WordNet

write by means of a keyboard with types; "type the acceptance letter, please" (同)typewrite
a small metal block bearing a raised character on one end; produces a printed character when inked and pressed on paper; "he dropped a case of type, so they made him pick them up"
(biology) the taxonomic group whose characteristics are used to define the next higher taxon
a subdivision of a particular kind of thing; "what type of sculpture do you prefer?"
all of the tokens of the same symbol; "the word `element contains five different types of character"
printed characters; "small type is hard to read"
identify as belonging to a certain type; "Such people can practically be typed" (同)typecast
an encapsulated neural structure consisting of a collection of cell bodies or neurons
writing done with a typewriter (同)typewriting

PrepTutorEJDIC

〈C〉(…の)『型』,タイプ,類型,種類(kind)《+of+名》 / 〈C〉(その種類の特質を最もよく表している)『典型』,手本,模範《+of+名》 / 〈U〉《集合的に》活字;〈C〉(1個の)活字 / 〈U〉(印刷された)字体,活字 / 〈C〉(貨幣・メダルなどの)模様,図柄 / 〈C〉血液型(blood group) / …‘を'タイプに打つ / (…として)…‘を'分類する《+名+as+名(doing)》 / …‘の'型を決める / タイプライターを打つ
神経節・ガングリオン，結節腫《主に手首にできる良性の嚢腫(のうしゆ)》・〔知的･産業的活動の〕中心，中枢〔of〕

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 手首および手のガングリオン嚢胞 ganglion cysts of the wrist and hand
2. 神経線維腫症I型（NF1）：病因、臨床的特徴、および診断 neurofibromatosis type 1 nf1 pathogenesis clinical features and diagnosis
3. 舞踏病の概要 overview of chorea
4. ペリツェウス・メルツバッハー病 pelizaeus merzbacher disease
5. 遺伝性運動失調の概要 overview of the hereditary ataxias

English Journal

Multiple endocrine neoplasia type 1 (MEN1) and type 4 (MEN4).

Thakker RV.Author information Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford OX3 7LJ, United Kingdom. Electronic address: rajesh.thakker@ndm.ox.ac.uk.AbstractMultiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previously MEN2A) due to mutations of a tyrosine kinase receptor encoded by the rearranged during transfection (RET) protoncogene; MEN3 (previously MEN2B) due to RET mutations; and MEN4 due to cyclin-dependent kinase inhibitor (CDNK1B) mutations. Each MEN type is associated with the occurrence of specific tumors. Thus, MEN1 is characterized by the occurrence of parathyroid, pancreatic islet and anterior pituitary tumors; MEN2 is characterized by the occurrence of medullary thyroid carcinoma (MTC) in association with phaeochromocytoma and parathyroid tumors; MEN3 is characterized by the occurrence of MTC and phaeochromocytoma in association with a marfanoid habitus, mucosal neuromas, medullated corneal fibers and intestinal autonomic ganglion dysfunction, leading to megacolon; and MEN4, which is also referred to as MENX, is characterized by the occurrence of parathyroid and anterior pituitary tumors in possible association with tumors of the adrenals, kidneys, and reproductive organs. This review will focus on the clinical and molecular details of the MEN1 and MEN4 syndromes. The gene causing MEN1 is located on chromosome 11q13, and encodes a 610 amino-acid protein, menin, which has functions in cell division, genome stability, and transcription regulation. Menin, which acts as scaffold protein, may increase or decrease gene expression by epigenetic regulation of gene expression via histone methylation. Thus, menin by forming a subunit of the mixed lineage leukemia (MLL) complexes that trimethylate histone H3 at lysine 4 (H3K4), facilitates activation of transcriptional activity in target genes such as cyclin-dependent kinase (CDK) inhibitors; and by interacting with the suppressor of variegation 3-9 homolog family protein (SUV39H1) to mediate H3K methylation, thereby silencing transcriptional activity of target genes. MEN1-associated tumors harbor germline and somatic mutations, consistent with Knudson's two-hit hypothesis. Genetic diagnosis to identify individuals with germline MEN1 mutations has facilitated appropriate targeting of clinical, biochemical and radiological screening for this high risk group of patients for whom earlier implementation of treatments can then be considered. MEN4 is caused by heterozygous mutations of CDNK1B which encodes the 196 amino-acid CDK1 p27Kip1, which is activated by H3K4 methylation.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Apr 5;386(1-2):2-15. doi: 10.1016/j.mce.2013.08.002. Epub 2013 Aug 8.
Multiple endocrine neoplasia (MEN) is characterized by the occurrence of tumors involving two or more endocrine glands within a single patient. Four major forms of MEN, which are autosomal dominant disorders, are recognized and referred to as: MEN type 1 (MEN1), due to menin mutations; MEN2 (previou
PMID 23933118

Novel role for carbamoyl phosphate synthetase 2 in cranial sensory circuit formation.

Cox JA1, Lamora A2, Johnson SL3, Voigt MM4.Author information 1Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA. Electronic address: coxj@slu.edu.2Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA. Electronic address: angie_lamora@hotmail.com.3Department of Genetics, Washington University of St. Louis, St. Louis, MO 63110, USA. Electronic address: sjohnson@genetics.wustl.edu.4Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 S. Grand Blvd, St. Louis, MO 63104, USA. Electronic address: voigtm@slu.edu.AbstractIn zebrafish, cranial sensory circuits form by 4 days post-fertilization. We used a forward genetic screen to identify genes involved in the formation of these circuits. In one mutant allele, sl23, axons arising from the epibranchial sensory ganglia do not form their stereotypical terminal fields in the hindbrain. These embryos also had small eyes and deformed jaws, suggesting a pleiotropic effect. Using positional cloning, a 20-nucleotide deletion in the carbamoyl-phosphate-synthetase2-aspartate-transcarbamylase-dihydroorotase (cad) gene was found. Injection of a CAD morpholino phenocopied the mutant and mutants were rescued by injection of cad RNA. Cad activity is required for pyrimidine biosynthesis, and thus is a prerequisite for nucleic acid production and UDP-dependent protein glycosylation. Perturbation of nucleic acid biosynthesis can result in cell death. sl23 mutants did not exhibit elevated cell death, or gross morphological changes, in their hindbrains. To determine if defective protein glycosylation was involved in the aberrant targeting of sensory axons, we treated wild type embryos with tunicamycin, which blocks N-linked protein glycosylation. Interference with glycosylation via tunicamycin treatment mimicked the sl23 phenotype. Loss of cad reveals a critical role for protein glycosylation in cranial sensory circuit formation.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience.Int J Dev Neurosci.2014 Apr;33:41-8. doi: 10.1016/j.ijdevneu.2013.11.003. Epub 2013 Nov 23.
In zebrafish, cranial sensory circuits form by 4 days post-fertilization. We used a forward genetic screen to identify genes involved in the formation of these circuits. In one mutant allele, sl23, axons arising from the epibranchial sensory ganglia do not form their stereotypical terminal fields in
PMID 24280100

Japanese Journal

A distinct effect of transient and sustained upregulation of cellular factor XIII in the goldfish retina and optic nerve on optic nerve regeneration

Sugitani Kayo,Ogai Kazuhiro,Hitomi Kiyotaka,Nakamura-Yonehara Kayo,Shintani Takafumi,Noda Masaharu,Koriyama Yoshiki,Tanii Hideji,Matsukawa Toru,Kato Satoru
Neurochemistry International 61(3), 423-432, 2012-08
… Unlike in mammals, fish retinal ganglion cells (RGCs) have a capacity to repair their axons even after optic nerve transection. … In our previous study, we isolated a tissue type transglutaminase (TG) from axotomized goldfish retina. …
NAID 120004754689