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1 V) isolates JHM.WU and JHM.SD promote severe central nervous system disease.
2  caused by Escherichia coli K1, is a serious central nervous system disease.
3 because of symptoms or signs consistent with central nervous system disease.
4  pathogen that causes devastating ocular and central nervous system disease.
5 invariably relapsed with disseminated and/or central nervous system disease.
6 r excess of either copper or iron results in central nervous system disease.
7 sfolded proteins, which leads to progressive central nervous system disease.
8  a basic requirement for X4 viruses to cause central nervous system disease.
9 ic marker for the development of HIV-induced central nervous system disease.
10 idely used for the treatment of a variety of central nervous system diseases.
11 0A inhibitors in clinical trials for various central nervous system diseases.
12 measure of neuroinflammation in a variety of central nervous system diseases.
13 tic agents in the brain for the treatment of central nervous system diseases.
14 utcomes for patients with cardiovascular and central nervous system diseases.
15  role for HHV-6 in the pathogenesis of these central nervous system diseases.
16 le of statins as a treatment of inflammatory central nervous system diseases.
17 ion in inflammatory conditions, particularly central nervous system diseases.
18 generation associated with several different central nervous system diseases.
19 pathogenesis of poorly understood idiopathic central nervous system diseases.
20 other nonantiepileptic drug (13%), and acute central nervous system disease (12%).
21 15.5 vs. 50.5 +/- 13.8 yrs, p < .001), acute central nervous system disease (21% vs. 4%, p = .001), m
22 mised macaques can cause fatal demyelinating central nervous system disease analogous to progressive
23 ress and future perspectives for modeling of central nervous system disease and brain development in
24 esence (type 2 and 3) or absence (type 1) of central nervous system disease and severity of clinical
25 CD4 in the brains of some AIDS patients with central nervous system disease and suggest that R5 varia
26 r the defining criteria of antibody-mediated central nervous system disease and the extent to which t
27 ction, and that mimic certain aspects of the central nervous system diseases and immunosuppression th
28 r evaluation of the potential of STS-E412 in central nervous system diseases and organ protection is
29 ast 60 years, immunocompromise, a history of central nervous system disease, and a history of seizure
30 , so as to generate a current picture of the central nervous system disease, and emphasize potential
31 ces in initial white blood cell (WBC) count, central nervous system disease, and risk group.
32 and connected with human metabolic diseases, central nervous system diseases, and neoplasms.
33   Infections, medications, and rare cases of central nervous system disease are much less common.
34 on may also underlie acquired peripheral and central nervous system diseases associated with small-ce
35 indered by the lack of objective measures of central nervous system disease burden.
36                                              Central nervous system disease continues to be difficult
37 netically modified cells in animal models of central nervous system disease encourage the continued d
38                                              Central nervous system disease frequently results in hig
39                                   Concurrent central nervous system disease has been correlated to a
40 e agent of toxoplasmosis, a leading cause of central nervous system disease in AIDS.
41             Identification of biomarkers for central nervous system disease in MPS patients would fac
42 criminators between those three inflammatory central nervous system diseases in adults and children t
43      They may also play a role in preventing central nervous system diseases in HIV-positive individu
44 the risk of neuronal injury for a variety of central nervous system diseases, including stroke and ne
45         A key hurdle for drug discoverers of central nervous system disease is a lack of high quality
46 f much significance was the finding that the central nervous system disease is brain autonomous.
47                   The effective treatment of central nervous system diseases is a major challenge due
48 nly drug that is effective for both types of central nervous system disease, is so toxic that it kill
49 protein (MOG) are associated with autoimmune central nervous system diseases like acute disseminated
50 ght that complex diseases such as cancer and central nervous system diseases may require complex ther
51 ith increased concentrations in inflammatory central nervous system diseases, may profoundly affect m
52 itis (EAE) is an animal model for autoimmune central nervous system disease mediated by CD4 T cells.
53 sclerosis is an inflammatory, demyelinating, central nervous system disease mediated by myelin-specif
54 alomyelitis (EAE) is an animal model for the central nervous system disease multiple sclerosis (MS).
55 reversible neurological decline in the human central nervous system disease, multiple sclerosis (MS).
56 he relevant oligoclonal IgGs in inflammatory central nervous system diseases of unknown cause.
57 nsus as to what exactly defines biologically central nervous system disease or what specific cerebros
58 vement such as renal disease (P < 0.0001) or central nervous system disease (P < 0.0025).
59 ary hypertension, pulmonary dysfunction, and central nervous system disease persisted, following trea
60              Death was associated with acute central nervous system disease, prolonged ventilation, t
61 's and Creutzfeldt-Jakob's disease and other central nervous system diseases such as Parkinson's and
62 and have been differentially associated with central nervous system diseases, suggesting an HHV-6 var
63 e susceptible to both neuronal infection and central nervous system disease than their immunocompeten
64 antly higher rate of disease progression and central nervous system disease than those infected with
65 g the underlying basis of the characteristic central nervous system disease that occurs following int
66 dentify patients with clinically distinctive central nervous system diseases that appear to benefit f
67 arizes the most recent published findings of central nervous system diseases that have evidence of a
68 V) and Nipah virus (NiV), which cause lethal central nervous system diseases-the addition of choleste
69 lation also had more frequent renal disease, central nervous system disease, thrombocytopenia, and cl
70  spectrum of diseases in humans ranging from central nervous system disease to lethal hemorrhagic fev
71 erated model of human immunodeficiency virus central nervous system disease was developed in which mo
72                                              Central nervous system disease was present at diagnosis
73 eurotrophic factor for the treatment of many central nervous system diseases, was delivered by IN fol
74 nical visit will extend the ability to model central nervous system disease while facilitating high-t

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