Physical Activity, Burnout, and Engagement in Latin American Students of Higher Education During the COVID-19 Pandemic.

The coronavirus-disease-2019 (COVID-19) pandemic has had a devastating physical and psychological impact on society, especially on students. In this study, we describe the levels of physical activity (Physical-Activity-Questionnaire-Short-Form (IPAQ-SF)), Burnout (School-Burnout-Inventory for students (SBI-U)) and engagement (Utrecht-Work-Engagement-Scale-9 items (UWES-9S)) in a cohort of Latin American higher education students during the COVID-19 pandemic in 2020. We also determined whether physical activity, Burnout, and engagement are related according to gender and area of study. Self-reported data from 571 Latin American students (64.79% women, 34.15% men; average age 25.24 ± 5.52 years) were collected via an online survey questionnaire. Spearman correlation analyses evaluated the associations between physical activity, Burnout, and engagement. Comparative analyses by gender and field of study were also performed. The results showed no correlation or association in the linear regression between the IPAQ-SF and SBI-U scores or between the IPAQ-SF and the UWES-9S scores. By gender, men had higher IPAQ-SF scores (p < 0.05) and reported higher intensity physical activity than women, but women had higher SBI-U scores (p < 0.05). No difference was found between men and women according to the UWES-9S scores (p = 0.28). There was also no difference in IPAQ-SF scores (p = 0.29) regarding the field of study. Our results suggest that women perform less physical activity than men, which is consistent with higher Burnout. However, physical activity was not associated with Burnout or engagement overall, which indicates that it was insufficient to prevent emotional stress in Latin American higher education students during a pandemic.

Purkinje cell dendritic atrophy induced by prenatal stress is mitigated by early environmental enrichment.

BACKGROUND: Prenatal stress (PS) in experimental animals causes long-lasting changes in Purkinje cell dendritic morphology. Furthermore, these structural changes are associated with an increase in anxiogenic behaviors in the elevated plus maze (EPM) and open-field (OF) test. OBJECTIVES: As environmental enrichment (EE) has significant restorative effects on brain neurons and behavior, the aim of this study was to evaluate if postweaning EE mitigates the decrease in Purkinje cell dendritic expansion and exploratory behavior induced by PS in mice. MATERIALS AND METHODS: Restraint stress was induced from gestational day 14 (G14) to G21. Approximately 50% of the PS animals were submitted to the EE paradigm between postnatal days 22 (P22) and P52. At P52 and P82, male animals were behaviorally evaluated, and then the morphology of the cerebellar vermal Purkinje cells was analyzed. RESULTS: We found that EE significantly ameliorates the Purkinje cell dendritic atrophy and anxiety-like behavior in the EPM. CONCLUSION: Our data show that long-lasting Purkinje cell dendritic impairments and anxiety-like behavior can be mitigated by postweaning EE.

Effects of a single course of prenatal betamethasone on dendritic development in dentate gyrus granular neurons and on spatial memory in rat offspring.

BACKGROUND: Preterm babies treated with synthetic glucocorticoids (sGC) in utero exhibit behavioral alterations and disturbances in brain maturation during infancy. However, the effects on dentate granule cell morphology and spatial memory in rats that were given clinically equivalent doses of antenatal betamethasone remain unclear. METHODS: Pregnant rats were randomly divided into the following two experimental groups: control (CON) and betamethasone-treated (BET) groups. At gestational day 20 (G20), BET dams were subcutaneously injected with a 0.17 mg/kg betamethasone solution, and CON animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CON offsprings were behaviorally evaluated in the Y-Maze test, and the dentate gyrus granular neurons were histologically analyzed. RESULTS: Animals prenatally treated with a single course of betamethasone exhibit a significant decrement in the dendritic outgrowth of dentate granule cells along with impaired spatial memory when evaluated at P52. Moreover, the body and brain weight of the BET group was significantly lower than the CON group at P0, P22, and P52. CONCLUSION: The current results indicate that a single course of betamethasone in pregnant rats produces significant neuronal and behavioral impairments of the offspring at adolescence along with a decrement in somatic and brain weights at each of the three ages evaluated.

Environmental enrichment reverses cerebellar impairments caused by prenatal exposure to a synthetic glucocorticoid.

During prenatal life, exposure to synthetic glucocorticoids (SGCs) can alter normal foetal development, resulting in disease later in life. Previously, we have shown alterations in the dendritic cytoarchitecture of Purkinje cells in adolescent rat progeny prenatally exposed to glucocorticoids. However, the molecular mechanisms underlying these alterations remain unclear. A possible molecular candidate whose deregulation may underlie these changes is the glucocorticoid receptor (GR) and neurotrophin 3/ tropomyosin receptor kinase C, neurotrophic complex (NT-3/TrkC), which specifically modulates the development of the neuronal connections in the cerebellar vermis. To date, no evidence has shown that the cerebellar expression levels of this neurotrophic complex are affected by exposure to a synthetic glucocorticoid in utero. Therefore, the first objective of this investigation was to evaluate the expression of GR, NT-3 and TrkC in the cerebellar vermis using immunohistochemistry and western blot techniques by evaluating the progeny during the postnatal stage equivalent to adolescence (postnatal Day 52). Additionally, we evaluated anxiety-like behaviours in progeny using the elevated plus maze and the marble burying test. In addition, an environmental enrichment (EE) can increase the expression of some neurotrophins and has anxiolytic power. Therefore, we wanted to assess whether an EE reversed the long-term alterations induced by prenatal betamethasone exposure. The major findings of this study were as follows: i) prenatal betamethasone (BET) administration decreases GR, NT-3 and TrkC expression in the cerebellar vermis ii) prenatal BET administration decreases GR expression in the cerebellar hemispheres and iii) enhances the anxiety-like behaviours in the same progeny, and iv) exposure to an EE reverses the reduced expression of GR, NT-3 and TrkC in the cerebellar vermis and v) decreases anxiety-like behaviours. In conclusion, an enriched environment applied 18 days post-weaning was able to restabilize GR, NT-3 and TrkC expression levels and reverse anxious behaviours observed in adolescent rats prenatally exposed to betamethasone.

Environmental enrichment restores the reduced expression of cerebellar synaptophysin and the motor coordination impairment in rats prenatally treated with betamethasone.

Preterm babies treated with synthetic glucocorticoids in utero exhibit behavioural alterations and disturbances in brain maturation during postnatal life. Accordingly, it has been shown in preclinical studies that SGC exposure at a clinical dose alters the presynaptic and postsynaptic structures and results in synaptic impairments. However, the precise mechanism by which SGC exposure impairs synaptic protein expression and its implications are not fully elucidated. Therefore, the purpose of this study was to investigate the effect of prenatal exposure to a clinical dose of betamethasone on the pre- and postsynaptic proteins expression in the developing rat cerebellum and prefrontal cortex, whose synchronized synaptic activity is crucial for motor control and learning. Consequently, the first objective of the present study was to determine whether prenatal betamethasone -equivalent to the clinically used dose- alters cerebellar vermal and cortical expression of synaptophysin, synaptotagmin I, post-synaptic density protein 95 and gephyrin - four important pre- and post-synaptic proteins, respectively- at a relevant adolescent stage. In addition, our second objective was to assess whether prenatal betamethasone administration induced coordination impairment using a rotarod test. On the other hand, it has been shown that the environmental enrichment is capable of improving synaptic transmission and recovering various behavioural impairments. Nevertheless, there is not enough information about the effect of this non-pharmacological preclinical approach on the regulation of this cerebellar and cortical synaptic proteins. Therefore, the third objective of this study was to examine whether environmental enrichment exposure could recover the possible molecular and behavioural impairments in the offspring at the same developmental stage. The principal data showed that adolescent rats prenatally treated with betamethasone exhibited underexpression of synaptophysin in the vermal cerebellum, but not change in levels of synaptotagmin I, post-synaptic density protein 95 and gephyrin. Analysis of the same pre- and post-synaptic proteins no showed differences in the frontal cortex of the same rats. These results were accompanied by an increase in the number of falls in the rotarod test, when the speed of rotation was fixed and when it was in acceleration, which means motor coordination impairments. Importantly, we found that environmental enrichment restores the betamethasone-induced reduction in the cerebellar synaptophysin together with a recover in the motor coordination impairments in prenatally betamethasone-exposed adolescent rats.

Influence of antenatal synthetic glucocorticoid administration on pyramidal cell morphology and microtubule-associated protein type 2 (MAP2) in rat cerebrocortical neurons.

Previous animal studies have indicated that excessive prenatal circulating glucocorticoid (GC) levels induced by the antenatal administration of synthetic GC (sGC) significantly alter neuronal development in the cerebellar and hippocampal neurons of the offspring. However, it is unknown whether antenatal sGC administration results in long-term neocortical pyramidal cell impairment. In the current study, we examined whether an equivalent therapeutic dose of antenatal betamethasone phosphate (BET) in pregnant rats alters the Golgi-stained basilar dendritic length and histochemical expression of dendritic microtubule-associated protein 2 (MAP2) of neocortical pyramidal cells in infant, adolescent, and young adult offspring. The results obtained showed that in utero BET exposure resulted in a significant reduction in the basilar dendritic length per neuron and a transient reduction in histochemical MAP2 immunoreactivity. Consistent with previous hippocampal and cerebellar data, the present findings suggest that prenatal BET administration alters the dendritic growth of cerebrocortical pyramidal cells.

Prenatal glucocorticoid administration persistently increased the immunohistochemical expression of type-1 metabotropic glutamate receptor and Purkinje cell dendritic growth in the cerebellar cortex of the rat.

Several studies have indicated that abnormal prenatal changes in the circulating glucocorticoids (GCs), induced by either maternal stress or exogenous GC administration, significantly alter the development of Purkinje cells (PCs). Among the suggested mechanisms that could mediate this GC-dependent PC susceptibility are changes in the expression of type-1 metabotropic glutamate receptors (mGluR1). In the current study, we analyzed whether a single course of prenatally administered betamethasone phosphate (BET) in pregnant rats increased the immunohistochemical expression of mGluR1 in PCs and decreased PC dendritic growth. The data obtained showed that in utero BET exposure resulted in a significant immunohistochemical overexpression of mGluR1 and a significant reduction in Purkinje cell dendritic outgrowth during postnatal life.

Antenatal betamethasone produces protracted changes in anxiety-like behaviors and in the expression of microtubule-associated protein 2, brain-derived neurotrophic factor and the tyrosine kinase B receptor in the rat cerebellar cortex.

Using classic Golgi staining methods, we previously showed that the administration of synthetic glucocorticoid betamethasone in equivalent doses to those given in cases of human premature birth generates long-term alterations in Purkinje cell dendritic development in the cerebellar cortex. In the present study, we evaluated whether betamethasone alters the immunohistochemical expression of proteins that participate in cerebellar Purkinje cell dendritic development and maintenance, including microtubule-associated protein 2 (MAP2), brain-derived neurotrophic factor (BDNF) and the tyrosine kinase B receptor (TrkB), which are located predominantly in the cerebellar molecular layer where Purkinje cell dendritogenesis occurs. Consistent with our previous Golgi stain studies, we observed that animals prenatally exposed to a single course of betamethasone showed long-term alterations in the expression of MAP2, BDNF and TrkB. Additionally, these protracted molecular changes were accompanied by anxiety-like behaviors in the elevated plus maze and marble burying tests.

Single course of antenatal betamethasone produces delayed changes in morphology and calbindin-D28k expression in a rat's cerebellar Purkinje cells.

In the current study, we analyzed the impact of antenatal betamethasone on macroscopic cerebellar development, Purkinje cell morphology and the expression of the neuroprotective protein calbindin-D28k. Pregnant rats (Sprague-Dawley) were randomly divided into two experimental groups: control (CONT) and betamethasone-treated (BET). At gestational day 20 (G20), BET dams were subcutaneously injected with a solution of 0.17 mg kg⁻¹ of betamethasone, while CONT animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CONT offspring were behaviorally evaluated, and the cerebella were histologically and immunohistochemically processed. Animals that were prenatally treated with a single course of betamethasone exhibited long-lasting behavioral changes consistent with anxiety-like behavior in the open-field test, together with (1) reduced cerebellar weight and volume, (2) Purkinje cell dendritic atrophy, and (3) an overexpression of calbindin-D28k. The current results indicate that an experimental single course of betamethasone in pregnant rats produces long-lasting anxiety-like behaviors, together with macroscopic and microscopic cerebellar alterations.

Stability inside hen eggs of a salmonella enterica serovar enteritidis bacteriophage

Background: Bacteriophages are viruses that infect bacteria and therefore are widespread in nature. Those that lyse the pathogen Salmonella enterica serovar Enteritidis (SE) should be expected in niches in which this bacterium thrives, among others the avian egg. Furthermore, bacteriophages could remain viable in this milieu. Results: Upon artificially infecting hen eggs with the SE bacteriophage f18 we found that the bacteriophage titer remains stable at least for up to 144 hrs post-infection , both in yolk and albumen at 25ºC. Conclusion: Bacteriophage f18 withstands the physico-chemical conditions of the egg inner milieu and could be considered for SE-controlling measures in the poultry industry.