A study of the interrelationship between Byron & Goethe : their promethean side

application/pdfdepartmental bulletin pape

Observation of b→dγ and Determination of |Vtd/Vts|

journal articl

アルコールCVD法による金属化合物内包ならびに“ティー型”カーボンナノチューブの成長

application/pdf三重大学大学院工学研究科博士前期課程分子素材工学専攻78thesi

mexicana

Scutellaria mexicana  (Torr.) A.J. PatonMexican bladdersage,  Papterbag bushSalazaria mexicananear s. entrance to Joshua Tree National MonumentIn gravel wash, side canyo

三池萬田炭坑計画

東京帝国大学工科大学種別:卒業論文thesi

1988年夏江南デルタ小城鎮紀行―科学研究費（国際学術研究）大学間（名古屋大学・南京大学）協力研究「江南デルタの中小都市―市鎮―の社会経済構造に関する歴史学的地理学的研究」第1年度調査の記録―

1990-03-31departmental bulletin pape

Neurons derived from transplanted neural stem cells restore disrupted neuronal circuitry in a mouse model of spinal cord injury

The body's capacity to restore damaged neural networks in the injured CNS is severely limited. Although various treatment regimens can partially alleviate spinal cord injury (SCI), the mechanisms responsible for symptomatic improvement remain elusive. Here, using a mouse model of SCI, we have shown that transplantation of neural stem cells (NSCs) together with administration of valproic acid (VPA), a known antiepileptic and histone deacetylase inhibitor, dramatically enhanced the restoration of hind limb function. VPA treatment promoted the differentiation of transplanted NSCs into neurons rather than glial cells. Transsynaptic anterograde corticospinal tract tracing revealed that transplant-derived neurons reconstructed broken neuronal circuits, and electron microscopic analysis revealed that the transplant-derived neurons both received and sent synaptic connections to endogenous neurons. Ablation of the transplanted cells abolished the recovery of hind limb motor function, confirming that NSC transplantation directly contributed to restored motor function. These findings raise the possibility that epigenetic status in transplanted NSCs can be manipulated to provide effective treatment for SCI.journal articl

A de novo nonsense variant in the DMD gene associated with X‐linked dystrophin‐deficient muscular dystrophy in a cat

Abstract Background X‐linked dystrophin‐deficient muscular dystrophy (MD) is a form of MD caused by variants in the DMD gene. It is a fatal disease characterized by progressive weakness and degeneration of skeletal muscles. Hypothesis/Objectives Identify deleterious genetic variants in DMD by whole‐genome sequencing (WGS) using a next‐generation sequencer. Animals One MD‐affected cat, its parents, and 354 cats from a breeding colony. Methods We compared the WGS data of the affected cat with data available in the National Center for Biotechnology Information database and searched for candidate high‐impact variants by in silico analyses. Next, we confirmed the candidate variants by Sanger sequencing using samples from the parents and cats from the breeding colony. We used 2 genome assemblies, the standard felCat9 (from an Abyssinian cat) and the novel AnAms1.0 (from an American Shorthair cat), to evaluate genome assembly differences. Results We found 2 novel high‐impact variants: a 1‐bp deletion in felCat9 and an identical nonsense variant in felCat9 and AnAms1.0. Whole genome and Sanger sequencing validation showed that the deletion in felCat9 was a false positive because of misassembly. Among the 357 cats, the nonsense variant was only found in the affected cat, which indicated it was a de novo variant. Conclusion and Clinical Importance We identified a de novo variant in the affected cat and next‐generation sequencing‐based genotyping of the whole DMD gene was determined to be necessary for affected cats because the parents of the affected cat did not have the risk variant

Genomic, transcript, and protein characteristics of the genes in silico

<p><b>Copyright information:</b></p><p>Taken from "Integrative characterization of germ cell-specific genes from mouse spermatocyte UniGene library"</p><p>http://www.biomedcentral.com/1471-2164/8/256</p><p>BMC Genomics 2007;8():256-256.</p><p>Published online 28 Jul 2007</p><p>PMCID:PMC1955454.</p><p></p> Gene structure and exon organization were determined using genome database searches. In exon organization, the boxes represent exons. The bars indicate regions amplified in the PCR analysis and used as probes in the Northern blot analysis. Coding regions were determined by selecting the longest open reading frames deduced from cDNA sequences. The predicted coding regions are shaded. The position of the poly A signal is marked by filled arrowheads, and the presence of poly A is indicated by 'A'. Chromosomal location was determined by searching the mouse and human genome databases. The predicted amino acid sequences of genes were analyzed using various bioinformatics tools (see Experimental Procedure). For annotation of genes with ontology terms, amino acid sequences were submitted to and subsequently obtained from exclusive web servers (Goblet), which use a variety of different protein databases and provide gene ontology codes. Each gene ontology code falls into one of the larger categories of molecular function (M), cellular component (C), or biological process (B)

Additional file 1: of A phase 1, first-in-human study of 18F-GP1 positron emission tomography for imaging acute arterial thrombosis

Table S1. Clinical laboratory parameters for safety assessment. Table S2. 18F-GP1 uptake over time. Figure S1. 18F-GP1 PET/CT images of a 76-year-old man with bypass surgery and stent placement. (PDF 499 kb