ライフサイエンスコーパス: motor neurone

1 rones, but caused no apparent loss of spinal motor neurones.

2 events driving the initial specification of motor neurones.

3 usion protein was created to target IGF-1 to motor neurones.

4 to provide target-derived trophic effects on motor neurones.

5 s from the NTS onto gastric-projecting vagal motor neurones.

6 inct populations of gastric-projecting vagal motor neurones.

7 ube of the chick embryo including developing motor neurones.

8 , which implied an oscillatory modulation of motor neurones.

9 Terminals of enteric motor neurones also form tight, synaptic-like contacts w

10 ctly and/or indirectly excite spinal phrenic motor neurones and hence are involved in inspiratory rhy

11 wed that the maximum projection length of CM motor neurones and interneurones along the bowel was 2.8

12 IGF-1 is a potent growth factor for both motor neurones and skeletal muscle.

13 e is insufficient to produce tonic firing of motor neurones and that excessive supraspinal excitation

14 e motor neurones, (ii) short circular muscle motor neurones, and (iii) ascending interneurones.

15 nsgenic expression of fluorescent protein in motor neurones as a morphological reporter.

16 taken of 47 children with a congenital upper motor neurone bulbar palsy (excluding pure speech dyspra

17 Spinal motor neurones can exhibit sustained depolarization in t

18 oped a cell culture model of FALS in which a motor neurone cell line (NSC34) has been stably transfec

19 been proposed to account for the progressive motor neurone death evident in amyotrophic lateral scler

20 involvement of apoptosis in SOD1-associated motor neurone death.

21 s do not explain the observed specificity of motor neurone death.

22 that overexpression of HSPB8 in immortalized motor neurones decreased the accumulation of TDP-25 and

23 to a combination of afferent target loss and motor neurone denervation from motor tracts originating

24 In 2003 the Motor Neurone Disease (MND) Association, together with T

25 ve study, the cause of the high incidence of motor neurone disease (MND) on Guam, and the relationshi

26 Subsequently, 32 patients with motor neurone disease (MND) were studied to identify fac

27 agnosed and electrophysiologically confirmed motor neurone disease (MND), in whom communication probl

28 In motor neurone disease (MND), respiratory muscle weakness

29 e toxins, anterior horn cell degeneration in motor neurone disease and genetic disorders.

30 te gene for neurological disorders including motor neurone disease and Parkinsons disease in addition

31 tion, University, and Research in Italy; the Motor Neurone Disease Association of England, Wales, and

32 reported that over expression of FUS causes motor neurone disease in mouse models hence mutations le

33 Motor neurone disease is caused by mutations in Cu/Zn su

34 were recruited through the national Scottish Motor Neurone Disease Register and were asked to complet

35 ted with Amyotrophic Lateral Sclerosis (ALS, motor neurone disease) (sporadic and familial) and Parki

36 Using a cellular model of familial motor neurone disease, the motor neuronal cell line NSC3

37 Spinal cord motor neurones effectively bound and internalized the IG

38 halitis is a related syndrome in which upper motor neurone features accompany the classic triad.

39 ones revealed that cholinergic and nitrergic motor neurones formed close contacts with ICC-IM in the

40 of physiologically identified gastric vagal motor neurones (gastric-DMN) involved in the gastric acc

41 ulation, including those provided by enteric motor neurones, hormones and paracrine substances.

42 ding microelectrode: (i) longitudinal muscle motor neurones, (ii) short circular muscle motor neurone

43 mutase (SOD1) lead to the selective death of motor neurones in familial amyotrophic lateral sclerosis

44 argets for neurokinins released from enteric motor neurones in the intestine.

45 imed to identify pathways that contribute to motor neurone injury and cell death.

46 ortant mechanism by which mutant SOD1 causes motor neurone injury involves inhibition of specific com

47 tochondrial abnormalities may develop during motor neurone injury, but several important questions re

48 , which is typically active in parallel with motor neurone input during muscular activity.

49 Their function in motor neurones is now under scrutiny.

50 current inhibition from soleus to quadriceps motor neurones is under at least two types of control: o

51 t inhibition reported in subjects with upper motor neurone lesions.

52 decline in muscle function stems partly from motor neurone loss, a tetanus toxin fragment-C (TTC) fus

53 rogression of, and it is hoped even reverse, motor neurone loss.

54 duced overexpression of IGF-1 in spinal cord motor neurones of ageing mice prevents muscle fibre spec

55 ontacts between ascending sensory fibres and motor neurones of the cervical enlargement are more effi

56 Spontaneous, synchronous activity occurs in motor neurones of the embryonic mouse hindbrain at the s

57 current inhibition from soleus to quadriceps motor neurones of the human lower limb.

58 mmon disorder characterized by loss of lower motor neurones of the spinal cord.

59 f TDP-43 and is upregulated in the surviving motor neurones of transgenic ALS mice and human patients

60 ells and vulva; pB directs expression in the motor neurone PDA, the amphid socket cells and the sperm

61 s to be studied specifically in cells with a motor neurone phenotype, without interference from genes

62 distinct populations of preganglionic vagal motor neurones, recordings were made from neurones whose

63 with markers for specific classes of enteric motor neurones revealed that cholinergic and nitrergic m

64 hy, autonomic neuropathy and upper and lower motor neurone signs including distal motor neuropathy an

65 the synaptic activation of many cholinergic motor neurones simultaneously, by synchronous firing in

66 sease is caused by mutations in the survival motor neurone ( SMN ) gene.

67 s and the other "negative" features of upper motor neurone syndrome, rather than muscle overactivity.

68 ections can, in selected patients with upper motor neurone syndrome, reduce spasticity and improve vo

69 ally within the DMV to directly excite vagal motor neurones that project to gastric fundus and corpus

70 modulate the activity of preganglionic vagal motor neurones that supply the stomach.

71 than the projection length of any single CM motor neurone, we suggest that the generation of each di