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1 tes JHM.WU and JHM.SD promote severe central nervous system disease.
2 by Escherichia coli K1, is a serious central nervous system disease.
3 of symptoms or signs consistent with central nervous system disease.
4 may shed new light on mechanisms underlying nervous system disease.
5 d therapeutic approaches to this challenging nervous system disease.
6 n that causes devastating ocular and central nervous system disease.
7 ly relapsed with disseminated and/or central nervous system disease.
8 at points to new strategies for treatment of nervous system disease.
9 of either copper or iron results in central nervous system disease.
10 proteins, which leads to progressive central nervous system disease.
11 requirement for X4 viruses to cause central nervous system disease.
12 r for the development of HIV-induced central nervous system disease.
13 ed for the treatment of a variety of central nervous system diseases.
14 itors in clinical trials for various central nervous system diseases.
15 ty's interests in ameliorating the impact of nervous system diseases.
16 of neuroinflammation in a variety of central nervous system diseases.
17 ts in the brain for the treatment of central nervous system diseases.
18 for patients with cardiovascular and central nervous system diseases.
19 ring neuronal development and upregulated in nervous system diseases.
20 r HHV-6 in the pathogenesis of these central nervous system diseases.
21 atins as a treatment of inflammatory central nervous system diseases.
22 nflammatory conditions, particularly central nervous system diseases.
23 on associated with several different central nervous system diseases.
24 esis of poorly understood idiopathic central nervous system diseases.
25 proaches to promote functional recovery from nervous system diseases.
27 50.5 +/- 13.8 yrs, p < .001), acute central nervous system disease (21% vs. 4%, p = .001), mechanica
28 caques can cause fatal demyelinating central nervous system disease analogous to progressive multifoc
30 future perspectives for modeling of central nervous system disease and brain development in vitro.
31 type 2 and 3) or absence (type 1) of central nervous system disease and severity of clinical manifest
32 he brains of some AIDS patients with central nervous system disease and suggest that R5 variants with
33 fining criteria of antibody-mediated central nervous system disease and the extent to which the psych
34 nd that mimic certain aspects of the central nervous system diseases and immunosuppression that can o
35 tion of the potential of STS-E412 in central nervous system diseases and organ protection is warrante
36 encephalitis and other complement-dependent nervous system diseases and thus underscore the need for
37 ears, immunocompromise, a history of central nervous system disease, and a history of seizure within
38 to generate a current picture of the central nervous system disease, and emphasize potential aspects
42 for the treatment of central and peripheral nervous system diseases associated with excess glutamate
43 lso underlie acquired peripheral and central nervous system diseases associated with small-cell lung
45 a progressive and severe human degenerative nervous system disease caused by a primary astroglial ab
46 system itself may have beneficial effects in nervous system diseases considered neurodegenerative.
48 y modified cells in animal models of central nervous system disease encourage the continued developme
53 mproved understanding of the pathogenesis of nervous system disease in these infections; more effecti
54 ors between those three inflammatory central nervous system diseases in adults and children to suppor
55 y may also play a role in preventing central nervous system diseases in HIV-positive individuals.
56 of neuronal injury for a variety of central nervous system diseases, including stroke and neurodegen
57 A key hurdle for drug discoverers of central nervous system disease is a lack of high quality neurona
60 that is effective for both types of central nervous system disease, is so toxic that it kills 5% of
61 (MOG) are associated with autoimmune central nervous system diseases like acute disseminated encephal
62 complex diseases such as cancer and central nervous system diseases may require complex therapeutic
63 eased concentrations in inflammatory central nervous system diseases, may profoundly affect microglia
65 s is an inflammatory, demyelinating, central nervous system disease mediated by myelin-specific T cel
68 vestigation included cancer (n = 31; 23.1%), nervous system diseases (n = 26; 19.4%), and injury and
70 experimentally supported associations about nervous system diseases (NSDs) and noncoding RNAs (ncRNA
72 to what exactly defines biologically central nervous system disease or what specific cerebrospinal fl
74 rtension, pulmonary dysfunction, and central nervous system disease persisted, following treatment.
76 emarkably similar to humans with sympathetic nervous system disease, raising the possibility that it
77 , chronic obstructive pulmonary disease, and nervous system disease relative to comparable US women.
78 reutzfeldt-Jakob's disease and other central nervous system diseases such as Parkinson's and Huntingt
79 been differentially associated with central nervous system diseases, suggesting an HHV-6 variant-spe
80 tible to both neuronal infection and central nervous system disease than their immunocompetent litter
81 gher rate of disease progression and central nervous system disease than those infected with HIV-1 al
82 derlying basis of the characteristic central nervous system disease that occurs following intracerebr
83 patients with clinically distinctive central nervous system diseases that appear to benefit from immu
84 he most recent published findings of central nervous system diseases that have evidence of a post-str
85 ipah virus (NiV), which cause lethal central nervous system diseases-the addition of cholesterol to a
86 lso had more frequent renal disease, central nervous system disease, thrombocytopenia, and clotting e
87 m of diseases in humans ranging from central nervous system disease to lethal hemorrhagic fevers with
88 for therapeutic applications, especially for nervous system disease, using successive application of
89 odel of human immunodeficiency virus central nervous system disease was developed in which more than
91 hic factor for the treatment of many central nervous system diseases, was delivered by IN followed by
92 y the pathogenesis of HIV-induced peripheral nervous system disease, we established a model in which
93 sit will extend the ability to model central nervous system disease while facilitating high-throughpu
94 ology will yield important insights into how nervous system diseases with systemic comorbidities aris
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