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 s in the LYST gene that involves progressive neurologic dysfunction.

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

4 >/= 10, and 62% showed clinical evidence of neurologic dysfunction.

5 liver failure during infancy without notable neurologic dysfunction.

6 atic incubation period precedes the onset of neurologic dysfunction.

7 pathways differ in patients with and without neurologic dysfunction.

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

9 which may lead to increased vulnerability to neurologic dysfunction.

10 he spinal fluid correlate with the degree of neurologic dysfunction.

11 tential benefits in reducing respiratory and neurologic dysfunction.

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

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

14 are currently available to treat age-related neurologic dysfunction although synaptic dysfunction occ

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

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

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

18 ination in multiple sclerosis contributes to neurologic dysfunction and neurodegeneration.

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

20 ator protein (CTMP) in Akt-signaling related neurologic dysfunction and skeletal muscle metabolism.

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Sudden neurologic dysfunction caused by focal brain ischemia wi

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

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

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

38 Severe neurologic dysfunction develops in Sepp1 null mice (Sepp

39 sed by relapsing/remitting (RRMS) attacks of neurologic dysfunction followed by variable resolution.

40 ing neuroinflammation could reduce long-term neurologic dysfunction following SAH.

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

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

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

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

45 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

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

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

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

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

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

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

52 neurons, not storage accumulation, underlies neurologic dysfunction in CLN3 disease.

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

54 performed by the Global Consortium Study of Neurologic Dysfunction in COVID-19 (GCS-NeuroCOVID) from

55 Our understanding of neurologic dysfunction in demyelinating diseases and the

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

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

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

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

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

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

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

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

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

65 Neurologic dysfunction may persist for years after acute

66 Neurologic dysfunction may result from leukemic infiltra

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

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

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

70 ients with cancer, often leading to malaise, neurologic dysfunction, or death.

71 athy syndrome with altered mental status and neurologic dysfunction, or hemophagocytic lymphohistiocy

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

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

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

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

76 S-CoV-2 infection induces a wide spectrum of neurologic dysfunction that emerges weeks after the acut

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

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

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

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

81 Neurologic dysfunction was assessed using a well-standar

82 nth surveillance: no overt constitutional or neurologic dysfunction was noted for any study animals.

83 Mild chronic neurologic dysfunction was reported in all three patient

84 Neurosensory and neurologic dysfunctions were assessed and results compar

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