ライフサイエンスコーパス: neurologic dysfunction

1 t distinct failures that could contribute to neurologic dysfunction.

2 ath and survived for 8 months despite severe neurologic dysfunction.

3 >/= 10, and 62% showed clinical evidence of neurologic dysfunction.

4 liver failure during infancy without notable neurologic dysfunction.

5 atic incubation period precedes the onset of neurologic dysfunction.

6 pathways differ in patients with and without neurologic dysfunction.

7 ion in the central nervous system and severe neurologic dysfunction.

8 on of propofol resulted in 1) aggravation of neurologic dysfunction, 2) increased 28-day mortality ra

9 itory-vestibular-visual deficits (6%), focal neurologic dysfunction (7.1%), and severe headaches (5.3

10 c defects, reduced pigmentation, progressive neurologic dysfunction and a bleeding diathesis.

11 logic examination in SLE for excluding overt neurologic dysfunction and assuring a non-NPSLE group se

12 The CMV-lambda6 transgenic mice develop neurologic dysfunction and Congophilic amyloid deposits

13 iasis patient who presented with progressive neurologic dysfunction and seizures after 2.5 years of f

14 reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or p

15 een advanced cerebral amyloid angiopathy and neurologic dysfunction and that such large-scale brain n

16 -cardiac arrest syndrome regarding survival, neurologic dysfunction, and histologic lesions (brain, h

17 nt myelin or myelin loss, lead to a range of neurologic dysfunctions, and can result in early death.

18 ting era of discovery in which substrates of neurologic dysfunction are being identified at the synap

19 to 0.15 Hz) heart rate power and severity of neurologic dysfunction (as assessed by the admission Gla

20 oglia, are key participants in mediating the neurologic dysfunction associated with HIV infection of

21 ldren at 18 mo of age: children with minimal neurologic dysfunction at age 18 mo had significantly hi

22 PrP) or Tg(DePrP) mice exhibited spontaneous neurologic dysfunction at more than 600 days of age.

23 The mice developed neurologic dysfunction between 380 and 660 days after in

24 Bilirubin-induced neurologic dysfunction (BIND) and kernicterus has been u

25 vels were the most significant predictors of neurologic dysfunction, but it is unclear if they are di

26 ssing both mutant and wt PrP did not exhibit neurologic dysfunction, but their brains revealed low le

27 eltaGPI) developed a late-onset, spontaneous neurologic dysfunction characterized by widespread amylo

28 manifestations include fever, splenomegaly, neurologic dysfunction, coagulopathy, liver dysfunction,

29 Post-transplantation progression of neurologic dysfunction depended significantly on the pre

30 Severe neurologic dysfunction develops in Sepp1 null mice (Sepp

31 Therefore, it may be that the neurologic dysfunction found in these animals is associa

32 ataxia telangiectasia (AT), associated with neurologic dysfunction, growth abnormalities, and extrem

33 with neurotropic pathogens, post-infectious neurologic dysfunction has traditionally been attributed

34 ensitivity reactions, cardiovascular events, neurologic dysfunction, hepatic and renal failure, and t

35 eficits (HR, 2.3; 95% CI, 1.3 to 4.0); focal neurologic dysfunction (HR, 4.9; 95% CI, 3.2 to 7.5); an

36 ity of blood clot (mg) in brain that produce neurologic dysfunction in 50% of the rabbits (P(50)), wi

37 spontaneously ill TgM83(+/+) mice developed neurologic dysfunction in approximately 210 d.

38 The child developed marked neurologic dysfunction in association with a seizure dis

39 and to distinguish them from other causes of neurologic dysfunction in cancer patients.

40 us, causes progressive immunosuppression and neurologic dysfunction in cats.

41 Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress d

42 The unknown biochemical basis for neurologic dysfunction in cobalamin deficiency and the f

43 Our understanding of neurologic dysfunction in demyelinating diseases and the

44 ately 8 months, and treatment often leads to neurologic dysfunction in long-term survivors, emphasizi

45 t give rise to cell death, inflammation, and neurologic dysfunction in patients of all demographics.

46 co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along wit

47 lerosis (MS) are common causes of visual and neurologic dysfunction in young adults.

48 but none with febrile illness had persistent neurologic dysfunction, including static encephalopathy

49 ignificantly correlated with the severity of neurologic dysfunction indicated by mJOA score (r(2) = 0

50 umulated low levels of PrPSc, they showed no neurologic dysfunction, indicating that low levels of Pr

51 ted Atm allele displayed growth retardation, neurologic dysfunction, male and female infertility seco

52 ist for years after acute infection, and new neurologic dysfunction may develop after acute illness.

53 Neurologic dysfunction may persist for years after acute

54 Neurologic dysfunction may result from leukemic infiltra

55 ary outcome included postoperative renal and neurologic dysfunction, nosocomial infections, length of

56 has been used to describe moderate to severe neurologic dysfunction observed in children exposed to e

57 mimicry could explain persistent or ongoing neurologic dysfunction occurring after elimination of th

58 yelitis (EAE), are characterized by episodic neurologic dysfunction, perivascular mononuclear cell in

59 tage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent

60 malities to subsequent stroke or progressive neurologic dysfunction requires further study.

61 ry-vestibular-visual sensory deficits, focal neurologic dysfunction, seizures, and serious headaches

62 ith Rett syndrome exhibit a delayed onset of neurologic dysfunction that manifests around the child's

63 ncillary testing to rule out other causes of neurologic dysfunction that mimic botulism, such as stro

64 g Efficacy of Targeted Sedation and Reducing Neurologic Dysfunction trial, which compared sedation wi

65 e at HCT was 91%, whereas that for boys with neurologic dysfunction was 66% (P = .08).

66 Neurologic dysfunction was assessed using a well-standar

67 Mild chronic neurologic dysfunction was reported in all three patient

68 Neurosensory and neurologic dysfunctions were assessed and results compar

69 of the central nervous system can result in neurologic dysfunction with devastating consequences in