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the 9th letter of the Roman alphabet (同)i

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『私は』私が
iodineの化学記号
Indiana

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/18 21:38:10」(JST)

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1. イソニアジド：概要 isoniazid an overview
2. イソニアジド肝毒性 isoniazid hepatotoxicity
3. イソニアジド（INH）中毒 isoniazid inh poisoning
4. HIV陰性成人における潜伏結核感染の治療 treatment of latent tuberculosis infection in hiv negative adults
5. 成人における非結核性抗酸菌による骨髄炎の治療 treatment of osteomyelitis due to nontuberculous mycobacteria in adults

English Journal

Metabolomics and transcriptomics demonstrate severe oxidative stress in both localized chemotherapy-treated and bystander tumors.

Morvan D1, Demidem A2.Author information 1UDA University, 49 Boulevard François Mitterrand, CS 60032, 63001 Clermont Ferrand Cedex 1, France; Centre Jean Perrin, 58 Rue Montalembert, F-63011 Clermont Ferrand, France. Electronic address: ademidem@clermont.inra.fr.2UMR 1019 INRA/UDA University, ECREIN, Laboratoire de Biochimie Biologie Moléculaire, Faculté de Pharmacie, 28 Place Henri Dunant, F-63001 Clermont Ferrand, France. Electronic address: Daniel.Morvan@udamail.fr.AbstractBACKGROUND: Localized radiotherapy is long known to cause damages to not only targeted but also non-targeted cells, the so-called bystander (BS) effect. Recently, BS effect was demonstrated in response to chemotherapy. To get further insight into the mechanism of chemotherapy-induced BS effect in vivo, we investigated the response of normal tissues and untreated BS melanomas, at distance from localized chemotherapy-treated melanomas.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Mar;1840(3):1092-104. doi: 10.1016/j.bbagen.2013.11.022. Epub 2013 Dec 1.
BACKGROUND: Localized radiotherapy is long known to cause damages to not only targeted but also non-targeted cells, the so-called bystander (BS) effect. Recently, BS effect was demonstrated in response to chemotherapy. To get further insight into the mechanism of chemotherapy-induced BS effect in vi
PMID 24296419

Polymorphism p.Val231Ile alters substrate selectivity of drug-metabolizing arylamine N-acetyltransferase 2 (NAT2) isoenzyme of rhesus macaque and human.

Tsirka T1, Boukouvala S1, Agianian B1, Fakis G2.Author information 1Democritus University of Thrace, Department of Molecular Biology and Genetics, Alexandroupolis, Greece.2Democritus University of Thrace, Department of Molecular Biology and Genetics, Alexandroupolis, Greece. Electronic address: gfakis@mbg.duth.gr.AbstractArylamine N-acetyltransferases (NATs) are polymorphic enzymes mediating the biotransformation of arylamine/arylhydrazine xenobiotics, including pharmaceuticals and environmental carcinogens. The NAT1 and NAT2 genes, and their many polymorphic variants, have been thoroughly studied in humans by pharmacogeneticists and cancer epidemiologists. However, little is known about the function of NAT homologues in other primate species, including disease models. Here, we perform a comparative functional investigation of the NAT2 homologues of the rhesus macaque and human. We further dissect the functional impact of a previously described rhesus NAT2 gene polymorphism, causing substitution of valine by isoleucine at amino acid position 231. Gene constructs of rhesus and human NAT2, bearing or lacking non-synonymous polymorphism c.691G>A (p.Val231Ile), were expressed in Escherichia coli for comparative enzymatic analysis against various NAT1- and NAT2-selective substrates. The results suggest that the p.Val231Ile polymorphism does not compromise the stability or overall enzymatic activity of NAT2. However, substitution of Val231 by the bulkier isoleucine appears to alter enzyme substrate selectivity by decreasing the affinity towards NAT2 substrates and increasing the affinity towards NAT1 substrates. The experimental observations are supported by in silico modelling localizing polymorphic residue 231 close to amino acid loop 125-129, which forms part of the substrate binding pocket wall and determines the substrate binding preferences of the NAT isoenzymes. The p.Val231Ile polymorphism is the first natural polymorphism demonstrated to affect NAT substrate selectivity via this particular mechanism. The study is also the first to thoroughly characterize the properties of a polymorphic NAT isoenzyme in a non-human primate model.
Gene.Gene.2014 Feb 15;536(1):65-73. doi: 10.1016/j.gene.2013.11.085. Epub 2013 Dec 11.
Arylamine N-acetyltransferases (NATs) are polymorphic enzymes mediating the biotransformation of arylamine/arylhydrazine xenobiotics, including pharmaceuticals and environmental carcinogens. The NAT1 and NAT2 genes, and their many polymorphic variants, have been thoroughly studied in humans by pharm
PMID 24333853

A systematic analysis of the complement pathways in patients with neuromyelitis optica indicates alteration but no activation during remission.

Veszeli N, Füst G, Csuka D, Trauninger A, Bors L, Rozsa C, Nagy Z, Jobbágy Z, Eizler K, Prohászka Z, Varga L, Illes Z.Author information 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.AbstractNeuromyelitis optica (NMO) is an autoimmune demyelinating inflammatory disorder, mediated by pathogenic autoantibodies against aquaporin 4 (AQP4), the main water channel of the central nervous system (CNS). NMO is characterized by local IgG deposition and complement activation within the CNS, but the three complement pathways have not been systematically investigated. We evaluated the overall activation of the classical, alternative, and MBL-lectin pathways in the peripheral blood of 25 patients with AQP4-seropositive NMO spectrum during remission and 113 healthy controls by three ways: (1) we measured the concentrations of native complement proteins of the three pathways [C1-inhibitor (C1-inh), C1q, C4, C3, C5, factor I, factor B, properdin]; (2) the concentrations of complement products suggesting in vivo activation (C1rC1sC1-inh, C3a, C3bBbP, and SC5b-9); and (3) the total activity of the three complement pathways. Additionally we measured levels of C1rC1sC1-inh, C3a, C3bBbP in cerebrospinal fluid (CSF) of 6 patients with relapsing NMO and of 18 patients with relapsing multiple sclerosis (MS). The serological studies indicated that total complement activity of the classical [median (interquartile range) 72 (61-82) vs. 65 (56-73) CH50/mL; p=0.0122] and of the lectin pathways [73 (59-111) vs. 49 (3-92)%; p=0.0078)] were elevated compared with the controls, whereas that of the alternative pathway was not significantly different. The levels of C3 [1.1 (0.9-1.3) vs. 1.4 (1.2-1.5)g/L; p<0.0001], factor B [89 (77-115) vs. 103 (93-113)%; p=0.0397] and factor I [85 (69-95) vs. 101 (93-107)%; p=0.0007], as well as of properdin [92 (74-104) vs. 108 (97-122)%; p=0.0028] were significantly lower in the patients than in the controls. The only increase in the patients was ascertained in the relative concentration of C1rC1sC1-inh vs. the C1-inhibitor (42.3 [31.9-65.0] vs. 30.8 [13.5-43.5] AU/mg; p=0.0007). The absolute and relative levels of the other complement activation products were not elevated in the patients. On the contrary, the serum concentrations of C3a, C3bBbP, and SC5b-9 of the patients were lower than those of the controls. The absolute concentration of the complement activation products (C1rC1sC1-inh, C3bBbP, C3a) and the ratio of C3bBbP/C1rC1sC1-inh did not differ in NMO and MS CSF samples. The ratio of C3bBbP/C1rC1sC1-inh was similar in NMO plasma and CSF samples. We found a higher ratio of C3bBbP/C1rC1sC1-inh in the plasma of control subjects compared to those in any pathological samples. Our results do not indicate substantial systemic complement activation if NMO activity is adequately controlled; nevertheless, the complement system is abnormally affected even during remission. The relative ancillarity of the alternative compared to the classical pathway may also suggest that suppression of the alternative pathway by treatment may be important to achieve remission.
Molecular immunology.Mol Immunol.2014 Feb;57(2):200-9. doi: 10.1016/j.molimm.2013.09.010. Epub 2013 Oct 26.
Neuromyelitis optica (NMO) is an autoimmune demyelinating inflammatory disorder, mediated by pathogenic autoantibodies against aquaporin 4 (AQP4), the main water channel of the central nervous system (CNS). NMO is characterized by local IgG deposition and complement activation within the CNS, but th
PMID 24172223

Japanese Journal

遺伝性血管性浮腫患者の歯根囊胞摘出術を行った1例

井口蘭,中澤龍一,諸井明徳,石原由梨,外堀恵,井川浩海,河阪明彦,丸川浩平,上木耕一郎
日本口腔診断学会雑誌 27(1), 22-26, 2014
… In accordance with the HAE guidelines, C1-INH was injected before surgery and tranexamic acid was administered long-term to avoid angioedema attacks. …
NAID 130003398154

20代の女性に発症したMycobacterium kansasii症の2例

出浦弦,吾妻俊彦,藤本圭作
信州医学雑誌 = The Shinshu medical journal 62(1), 51-57, 2014
NAID 120005373331

インターフェロンγ遊離試験T-スポット<SUP>®</SUP>.<I>TB</I>が結核症の診断に有用であった透析患者の1例

甲田亮,吉野篤範,今西優仁 [他],川本進也,竹田徹朗,水口真理,笛木直人,相良博典
日本透析医学会雑誌 46(7), 681-686, 2013
69歳，女性，抗基底膜抗体型急速進行性糸球体腎炎のため8か月前に血液透析導入．近医で週3回の維持血液透析を受けていた．血液透析導入後も抗基底膜抗体価は高値を持続しプレドニゾロン，シクロホスファミドの内服を継続していた．入院2か月前から微熱あり．咳，痰などの呼吸器症状はなかった．精査のため当院入院，両肺野にびまん性の小結節影あり，肺結核症が疑われた．入院翌日血液透析開始時にT-スポット<SUP …
NAID 130003372799

Related Pictures

★リンクテーブル★

国試過去問	「080B082」
リンク元	「ビタミン」「紅皮症」「鉄芽球性貧血」「イソニアジドメタンスルホン酸ナトリウム」「イソニアジド」
拡張検索	「C1 INH欠損症」
関連記事	「I」

「080B082」

　　[★]

ペラグラの原因となるのはどれか？

「ビタミン」

　　[★]

英: vitamin

ビタミン、生物の生存・生育に必要な栄養素のうち、炭水化物やタンパク質、脂質、ミネラル以外の栄養素であり、微量ではあるが生理作用を円滑に行うために必須な有機化合物の総称 wiki

ビタミン

性状	ビタミン名	化合物名	機能			補酵素名	欠乏症	過剰症
性状	ビタミン名	化合物名		アミノ酸代謝	補酵素前駆体	補酵素名	欠乏症	過剰症
水溶性ビタミン	ビタミンB1	チアミン	糖代謝		○	チアミン二リン酸	脚気 (多発性神経炎、脚気心による動悸・息切れ) ウェルニッケ脳症コルサコフ症候群
	ビタミンB2	リボフラビン	酸化還元反応	アミノ酸オキシダーゼ	○	フラビンアデニンジヌクレオチド	口角炎、舌炎、結膜炎、角膜炎、脂漏性皮膚炎
	ビタミンB6	ピリドキシン	転移反応、脱炭酸反応、離脱反応、ラセミ化	多くのアミノ酸	○	ピリドキサルリン酸	末梢神経障害（INHの副作用)
	ビタミンB12	シアノコバラミン	C1転移	メチオニン、分岐アミノ酸	○	コバルト補酵素	巨赤芽球性貧血
	ビタミンC	アスコルビン酸	抗酸化		○		壊血病易出血性、骨・筋の脆弱化
	ビタミンB5	パントテン酸	CoAの骨格
	ビタミンB9	葉酸	C1転移	グリシン、セリン	○		巨赤芽球性貧血
	ビタミンB3	ナイアシンニコチン酸	酸化還元反応		○	ニコチンアミドアデニンジヌクレオチド	ペラグラ (1)光過敏性皮膚炎、(2)下痢、(3)認知症
	ビタミンB7	ビオチン	炭素固定反応		○	ビオチン酵素	脂漏性皮膚炎、鱗屑状皮膚炎
脂溶性ビタミン	ビタミンA	レチノイド	転写因子、視覚				夜盲症眼球乾燥症・角膜軟化症(Bitot斑)・毛孔性角化症	脳圧亢進、四肢疼痛性腫脹、肝性皮膚落屑、悪心・嘔吐、食欲不振、催奇形性
	ビタミンD	コレカルシフェロール等	骨形成				くる病、骨軟化症	腎臓・血管壁への石灰沈着、多尿、↑尿Ca、高Ca血症、高P血症
	ビタミンE	トコフェロール	抗酸化				未熟児の溶血性貧血
	ビタミンK	フィロキノン、メナキノン等	血液凝固因子やオステオカルシンの成熟		○		出血傾向	溶血、核黄疸

ビタミンと欠乏症、過剰症

「紅皮症」

　　[★]

英: erythroderma
同: 剥脱性皮膚炎 exfoliative dermatitis

定義

(1)全身(体表の80%以上)の持続性の炎症性発赤(潮紅)し、健常部皮膚を殆ど残さず、(2)粃糠様・落葉状の落屑が持続する病態

原因

起こしやすい疾患 (2009 CBT QB2 p.116)

(%)は紅皮症に占める割合

湿疹続発性(約50%)	アトピー性皮膚炎、自家感作性皮膚炎など
各種疾患続発性	乾癬(数%)、毛孔性紅色粃糠疹、天疱瘡など
中毒性	薬疹(約10%)(ピラゾロン、INH、SMなど)、ウイルスなどの感染症、GVHD
落屑性	ビタミンB群欠乏症
腫瘍性	T細胞リンパ腫(Sezary症候群、菌状息肉腫)

起こしうる疾患 (NDE.122)

炎症性疾患

腫瘍性疾患

菌状息肉症
Sezary症候群
成人T 細胞白血病・リンパ腫
白血病(急性，慢性)
悪性リンパ腫(Hodgkin病を含む)
多発性骨髄腫
各種内臓悪性腫瘍

「鉄芽球性貧血」

　　[★]

英: sideroblastic anemia SA
ラ: anemia sideroblastica
同: 鉄不応性貧血 sideroachrestic anemia
関: 環状鉄芽球、貧血、続発性鉄芽球性貧血

概念

ヘム合成障害による無効造血によって貧血を来す症候群

病因

原発性

後天性
先天性

続発性

薬剤性：INH、サイクロセリン、アザチオプリン、クロラムフェニコール
症候性：関節リウマチ、悪性腫瘍、骨髄異形成症 MDS(骨髄線維症)、白血病、多発性骨髄腫、サラセミア
中毒性：アルコール中毒、鉛中毒

ピリドキシン反応性：ビタミンB6投与により改善(ピリドキシン反応性貧血)

検査

(根拠無き解釈)骨髄では鉄が赤芽球に取り込まれてはアポトーシスに至り無効造血が続いており、鉄の需要はない。このため、末梢血中の鉄は使用されないため増加、また網内系の貯蔵鉄も使用されないまま蓄積するので血清フェリチンが増加する。総鉄結合能はトランスフェリンの全体量は変化せず不変。骨髄ではなんとか赤血球を作ろうと、過形成となっており、赤芽球が著明にみられる。