplinary knowledge in physiology. Subjects and methods. In this work we developed and applied a self-assessment tool to second-year medical students in the physiology course of the Faculty of Medicine of the National Autonomous University of Mexico. We then collected feedback and divided it into ratings categorized as: ‘high scores’ and ‘low scores.’ Finally, we compared the results of the self-assessment with those of an objective test (standardized test) that assesses disciplinary knowledge of physiology. Result: Students who consider that they have made a constant effort and work during the course value themselves better than students who do not. On the other hand, we found significant differences between the objective test and the selfassessment. Conclusions: Criteria-based self-assessment can help assess qualities beyond disciplinary knowledge.(AU)

Neuroprotection of Thioredoxin1 in the Brain.

Thioredoxin1 (Trx1) is a ubiquitous antioxidant protein that regulates the cell's redox status. Trx1's thiol redox activity protects neurons from various physiological processes that cause neuronal damage and neurodegeneration, including oxidative stress, apoptosis, and inflammation. Several studies have found that direct or indirect Trx1 regulation has neuroprotective effects in the brain, protecting against, preventing, or delaying neurodegenerative processes or brain traumas. This review focuses on the term neuroprotection, Trx1 localization, and expression in the brain, as well as its modulation concerning its neuroprotective effect in both animal and clinical models of ischemia, hypoxia, hemorrhage, traumatic brain injury, epilepsy, Alzheimer's disease, and Parkinson's disease.

The effect of thioredoxin-1 in a rat model of traumatic brain injury depending on diurnal variation.

INTRODUCTION: Traumatic brain injury (TBI) is a public health concern with limited treatment options because it causes a cascade of side effects that are the leading cause of hospital death. Thioredoxin is an enzyme with neuroprotective properties such as antioxidant, antiapoptotic, immune response modulator, and neurogenic, among others; it has been considered a therapeutic target for treating many disorders. METHODS: The controlled cortical impact (CCI) model was used to assess the effect of recombinant human thioredoxin 1 (rhTrx1) (1 µg/2 µL, intracortical) on rats subjected to TBI at two different times of the light-dark cycle (01:00 and 13:00 h). We analyzed the food intake, body weight loss, motor coordination, pain perception, and histology in specific hippocampus (CA1, CA2, CA3, and Dental Gyrus) and striatum (caudate-putamen) areas. RESULTS: Body weight loss, reduced food intake, spontaneous pain, motor impairment, and neuronal damage in specific hippocampus and striatum regions are more evident in rats subjected to TBI in the light phase than in the dark phase of the cycle and in groups that did not receive rhTrx1 or minocycline (as positive control). Three days after TBI, there is a recovery in body weight, food intake, motor impairment, and pain, which is more pronounced in the rats subjected to TBI at the dark phase of the cycle and those that received rhTrx1 or minocycline. CONCLUSIONS: Knowing the time of day a TBI occurs in connection to the neuroprotective mechanisms of the immune response in diurnal variation and the usage of the Trx1 protein might have a beneficial therapeutic impact in promoting quick recovery after a TBI.

Activation of dopamine D2 receptors attenuates neuroinflammation and ameliorates the memory impairment induced by rapid eye movement sleep deprivation in a murine model.

The proinflammatory state, which may be induced by sleep deprivation, seems to be a determining factor in the development of neurodegenerative processes. Investigations of mechanisms that help to mitigate the inflammatory effects of sleep disorders are important. A new proposal involves the neurotransmitter dopamine, which may modulate the progression of the immune response by activating receptors expressed on immune cells. This study aimed to determine whether dopamine D2 receptor (D2DR) activation attenuates the proinflammatory response derived from rapid eye movement (REM) sleep deprivation in mice. REM sleep deprivation (RSD) was induced in 2-month-old male CD1 mice using the multiple platform model for three consecutive days; during this period, the D2DR receptor agonist quinpirole (QUIN) was administered (2 mg/kg/day i.p.). Proinflammatory cytokine levels were assessed in serum and homogenates of the brain cortex, hippocampus, and striatum using ELISAs. Long-term memory deficits were identified using the Morris water maze (MWM) and novel object recognition (NOR) tests. Animals were trained until learning criteria were achieved; then, they were subjected to RSD and treated with QUIN for 3 days. Memory evocation was determined afterward. Moreover, we found RSD induced anhedonia, as measured by the sucrose consumption test, which is commonly related to the dopaminergic system. Our data revealed increased levels of proinflammatory cytokines (TNFα and IL-1ß) in both the hippocampus and serum from RSD mice. However, QUIN attenuated the increased levels of these cytokines. Furthermore, RSD caused a long-term memory evocation deficit in both the MWM and NOR tests. In contrast, QUIN coadministration during the RSD period significantly improved the performance of the animals. On the other hand, QUIN prevented the anhedonic condition induced by RSD. Based on our results, D2DR receptor activation protects against memory impairment induced by disturbed REM sleep by inhibiting neuroinflammation.

Cannabinoid receptors are differentially regulated in the pancreatic islets during the early development of metabolic syndrome.

The endocannabinoid system is found in tissues that regulate the glycemia, including adipose tissue, muscle, and pancreatic islets. Diet-induced metabolic syndrome changes the expression of the CB receptors in muscle, adipose tissue, and liver. However, it is poorly understood whether metabolic syndrome (MetS) affects the expression of CB receptors in pancreatic ß cells. We analyzed the expression of CB receptors in pancreatic ß cells under chronic high-sucrose diet (HSD)-induced MetS. Wistar rats fed an HSD as a model of MetS were used to investigate changes in cannabinoid receptors. After 8 weeks of treatment, we evaluated the appearance of the following MetS biomarkers: glucose intolerance, hyperinsulinemia, insulin resistance, hypertriglyceridemia, and an increase in visceral adiposity. To determine the presence of CB1 and CB2 receptors in pancreatic ß cells, immunofluorescence of primary cell cultures and pancreatic sections was performed. For whole-islet quantification of membrane-bound CB1 and CB2 receptors, western-blotting following differential centrifugation was conducted. Our results revealed that an HSD treatment closely mimics the alterations seen in MetS. We observed that in primary cell culture, CB1 and CB2 receptors were expressed at a higher level in pancreatic ß cells compared with non-ß cells. MetS resulted in a reduction of CB1 in the islet, whereas abundant CB2 was observed after the treatment. CB1 and CB2 receptors are differentially expressed in pancreatic ß cells during MetS development.

Diurnal Variation Induces Neurobehavioral and Neuropathological Differences in a Rat Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) induces two types of brain damage: primary and secondary. Damage initiates a series of pathophysiological processes, such as metabolic crisis, excitotoxicity with oxidative stress-induced damage, and neuroinflammation. The long-term perpetuation of these processes has deleterious consequences for neuronal function. However, it remains to be elucidated further whether physiological variation in the brain microenvironment, depending on diurnal variations, influences the damage, and consequently, exerts a neuroprotective effect. Here, we established an experimental rat model of TBI and evaluated the effects of TBI induced at two different time points of the light-dark cycle. Behavioral responses were assessed using a 21-point neurobehavioral scale and the cylinder test. Morphological damage was assessed in different regions of the central nervous system. We found that rats that experienced a TBI during the dark hours had better behavioral performance than those injured during the light hours. Differences in behavioral performance correlated with less morphological damage in the perilesional zone. Moreover, certain brain areas (CA1 and dentate gyrus subregions of the hippocampus) were less prone to damage in rats that experienced a TBI during the dark hours. Our results suggest that diurnal variation is a crucial determinant of TBI outcome, and the hour of the day at which an injury occurs should be considered for future research.

Metabolic Physiological Networks: The Impact of Age.

Metabolic homeostasis emerges from the interplay between several feedback systems that regulate the physiological variables related to energy expenditure and energy availability, maintaining them within a certain range. Although it is well known how each individual physiological system functions, there is little research focused on how the integration and adjustment of multiple systems results in the generation of metabolic health. The aim here was to generate an integrative model of metabolism, seen as a physiological network, and study how it changes across the human lifespan. We used data from a transverse, community-based study of an ethnically and educationally diverse sample of 2572 adults. Each participant answered an extensive questionnaire and underwent anthropometric measurements (height, weight, and waist), fasting blood tests (glucose, HbA1c, basal insulin, cholesterol HDL, LDL, triglycerides, uric acid, urea, and creatinine), along with vital signs (axillar temperature, systolic, and diastolic blood pressure). The sample was divided into 6 groups of increasing age, beginning with less than 25 years and increasing by decades up to more than 65 years. In order to model metabolic homeostasis as a network, we used these 15 physiological variables as nodes and modeled the links between them, either as a continuous association of those variables, or as a dichotomic association of their corresponding pathological states. Weight and overweight emerged as the most influential nodes in both types of networks, while high betweenness parameters, such as triglycerides, uric acid and insulin, were shown to act as gatekeepers between the affected physiological systems. As age increases, the loss of metabolic homeostasis is revealed by changes in the network's topology that reflect changes in the system-wide interactions that, in turn, expose underlying health stages. Hence, specific structural properties of the network, such as weighted transitivity, i.e., the density of triangles in the network, can provide topological indicators of health that assess the whole state of the system. Overall, our findings show the importance of visualizing health as a network of organs and/or systems, and highlight the importance of triglycerides, insulin, uric acid and glucose as key biomarkers in the prevention of the development of metabolic disorders.

The Impact of Education and Age on Metabolic Disorders.

Metabolic disorders, such as obesity, elevated blood pressure, dyslipidemias, insulin resistance, hyperglycemia, and hyperuricemia have all been identified as risk factors for an epidemic of important and widespread chronic-degenerative diseases, such as type 2 diabetes and cardiovascular disease, that constitute some of the world's most important public health challenges. Their increasing prevalence can be associated with an aging population and to lifestyles within an obesogenic environment. Taking educational level as a proxy for lifestyle, and using both logistic and linear regressions, we study the relation between a wide set of metabolic biomarkers, and educational level, body mass index (BMI), age, and sex as correlates, in a population of 1,073 students, academic and non-academic staff at Mexico's largest university (UNAM). Controlling for BMI and sex, we consider educational level and age as complementary measures-degree and duration-of exposure to metabolic insults. Analyzing the role of education across a wide spectrum of educational levels (from primary school to doctoral degree), we show that higher education correlates to significantly better metabolic health when compared to lower levels, and is associated with significantly less risk for waist circumference, systolic blood pressure, glucose, glycosylated hemoglobin, triglycerides, high density lipoprotein and metabolic syndrome (all p < 0.05); but not for diastolic blood pressure, basal insulin, uric acid, low density lipoprotein, and total cholesterol. We classify each biomarker, and corresponding metabolic disorder, by its associated set of statistically significant correlates. Differences among the sets of significant correlates indicate various aetiologies and the need for targeted population-specific interventions. Thus, variables strongly linked to educational level are candidates for lifestyle change interventions. Hence, public policy efforts should be focused on those metabolic biomarkers strongly linked to education, while adopting a different approach for those biomarkers not linked as they may be poor targets for educational campaigns.

Differences in Diurnal Variation of Immune Responses in Microglia and Macrophages: Review and Perspectives.

Biological rhythms, especially those that last close to 24 h, better known as circadian rhythms, are highly regulated phenomena, maintained throughout evolution in various organisms which allow organisms to predict, prepare for, and adapt to environmental changes. One of these phenomena that exhibit biological rhythms is the immune response to external agents. Immune cells (neutrophils, lymphocytes, macrophages, among others), as well as their mediators such as cytokines and chemokines, undergo variations in tissue and blood concentrations during the day. These rhythms are still being elucidated in microglia, the resident macrophages of the central nervous system, but since these cells share a common origin with peripheral macrophages, they are expected to behave similarly. In this review, we will discuss the possible differences in the responses between peripheral macrophages and microglia, their relationship with the circadian clock, and whether these rhythms can influence therapeutic choices.

Correction to: Differences in Diurnal Variation of Immune Responses in Microglia and Macrophages: Review and Perspectives.

The original version of this article unfortunately contained an error in the author group. The given name and family name was interchanged for the two co-authors. The author name should be Anahí Chavarría and Luz Navarro instead it was published incorrectly as Chavarría Anahí and Navarro Luz. The original article has been corrected.

Neuroinflamación: el ying-yang de la neuroinmunología / Neuroinflammation: the ying-yang of neuroimmunology

Resumen El área de la neuroinmunología es un campo que se encuentra en gran desarrollo y que tiene como objetivo el entender las interacciones fisiológicas entre el sistema nervioso central (SNC) y el sistema inmune periférico, llegándose a encontrar que estas relaciones son más importantes de lo que se creía y que por lo tanto son 2 sistemas íntimamente conectados y con una gran dinámica. Por otro lado, la neuroinflamación es activada después de cualquier reto inmunológico, tanto dentro como fuera del SNC, y que puede llevar a generar tanto respuestas enfocadas a la limitación del daño y la restauración del tejido, como a ser un riesgo para el desarrollo de enfermedades neurodegenerativas en el caso de que este estímulo permanezca de manera crónica.

Abstract The field of neuroimmunology has recently had a development, and its primary goal is to understand the physiological interactions between the central nervous system (CNS) and the peripheral immune system. Various data has found that these relations are more important than what was previously thought. Also, that both systems are highly dynamic and are intimately connected. On the other hand, neuroinflammation is activated after any immune challenge, both inside and outside the CNS, leading to responses focused on limiting tissue damage and restoration; as well as being a risk for developing neurodegenerative diseases when this stimulus remains chronic.

Models used in the study of traumatic brain injury.

Traumatic brain injury (TBI) is a contemporary health problem and a leading cause of mortality and morbidity worldwide. Survivors of TBI frequently experience disabling long-term changes in cognition, sensorimotor function, and personality. A crucial step in understanding TBI and providing better treatment has been the use of models to mimic the event under controlled conditions. Here, we describe the known head injury models, which can be classified as whole animal (in vivo), in vitro, and mathematical models. We will also review the ways in which these models have advanced the knowledge of TBI.

Sleep deprivation has a neuroprotective role in a traumatic brain injury of the rat.

During the process of a brain injury, responses to produce damage and cell death are activated, but self-protective responses that attempt to maintain the integrity and functionality of the brain are also activated. We have previously reported that the recovery from a traumatic brain injury (TBI) is better in rats if it occurs during the dark phase of the diurnal cycle when rats are in the waking period. This suggests that wakefulness causes a neuroprotective role in this type of injury. Here we report that 24h of total sleep deprivation after a TBI reduces the morphological damage and enhances the recovery of the rats, as seen on a neurobiological scale.