ライフサイエンスコーパス: end plate

1 fluence removal of excess innervation at the end plate.

2 omposition depends on the orientation of the end plate.

3 inage fistula and shunts aqueous humor to an end plate.

4 splaying acetylcholinesterase-positive motor end plates.

5 from C6 were the sole input to reinnervated end plates.

6 there are morphological changes at the motor end-plates.

7 ease in gamma-subunit mRNA expression at CMS end-plates.

8 silon, delta, beta and alpha subunits of the end plate acetylcholine (ACh) receptor (AChR) are descri

9 ain of function mutations in subunits of the end-plate acetylcholine receptor (AChR).

10 Congenital end-plate acetylcholinesterase (AChE) deficiency (CEAD),

11 tion in the ColQ deficient mouse, a model of end-plate acetylcholinesterase deficiency.

12 Human end-plate AChE deficiency was recently shown to be cause

13 nine novel COLQ mutations in 7 patients with end-plate AChE deficiency.

14 on of the foetal-specific gamma-subunit into end-plate AChR.

15 d by the binding of complement-fixing IgG to end-plate AChRs.

16 nded on accurate identification of vertebral end plates and posterior elements.

17 , 57, and 66 years) containing cartilaginous end plates and subchondral bone were prepared.

18 in areas surrounding the nuclei of the motor end plate, and in perisynaptic Schwann cells, and locali

19 occurs across the fibrous capsule around the end plate, and the major determinants of the final intra

20 on may be achieved with implants with larger end plates, and valved implants appear to reduce the ris

21 Samples were imaged with the end plate at three orientations with respect to the cons

22 c neuregulin expression and maintains normal end plate band architecture in the presence of activity

23 synaptic differentiation and formation of an end-plate band require MuSK and rapsyn, but are not depe

24 , or why most synapses are restricted to an 'end-plate band' in the middle of the muscle remains unkn

25 When end-plate border properties of fibers from 3 MG patients

26 At the end-plate border we examined miniature end-plate potenti

27 evels of mRNA for AChR subunits at the motor end-plates by in situ hybridization.

28 d in articular cartilage from older mice, in end-plate cartilage from mice, and in chondrocytes from

29 growth and/or a fall in blood supply through end plate changes could instigate NC disappearance.

30 ransition from C7- to C6-dominated input, at end plates coinnervated by C6 and C7 axons, the average

31 udies demonstrated that changes in the inlet end plate configuration designed to ensure uniform flow

32 second denervation, most of the reinnervated end plates contained only axons from the C7 branch; the

33 End plate current simulations suggest that the higher af

34 ure end-plate potential (MEPP) and miniature end-plate current (MEPC); at 5 x 10(-3) M, the MEPP beca

35 All three had prolonged end plate currents and AChR channel opening episodes and

36 er, the quantal size (amplitude of miniature end-plate currents) and the kinetic properties of synapt

37 s a hitherto unrecognized consequence of the end-plate damage initiated by the binding of complement-

38 ons in the nicotinic receptor from the motor end plate decreases unitary conductance up to 80%.

39 eaching experiments carried out a frog motor end-plates demonstrated lack of lateral intermixing of s

40 Motor end plates denervated by axonal retraction of dying moto

41 by MRI, including Romanus lesions (RLs) and end-plate, diffuse vertebral body, posterior element, an

42 nels is associated with the phenotype "motor end plate disease," which is characterized by a progress

43 parameters, like ESI voltage and ESI tip-to-end plate distance, were optimized for very low flow rat

44 End-plate edema, degenerative discs, and RLs were freque

45 unrelated patients with very small miniature end plate (EP) potentials, but with normal EP AChR densi

46 l myasthenic syndrome associated with severe end-plate (EP) acetylcholine receptor (AChR) deficiency

47 d quantitative electron microscopy EM of 409 end plates (EPs), and by mutation analysis, and expressi

48 In cartilage end plates/GPs, TonEBP deletion induced cell death, but

49 ion of the degeneration of the cartilaginous end plate; however, the accuracy of T2*-based estimates

50 s of voltage-gated Na+ channels at the motor end plate in both patients with MG and in rats with PTMG

51 vidence of more degeneration of the disc and end plate in the spines of Col9a1(-/-) mice compared wit

52 Amplitudes of MEPPs and INa at the end plate indicated that loss of AChRs was greater than

53 ter 6 d, the pattern was reversed, with most end plates innervated exclusively by C6.

54 Classic signs include vertebral end plate irregularity, disk space narrowing, and anteri

55 cases a destruction of vertebral bodies with end plates loss restriction and cortical layer discontin

56 rately positioned using holes drilled in two end plates made of plastic.

57 Reelin is required for motor end-plate maturation and proper nerve-muscle connectivit

58 The end plate myopathy stems from cationic overloading of th

59 nts and AChR channel opening episodes and an end plate myopathy with loss of AChR from degenerating j

60 el, leading to a depolarization block and an end-plate myopathy.

61 Compared with WT mice, motor end-plates of mdx mice demonstrated less continuous morp

62 ssion of alpha- and epsilon-subunit mRNAs at end-plates of patient and control muscles, suggesting th

63 MS parameters, including capillary voltage, end plate offset, ion energy, and "collision energy".

64 Higher end plate porosity in discs with NCs suggested greater n

65 used scanning electron microscopy to examine end plate porosity of discs with NCs and those with MNPC

66 Furthermore, the decreased end plate potential (EPP) amplitude in these 30-month-ol

67 not after a tetanus, increased the speed of end plate potential (EPP) amplitude rundown, and greatly

68 namely, decreased quantal content, decreased end plate potential (EPP) amplitude with prolonged rise

69 End plate potential (EPP) amplitudes were used to follow

70 rise and decay time, and prolonged miniature end plate potential (mEPP) rise and decay time.

71 rise and decay time, and, although miniature end plate potential (mEPPs) amplitude and frequency were

72 ionally, miniature end plate potential size, end plate potential size, and quantal content did not di

73 Functionally, miniature end plate potential size, end plate potential size, and

74 Evoked end-plate potential (EPP) remained similar at the NMJs i

75 plitude and decay time constant of miniature end-plate potential (MEPP) and miniature end-plate curre

76 itude but increase in frequency of miniature end-plate potential (mEPP) at the NMJs in Acta1+/Ki mice

77 ulation frequencies (P < 0.05) and miniature end-plate potential amplitude analysis (P < 0.01) showed

78 loroquine reduced the quantal content of the end-plate potential by 37-45%.

79 ock owing to temporal summation of prolonged end plate potentials at physiologic rates of stimulation

80 End-plate potentials (EPPs) and miniature end-plate pote

81 as the frequency of occurrence of miniature end-plate potentials (MEPP(f)), were evoked by high pota

82 Miniature end-plate potentials (MEPPs) were focally recorded from

83 End-plate potentials (EPPs) and miniature end-plate potentials (MEPPs) were recorded from neuromus

84 t the end-plate border we examined miniature end-plate potentials (MEPPs), sodium current (INa) ampli

85 ed to 10-30% of normal levels, the miniature end-plate potentials are correspondingly reduced, and th

86 ronous ACh release evoked by nerve impulses (end-plate potentials, EPPs) follow a simple binomial dis

87 Devices with larger end plates produce greater IOP reduction, and the presen

88 om the C7 branch; the remaining reinnervated end plates received input from C6 only or were multiply

89 <0.01) and at 12 months (P<0.10) and for the end plate region only at 6 months (P<0.10).

90 as acetylcholine receptors (AChRs) from the end-plate region in patients with acquired myasthenia gr

91 cence and ultrastructural analyses of muscle end-plate regions showed synaptic remodelling with dener

92 ed; rather, it resulted from a lack of motor end plate reinnervation.

93 tween CAV-1 and alphaC418W that could confer end plates rich in alphaC418W nAChRs to a susceptibility

94 Larger end-plate size is associated with greater intraocular pr

95 The end-plate species of acetylcholinesterase (AChE) is an a

96 cycling in the neuromuscular junction (NMJ), end-plate structure of NMJs and muscle contractility of

97 Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junctio

98 Degeneration in the end plates was associated with more cell proliferation,

99 End plates were 14% smaller in N-CAM-deficient mice than

100 Smaller axons and motor end plates were also demonstrated in SM, using NADPH-dia

101 omical analysis indicated that 50% of soleus end plates were completely denervated 1-4 weeks post-par

102 nsmission is ensured by the large INa at the end plate, which reduces the AP threshold.

103 ntering through an aperture in the dc-biased end plate, which was also operated as an ion gate.

104 ion showed thickened bone in the Cupid's bow end plate with annular fibers inserting into this region

105 Axons terminating in motor end plates within SM bundles were immunoreactive to PHA-