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
a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
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
=sense organ / 受信装置

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. 小児における原発性副腎不全の原因および臨床症状 causes and clinical manifestations of primary adrenal insufficiency in children
2. 副腎不全の稀な原因 unusual causes of adrenal insufficiency
3. 小児における中枢性副腎不全の原因および臨床症状 causes and clinical manifestations of central adrenal insufficiency in children
4. 高身長や異常に急激な成長がみられる小児 the child with tall stature and or abnormally rapid growth
5. 副腎皮質腫瘍の臨床症状および評価 clinical presentation and evaluation of adrenocortical tumors

English Journal

Neural melanocortin receptors in obesity and related metabolic disorders.

Girardet C1, Butler AA2.Author information 1Department of Metabolism and Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, USA.2Department of Metabolism and Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, USA. Electronic address: AButler@Scripps.edu.AbstractObesity is a global health issue, as it is associated with increased risk of developing chronic conditions associated with disorders of metabolism such as type 2 diabetes and cardiovascular disease. A better understanding of how excessive fat accumulation develops and causes diseases of the metabolic syndrome is urgently needed. The hypothalamic melanocortin system is an important point of convergence connecting signals of metabolic status with the neural circuitry that governs appetite and the autonomic and neuroendocrine system controling metabolism. This system has a critical role in the defense of body weight and maintenance of homeostasis. Two neural melanocortin receptors, melanocortin 3 and 4 receptors (MC3R and MC4R), play crucial roles in the regulation of energy balance. Mutations in the MC4R gene are the most common cause of monogenic obesity in humans, and a large literature indicates a role in regulating both energy intake through the control of satiety and energy expenditure. In contrast, MC3Rs have a more subtle role in energy homeostasis. Results from our lab indicate an important role for MC3Rs in synchronizing rhythms in foraging behavior with caloric cues and maintaining metabolic homeostasis during periods of nutrient scarcity. However, while deletion of the Mc3r gene in mice alters nutrient partitioning to favor accumulation of fat mass no obvious role for MC3R haploinsufficiency in human obesity has been reported. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Mar;1842(3):482-94. doi: 10.1016/j.bbadis.2013.05.004. Epub 2013 May 13.
Obesity is a global health issue, as it is associated with increased risk of developing chronic conditions associated with disorders of metabolism such as type 2 diabetes and cardiovascular disease. A better understanding of how excessive fat accumulation develops and causes diseases of the metaboli
PMID 23680515

Identification of tetrapeptides from a mixture based positional scanning library that can restore nM full agonist function of the L106P, I69T, I102S, A219V, C271Y, and C271R human melanocortin-4 polymorphic receptors (hMC4Rs).

Haslach E, Huang H, Dirain ML, Debevec G, Geer P, Santos RG, Giulianotti MA, Pinilla C, Appel JR, Doering SR, Walters MA, Houghten RA, Haskell-Luevano C.AbstractHuman obesity has been linked to genetic factors and single nucleotide polymorphisms (SNPs). Melanocortin-4 receptor (MC4R) SNPs have been associated with up to 6% frequency in morbidly obese children and adults. A potential therapy for individuals possessing such genetic modifications is the identification of molecules that can restore proper receptor signaling and function. These compounds could serve as personalized medications improving quality of life issues as well as alleviating diseases symptoms associated with obesity including type 2 diabetes. Several hMC4 SNP receptors have been pharmacologically characterized in vitro to have a decreased, or a lack of response, to endogenous agonists such as -, -, 2-melanocyte stimulating hormones (MSH) and adrenocorticotropin hormone (ACTH). Herein we report the use of a mixture based positional scanning combinatorial tetrapeptide library to discover molecules with nM full agonist potency and efficacy to the L106P, I69T, I102S, A219V, C271Y, and C271R hMC4Rs. The most potent compounds at all these hMC4R SNPs include Ac-His-(pI)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Tic-(pNO2)DPhe-NH2, Ac-His-(pCl)DPhe-Arg-(pI)Phe-NH2, and Ac-Arg-(pCl)DPhe-Tic-(pNO2)DPhe-NH2, revealing new ligand pharmacophore models for melanocortin receptor drug design strategies.
Journal of medicinal chemistry.J Med Chem.2014 Feb 11. [Epub ahead of print]
Human obesity has been linked to genetic factors and single nucleotide polymorphisms (SNPs). Melanocortin-4 receptor (MC4R) SNPs have been associated with up to 6% frequency in morbidly obese children and adults. A potential therapy for individuals possessing such genetic modifications is the identi
PMID 24517312

Allopregnanolone in the brain: Protecting pregnancy and birth outcomes.

Brunton PJ1, Russell JA2, Hirst JJ3.Author information 1Division of Neurobiology, The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland, UK. Electronic address: p.j.brunton@ed.ac.uk.2Centre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Scotland, UK.3Mothers and Babies Research Centre, School of Biomedical Sciences, University of Newcastle, Newcastle, N.S.W., Australia.AbstractA successful pregnancy requires multiple adaptations in the mother's brain that serve to optimise foetal growth and development, protect the foetus from adverse prenatal programming and prevent premature delivery of the young. Pregnancy hormones induce, organise and maintain many of these adaptations. Steroid hormones play a critical role and of particular importance is the progesterone metabolite and neurosteroid, allopregnanolone. Allopregnanolone is produced in increasing amounts during pregnancy both in the periphery and in the maternal and foetal brain. This review critically examines a role for allopregnanolone in both the maternal and foetal brain during pregnancy and development in protecting pregnancy and birth outcomes, with particular emphasis on its role in relation to stress exposure at this time. Late pregnancy is associated with suppressed stress responses. Thus, we begin by considering what is known about the central mechanisms in the maternal brain, induced by allopregnanolone, that protect the foetus(es) from exposure to harmful levels of maternal glucocorticoids as a result of stress during pregnancy. Next we discuss the central mechanisms that prevent premature secretion of oxytocin and consider a role for allopregnanolone in minimising the risk of preterm birth. Allopregnanolone also plays a key role in the foetal brain, where it promotes development and is neuroprotective. Hence we review the evidence about disruption to neurosteroid production in pregnancy, through prenatal stress or other insults, and the immediate and long-term adverse consequences for the offspring. Finally we address whether progesterone or allopregnanolone treatment can rescue some of these deficits in the offspring.
Progress in neurobiology.Prog Neurobiol.2014 Feb;113:106-36. doi: 10.1016/j.pneurobio.2013.08.005. Epub 2013 Sep 4.
A successful pregnancy requires multiple adaptations in the mother's brain that serve to optimise foetal growth and development, protect the foetus from adverse prenatal programming and prevent premature delivery of the young. Pregnancy hormones induce, organise and maintain many of these adaptation
PMID 24012715