WordNet

to be on base at the end of an inning, of a player
pass from physical life and lose all bodily attributes and functions necessary to sustain life; "She died from cancer"; "The children perished in the fire"; "The patient went peacefully"; "The old guy kicked the bucket at the age of 102" (同)decease, perish, go, exit, pass_away, expire, pass, kick the bucket, cash in one''s chips, buy the farm, conk, give-up the ghost, drop dead, pop_off, choke, croak, snuff it
disappear or come to an end; "Their anger died"; "My secret will die with me!"
suffer spiritual death; be damned (in the religious sense); "Whosoever..believes in me shall never die"
a small cube with 1 to 6 spots on the six faces; used in gambling to generate random numbers (同)dice
a cutting tool that is fitted into a diestock and used for cutting male (external) screw threads on screws or bolts or pipes or rods
a device used for shaping metal
cut or shape with a die; "Die out leather for belts" (同)die_out
lose sparkle or bouquet; "wine and beer can pall" (同)pall, become flat
be brought to or as if to the point of death by an intense emotion such as embarrassment, amusement, or shame; "I was dying with embarrassment when my little lie was discovered"; "We almost died laughing during the show"
feel indifferent towards; "She died to worldly things and eventually entered a monastery"
languish as with love or desire; "She dying for a cigarette"; "I was dying to leave"
suffer or face the pain of death; "Martyrs may die every day for their faith"

PrepTutorEJDIC

〈人・動物が〉『死ぬ』,〈植物が〉『枯れる』 / 《副詞[句]を伴って》〈音・光・風などが〉消えてゆく《+『away』》;〈火・感情などが〉次第に収まる《+『down』》;〈家系・習慣などが〉絶えてなくなる《+『out』》 / 〈機械が〉動かなくなる,止まる / 《話》《進行形で》死ぬほど望む
さい,さいころ / ダイス,雄ねじ切り / (貨幣・メダルなどの)打ち型,打ち抜き型
(おもに人称代名詞・固有名詞(人名),thereの後で)had, wouldの短縮形 / (疑問文でwhere,what,whenの後で)didの短縮形;Where'd he go?=Where did he go?

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/12/11 15:38:13」(JST)

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1. ダグラス窩深部または腸管子宮内膜症 rectovaginal or bowel endometriosis
2. 子宮内膜症の治療の概要 overview of the treatment of endometriosis
3. 子宮内膜症の病因、臨床的特徴、および診断 pathogenesis clinical features and diagnosis of endometriosis
4. 無脳症 anencephaly
5. 終末期ケア：栄養および水分補給の停止 end of life care stopping nutrition and hydration

English Journal

Loss of proteostasis induced by amyloid beta peptide in brain endothelial cells.

Fonseca AC1, Oliveira CR2, Pereira CF2, Cardoso SM3.Author information 1Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal; Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, Apartado 3046, 3001-401 Coimbra, Portugal.2Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal; Faculty of Medicine, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal.3Center for Neuroscience and Cell Biology, University of Coimbra, Largo Marquês de Pombal, 3004-517 Coimbra, Portugal; Faculty of Medicine, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal. Electronic address: cardoso.sandra.m@gmail.com.AbstractAbnormal accumulation of amyloid-β (Aβ) peptide in the brain is a pathological hallmark of Alzheimer's disease (AD). In addition to neurotoxic effects, Aβ also damages brain endothelial cells (ECs) and may thus contribute to the degeneration of cerebral vasculature, which has been proposed as an early pathogenic event in the course of AD and is able to trigger and/or potentiate the neurodegenerative process and cognitive decline. However, the mechanisms underlying Aβ-induced endothelial dysfunction are not completely understood. Here we hypothesized that Aβ impairs protein quality control mechanisms both in the secretory pathway and in the cytosol in brain ECs, leading cells to death. In rat brain RBE4 cells, we demonstrated that Aβ1-40 induces the failure of the ER stress-adaptive unfolded protein response (UPR), deregulates the ubiquitin-proteasome system (UPS) decreasing overall proteasome activity with accumulation of ubiquitinated proteins and impairs the autophagic protein degradation pathway due to failure in the autophagic flux, which culminates in cell demise. In conclusion, Aβ deregulates proteostasis in brain ECs and, as a consequence, these cells die by apoptosis.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jun;1843(6):1150-61. doi: 10.1016/j.bbamcr.2014.02.016. Epub 2014 Feb 28.
Abnormal accumulation of amyloid-β (Aβ) peptide in the brain is a pathological hallmark of Alzheimer's disease (AD). In addition to neurotoxic effects, Aβ also damages brain endothelial cells (ECs) and may thus contribute to the degeneration of cerebral vasculature, which has been proposed as an
PMID 24589617

The syndrome of excited delirium.

Gill JR.Author information State of Connecticut, Office of the Chief Medical Examiner, 11 Shuttle Rd, Farmington, CT, 06032, USA, jgill@ocme.org.AbstractThe excited delirium syndrome (EDS) is a life-threatening condition caused by a variety of factors including drug intoxication and psychiatric illness. Fatal instances of excited delirium frequently come to the attention of the medical examiner/coroner due to the circumstances and potential causes. Excited delirium may include paranoid, aggressive, and incoherent behavior which may lead to an encounter with law enforcement. In some instances, the person may die while in the presence of law enforcement. This circumstance further broadens the potential causes of death particularly as EDS has no pathognomonic autopsy finding. Although the syndrome of excited delirium is sufficient to explain death, other intervening causes need to be considered. These include chest or neck compression during restraint, blunt trauma, and underlying natural disease. Since chest/neck compression, natural disease (e.g., atherosclerosis), blunt trauma, and excited delirium are not mutually exclusive, all may be present in one death. The forensic pathologist's role is to determine what caused and/or contributed to the death. When attempting to determine the proximate cause of death in instances with multiple potential causes, determining the mechanism of death often is useful. As not all causes of death have pathologically-demonstrable mechanisms of death, examination of the circumstances of the death often are diagnostically important. The main goal of the autopsy of deaths suspected to be due to EDS is to identify (or exclude) intervening diseases or injuries sufficient to explain the death in the context of the investigated circumstances.
Forensic science, medicine, and pathology.Forensic Sci Med Pathol.2014 Jun;10(2):223-8. doi: 10.1007/s12024-014-9530-2. Epub 2014 Feb 14.
The excited delirium syndrome (EDS) is a life-threatening condition caused by a variety of factors including drug intoxication and psychiatric illness. Fatal instances of excited delirium frequently come to the attention of the medical examiner/coroner due to the circumstances and potential causes.
PMID 24526411

Perspectives on the therapeutic modulation of an alternative cell death, programmed necrosis (Review).

Cho YS.Author information College of Pharmacy, Keimyung University, Dalseo-gu, Daegu 704-701, Republic of Korea.AbstractIn response to overwhelming external stimuli, cells are forced to die in different ways. By default, cells are prone to apoptosis, a programmed cell death through the activation of the caspase cascade. However, this process would be blocked if one of the proteins involved in executing apoptosis was genetically impaired or chemically inhibited, or if the apoptotic machinery was not properly operated under specific conditions, such as ischemia and microbial infection. To address these issues, the paradigm of programmed cell death needs to be revised; thus, an alternative form of cell death, programmed necrosis (termed necroptosis, through the caspase-independent pathway), which is distinct from apoptosis in many aspects, has recently been adopted. There is much interest in programmed necrosis as it is very closely associated with pathophysiological conditions, such as stroke, heart attack and septic shock. In an effort to identify target molecules of small compounds interfering with the signaling downstream of tumor necrosis factor-α (TNF-α), necrostatin-1 (Nec-1) was first identified to be a selective allosteric inhibitor of the death domain receptor-associated adaptor kinase, receptor interacting protein 1 (RIP1) in vitro. Since then, some novel scaffolds with selective and distinctive activity have been proposed. In this review, the significant advancement and state-of-art direction for the development of small molecules that can control programmed necrosis is discussed. Furthermore, the perspectives on novel strategies harnessing therapeutic targets identified thus far, are also discussed.
International journal of molecular medicine.Int J Mol Med.2014 Jun;33(6):1401-6. doi: 10.3892/ijmm.2014.1716. Epub 2014 Mar 27.
In response to overwhelming external stimuli, cells are forced to die in different ways. By default, cells are prone to apoptosis, a programmed cell death through the activation of the caspase cascade. However, this process would be blocked if one of the proteins involved in executing apoptosis was
PMID 24676489

Packaging commercial CMOS chips for lab on a chip integration.

Datta-Chaudhuri T1, Abshire P, Smela E.Author information 1Department of Electrical and Computer Engineering, 2160 A.V. Williams, College Park, Maryland, USA.AbstractCombining integrated circuitry with microfluidics enables lab-on-a-chip (LOC) devices to perform sensing, freeing them from benchtop equipment. However, this integration is challenging with small chips, as is briefly reviewed with reference to key metrics for package comparison. In this paper we present a simple packaging method for including mm-sized, foundry-fabricated dies containing complementary metal oxide semiconductor (CMOS) circuits within LOCs. The chip is embedded in an epoxy handle wafer to yield a level, large-area surface, allowing subsequent photolithographic post-processing and microfluidic integration. Electrical connection off-chip is provided by thin film metal traces passivated with parylene-C. The parylene is patterned to selectively expose the active sensing area of the chip, allowing direct interaction with a fluidic environment. The method accommodates any die size and automatically levels the die and handle wafer surfaces. Functionality was demonstrated by packaging two different types of CMOS sensor ICs, a bioamplifier chip with an array of surface electrodes connected to internal amplifiers for recording extracellular electrical signals and a capacitance sensor chip for monitoring cell adhesion and viability. Cells were cultured on the surface of both types of chips, and data were acquired using a PC. Long term culture (weeks) showed the packaging materials to be biocompatible. Package lifetime was demonstrated by exposure to fluids over a longer duration (months), and the package was robust enough to allow repeated sterilization and re-use. The ease of fabrication and good performance of this packaging method should allow wide adoption, thereby spurring advances in miniaturized sensing systems.
Lab on a chip.Lab Chip.2014 May 21;14(10):1753-66. doi: 10.1039/c4lc00135d. Epub 2014 Mar 28.
Combining integrated circuitry with microfluidics enables lab-on-a-chip (LOC) devices to perform sensing, freeing them from benchtop equipment. However, this integration is challenging with small chips, as is briefly reviewed with reference to key metrics for package comparison. In this paper we pre
PMID 24682025

Japanese Journal

単一ノード故障時におけるマルチコアプロセッサシステムの回復時間を最小化するタスクスケジューリング

柴田直樹,後藤田祥平,伊藤実
情報処理学会論文誌 55(2), 575-586, 2014-02-15
本論文では,各計算ノードがマルチコアプロセッサであるような並列処理システムにおいて,ネットワークの輻輳を考慮しつつ,マルチコアプロセッサの単一停止故障時の回復時間を最小化するタスクスケジューリングアルゴリズムを提案する.最近開発されたプロセッサのほとんどはマルチコアであり,マルチコアプロセッサが故障した場合は,その上で実行されているタスクをすべてやり直す必要が発生する.ここでは,リカバリのために, …
NAID 110009664968