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1                                              SSPE cases had clinically compatible symptoms and measle
2                                              SSPE cases in California occurred at a high rate among u
3                                              SSPE demonstrates the high human cost of "natural" measl
4                                              SSPE patients were contrasted to patients with more prox
5                                              SSPE was diagnosed at a median age of 12 years (3-35 yea
6                                              SSPE was diagnosed in 15/44 (34.09%) patients in HP-PECG
7                                              SSPE-causing MeVs are characterized by a hypermutated ge
8 sles virus, and selected the library against SSPE brain sections.
9                         No treatment against SSPE is available, but the nucleoside analog remdesivir
10 tion of the measles virus (MeV) genome in an SSPE case suggested that the matrix (M) protein mutation
11  protein F50S, drove neuropathogenesis in an SSPE case.
12                 We show that treatment of an SSPE patient with remdesivir led to transient clinical i
13 panned on IgG extracted from the brain of an SSPE patient, or on a monospecific recombinant Fab ident
14 are complications of MeV infection, MIBE and SSPE are lethal.
15 usion complexes confirmed that both MIBE and SSPE F protein mutations promoted fusion with less depen
16 neurological complications, such as MIBE and SSPE.
17 propriate treatment of incidentally detected SSPE, for which the data are sparse.
18             The estimated risk of developing SSPE was 10-fold higher than the previous estimate repor
19 sles and to calculate the risk of developing SSPE.
20  antibodies immunostained cells in different SSPE brains but not in control brain.
21 etection of subsegmental pulmonary embolism (SSPE) in patients suspected of acute pulmonary embolism
22 ificance of subsegmental pulmonary embolism (SSPE) remains to be determined.
23  were found to be independent predictors for SSPE, and patients with SSPE were at an increased risk o
24 the patterns of infection that are risks for SSPE, early infection and a close temporal relationship
25 1 recombinant antibodies (rAbs) derived from SSPE brain plasma cell clones recognized the measles vir
26      This case, diametrically different from SSPE, has 2 unique features, its focal nature and its pe
27 monospecific recombinant Fab identified from SSPE brain.
28        Based on studies of brain tissue from SSPE patients and our work with MV-infected NSE-CD46(+)
29 irmed in 748 patients, of whom 116 (16%) had SSPE; PE was ruled out in 2980 patients.
30  CSF/serum ratios of IL-1beta and sICAM-1 in SSPE indicate synthesis of IL-1beta and sICAM-1 in the c
31 ith mutations that are typically detected in SSPE, characterized by a hypermutated M gene.
32 toire of IgG V region sequences expressed in SSPE brain.
33  encouraging the future use of remdesivir in SSPE patients.
34 in, confirming that the antibody response in SSPE targets primarily the agent causing disease.
35 lk of available data suggest that incidental SSPE is associated with recurrent venous thromboembolism
36 her interpreted the images for assessment of SSPE, image quality, and quantitative parameters.
37                Clinicians should be aware of SSPE in patients with compatible symptoms, even in older
38 as conducted to identify reports of cases of SSPE in persons residing in the United States who had me
39 ation against measles prevents more cases of SSPE than was originally estimated.
40 f the present study was to identify cases of SSPE that were associated with the resurgence of measles
41 the nucleocapsid protein of MV, the cause of SSPE.
42 arteries, which allows enhanced detection of SSPE.
43 s, it was determined that the development of SSPE was associated with the measles resurgence that occ
44  11 patients with a presumptive diagnosis of SSPE were tested for the presence of measles virus RNA.
45 atients with SSPE confirmed the diagnosis of SSPE.
46 uid (CSF) or medical record documentation of SSPE.
47 e model that mimics the cardinal features of SSPE.
48 d to CDPH during 1988-1991, the incidence of SSPE was 1:1367 for children <5 years, and 1:609 for chi
49  to the understanding of the pathogenesis of SSPE and the mechanism enabling viruses to evade the imm
50 o both molecularly probe the pathogenesis of SSPE and to test a variety of therapies to treat the dis
51 eins sheds light on the shared properties of SSPE-causing MeVs and further contributes to understandi
52                         The specificities of SSPE rAbs to these regions of the MV nucleocapsid protei
53 on of remdesivir as a potential treatment of SSPE and highlights the necessity to functionally unders
54 e are no drugs approved for the treatment of SSPE.
55 wed the clinical progression of a 5-year-old SSPE patient after treatment with the nucleoside analog
56 ally, recombinant viruses expressing MIBE or SSPE fusion complexes spread in the absence of known MeV
57 rom brain tissue of individuals with MIBE or SSPE, infected during the same epidemic, after the onset
58 mbed to subacute sclerosing panencephalitis (SSPE) about 20 years after acute measles virus (MeV) inf
59         Subacute sclerosing panencephalitis (SSPE) is a fatal complication of measles.
60         Subacute sclerosing panencephalitis (SSPE) is a lethal neurological disorder occurring severa
61         Subacute sclerosing panencephalitis (SSPE) is a progressive fatal neurodegenerative disease a
62         Subacute sclerosing panencephalitis (SSPE) is a rare but fatal late neurological complication
63         Subacute sclerosing panencephalitis (SSPE) is caused by atypical measles infection.
64 nce and subacute sclerosing panencephalitis (SSPE) occur even in the face of an intact immune respons
65 such as subacute sclerosing panencephalitis (SSPE) or cryptococcal meningitis have been shown to repr
66 such as subacute sclerosing panencephalitis (SSPE) or cryptococcal meningitis have been shown to repr
67  causes subacute sclerosing panencephalitis (SSPE) several years after acute infection.
68 an with subacute sclerosing panencephalitis (SSPE), a chronic encephalitis caused by measles virus, a
69 tion is subacute sclerosing panencephalitis (SSPE), a fatal disease of the central nervous system tha
70  causes subacute sclerosing panencephalitis (SSPE), a progressive, relentless fatal disorder.
71 ts with subacute sclerosing panencephalitis (SSPE), multiple sclerosis (MS), or other neurologic dise
72 cation, subacute sclerosing panencephalitis (SSPE), occurs during persistent MV infection of the CNS
73 ts with subacute sclerosing panencephalitis (SSPE), which is associated with persistent measles virus
74 ng with subacute sclerosing panencephalitis (SSPE).
75 nt with subacute sclerosing panencephalitis (SSPE).
76 isorder subacute sclerosing panencephalitis (SSPE).
77 significance of symptomatic subsegmental PE (SSPE) are conflicting, making it difficult to draw concl
78                                    Seventeen SSPE cases were identified.
79 alyzed from brain tissue samples of a single SSPE case and compared with MIBE sequences previously ob
80 rs, including various concentrations of SSC, SSPE, PBS, TRIS, MES, sodium phosphate, and potassium ph
81                                     Both the SSPE and the MIBE viruses had amino acid substitutions i
82                CSF sICAM-1 was higher in the SSPE group than in the MS or OND group.
83 IL-1beta CSF/serum ratios were higher in the SSPE than in the MS or OND group.
84  sICAM-1 CSF/serum ratios were higher in the SSPE than the OND group.
85 ta was significantly increased in CSF of the SSPE group compared with levels in the MS or OND group.
86                              All four of the SSPE rAbs enriched phage-displayed peptide sequences tha
87                                    While the SSPE F required the presence of a homotypic attachment p
88 ly, recombinant wild-type-based MeV with the SSPE-F gene or the F gene with the N465I mutation was no
89 ed by diluting the positive clones from this SSPE phage-displayed library at a ratio of 10(-6) into a
90 hts the necessity to functionally understand SSPE-causing MeV.IMPORTANCEMeasles virus (MeV) causes ac
91                                        Using SSPE as a model system, we developed a strategy to ident
92                                        Using SSPE as a model system, we have developed a PCR-based st
93      This study aimed to investigate whether SSPE forms a distinct subset of thromboembolic disease c
94 ucleocapsid protein could be identified with SSPE brain rAbs.
95 0.7% vs 6.5%; P = .17) between patients with SSPE and those with more proximal PE.
96 issue samples obtained from 11 patients with SSPE confirmed the diagnosis of SSPE.
97      This study indicates that patients with SSPE mimic those with more proximally located PE in rega
98 ndent predictors for SSPE, and patients with SSPE were at an increased risk of VTE during follow-up (
99                For 5 of the 11 patients with SSPE who had samples tested by RT-PCR and for 7 patients
100 les tested by RT-PCR and for 7 patients with SSPE who were identified in published case reports, it w