ライフサイエンスコーパス: LEMS

1 LEMS analyses of single analytes as a function of concen

2 LEMS analysis of the powders revealed several new mass s

3 LEMS antibodies inhibit Ca2+ currents in excitable cells

4 LEMS antibody treatment increased the percentage of trai

5 LEMS imaging of the spatial distribution of an oxycodone

6 cit in neurotransmitter release magnitude at LEMS model NMJs.

7 tive increase in neurotransmitter release at LEMS model NMJs.

8 symptoms and signs cannot be used to exclude LEMS from the differential diagnosis.

9 There is no cure for LEMS, and the current most commonly used symptomatic tre

10 represents a promising treatment option for LEMS and potentially for other disorders of the NMJ.

11 possible alternative treatment strategy for LEMS.

12 -type channels was abolished by four of four LEMS IgG preparations, that subserved by Q-type channels

13 vas deferens of mice injected with IgG from LEMS patients or from controls.

14 ce by repeated administration of plasma from LEMS patients reduces the amplitude of the perineurial P

15 The pathogenic role of anti-VGCC antibody in LEMS is well established.

16 ponse of the ACh release apparatus occurs in LEMS.

17 elp distinguish between tumour and nontumour LEMS.

18 dissuade some colleagues from a diagnosis of LEMS.

19 The effect of LEMS antibodies on Ca2+ currents and exocytosis was stud

20 The hallmark of LEMS is a large potentiation of neuromuscular transmissi

21 esis using a mouse passive transfer model of LEMS.

22 characteristic electrophysiological signs of LEMS: reduced quantal content and facilitation of EPP am

23 on to ACh release during passive transfer of LEMS appears to occur only after quantal release is sign

24 Passive transfer of LEMS to mice by repeated administration of plasma from L

25 treated for 2 or 24 h with either control or LEMS plasma, or following chronic treatment with control

26 in 8 patients, also were observed among our LEMS population.

27 al oculobulbar feature occurred in 13 of our LEMS patients.

28 Purified LEMS IgGs from five patients inhibited N- and P/Q-type C

29 ion of the laser electrospray mass spectral (LEMS) measurements resulted in perfect classification of

30 ed for laser electrospray mass spectrometry (LEMS) and electrospray ionization-mass spectrometry (ESI

31 Laser electrospray mass spectrometry (LEMS) coupled with offline multivariate statistical anal

32 second laser electrospray mass spectrometry (LEMS) experiments, suggesting that the fiber-based femto

33 Laser electrospray mass spectrometry (LEMS) is demonstrated for pharmaceutical samples at atmo

34 using laser electrospray mass spectrometry (LEMS) reveal monotonic signal response as a function of

35 using laser electrospray mass spectrometry (LEMS).

36 including Lambert-Eaton myasthenic syndrome (LEMS) and paraneoplastic cerebellar ataxia (PCA).

37 Lambert-Eaton myasthenic syndrome (LEMS) is a paraneoplastic disorder in which autoantibodi

38 Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that affects neurotransmi

39 Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder in which a significant f

40 (78%) of Lambert-Eaton myasthenic syndrome (LEMS) patients evaluated at the Lahey Clinic (Table).

41 In Lambert-Eaton myasthenic syndrome (LEMS), SOX antibodies help distinguish between tumour an

42 utoimmune Lambert-Eaton myasthenic syndrome (LEMS).

43 utoimmune Lambert-Eaton myasthenic syndrome (LEMS).

44 ificant charge reduction was observed in the LEMS experiment while the ESI measurement revealed charg

45 component analysis and discrimination of the LEMS mass spectral measurements resulted in perfect clas

46 In contrast to the LEMS experiments, the intensity ratios from control expe

47 Thus, LEMS IgG impairs transmitter release from parasympatheti

48 even after very short periods of exposure to LEMS plasma.

49 ers and fillers in intact formulations using LEMS.

50 so reduced in muscles incubated acutely with LEMS plasma.

51 Incubation for 18 h with LEMS IgG (2 mg/ml) caused a significant dose-dependent r

52 aphragms from naive mice were incubated with LEMS or control human plasma for 2 or 24 h.

53 Treatment of mice with LEMS plasma evoked the characteristic electrophysiologic

54 ubated cultured rat cerebellar neurones with LEMS IgG and observed a reduction in P-type current in P

55 from healthy human controls or patients with LEMS.

56 However, following 30 days treatment with LEMS plasma, nimodipine significantly reduced the remain

57 after chronic, but not acute treatment with LEMS plasma.