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1 ere depressed with age (PDI and intensity of Nissl staining).
2 P days) 4 and 6 using cytochrome oxidase and Nissl staining.
3 ppaB, protein disulfide isomerase (PDI), and Nissl staining.
4 s determined by MAP2 immunocytochemistry and Nissl staining.
5 e defined by histological markers other than Nissl staining.
6 of neurons in brain sections was examined by Nissl staining.
7 eatments were evaluated using cresyl violet (Nissl) staining.
8 orphology were assessed using Cresyl violet (Nissl) staining.
10 n of a rhesus and 11 cynomolgus monkeys with Nissl staining and immunohistochemistry for neuron-speci
11 rew's brain, we sectioned brains and applied Nissl staining and NeuN (neuronal nuclei) antibody stain
15 ent regions of the ganglion cell layer using Nissl staining and tetramethylrhodamine dextran amine ba
19 ination of Tbr1 and Lmx1a immunolabeling and Nissl staining confirmed the loss of CN neurons from the
23 ranule cell axon reorganization and by using Nissl staining, immunocytochemistry, and the optical fra
24 s of NeuN and DARPP-32 immunoreactivity, and Nissl staining, in the striatum showed no striatal neuro
25 ed SE, bromodeoxyuridine (BrdU) labeling and Nissl staining increased in the rostral forebrain SVZ.
31 DA cells/section by immunohistochemistry and Nissl staining [TH-labeled cells and thionin-stained cel
32 sparrows (Zonotrichia leucophrys gambelii): Nissl staining, the distribution of acetylcholinesterase
33 re removed after perfusion and processed for Nissl staining, the samples were randomized, and the inv
35 n after 6 hours of ischemia, as evaluated by Nissl staining, was significantly less in HSP70tg mice c
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