Teachers’ perspectives on optimizing manipulatives in teaching 21st century skills in kindergarten

Kindergarten teachers optimize manipulatives in teaching young children. These manipulatives can be tools in developing essential skills needed to meet the demands of 21st century society. A descriptive mixed method design was employed in this study. Qualitative data were gathered using interviews and classroom observations, while quantitative data were extracted from questionnaire and classroom inventory checklist. Quantitative data were analyzed using descriptive statistics, whereas qualitative data were transcribed, coded, and categorized by themes. Research respondents were the 25 kindergarten teachers from public schools (n=8) and private schools (n=3) in Pulilan, Bulacan. Results showed that teachers use manipulatives in the teaching and learning process as these provide many opportunities for children to learn and acquire different skills. Several manipulatives develop more than one skill, depending on their characteristics and nature. Moreover, skill development varies depending on the activity and type of manipulatives used.  The research finds that manipulatives continue to be relevant and can be used to develop 21st century skills in kindergarten. However, teachers need to undergo training on the optimization of manipulatives that are readily available in the kindergarten classroom. Furthermore, there is a need for schools to invest in different manipulatives for use in kindergarten

Microglial Cells Prevent Hemorrhage in Neonatal Focal Arterial Stroke

Perinatal stroke leads to significant morbidity and long-term neurological and cognitive deficits. The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. To understand whether microglial cells limit injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/ALK5 signaling, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO). Microglial depletion by intracerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage and triggered hemorrhages in injured regions 24 h after tMCAO. Lack of microglia did not alter expression or intracellular redistribution of several tight junction proteins, did not affect degradation of collagen IV induced by the tMCAO, but altered cell types producing TGFβ1 and the phosphorylation and intracellular distribution of SMAD2/3. Selective inhibition of TGFbr2/ALK5 signaling in microglia via intracerebral liposome-encapsulated SB-431542 delivery triggered hemorrhages after tMCAO, demonstrating that TGFβ1/TGFbr2/ALK5 signaling in microglia protects from hemorrhages. Consistent with observations in neonatal rats, depletion of microglia before tMCAO in P9 Cx3cr1(GFP/+)/Ccr2(RFP/+) mice exacerbated injury and induced hemorrhages at 24 h. The effects were independent of infiltration of Ccr2(RFP/+) monocytes into injured regions. Cumulatively, in two species, we show that microglial cells protect neonatal brain from hemorrhage after acute ischemic stroke. SIGNIFICANCE STATEMENT The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. We assessed whether microglial cells preserve neurovascular integrity after neonatal stroke. In neonatal rats, microglial depletion or pharmacological inhibition of TGFbr2/ALK5 signaling in microglia triggered hemorrhages in injured regions. The effect was not associated with additional changes in expression or intracellular redistribution of several tight junction proteins or collagen IV degradation induced by stroke. Consistent with observations in neonatal rats, microglial depletion in neonatal mice exacerbated stroke injury and induced hemorrhages. The effects were independent of infiltration of monocytes into injured regions. Thus, microglia protect neonatal brain from ischemia-induced hemorrhages, and this effect is consistent across two species

Microglial Cells Prevent Hemorrhage in Neonatal Focal Arterial Stroke

Perinatal stroke leads to significant morbidity and long-term neurological and cognitive deficits. The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. To understand whether microglial cells limit injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/ALK5 signaling, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO). Microglial depletion by intracerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage and triggered hemorrhages in injured regions 24 h after tMCAO. Lack of microglia did not alter expression or intracellular redistribution of several tight junction proteins, did not affect degradation of collagen IV induced by the tMCAO, but altered cell types producing TGFβ1 and the phosphorylation and intracellular distribution of SMAD2/3. Selective inhibition of TGFbr2/ALK5 signaling in microglia via intracerebral liposome-encapsulated SB-431542 delivery triggered hemorrhages after tMCAO, demonstrating that TGFβ1/TGFbr2/ALK5 signaling in microglia protects from hemorrhages. Consistent with observations in neonatal rats, depletion of microglia before tMCAO in P9 Cx3cr1(GFP/+)/Ccr2(RFP/+) mice exacerbated injury and induced hemorrhages at 24 h. The effects were independent of infiltration of Ccr2(RFP/+) monocytes into injured regions. Cumulatively, in two species, we show that microglial cells protect neonatal brain from hemorrhage after acute ischemic stroke. SIGNIFICANCE STATEMENT The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. We assessed whether microglial cells preserve neurovascular integrity after neonatal stroke. In neonatal rats, microglial depletion or pharmacological inhibition of TGFbr2/ALK5 signaling in microglia triggered hemorrhages in injured regions. The effect was not associated with additional changes in expression or intracellular redistribution of several tight junction proteins or collagen IV degradation induced by stroke. Consistent with observations in neonatal rats, microglial depletion in neonatal mice exacerbated stroke injury and induced hemorrhages. The effects were independent of infiltration of monocytes into injured regions. Thus, microglia protect neonatal brain from ischemia-induced hemorrhages, and this effect is consistent across two species

Fluoruro en el agua subterránea: niveles, origen y control natural en la región de Tenextepango, Morelos, México

El agua subterránea que consume la población en la región de Tenextepango, Morelos, contiene fluoruro en concentración que varía de 0.5 a 1.9 mg/L, causando problema de fluororis dental a la población. El objetivo de este trabajo es conocer los niveles de fluoruro en el agua subterránea, su distribución y su procedencia en la región de Tenexpenango, Morelos, México. Para esto se elaboró el modelo hidrogeológico soportado con análisis químicos del agua obtenida en 17 pozos y cinco manantiales; el pH, alcalinidad, CE y temperatura del agua se registraron en campo. La concentración de cationes, aniones y elementos traza se determinó por ICP-MS. Los resultados indican que la concentración de fluoruro, y temperatura del agua subterránea, son mayores en los pozos que extraen agua sin interrupción y menor en aquéllos que bombean solo nueve horas-día. La variación de estos parámetros sugiere que los primeros extraen agua de un flujo con mayor profundidad de recorrido con respecto al agua de otros pozos, indicando que el incremento en el tiempo de extracción induce un flujo vertical de agua (ascendente) permitiendo que en tales pozos se descargue un sistema de flujo más profundo, cuyo contenido de fluoruro y valor de temperatura son sensiblemente mayores al resto de los demás pozos. Como conclusión, la fuente del fluoruro al agua subterránea en esta región está en las rocas que conforman del relieve que rodea la planicie y principalmente en aquel ubicado fuera de la planicie hacia el noreste (Sierra Nevada). El fluoruro es liberado al agua subterránea por el proceso del intemperismo químico de rocas ígneas intermedias y félsicas

Fluoruro en el agua subterránea: niveles, origen y control natural en la región de Tenextepango, Morelos, México

El agua subterránea que consume la población en la región de Tenextepango, Morelos, contiene fluoruro en concentración que varía de 0.5 a 1.9 mg/L, causando problema de fluororis dental a la población. El objetivo de este trabajo es conocer los niveles de fluoruro en el agua subterránea, su distribución y su procedencia en la región de Tenexpenango, Morelos, México. Para esto se elaboró el modelo hidrogeológico soportado con análisis químicos del agua obtenida en 17 pozos y cinco manantiales; el pH, alcalinidad, CE y temperatura del agua se registraron en campo. La concentración de cationes, aniones y elementos traza se determinó por ICP-MS. Los resultados indican que la concentración de fluoruro, y temperatura del agua subterránea, son mayores en los pozos que extraen agua sin interrupción y menor en aquéllos que bombean solo nueve horas-día. La variación de estos parámetros sugiere que los primeros extraen agua de un flujo con mayor profundidad de recorrido con respecto al agua de otros pozos, indicando que el incremento en el tiempo de extracción induce un flujo vertical de agua (ascendente) permitiendo que en tales pozos se descargue un sistema de flujo más profundo, cuyo contenido de fluoruro y valor de temperatura son sensiblemente mayores al resto de los demás pozos. Como conclusión, la fuente del fluoruro al agua subterránea en esta región está en las rocas que conforman del relieve que rodea la planicie y principalmente en aquel ubicado fuera de la planicie hacia el noreste (Sierra Nevada). El fluoruro es liberado al agua subterránea por el proceso del intemperismo químico de rocas ígneas intermedias y félsicas

Neonatal Stroke and TLR1/2 Ligand Recruit Myeloid Cells through the Choroid Plexus in a CX3CR1-CCR2- and Context-Specific Manner.

Neonatal stroke is as frequent as stroke in the elderly, but many pathophysiological injury aspects are distinct in neonates, including immune signaling. While myeloid cells can traffic into the brain via multiple routes, the choroid plexus (CP) has been identified as a uniquely educated gate for immune cell traffic during health and disease. To understand the mechanisms of myeloid cell trafficking via the CP and their influence on neonatal stroke, we characterized the phenotypes of CP-infiltrating myeloid cells after transient middle cerebral artery occlusion (tMCAO) in neonatal mice of both sexes in relation to blood-brain barrier permeability, injury, microglial activation, and CX3CR1-CCR2 signaling, focusing on the dynamics early after reperfusion. We demonstrate rapid recruitment of multiple myeloid phenotypes in the CP ipsilateral to the injury, including inflammatory CD45+CD11b+Ly6chighCD86+, beneficial CD45+CD11b+Ly6clowCD206+, and CD45+CD11b+Ly6clowLy6ghigh cells, but only minor leukocyte infiltration into acutely ischemic-reperfused cortex and negligible vascular albumin leakage. We report that CX3CR1-CCR2-mediated myeloid cell recruitment contributes to stroke injury. Considering the complexity of inflammatory cascades triggered by stroke and a role for TLR2 in injury, we also used direct TLR2 stimulation as an independent injury model. TLR2 agonist rapidly recruited myeloid cells to the CP, increased leukocytosis in the CSF and blood, but infiltration into the cortex remained low over time. While the magnitude and the phenotypes of myeloid cells diverged between tMCAO and TLR2 stimulation, in both models, disruption of CX3CR1-CCR2 signaling attenuated both monocyte and neutrophil trafficking to the CP and cortex.SIGNIFICANCE STATEMENT Stroke during the neonatal period leads to long-term disabilities. The mechanisms of ischemic injury and inflammatory response differ greatly between the immature and adult brain. We examined leukocyte trafficking via the choroid plexus (CP) following neonatal stroke in relation to blood-brain barrier integrity, injury, microglial activation, and signaling via CX3CR1 and CCR2 receptors, or following direct TLR2 stimulation. Ischemia-reperfusion triggered marked unilateral CX3CR1-CCR2 dependent accumulation of diverse leukocyte subpopulations in the CP without inducing extravascular albumin leakage or major leukocyte infiltration into the brain. Disrupted CX3CR1-CCR2 signaling was neuroprotective in part by attenuating monocyte and neutrophil trafficking. Understanding the migratory patterns of CP-infiltrating myeloid cells with intact and disrupted CX3CR1-CCR2 signaling could identify novel therapeutic targets to protect the neonatal brain

The Relationship between Rhombomeres and Vestibular Neuron Populations as Assessed in Quail–Chicken Chimeras

AbstractThe aim of this study was to evaluate the role segmentation plays in the determination of neuronal identity in the hindbrain. We focused on two specific sets of hindbrain neurons, namely, the vestibulospinal and vestibulo-ocular neurons, which comprise distinct groups that can be identified and distinguished by virtue of their axonal projection pathways. The relationship between rhombomeres and the vestibular neuron groups was assessed by a combination of quail–chicken chimeric grafting and selective retrograde axonal tracing. Individual quail hemirhombomeres were transplanted homotopically and isochronically into a chicken embryo host. Subsequently, vestibulospinal and vestibulo-ocular neurons with specific axon trajectories were labeled retrogradely with biotin-conjugated dextran-amines. The relationship between the spatial domains of the vestibular neuron groups and rhombomere-derived domains had the following features: (1) some groups were derived from single rhombomeres; (2) some groups were derived from multiple contiguous rhombomeres; (3) two groups occupied domains that could not be defined in terms of whole rhombomere lengths; (4) some groups spanning multiple rhombomeres exhibited an internal cytoarchitectonic organization that related to individual rhombomeres; and (5) some groups exhibited limited boundary violation. These results support the notion that positional information within defined domains of the neural tube provides a groundplan for the regional determination of neuronal identity and axon pathfinding, and that hindbrain segmentation contributes to this process. But they also indicate that segmentation is not the only mechanism that defines the rostrocaudal domains of neuron types. Moreover, they emphasize that the relationship between rhombomeres and neuronal determination cannot be couched simply in terms of segmental iteration or of bimeric (paired rule) specification