ライフサイエンスコーパス: SSPE

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 sles virus, and selected the library against SSPE brain sections.

7 panned on IgG extracted from the brain of an SSPE patient, or on a monospecific recombinant Fab ident

8 propriate treatment of incidentally detected SSPE, for which the data are sparse.

9 The estimated risk of developing SSPE was 10-fold higher than the previous estimate repor

10 sles and to calculate the risk of developing SSPE.

11 antibodies immunostained cells in different SSPE brains but not in control brain.

12 ificance of subsegmental pulmonary embolism (SSPE) remains to be determined.

13 were found to be independent predictors for SSPE, and patients with SSPE were at an increased risk o

14 the patterns of infection that are risks for SSPE, early infection and a close temporal relationship

15 1 recombinant antibodies (rAbs) derived from SSPE brain plasma cell clones recognized the measles vir

16 This case, diametrically different from SSPE, has 2 unique features, its focal nature and its pe

17 monospecific recombinant Fab identified from SSPE brain.

18 Based on studies of brain tissue from SSPE patients and our work with MV-infected NSE-CD46(+)

19 irmed in 748 patients, of whom 116 (16%) had SSPE; PE was ruled out in 2980 patients.

20 CSF/serum ratios of IL-1beta and sICAM-1 in SSPE indicate synthesis of IL-1beta and sICAM-1 in the c

21 toire of IgG V region sequences expressed in SSPE brain.

22 in, confirming that the antibody response in SSPE targets primarily the agent causing disease.

23 lk of available data suggest that incidental SSPE is associated with recurrent venous thromboembolism

24 Clinicians should be aware of SSPE in patients with compatible symptoms, even in older

25 as conducted to identify reports of cases of SSPE in persons residing in the United States who had me

26 ation against measles prevents more cases of SSPE than was originally estimated.

27 f the present study was to identify cases of SSPE that were associated with the resurgence of measles

28 the nucleocapsid protein of MV, the cause of SSPE.

29 s, it was determined that the development of SSPE was associated with the measles resurgence that occ

30 11 patients with a presumptive diagnosis of SSPE were tested for the presence of measles virus RNA.

31 atients with SSPE confirmed the diagnosis of SSPE.

32 uid (CSF) or medical record documentation of SSPE.

33 e model that mimics the cardinal features of SSPE.

34 d to CDPH during 1988-1991, the incidence of SSPE was 1:1367 for children <5 years, and 1:609 for chi

35 to the understanding of the pathogenesis of SSPE and the mechanism enabling viruses to evade the imm

36 o both molecularly probe the pathogenesis of SSPE and to test a variety of therapies to treat the dis

37 The specificities of SSPE rAbs to these regions of the MV nucleocapsid protei

38 Subacute sclerosing panencephalitis (SSPE) is a fatal complication of measles.

39 Subacute sclerosing panencephalitis (SSPE) is a progressive fatal neurodegenerative disease a

40 Subacute sclerosing panencephalitis (SSPE) is caused by atypical measles infection.

41 such as subacute sclerosing panencephalitis (SSPE) or cryptococcal meningitis have been shown to repr

42 such as subacute sclerosing panencephalitis (SSPE) or cryptococcal meningitis have been shown to repr

43 an with subacute sclerosing panencephalitis (SSPE), a chronic encephalitis caused by measles virus, a

44 tion is subacute sclerosing panencephalitis (SSPE), a fatal disease of the central nervous system tha

45 causes subacute sclerosing panencephalitis (SSPE), a progressive, relentless fatal disorder.

46 ts with subacute sclerosing panencephalitis (SSPE), multiple sclerosis (MS), or other neurologic dise

47 cation, subacute sclerosing panencephalitis (SSPE), occurs during persistent MV infection of the CNS

48 ts with subacute sclerosing panencephalitis (SSPE), which is associated with persistent measles virus

49 nt with subacute sclerosing panencephalitis (SSPE).

50 significance of symptomatic subsegmental PE (SSPE) are conflicting, making it difficult to draw concl

51 Seventeen SSPE cases were identified.

52 rs, including various concentrations of SSC, SSPE, PBS, TRIS, MES, sodium phosphate, and potassium ph

53 CSF sICAM-1 was higher in the SSPE group than in the MS or OND group.

54 IL-1beta CSF/serum ratios were higher in the SSPE than in the MS or OND group.

55 sICAM-1 CSF/serum ratios were higher in the SSPE than the OND group.

56 ta was significantly increased in CSF of the SSPE group compared with levels in the MS or OND group.

57 All four of the SSPE rAbs enriched phage-displayed peptide sequences tha

58 ed by diluting the positive clones from this SSPE phage-displayed library at a ratio of 10(-6) into a

59 Using SSPE as a model system, we developed a strategy to ident

60 Using SSPE as a model system, we have developed a PCR-based st

61 This study aimed to investigate whether SSPE forms a distinct subset of thromboembolic disease c

62 ucleocapsid protein could be identified with SSPE brain rAbs.

63 0.7% vs 6.5%; P = .17) between patients with SSPE and those with more proximal PE.

64 issue samples obtained from 11 patients with SSPE confirmed the diagnosis of SSPE.

65 This study indicates that patients with SSPE mimic those with more proximally located PE in rega

66 ndent predictors for SSPE, and patients with SSPE were at an increased risk of VTE during follow-up (

67 For 5 of the 11 patients with SSPE who had samples tested by RT-PCR and for 7 patients

68 les tested by RT-PCR and for 7 patients with SSPE who were identified in published case reports, it w