29 research outputs found
Introducing E-learning to Lower Level Learners of English: A Preliminary Study
本稿は大学の授業における下位英語学習者へのe-learning 教材導入の有効性及びその効
果的活用方法を検証し考察するものである。E-learning導入後のTOEICスコア変化と自律
学習アンケート結果を、統制群を用いて比較検証した。その結果、distance learning モデ
ルである実験群では、TOEIC スコアに大きな伸びがみられたが、GTEC テストを用いた統
制群では、実験群のような著しい伸びは認められなかった。また、実験群では自律学習の
アンケート結果から「意識要因」のMotivation とIdeal-Self の値が微増していることが分
かった。本研究は学内COE 教育支援経費を受けての予備調査であるものの、教員の適切な
指導と助言があれば、下位英語学習者へのdistance learning モデルにおいて効果的に
e-learning教材が活用出来ることを示唆している
Bilateral Cataract in a Cynomolgus Monkey
Severe bilateral cataract was found in a 7 year-old naïve female cynomolgus monkey
(Macaca fascicularis) 3 months before necropsy. During macroscopic
examination, severe opacity and thinning of the lens were observed in both eyes.
Histopathology revealed that the lens nuclei and majority of cortex lens fibers had
disappeared and become excavated, while the lens fibers in the subcapsular area were
swollen and distorted. Other observations included atrophy and vacuolation in the lens
epithelial cells and proliferation of spindle cells and collagen fiber beneath the
anterior capsule of the right eye. Immunohistochemical staining of these spindle cells
revealed the presence of vimentin, cytokeratin and α-smooth muscle actin (α-SMA), which
were considered to be derived from lens epithelial cells. This is a rare case of
spontaneous, bilateral, hypermature cataract in a cynomolgus monkey
Porencephaly in a Cynomolgus Monkey (Macaca Fascicularis)
Porencephaly was observed in a female cynomolgus monkey (Macaca fascicularis) aged 5 years and 7 months. The cerebral hemisphere exhibited diffuse brownish excavation with partial defects of the full thickness of the hemispheric wall, and it constituted open channels between the lateral ventricular system and arachnoid space. In addition, the bilateral occipital lobe was slightly atrophied. Histopathologically, fibrous gliosis was spread out around the excavation area and its periphery. In the roof tissue over the cavity, small round cells were arranged in the laminae. They seemed to be neural or glial precursor cells because they were positive for Musashi 1 and negative for NeuN and GFAP. In the area of fibrous gliosis, hemosiderin or lipofuscin were deposited in the macrophages, and activated astroglias were observed extensively around the excavation area
Thyroid Hormone Induces PGC-1α during Dendritic Outgrowth in Mouse Cerebellar Purkinje Cells
Thyroid hormone 3,3′,5-Triiodo-L-thyronine (T3) is essential for proper brain development. Perinatal loss of T3 causes severe growth defects in neurons and glia, including strong inhibition of dendrite formation in Purkinje cells in the cerebellar cortex. Here we show that T3 promotes dendritic outgrowth of Purkinje cells through induction of peroxisome proliferator-activated receptor gamma (PPARγ) co-activator 1α (PGC-1α), a master regulator of mitochondrial biogenesis. PGC-1α expression in Purkinje cells is upregulated during dendritic outgrowth in normal mice, while it is significantly retarded in hypothyroid mice or in cultures depleted of T3. In cultured Purkinje cells, PGC-1α knockdown or molecular perturbation of PGC-1α signaling inhibits enhanced dendritic outgrowth and mitochondrial generation and activation caused by T3 treatment. In contrast, PGC-1α overexpression promotes dendrite extension even in the absence of T3. PGC-1α knockdown also downregulates dendrite formation in Purkinje cells in vivo. Our findings suggest that the growth-promoting activity of T3 is partly mediated by PGC-1α signaling in developing Purkinje cells
Thyroid hormone induces PGC-1α during dendritic outgrowth in mouse cerebellar purkinje cells
Thyroid hormone 3, 3′, 5-Triiodo-L-thyronine (T3) is essential for proper brain development. Perinatal loss of T3 causes severe growth defects in neurons and glia, including strong inhibition of dendrite formation in Purkinje cells in the cerebellar cortex. Here we show that T3 promotes dendritic outgrowth of Purkinje cells through induction of peroxisome proliferator-activated receptor gamma (PPARγ) co-activator 1α (PGC-1α), a master regulator of mitochondrial biogenesis. PGC-1α expression in Purkinje cells is upregulated during dendritic outgrowth in normal mice, while it is significantly retarded in hypothyroid mice or in cultures depleted of T3. In cultured Purkinje cells, PGC-1α knockdown or molecular perturbation of PGC-1α signaling inhibits enhanced dendritic outgrowth and mitochondrial generation and activation caused by T3 treatment. In contrast, PGC-1α overexpression promotes dendrite extension even in the absence of T3. PGC-1α knockdown also downregulates dendrite formation in Purkinje cells in vivo. Our findings suggest that the growth-promoting activity of T3 is partly mediated by PGC-1α signaling in developing Purkinje cells