Megumi ogawa biography for kids
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List of hāfu people
Hāfu (ハーフ, "half") describes an individual who fryst vatten either the child of one Japanese and one non-Japanese parent or, less commonly, two half Japanese parents. Because the begrepp is specific to individuals of ethnic Japanese (Yamato) ancestry, individuals whose Japanese ancestry is not of ethnic Japanese origin, such as Zainichi Koreans (e.g. Crystal Kay Williams and Kiko Mizuhara) will not be listed.[1][2] This list is only for notable Hāfu.
Academics, science, and technology
[edit]- Kusumoto Ine (1827–1903), Japanese physician (German father)[3]
- Edwin McClellan (1925–2009), British Japanologist (British father)[4]
- Marie Morisawa (1919–1994), American geomorphologist (American mother)
- Samaya Nissanke, British astrophysicist (Sri Lankan father)
- Marian Irwin Osterhout (1888–1973), American plant physiologist (American father)[5]
- Charles John "Yoshio" Pedersen (1904–1989), American organic chemist and rec
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Abstract
Purpose
Ablation of short single cones (SSCs) expressing short-wavelength-sensitive opsin (SWS1) fryst vatten well analyzed in the field of regenerative retinal cells. In contrast with ablation studies, the phenomena caused by the complete deletion of SWS1 are less well-understood. To assess the effects of SWS1 deficiency on retinal structure, we established and analyzed sws1-mutant medaka.
Methods
To visualize SWS1, a monoclonal anti-SWS1 antibody and transgenic reporter fish (Tg(sws1:mem-egfp)) were generated. We also developed a CRISPR/Cas-driven sws1-mutant line. Retinal structure of sws1 mutant was visualized using anti-SWS1, 1D4, and ZPR1 antibodies and coumarin derivatives and compared with wild type, Tg(sws1:mem-egfp), and another opsin (lws) mutant.
Results
Our rat monoclonal antibody specifically recognized medaka SWS1. Sws1 mutant retained regularly arranged cone mosaic as lws mutant and its SSCs had neither SWS1 nor long wavelength sensitive op
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Lennart Mucke, MD
Lennart Mucke’s lab focuses on how major neurological and psychiatric conditions cause cognitive deficits, behavioral abnormalities, and other disabling symptoms, with an emphasis on dementias, epilepsy, and autism. The group uses mouse models and brain cell cultures to study disease-causing factors and pathways at molecular, cellular, network, and behavioral levels. Such models are also used to identify and validate novel entry points for therapeutic interventions. The clinical relevance of discoveries made is assessed through collaborative studies of human patients and brain tissues. The most informative experimental models have been used to identify novel strategies to counteract the development of brain dysfunctions and neurological decline.
Disease Areas
Alzheimer’s Disease
Other Dementias
Epilepsy
Autism Spectrum Disorders
Areas of Expertise
Development of Interdisciplinary Research Programs
Identification and Preclinical Assessment of Nov