WordNet

unusually great in degree or quantity or number; "heavy taxes"; "a heavy fine"; "heavy casualties"; "heavy losses"; "heavy rain"; "heavy traffic"
a serious (or tragic) role in a play
an actor who plays villainous roles
slowly as if burdened by much weight; "time hung heavy on their hands" (同)heavily
requiring or showing effort; "heavy breathing"; "the subject made for labored reading" (同)labored, laboured
lacking lightness or liveliness; "heavy humor"; "a leaden conversation" (同)leaden
darkened by clouds; "a heavy sky" (同)lowering, sullen, threatening
slow and laborious because of weight; "the heavy tread of tired troops"; "moved with a lumbering sag-bellied trot"; "ponderous prehistoric beasts"; "a ponderous yawn" (同)lumbering, ponderous
(of sleep) deep and complete; "a heavy sleep"; "fell into a profound sleep"; "a sound sleeper"; "deep wakeless sleep" (同)profound, sound, wakeless
full and loud and deep; "heavy sounds"; "a herald chosen for his sonorous voice" (同)sonorous
full of; bearing great weight; "trees heavy with fruit"; "vines weighed down with grapes" (同)weighed down
(of an actor or role) being or playing the villain; "Iago is the heavy role in `Othello"
(physics, chemistry) being or containing an isotope with greater than average atomic mass or weight; "heavy hydrogen"; "heavy water"
dense or inadequately leavened and hence likely to cause distress in the alimentary canal; "a heavy pudding"
large and powerful; especially designed for heavy loads or rough work; "a heavy truck"; "heavy machinery"
made of fabric having considerable thickness; "a heavy coat"
marked by great psychological weight; weighted down especially with sadness or troubles or weariness; "a heavy heart"; "a heavy schedule"; "heavy news"; "a heavy silence"; "heavy eyelids"
of comparatively great physical weight or density; "a heavy load"; "lead is a heavy metal"; "heavy mahogany furniture"
of great intensity or power or force; "a heavy blow"; "the fighting was heavy"; "heavy seas"
of relatively large extent and density; "a heavy line"
of the military or industry; using (or being) the heaviest and most powerful armaments or weapons or equipment; "heavy artillery"; "heavy infantry"; "a heavy cruiser"; "heavy guns"; "heavy industry involves large-scale production of basic products (such as steel) used by other industries"
sharply inclined; "a heavy grade"
fasten or secure with chains; "Chain the chairs together"
a unit of length
a necklace made by a stringing objects together; "a string of beads"; "a strand of pearls"; (同)string, strand
a linked or connected series of objects; "a chain of daisies"
a series of (usually metal) rings or links fitted into one another to make a flexible ligament
anything that acts as a restraint
(chemistry) a series of linked atoms (generally in an organic molecule) (同)chemical chain
a series of things depending on each other as if linked together; "the chain of command"; "a complicated concatenation of circumstances" (同)concatenation
(business) a number of similar establishments (stores or restaurants or banks or hotels or theaters) under one ownership
connect or arrange into a chain by linking
(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
British biochemist (born in Germany) who isolated and purified penicillin, which had been discovered in 1928 by Sir Alexander Fleming (1906-1979) (同)Ernst Boris Chain, Sir Ernst Boris Chain

PrepTutorEJDIC

『重い』,重量のある / (分量・程度・規模・強さなどが)『激しい』,大きい, / 『厳しい』,耐えがたい,つらい / 悲しい,陰気な / (動作が)のろい,ぎこちない / ものうい,だるい / (空が)曇った,うっとうしい,(海が)荒れた / (食物が)消化の悪い / 敵役,悪役
『鎖』;(装飾用の)鎖 / 《複数形で》『束縛』,拘束;囚人をつなぐ鎖 / (物事の)『連続』,つながり《+『of』+『名』》 / (商店・銀行・ホテルなどの)チェーン(一連の店が同一資本のもとで連携して経営される方式;その店) / チェーン(測量で用いられる単位;約21.7m) / …'を'『鎖でつなぐ』《+『up』(『together』)+『名,』+『名』+『up』(『together』)》
遺伝子

UpToDate Contents

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1. 肥大型心筋症：遺伝子変異および臨床遺伝子検査 hypertrophic cardiomyopathy gene mutations and clinical genetic testing
2. 拡張型心筋症の遺伝学 genetics of dilated cardiomyopathy
3. 免疫グロブリン軽鎖（AL）アミロイドーシスおよび軽鎖重鎖沈着症の病因 pathogenesis of immunoglobulin light chain al amyloidosis and light and heavy chain deposition diseases
4. 多発性骨髄腫の病理生物学 pathobiology of multiple myeloma
5. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia

English Journal

Identification of ecdysteroid signaling late-response genes from different tissues of the Pacific white shrimp, Litopenaeus vannamei.

Qian Z1, He S1, Liu T1, Liu Y1, Hou F1, Liu Q1, Wang X1, Mi X1, Wang P2, Liu X3.Author information 1College of Animal Science and Technology, Northwest A & F University, Shaanxi Key Laboratory of Molecular Biology for Agriculture, Shaanxi Yangling 712100, China.2Nanjiang Marine Biotechnology Company Limited, Sanya, Hainan 572000, China.3College of Animal Science and Technology, Northwest A & F University, Shaanxi Key Laboratory of Molecular Biology for Agriculture, Shaanxi Yangling 712100, China. Electronic address: liuxiaolin@nwsuaf.edu.cn.AbstractEcdysteroids initiate signaling along multiple pathways that regulate various aspects of development, maturation, and reproduction in arthropods. This study was carried out to seek the late target genes of ecdysteroid signaling from different tissues of the Pacific white shrimp, Litopenaeus vannamei. In the present study, eight isoforms of ecdysteroid receptor (EcR), two isoforms of retinoic acid X receptor (RXR), and one homolog of E75 were characterized from L. vannamei. The overall protein sequences and specific functional sites of EcR, RXR and E75 among crustacean species were found highly conserved. Tissue-specific, development stage-specific, and molt stage-specific expression patterns of LvEcR, LvRXR, and LvE75 were detected by qPCR. Double stranded RNA (dsRNA)-mediated RNA interference (RNAi) of any one of the three genes LvEcR, LvRXR and LvE75 caused specific expression changes of the other two, and resulted in corresponding expression changes of two molting related genes Cathepsin-L (LvCHSL) and Hemocyanin (LvHCyn) in the hepatopancreas, two chitin metabolism related genes chitin synthase (LvChS) and chitinase isoenzyme (LvChi2) in the epidermis, and two muscle growth related genes LvActin and myosin heavy chain (LvMHC) in the muscle. In correspondence, after in vivo injections of 20 hydroxyecdysone, specific expression changes of LvEcR, LvRXR, LvE75, LvCHSL and LvHCyn in the hepatopancreas, LvEcR, LvRXR, LvE75, LvChS and LvChi2 in the epidermis, and LvEcR, LvRXR, LvE75, LvActin and LvMHC in the muscle were also observed, respectively. Results in our study indicate multiple functions of ecdysteroids signaling in L. vannamei and the function may be time- and space-specific; ecdysteroids may act through different pathways via its functional receptor heterodimer EcR-RXR and the early responsive gene E75 to perform specific regulation roles on the target genes in different shrimp tissues; LvCHSL and LvHCyn in the hepatopancreas, LvChS and LvChi2 in the epidermis, and LvActin and LvMHC in the muscle are potential targets for ecdysteroid control. This is the first report on nuclear receptors in the economically important shrimp L. vannamei.
Comparative biochemistry and physiology. Part A, Molecular & integrative physiology.Comp Biochem Physiol A Mol Integr Physiol.2014 Jun;172:10-30. doi: 10.1016/j.cbpa.2014.02.011. Epub 2014 Feb 17.
Ecdysteroids initiate signaling along multiple pathways that regulate various aspects of development, maturation, and reproduction in arthropods. This study was carried out to seek the late target genes of ecdysteroid signaling from different tissues of the Pacific white shrimp, Litopenaeus vannamei
PMID 24556071

Clinical significance of minimal residual disease in young adults with standard-risk/Ph-negative precursor B-acute lymphoblastic leukemia: results of prospective study.

Salah-Eldin M1, Abousamra NK, Azzam H.Author information 1Department of Medical Oncology, Oncology Center, Mansoura University, Mansoura, Egypt, msmk124@hotmail.com.AbstractClinical risk classification is inaccurate in predicting outcome in adult patients with acute lymphoblastic leukemia (ALL), sometimes resulting in patients receiving inappropriate chemotherapy or stem cell transplantation. To identify complementary markers suitable for further treatment stratification in patients with standard-risk (SR)/philadelphia-negative (Ph-negative) precursor B-ALL, we evaluated the predictive value of minimal residual disease (MRD) after induction and consolidation chemotherapy in strictly defined SR/Ph-negative precursor B-ALL patients who were treated with a standard protocol using quantitative real-time polymerase chain reaction with the rearranged immunoglobulin heavy chain gene as a molecular marker. The cytologic complete response (CR) rate was 92.3 % after induction. At this time point, the molecular CR rate was 73.9 %. Patients with molecular CR (MolCR) after induction had a significantly higher probability of disease-free survival (DFS; 78.8 vs 30.8 %; P = .001) and of overall survival (OS; 82.4 vs 41.7 %; P < .0001) compared to patients with molecular failure (MolFail). MRD at end consolidation had the same significance. Quantitative MRD assessment identified patients with MolFail after induction and/or consolidation as a high-risk group, with 3-year DFS and OS rates of 28.6 and 35.7 %, respectively. Patients with MolCR after induction and consolidation were classified as low-risk and had 3-year DFS rate of 89.7 % and OS rate of 93.3 %. Thus, MRD quantification during treatment identified prognostic subgroups within the otherwise homogeneous SR/Ph-negative precursor B-ALL population who may benefit from individualized treatment.
Medical oncology (Northwood, London, England).Med Oncol.2014 May;31(5):938. doi: 10.1007/s12032-014-0938-z. Epub 2014 Apr 2.
Clinical risk classification is inaccurate in predicting outcome in adult patients with acute lymphoblastic leukemia (ALL), sometimes resulting in patients receiving inappropriate chemotherapy or stem cell transplantation. To identify complementary markers suitable for further treatment stratificati
PMID 24692146

Metabotropic glutamate receptor 5 knockout promotes motor and biochemical alterations in a mouse model of Huntington's disease.

Ribeiro FM1, Devries RA, Hamilton A, Guimaraes IM, Cregan SP, Pires RG, Ferguson SS.Author information 1Departamento de Bioquimica e Imunologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil.AbstractHuntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by a polyglutamine expansion in the amino-terminal region of the huntingtin protein, which promotes progressive neuronal cell loss, neurological symptoms and death. In the present study, we show that blockade of mGluR5 with MTEP promotes increased locomotor activity in both control (Hdh(Q20/Q20)) and mutant HD (Hdh(Q111/Q111)) mice. Although acute injection of MTEP increases locomotor activity in both control and mutant HD mice, locomotor activity is increased in only control mice, not mutant HD mice, following the genetic deletion of mGluR5. Interestingly, treatment of mGluR5 knockout mice with either D1 or D2 dopamine antagonists eliminates the increased locomotor activity of mGluR5 knockout mice. Amphetamine treatment increases locomotor activity in control mice, but not mGluR5 null mutant HD mice. However, the loss of mGluR5 expression improves rotarod performance and decreases the number of huntingtin intranuclear inclusions in mutant HD mice. These adaptations may be due to mutant huntingtin-dependent alterations in gene expression, as microarray studies have identified several genes that are altered in mutant, but not wild-type HD mice lacking mGluR5 expression. qPCR experiments confirm that the mRNA transcript levels of dynein heavy chain, dynactin 3 and dynein light chain-6 are altered following the genetic deletion of mGluR5 in mutant HD mice, as compared with wild-type mutant HD mice. Thus, our data suggest that mutant huntingtin protein and mGluR5 exhibit a functional interaction that may be important for HD-mediated alterations in locomotor behavior and the development of intranuclear inclusions.
Human molecular genetics.Hum Mol Genet.2014 Apr 15;23(8):2030-42. doi: 10.1093/hmg/ddt598. Epub 2013 Nov 26.
Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by a polyglutamine expansion in the amino-terminal region of the huntingtin protein, which promotes progressive neuronal cell loss, neurological symptoms and death. In the present study, we show that blockade of mGl
PMID 24282028