self-limiting

出典: meddic

  • 自ら制限する、自己制御式の
Symptomatic therapy is recommended in simple self-limiting GI infections where diarrhea is frequent or troublesome, while diagnostic workup is in progress, when specific management fails to improve symptoms, or when a specific etiology is not identified.(WMM.465)
self-limited

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/08/26 01:09:05」(JST)

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英文文献

  • Assessment of dried blood samples as an alternative less invasive method for detection of Hepatitis E virus marker in an outbreak setting.
  • Singh MP1, Majumdar M, Budhathoki B, Goyal K, Chawla Y, Ratho RK.Author information 1Department of Virology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.AbstractHepatitis E virus (HEV) is the causative agent of hepatitis E. It can be asymptomatic, associated with acute self-limiting hepatitis or acute liver failure. The conventional diagnosis of HEV infection relies on anti-HEV IgM serology. The collection of blood samples by venepunture for laboratory confirmation is often difficult during an outbreak. Thus, testing the specimens of dried blood spots (DBS) on filter papers can prove to be a feasible alternative. The present study aimed to evaluate the applicability of anti-HEV IgM detection from DBS samples and the stability of anti-HEV IgM detection at varied time interval, at various storage temperatures. Paired blood and DBS sample were collected from 44 jaundiced patients and eight healthy controls during HEV outbreaks. The DBS were tested for anti-HEV IgM by available ELISA kit with in-house modifications. Three cut offs were determined, that is, the CO1: kit cut-off, CO2: mean of negative controls above 3SD and CO3: area under Receiver operating Curve. The sensitivity of anti-HEV IgM detection ranged from 86-91%. The maximum sensitivity (91%) and specificity (100%) was obtained using CO3. Maximum stability of anti-HEV IgM antibodies (100%) was observed till 65 days at 4°C. Storage at 37°C significantly reduced anti-HEV IgM positivity, wherein 42.85% sample became negative by 45 days. DBS showed good sensitivity and specificity for detecting anti-HEV IgM and can be considered an alternate to serum sample. Moreover, anti-HEV IgM was stable at 4°C, which makes DBS a preferred method for storage and transportation of the sample to reference laboratory. J. Med. Virol. 86:713-719, 2014. © 2013 Wiley Periodicals, Inc.
  • Journal of medical virology.J Med Virol.2014 Apr;86(4):713-9. doi: 10.1002/jmv.23874. Epub 2013 Dec 30.
  • Hepatitis E virus (HEV) is the causative agent of hepatitis E. It can be asymptomatic, associated with acute self-limiting hepatitis or acute liver failure. The conventional diagnosis of HEV infection relies on anti-HEV IgM serology. The collection of blood samples by venepunture for laboratory conf
  • PMID 24375126
  • 1.61 T-cells expressing TLR4 and CXCR4 are associated with an RA diagnostic in early inflammatory arthritis.
  • Parmar R1, Burska A, Emery P, Mellado M, Sacre S, Ponchel F.Author information 1Department of Immunology & Oncology, National Centre of Biotechnology/CSIC, Madrid, Spain.AbstractBACKGROUND: Biomarkers for the early diagnosis of RA are still needed despite the improvement brought about by ACR/EULAR-2010 criteria which include the ACPA biomarker. T-cell subset dys-regulation was shown to occur early in the RA disease continuum (Blood, 2002), to predict response to MTX (ARD, 2013) and safe discontinuation of biological when in clinical remission (ARD 2010). The aim of the current study is to determine whether T-cell subset phenotyping adding novel cell surface markers for TLR2, TLR4, IL-6R and 4 chemokine receptors (CCR3, CXCR4 CCR5 and CCR6) can discriminate between patients who are clearly RA from those with other (inflammatory) rheumatic diseases in an early arthritis clinic.
  • Annals of the rheumatic diseases.Ann Rheum Dis.2014 Mar 1;73 Suppl 1:A26-7. doi: 10.1136/annrheumdis-2013-205124.60.
  • BACKGROUND: Biomarkers for the early diagnosis of RA are still needed despite the improvement brought about by ACR/EULAR-2010 criteria which include the ACPA biomarker. T-cell subset dys-regulation was shown to occur early in the RA disease continuum (Blood, 2002), to predict response to MTX (ARD, 2
  • PMID 24489177
  • Caffey disease: New perspectives on old questions.
  • Nistala H1, Mäkitie O2, Jüppner H3.Author information 1Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA.2Division of Pediatric Endocrinology and Metabolic Bone Diseases, Helsinki University Central Hospital and University of Helsinki, Helsinki, Finland; Folkhälsan Institute of Genetics, Helsinki, Finland.3Pediatric Nephrology Unit and Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: hjueppner@partners.org.AbstractThe autosomal dominant form of Caffey disease is a largely self-limiting infantile bone disorder characterized by acute inflammation of soft tissues and localized thickening of the underlying bone cortex. It is caused by a recurrent arginine-to-cysteine substitution (R836C) in the α1(I) chain of type I collagen. However, the functional link between this mutation and the underlying pathogenetic mechanisms still remains elusive. Importantly, it remains to be established as to how a point-mutation in type I collagen leads to a cascade of inflammatory events and spatio-temporally limited hyperostotic bone lesions, and how structural and inflammatory components contribute to the different organ-specific manifestations in Caffey disease. In this review we attempt to shed light on these questions based on the current understanding of other mutations in type I collagen, their role in perturbing collagen biogenesis, and consequent effects on cell-cell and cell-matrix interactions.
  • Bone.Bone.2014 Mar;60C:246-251. doi: 10.1016/j.bone.2013.12.030. Epub 2013 Dec 31.
  • The autosomal dominant form of Caffey disease is a largely self-limiting infantile bone disorder characterized by acute inflammation of soft tissues and localized thickening of the underlying bone cortex. It is caused by a recurrent arginine-to-cysteine substitution (R836C) in the α1(I) chain of ty
  • PMID 24389367
  • ALK inhibitors in the treatment of advanced NSCLC.
  • Gridelli C1, Peters S, Sgambato A, Casaluce F, Adjei AA, Ciardiello F.Author information 1Division of Medical Oncology, "S.G. Moscati" Hospital, Avellino, Italy. Electronic address: cgridelli@libero.it.AbstractPharmacologic agents that target protein products of oncogenes in tumors are playing an increasing clinical role in the treatment of cancer. Currently, the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represent the standard of care for patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) harboring activating EGFR mutations. Subsequently other genetic abnormalities with "driver" characteristics - implying transforming and tumor maintenance capabilities have been extensively reported in several small distinct subsets of NSCLC. Among these rare genetic changes, anaplastic lymphoma kinase (ALK) gene rearrangements, most often consisting in a chromosome 2 inversion leading to a fusion with the echinoderm microtubule-associated protein like 4 (EML4) gene, results in the abnormal expression and activation of this tyrosine kinase in the cytoplasm of cancer cells. This rearrangement occurs in 2-5% of NSCLC, predominantly in young (50 years or younger), never- or former-smokers with adenocarcinoma. This aberration most commonly occurs a independently of EGFR and KRAS gene mutations. A fluorescent in situ hybridization assay was approved by the US Food and Drug Administration (FDA) as the standard method for the detection of ALK gene rearrangement in clinical practice and is considered the gold standard. Crizotinib, a first-in-class dual ALK and c-MET inhibitor, has been shown to be particularly effective against ALK positive NSCLC, showing dramatic and prolonged responses with low toxicity, predominantly restricted to the gastro-intestinal and visual systems, and generally self-limiting or easily managed. However, resistance to crizotinib inevitably emerges. The molecular mechanisms of resistance are currently under investigation, as are therapeutic approaches including crizotinib-based combination therapy and novel agents such as Hsp90 inhibitors. This review aims to present the current knowledge on this fusion gene, the clinic-pathological profile of ALK rearranged NSCLC, and to review the existing literature on ALK inhibitors, focusing on their role in the treatment of NSCLC.
  • Cancer treatment reviews.Cancer Treat Rev.2014 Mar;40(2):300-6. doi: 10.1016/j.ctrv.2013.07.002. Epub 2013 Aug 7.
  • Pharmacologic agents that target protein products of oncogenes in tumors are playing an increasing clinical role in the treatment of cancer. Currently, the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represent the standard of care for patients with locally advanced or m
  • PMID 23931927

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★リンクテーブル★
関連記事self」「limiting」「selfing

self」

  [★]

  • n.
  • セルフ
  • adj.
自己の


WordNet   license wordnet

「(used as a combining form) relating to--of or by or to or from or for--the self; "self-knowledge"; "self-proclaimed"; "self-induced"」

WordNet   license wordnet

「your consciousness of your own identity」
ego

WordNet   license wordnet

「a person considered as a unique individual; "one''s own self"」

PrepTutorEJDIC   license prepejdic

「(他人と区別して)『自己』,自分,自身 / 〈C〉(人・物の)本質,個性;性格の一面 / 〈U〉私利,私欲,私心 / 同じ材料でできた,共ぎれの」


limiting」

  [★]

  • 極限の、律速の
rate-determiningrate-limitingutmost

WordNet   license wordnet

「strictly limiting the reference of a modified word or phrase; "the restrictive clause in `Each made a list of the books that had influenced him'' limits the books on the list to only those particular ones defined by the clause"」

PrepTutorEJDIC   license prepejdic

「制限する,限定する」


selfing」

  [★]

  • n.
self-pollination




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