WordNet

an immature childish person; "he remained a child in practical matters as long as he lived"; "stop being a baby!" (同)baby
a human offspring (son or daughter) of any age; "they had three children"; "they were able to send their kids to college" (同)kid
a young person of either sex; "she writes books for children"; "theyre just kids"; "`tiddler is a British term for youngster" (同)kid, youngster, minor, shaver, nipper, small_fry, tiddler, tike, tyke, fry, nestling
a member of a clan or tribe; "the children of Israel"
processes and functions of an organism
the branch of the biological sciences dealing with the functioning of organisms
(physiology) the organic process of nourishing or being nourished; the processes by which an organism assimilates food and uses it for growth and maintenance
the scientific study of food and drink (especially in humans)
the 22nd letter of the Greek alphabet (同)khi

PrepTutorEJDIC

(おとなに対して)『子供』,幼児,児童;(小学・中学・高校の)児童 / (親に対して)子,子孫;息子,娘 / (ある環鏡・時代の)影響を受けて生まれた人,(…の)申し子《+『of』+『名』》 / (頭脳・空想などが)産み出したものの,所産《+『of』+『名』》
生理学 / 生理,機能
(生物の)栄養摂取 / 栄養分,食物
キー(ギリシア語アルファベットの第22字X,x;英語のchに相当)

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1. 乳児および小児における経静脈栄養法 parenteral nutrition in infants and children
2. 早産児における経腸栄養に対するアプローチ approach to enteral nutrition in the premature infant
3. 嚢胞性線維症：栄養上の問題 cystic fibrosis nutritional issues
4. 中等症から重症熱傷患者に対する栄養サポートの概要 overview of nutritional support for moderate to severe burn patients
5. 乳児および幼児における経腸栄養 enteral nutrition in infants and children

English Journal

Activation of focal adhesion kinase via M1 muscarinic acetylcholine receptor is required in restitution of intestinal barrier function after epithelial injury.

Khan MR1, Yazawa T2, Anisuzzaman AS3, Semba S2, Ma Y4, Uwada J5, Hayashi H6, Suzuki Y7, Ikeuchi H8, Uchino M8, Maemoto A9, Muramatsu I10, Taniguchi T11.Author information 1Division of Cellular Signal Transduction, Department of Biochemistry, Asahikawa Medical University, Asahikawa, Japan; Department of Pharmacy, University of Rajshahi, Rajshahi, Bangladesh.2Division of Cellular Signal Transduction, Department of Biochemistry, Asahikawa Medical University, Asahikawa, Japan.3Department of Pharmacy, University of Rajshahi, Rajshahi, Bangladesh.4Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, China.5Division of Pharmacology, Department of Biochemistry and Bioinformative Sciences, University of Fukui, Fukui, Japan.6Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka, Japan.7Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka, Japan; Division of Health and Nutrition, Sendai Shirayuri Women's College, Sendai, Japan.8Inflammatory Bowel Disease Center, Hyogo College of Medicine, Nishinomiya, Japan.9Department of Gastrointestinal Immunology and Regenerative Medicine, Asahikawa Medical University, Asahikawa, Japan; Inflammatory Bowel Disease Center, Sapporo Higashi Tokushukai Hospital, Sapporo, Japan.10Division of Pharmacology, Department of Biochemistry and Bioinformative Sciences, University of Fukui, Fukui, Japan; Organization for Life Science Advancement Programs, University of Fukui, Fukui, Japan; Research Center for Child Mental Development, University of Fukui, Fukui, Japan.11Division of Cellular Signal Transduction, Department of Biochemistry, Asahikawa Medical University, Asahikawa, Japan. Electronic address: takotago@asahikawa-med.ac.jp.AbstractImpairment of epithelial barrier is observed in various intestinal disorders including inflammatory bowel diseases (IBD). Numerous factors may cause temporary damage of the intestinal epithelium. A complex network of highly divergent factors regulates healing of the epithelium to prevent inflammatory response. However, the exact repair mechanisms involved in maintaining homeostatic intestinal barrier integrity remain to be clarified. In this study, we demonstrate that activation of M1 muscarinic acetylcholine receptor (mAChR) augments the restitution of epithelial barrier function in T84 cell monolayers after ethanol-induced epithelial injury, via ERK-dependent phosphorylation of focal adhesion kinase (FAK). We have shown that ethanol injury decreased the transepithelial electrical resistance (TER) along with the reduction of ERK and FAK phosphorylation. Carbachol (CCh) increased ERK and FAK phosphorylation with enhanced TER recovery, which was completely blocked by either MT-7 (M1 antagonist) or atropine. The CCh-induced enhancement of TER recovery was also blocked by either U0126 (ERK pathway inhibitor) or PF-228 (FAK inhibitor). Treatment of T84 cell monolayers with interferon-γ (IFN-γ) impaired the barrier function with the reduction of FAK phosphorylation. The CCh-induced ERK and FAK phosphorylation were also attenuated by the IFN-γ treatment. Immunological and binding experiments exhibited a significant reduction of M1 mAChR after IFN-γ treatment. The reduction of M1 mAChR in inflammatory area was also observed in surgical specimens from IBD patients, using immunohistochemical analysis. These findings provide important clues regarding mechanisms by which M1 mAChR participates in the maintenance of intestinal barrier function under not only physiological but also pathological conditions.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Apr;1842(4):635-45. doi: 10.1016/j.bbadis.2013.12.007. Epub 2013 Dec 21.
Impairment of epithelial barrier is observed in various intestinal disorders including inflammatory bowel diseases (IBD). Numerous factors may cause temporary damage of the intestinal epithelium. A complex network of highly divergent factors regulates healing of the epithelium to prevent inflammator
PMID 24365239

Gestational vitamin A deficiency reduces the intestinal immune response by decreasing the number of immune cells in rat offspring.

Liu X1, Li Y1, Wang Y1, Wang Q2, Li X2, Bi Y1, Liu L3, Wei X1, Li T1, Chen J4.Author information 1Children Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, CSTC2009 CA5002, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, P.R. China.2Institute of Pediatrics, Children's Hospital of Chongqing Medical University, Chongqing, P.R. China.3Laboratory of Intestinal Physiology and Pathology, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA.4Children Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, CSTC2009 CA5002, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children's Hospital of Chongqing Medical University, Chongqing, P.R. China. Electronic address: jchen010@gmail.com.AbstractOBJECTIVES: Vitamin A (VA) is a critical micronutrient for life, especially during growth and development. There is a close relationship between VA deficiency (VAD) and the morbidity of diarrhea in the clinical setting. However, the regulatory mechanisms of VA are not clearly understood.
Nutrition (Burbank, Los Angeles County, Calif.).Nutrition.2014 Mar;30(3):350-7. doi: 10.1016/j.nut.2013.09.008. Epub 2013 Dec 27.
OBJECTIVES: Vitamin A (VA) is a critical micronutrient for life, especially during growth and development. There is a close relationship between VA deficiency (VAD) and the morbidity of diarrhea in the clinical setting. However, the regulatory mechanisms of VA are not clearly understood.METHODS: Spe
PMID 24373915

A genome-wide association study of anorexia nervosa.

Boraska V1, Franklin CS2, Floyd JA3, Thornton LM4, Huckins LM2, Southam L2, Rayner NW5, Tachmazidou I2, Klump KL6, Treasure J7, Lewis CM8, Schmidt U7, Tozzi F4, Kiezebrink K9, Hebebrand J10, Gorwood P11, Adan RA12, Kas MJ13, Favaro A14, Santonastaso P14, Fernández-Aranda F15, Gratacos M16, Rybakowski F17, Dmitrzak-Weglarz M18, Kaprio J19, Keski-Rahkonen A20, Raevuori A21, Van Furth EF22, Slof-Op 't Landt MC23, Hudson JI24, Reichborn-Kjennerud T25, Knudsen GP26, Monteleone P27, Kaplan AS28, Karwautz A29, Hakonarson H30, Berrettini WH31, Guo Y32, Li D32, Schork NJ33, Komaki G34, Ando T35, Inoko H36, Esko T37, Fischer K37, Männik K38, Metspalu A39, Baker JH4, Cone RD40, Dackor J41, Desocio JE42, Hilliard CE4, O'Toole JK43, Pantel J44, Szatkiewicz JP41, Taico C4, Zerwas S4, Trace SE4, Davis OS45, Helder S8, Bühren K46, Burghardt R47, de Zwaan M48, Egberts K49, Ehrlich S50, Herpertz-Dahlmann B46, Herzog W51, Imgart H52, Scherag A53, Scherag S10, Zipfel S54, Boni C55, Ramoz N55, Versini A55, Brandys MK12, Danner UN56, de Kovel C57, Hendriks J13, Koeleman BP57, Ophoff RA58, Strengman E57, van Elburg AA59, Bruson A60, Clementi M60, Degortes D14, Forzan M60, Tenconi E14, Docampo E16, Escaramís G16, Jiménez-Murcia S15, Lissowska J61, Rajewski A62, Szeszenia-Dabrowska N62, Slopien A18, Hauser J18, Karhunen L63, Meulenbelt I64, Slagboom PE65, Tortorella A66, Maj M66, Dedoussis G67, Dikeos D68, Gonidakis F69, Tziouvas K67, Tsitsika A70, Papezova H71, Slachtova L72, Martaskova D71, Kennedy JL28, Levitan RD28, Yilmaz Z73, Huemer J29, Koubek D29, Merl E29, Wagner G29, Lichtenstein P74, Breen G8, Cohen-Woods S8, Farmer A8, McGuffin P8, Cichon S75, Giegling I76, Herms S77, Rujescu D76, Schreiber S78, Wichmann HE79, Dina C80, Sladek R81, Gambaro G82, Soranzo N2, Julia A83, Marsal S83, Rabionet R16, Gaborieau V84, Dick DM85, Palotie A86, Ripatti S87, Widén E87, Andreassen OA88, Espeseth T89, Lundervold A90, Reinvang I91, Steen VM92, Le Hellard S92, Mattingsdal M88, Ntalla I67, Bencko V93, Foretova L94, Janout V95, Navratilova M94, Gallinger S96, Pinto D97, Scherer SW98, Aschauer H99, Carlberg L99, Schosser A99, Alfredsson L100, Ding B100, Klareskog L101, Padyukov L101, Courtet P102, Guillaume S102, Jaussent I102, Finan C2, Kalsi G8, Roberts M8, Logan DW2, Peltonen L2, Ritchie GR103, Barrett JC2; The Wellcome Trust Case Control Consortium 3, Estivill X16, Hinney A10, Sullivan PF104, Collier DA105, Zeggini E2, Bulik CM106.Collaborators (42)Anderson CA, Barrett JC, Floyd JA, Franklin CS, McGinnis R, Soranzo N, Zeggini E, Sambrook J, Stephens J, Ouwehand WH, McArdle WL, Ring SM, Strachan DP, Alexander G, Bulik CM, Collier DA, Conlon PJ, Dominiczak A, Duncanson A, Hill A, Langford C, Lord G, Maxwell AP, Morgan L, Peltonen L, Sandford RN, Sheerin N, Soranzo N, Vannberg FO, Barrett JC, Blackburn H, Chen WM, Edkins S, Gillman M, Gray E, Hunt SE, Langford C, Onengut-Gumuscu S, Potter S, Rich SS, Simpkin D, Whittaker P.
Molecular psychiatry.Mol Psychiatry.2014 Feb 11. doi: 10.1038/mp.2013.187. [Epub ahead of print]
Anorexia nervosa (AN) is a complex and heritable eating disorder characterized by dangerously low body weight. Neither candidate gene studies nor an initial genome-wide association study (GWAS) have yielded significant and replicated results. We performed a GWAS in 2907 cases with AN from 14 countri
PMID 24514567