Forest structure and the unevenness of seed dispersal by birds

本研究は, 森林構造と鳥類による種子散布の関係を明らかにすることを目的とする. 季節によって鳥類による種子散布が集中する場所が異なり, 秋においては年によっても異なる分布を示した. これらのことから, 季節や年ごとの結実個体の生育分布の違いが鳥散布種子の集中分布に影響していると考えられる. しかし春においては, 結実個体のない場所でも鳥散布種子数が多くなる場所がみられたため, そのような場所では結実個体とは別の要因が鳥類の行動に影響したと考えられる. 1年を通して確認頻度の高かったヒヨドリが種子散布者として最も貢献していると考えられる. 春に採餌が観察されたヒヨドリはほとんどの個体が亜高木層と高木層で観察された. したがって, 春の鳥類の行動は亜高木層や高木層の密度の違いに影響を受けると考えられる. 草本層から高木層の密度と自然落下種子数を説明変数, 鳥散布種子数を目的変数とし, 重回帰分析を行った結果, 春において高木層の密度が高い場所で鳥散布種子数が多くなる正の相関が認められた. これは, 繁殖期の鳥類がソングポストになり得る高木を好むためだと考えられる. 森林の鳥散布種子の分布に最も影響を与える要因は, どの季節においても結実個体の生育場所の違いであり, 鳥類の繁殖期にあたる春においては, 森林構造の違いが鳥類による種子散布の不均一性に影響を与えることが示唆された

Random phase-free kinoform for large objects

We propose a random phase-free kinoform for large objects. When not using the random phase in kinoform calculation, the reconstructed images from the kinoform are heavy degraded, like edge-only preserved images. In addition, the kinoform cannot record an entire object that exceeds the kinoform size because the object light does not widely spread. In order to avoid this degradation and to widely spread the object light, the random phase is applied to the kinoform calculation; however, the reconstructed image is contaminated by speckle noise. In this paper, we overcome this problem by using our random phase-free method and error diffusion method

Evaluation of the Relationship Between Cognitive Impairment, Glycometabolism, and Nicotinic Acetylcholine Receptor Deficits in a Mouse Model of Alzheimer's Disease

PURPOSE: In patients with Alzheimer's disease (AD), the loss of cerebral nicotinic acetylcholine receptors (nAChRs) that are implicated in higher brain functions has been reported. However, it is unclear if nAChR deficits occur in association with cognitive impairments. The purpose of this study was to assess the relationship between nAChR deficits and cognitive impairments in a mouse model of AD (APP/PS2 mice). PROCEDURES: The cognitive abilities of APP/PS2 and wild-type mice (aged 2-16 months) were evaluated using the novel object recognition test. Double-tracer autoradiography analyses with 5-[125I]iodo-A-85380 ([125I]5IA: α4β2 nAChR imaging probe) and 2-deoxy-2-[18F]fluoro-D-glucose were performed in both mice of different ages. [123I]5IA-single-photon emission tomography (SPECT) imaging was also performed in both mice at 12 months of age. Furthermore, each age cohort was investigated for changes in cognitive ability and expression levels of α7 nAChRs and N-methyl-D-aspartate receptors (NMDARs). RESULTS: No significant difference was found between the APP/PS2 and wild-type mice at 2-6 months of age in terms of novel object recognition memory; subsequently, however, APP/PS2 mice showed a clear cognitive deficit at 12 months of age. [125I]5IA accumulation decreased in the brains of 12-month-old APP/PS2 mice, i.e., at the age at which cognitive impairments were first observed; this result was supported by a reduction in the protein levels of α4 nAChRs using Western blotting. nAChR deficits could be noninvasively detected by [123I]5IA-SPECT in vivo. In contrast, no significant changes in glycometabolism, expression levels of α7 nAChRs, or NMDARs were associated with cognitive impairments in APP/PS2 mice. CONCLUSION: A decrease in cerebral α4β2 nAChR density could act as a biomarker reflecting cognitive impairments associated with AD pathology