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BACKGROUND: Air pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially alzheimers disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution. RESULTS: 6 month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract. CONCLUSIONS: In conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve may be another direct invasion route in addition to olfactory nerve.

Although numerous epidemiological studies revealed an association between ambient fine particulate matter (PM2.5) exposure and Alzheimers disease (AD), the PM2.5-induced neuron toxicity and associated mechanisms were not fully elucidated. The present study assessed brain toxicity in 6-month-old female triple-transgenic AD (3xTg-AD) mice following subchronic exposure to PM2.5 via an inhalation system. The treated mice were whole-bodily and continuously exposed to real-world PM2.5 for 3 months, while the control mice inhaled filtered air. Changes in cognitive and motor functions were evaluated using the Morris Water Maze and rotarod tests. Magnetic resonance imaging analysis was used to record gross brain volume alterations, and tissue staining with hematoxylin and eosin, Nissl, and immunohistochemistry methods were used to monitor pathological changes in microstructures after PM2.5 exposure. The levels of AD-related hallmarks and the oxidative stress biomarker malondialdehyde (MDA) were assessed using Western blot analysis and liquid chromatography-mass spectrometry, respectively. Our results showed that subchronic exposure to environmental levels of PM2.5 induced obvious neuronal loss in the cortex of exposed mice, but without significant impairment of cognitive and motor function. Increased levels of phosphorylated-tau and MDA were also observed in olfactory bulb or hippocampus after PM2.5 exposure, but no amyloid pathology was detected, as reported in previous studies. These results revealed that a relatively lower level of PM2.5 subchronic exposure from the environmental atmosphere still induced certain neurodegenerative changes in the brains of AD mice, especially in the olfactory bulb, entorhinal cortex and hippocampus, which is consistent with the nasal entry and spreading route for PM exposure. Systemic factors may also contribute to the neuronal toxicity. The effects of PM2.5 after a more prolonged exposure period are needed to establish a more comprehensive picture of the PM2.5-mediated development of AD.

Reform efforts in Taiwan have added a mandatory 'Scientific Inquiry and Practice' curriculum for all high school students, emphasising 'inquiry-based learning content' including observing and questioning, planning and carrying out an investigation, argumentation and modelling, and expression and sharing. The purpose of this study was to develop an inquiry-based laboratory curriculum and to explore students' performance by emphasising 'expression and sharing' during the planning of their investigations and argumentation. This 'Scientific Inquiry and Practice' curriculum lasted 60 h with 17 10th graders. We employed Science Writing Heuristics to help students integrate inquiry, argumentation, and writing practice into laboratory contexts. Data collected via a Multimedia-based Assessment of Scientific Inquiry Abilities, an Achievement Test, students' writing in their Argumentation Writing Journal, and semi-structured interviews showed that some of the students' scientific inquiry abilities, argumentation abilities, and content learning were improved after participating. Moreover, engaging students in the practice of 'expression and sharing' provided them with opportunities to develop competency in designing and evaluating the scientific inquiry, and scientifically interpreting data and evidence. Various interpretations of these results are discussed, and the implications of this study can provide a template for the development of an inquiry-based laboratory curriculum in education and research.

The central dogma of biology is difficult to learn because its microscopic processes cannot be visualized. This study aimed to devise two inquiry activities: 'Button Code' and 'Beaded Bracelet Making,' involving the concepts of DNA replication and protein synthesis based on the Metacognitive Learning Cycle (MLC) for students, and to explore the effectiveness of concept learning of the central dogma, how students' metacognition may be expressed, and students' perceptions of their inquiry performance. We developed a 'Concept journal' including metacognitive scaffolds, and employed the 'Central Dogma Achievement Test' as a tool for the above purpose. A total of 18 junior high school students participated in this inquiry course instructed by two of the authors. The results showed that students' achievement performance was significantly improved on the whole, the students' metacognition was expressed during the process of inquiry with scaffolding, and most students gave positive responses about their learning performance. According to the results, this inquiry course could develop students' comprehension of the central dogma concept, and give students opportunities to practice metacognition that might lead to effective learning in inquiry activities. The implications and expandability of this course are discussed.

Although numerous epidemiological studies revealed an association between ambient fine particulate matter (PM2.5) exposure and Alzheimer's disease (AD), the PM2.5-induced neuron toxicity and associated mechanisms were not fully elucidated. The present study assessed brain toxicity in 6-month-old female triple-transgenic AD (3xTg-AD) mice following subchronic exposure to PM2.5 via an inhalation system. The treated mice were whole-bodily and continuously exposed to real-world PM2.5 for 3 months, while the control mice inhaled filtered air. Changes in cognitive and motor functions were evaluated using the Morris Water Maze and rotarod tests. Magnetic resonance imaging analysis was used to record gross brain volume alterations, and tissue staining with hematoxylin and eosin, Nissl, and immunohistochemistry methods were used to monitor pathological changes in microstructures after PM2.5 exposure. The levels of AD-related hallmarks and the oxidative stress biomarker malondialdehyde (MDA) were assessed using Western blot analysis and liquid chromatography-mass spectrometry, respectively. Our results showed that subchronic exposure to environmental levels of PM2.5 induced obvious neuronal loss in the cortex of exposed mice, but without significant impairment of cognitive and motor function. Increased levels of phosphorylated-tau and MDA were also observed in olfactory bulb or hippocampus after PM2.5 exposure, but no amyloid pathology was detected, as reported in previous studies. These results revealed that a relatively lower level of PM2.5 subchronic exposure from the environmental atmosphere still induced certain neurodegenerative changes in the brains of AD mice, especially in the olfactory bulb, entorhinal cortex and hippocampus, which is consistent with the nasal entry and spreading route for PM exposure. Systemic factors may also contribute to the neuronal toxicity. The effects of PM2.5 after a more prolonged exposure period are needed to establish a more comprehensive picture of the PM2.5-mediated development of AD. [ABSTRACT FROM AUTHOR]

The central dogma of biology is difficult to learn because its microscopic processes cannot be visualized. This study aimed to devise two inquiry activities: 'Button Code' and 'Beaded Bracelet Making,' involving the concepts of DNA replication and protein synthesis based on the Metacognitive Learning Cycle (MLC) for students, and to explore the effectiveness of concept learning of the central dogma, how students' metacognition may be expressed, and students' perceptions of their inquiry performance. We developed a 'Concept journal' including metacognitive scaffolds, and employed the 'Central Dogma Achievement Test' as a tool for the above purpose. A total of 18 junior high school students participated in this inquiry course instructed by two of the authors. The results showed that students' achievement performance was significantly improved on the whole, the students' metacognition was expressed during the process of inquiry with scaffolding, and most students gave positive responses about their learning performance. According to the results, this inquiry course could develop students' comprehension of the central dogma concept, and give students opportunities to practice metacognition that might lead to effective learning in inquiry activities. The implications and expandability of this course are discussed. [ABSTRACT FROM AUTHOR]

Zinc oxide (ZnO) particles induce acute occupational inhalation illness in humans and rats. However, the possible molecular mechanisms of ZnO particles on the respiratory system remain unclear. In this study, metabolic responses of the respiratory system of rats inhaled ZnO particles were investigated by a nuclear magnetic resonance (NMR)-based metabolomic approach. Male Sprague-Dawley rats were treated with a series of doses of nano-sized (35 nm) or fine-sized (250 nm) ZnO particles. The corresponding control groups inhaled filtered air. After 24 h, bronchoalveolar lavage fluid (BALF) and lung tissues were collected, extracted and prepared for 1H and J-resolved NMR analysis, followed by principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA). PCA and PLSDA models from analysis of BALF and hydrophilic lung NMR spectra demonstrated that dose response trends were restricted to the 250nm ZnO particle exposure group and were not observed in the 35nm ZnO particle exposure group. Increased isoleucine and valine, as well as decreased acetate, trimethylamine n-oxide, taurine, glycine, formate, ascorbate and glycerophosphocholine, were recorded in the BALF of rats treated with moderate and high dose 250nm ZnO exposures. Decreases in taurine and glucose, as well as an increase of phosphorylcholine-containing lipids and fatty acyl chains, were detected in the lung tissues from 250nm ZnO-treated rats. These metabolic changes may be associated with cell anti-oxidation, energy metabolism, DNA damage and membrane stability. We also concluded that a metabolic approach provides more complete measurements and suggests potential molecular mechanisms of adverse effects. [ABSTRACT FROM AUTHOR]