WordNet

establish as valid or genuine; "Can you back up your claims?" (同)back_up
strengthen by providing with a back or backing
a support that you can lean against while sitting; "the back of the dental chair was adjustable" (同)backrest
(American football) the position of a player on a football team who is stationed behind the line of scrimmage
the part of a garment that covers the back of your body; "they pinned a `kick me sign on his back"
travel backward; "back into the driveway"; "The car backed up and hit the tree"
the posterior part of a human (or animal) body from the neck to the end of the spine; "his back was nicely tanned" (同)dorsum
the part of something that is furthest from the normal viewer; "he stood at the back of the stage"; "it was hidden in the rear of the store" (同)rear
(football) a person who plays in the backfield
in or to or toward a past time; "set the clocks back an hour"; "never look back"; "lovers of the past looking fondly backward" (同)backward
at or to or toward the back or rear; "he moved back"; "tripped when he stepped backward"; "she looked rearward out the window of the car" (同)backward, backwards, rearward, rearwards
be behind; approve of; "He plumped for the Labor Party"; "I backed Kennedy in 1960" (同)endorse, indorse, plump for, plunk for, support
located at or near the back of an animal; "back (or hind) legs"; "the hinder part of a carcass" (同)hind, hinder
be in back of; "My garage backs their yard"
cause to travel backward; "back the car into the parking spot"
in or to or toward a former location; "she went back to her parents house"
in or to or toward an original condition; "he went back to sleep"
in repayment or retaliation; "we paid back everything we had borrowed"; "he hit me and I hit him back"; "I was kept in after school for talking back to the teacher"
in reply; "he wrote back three days later"
of an earlier date; "back issues of the magazine"
related to or located at the back; "the back yard"; "the back entrance"
shift to a counterclockwise direction; "the wind backed"
support financial backing for; "back this enterprise"
the act of providing approval and support; "his vigorous backing of the conservatives got him in trouble with progressives" (同)backup, championship, patronage
something forming a back that is added for strengthening (同)mount
in or associated with the process of passing from life or ceasing to be; "a dying man"; "his dying wish"; "a dying fire"; "a dying civilization"
used of film that is coated on the side opposite the emulsion with a substance to absorb light
having a back or backing, usually of a specified type
any pathology of the peripheral nerves

PrepTutorEJDIC

〈C〉(人・動物の)『背』,『背中』,背部 / 《通例the~》(正面に対して)(…の)『後ろ』,『裏』,奥,後部《+『of』+『名』》 / 《通例the back》背に似たもの;(手足の)甲;(刀の)みね;(いす・本の)背 / 〈C〉〈U〉(フットボール・ホッケーなどの)後衛 / 《名詞の前にのみ用にて》『後ろの』,後部にある,裏の / 後もどりする,逆の / 遅れている,未払いの / (中心から)遠い,へんぴな,奥地の / (音声が)後舌音の / 『後方へ』,『後ろに』(backward) / (場所・状態が)『もとへ』,帰って,返して / (時間的に)『さかのぼって』,今から…前に(ago) / 〈車など〉'を'『後退させる』 / (…で)〈人・計画など〉'を'『後援する』,支持する(support)《+『名』+『in』+『名』》 / (競馬で)…に賭ける / (…で)…‘の'伴奏をする《+『名』+『by』+『名』》 / …‘の'裏手にある,背景をなす / 〈手形など〉‘に'裏書きする(endorse) / 《しばしば受動態で》〈本〉‘に'背をつける,(…で)…'を'裏打ちする《+『名』+『with』+『名』》 / 後ずさりする,後退する(move backward)
〈U〉(本などの)裏打ち,背付け / 〈U〉後援,支持;《集合的に》後援者たち / 〈C〉(ポピュラー音楽で)伴奏
dieの現在分詞 / 死にかかっている,ひん死の / 消えかかっている,滅びかけている / 臨終の

UpToDate Contents

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1. 小児における後天性末梢性ニューロパチーの概要 overview of acquired peripheral neuropathies in children
2. 多発性神経障害の概要 overview of polyneuropathy
3. 遺伝性ニューロパチーの概要 overview of hereditary neuropathies
4. 糖尿病性多発性神経障害の病因および予防 pathogenesis and prevention of diabetic polyneuropathy
5. HIV関連末梢神経障害の疫学、臨床症状、診断、および治療 epidemiology clinical manifestations diagnosis and treatment of hiv associated peripheral neuropathy

English Journal

Pathophysiology of X-linked adrenoleukodystrophy.

Berger J1, Forss-Petter S2, Eichler FS3.Author information 1Pathobiology of the Nervous System, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria. Electronic address: johannes.berger@meduniwien.ac.at.2Pathobiology of the Nervous System, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria.3Department for Neurology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street ACC 708, Boston, MA 02114, USA.AbstractCurrently the molecular basis for the clinical heterogeneity of X-linked adrenoleukodystrophy (X-ALD) is poorly understood. The genetic bases for all different phenotypic variants of X-ALD are mutations in the gene encoding the peroxisomal ATP-binding cassette (ABC) transporter, ABCD1 (formerly adrenoleukodystrophy protein, ALDP). ABCD1 transports CoA-activated very long-chain fatty acids from the cytosol into the peroxisome for degradation. The phenotypic variability is remarkable ranging from cerebral inflammatory demyelination of childhood onset, leading to death within a few years, to adults remaining pre-symptomatic through more than five decades. There is no general genotype-phenotype correlation in X-ALD. The default manifestation of mutations in ABCD1 is adrenomyeloneuropathy, a slowly progressive dying-back axonopathy affecting both ascending and descending spinal cord tracts as well as in some cases, a peripheral neuropathy. In about 60% of male X-ALD patients, either in childhood (35-40%) or in adulthood (20%), an initial, clinically silent, myelin destabilization results in conversion to a devastating, rapidly progressive form of cerebral inflammatory demyelination. Here, ABCD1 remains a susceptibility gene, necessary but not sufficient for inflammatory demyelination to occur. Although the accumulation of very long-chain fatty acids appears to be essential for the pathomechanism of all phenotypes, the molecular mechanisms underlying these phenotypes are fundamentally different. Cell autonomous processes such as oxidative stress and energy shortage in axons as well as non-cell autonomous processes involving axon-glial interactions seem pertinent to the dying-back axonopathy. Various dynamic mechanisms may underlie the initiation of inflammation, the altered immune reactivity, the propagation of inflammation, as well as the mechanisms leading to the arrest of inflammation after hematopoietic stem cell transplantation. An improved understanding of the molecular mechanisms involved in these events is required for the development of urgently needed therapeutics.
Biochimie.Biochimie.2014 Mar;98:135-42. doi: 10.1016/j.biochi.2013.11.023. Epub 2013 Dec 4.
Currently the molecular basis for the clinical heterogeneity of X-linked adrenoleukodystrophy (X-ALD) is poorly understood. The genetic bases for all different phenotypic variants of X-ALD are mutations in the gene encoding the peroxisomal ATP-binding cassette (ABC) transporter, ABCD1 (formerly adre
PMID 24316281

Direct effect of radiation on the peripheral nerve in a rat model.

Okuhara Y1, Shinomiya R, Peng F, Kamei N, Kurashige T, Yokota K, Ochi M.Author information 1Department of Orthopaedic Surgery, Hiroshima University Graduate School of Biomedical & Health Science , Hiroshima , Japan.AbstractAbstract Radiation neuropathy is one of the severe complications of radiotherapy. Entrapment neuropathy, caused by surrounding soft tissue fibrosis induced by radiation, plays a key role in the onset of this neuropathy. Meanwhile, the pathophysiology of the direct effect of radiation on the peripheral nerve is not yet fully understood. The aim of this study is to investigate the direct effects of radiation on rat sciatic nerves that are isolated from surrounding soft tissue. In the radiation group (R group), only the exposed sciatic nerve was irradiated with 90 Gy X-radiation. In the sham group (S group), the surgical procedures were completed without radiation. The sciatic functional index (SFI) result demonstrated no statistical differences between the R group and S group. However, even though the surrounding soft tissue was not irradiated, the macroscopic and histological findings of the R group at 24 weeks after radiation showed scar formation around the radiated nerve. These findings on radiation neuropathy indicate that neurohumoral factors derived from the radiated nerve itself may cause fibrosis. The electromyographic and histological examination showed axonal degeneration in the R group. Furthermore, the axon diameter and axon packing density in the R group demonstrated the axonal degeneration, even though it was 0.5 cm more proximal to the radiated portion than the axon packing density in the S group. This appearance was assumed to be "dying-back" neuropathy. It is believed that this study is a first step toward identifying an accurate pathophysiology for intractable radiation-induced peripheral neuropathy.
Journal of plastic surgery and hand surgery.J Plast Surg Hand Surg.2014 Jan 30. [Epub ahead of print]
Abstract Radiation neuropathy is one of the severe complications of radiotherapy. Entrapment neuropathy, caused by surrounding soft tissue fibrosis induced by radiation, plays a key role in the onset of this neuropathy. Meanwhile, the pathophysiology of the direct effect of radiation on the peripher
PMID 24479792

The Molecular and Pharmacological Mechanisms of HIV-Related Neuropathic Pain.

Hao S.Author information Department of Anesthesiology, University of Miami Miller School of Medicine, Miami, FL33136.AbstractInfection of the nervous system with the human immunodeficiency virus (HIV-1) can lead to cognitive, motor and sensory disorders. HIV-related sensory neuropathy (HIV-SN) mainly contains the HIV infection-related distal sensory polyneuropathy (DSP) and antiretroviral toxic neuropathies (ATN). The main pathological features that characterize DSP and ATN include retrograde ("dying back") axonal degeneration of long axons in distal regions of legs or arms, loss of unmyelinated fibers, and variable degree of macrophage infiltration in peripheral nerves and dorsal root ganglia (DRG). One of the most common complaints of HIV-DSP is pain. Unfortunately, many conventional agents utilized as pharmacologic therapy for neuropathic pain are not effective for providing satisfactory analgesia in painful HIV-related distal sensory polyneuropathy, because the molecular mechanisms of the painful HIV-SDP are not clear in detail. The HIV envelope glycoprotein, gp120, appears to contribute to this painful neuropathy. Recently, preclinical studies have shown that glia activation in the spinal cord and DRG has become an attractive target for attenuating chronic pain. Cytokines/chemokines have been implicated in a variety of painful neurological diseases and in animal models of HIV-related neuropathic pain. Mitochondria injured by ATN and/or gp120 may be also involved in the development of HIV-neuropathic pain. This review discusses the neurochemical and pharmacological mechanisms of HIV-related neuropathic pain based on the recent advance in the preclinical studies, providing insights into novel pharmacological targets for future therapy.
Current neuropharmacology.Curr Neuropharmacol.2013 Sep;11(5):499-512. doi: 10.2174/1570159X11311050005.
Infection of the nervous system with the human immunodeficiency virus (HIV-1) can lead to cognitive, motor and sensory disorders. HIV-related sensory neuropathy (HIV-SN) mainly contains the HIV infection-related distal sensory polyneuropathy (DSP) and antiretroviral toxic neuropathies (ATN). The mai
PMID 24403874