Detection of somatic muscle fasciculation on electrocardiograms

BMJ ◽  
1976 ◽  
Vol 1 (6013) ◽  
pp. 836-836 ◽  
Author(s):  
R W Gilliatt ◽  
R G Willison
BMJ ◽  
1976 ◽  
Vol 1 (6009) ◽  
pp. 557-559 ◽  
Author(s):  
D J Thomas ◽  
D O Williams

Parasitology ◽  
1990 ◽  
Vol 101 (2) ◽  
pp. 265-271 ◽  
Author(s):  
L. Dye-Holden ◽  
R. J. Walker

The mechanism underlying the ability of the anthelmintic avermectin to paralyse the nematode Ascaris is not yet fully understood. Using conventional two-electrode electrophysiological recording techniques we have demonstrated that micromolar concentrations of ivermectin block the inhibitory GABA response on the muscle cells of the parasitic nematode Ascaris. The ability of a number of avermectin derivatives to act as receptor antagonists for the Ascaris muscle GABA receptor has been determined. This provides useful information to compare with the in vivo anthelmintic potency of these compounds. Abamectin, the most potent anthelmintic, was the most potent compound at inhibiting the GABA response whilst octahydroavermectin, a compound which lacks anthelmintic activity, did not block the GABA receptor. This is consistent with the notion that the GABA receptor antagonist properties of the avermectins could contribute to their anthelmintic action.


1969 ◽  
Vol 51 (1) ◽  
pp. 107-118
Author(s):  
Y. ITO ◽  
H. KURIYAMA ◽  
N. TASHIRO

1. Miniature excitatory junction potentials (m.e.j.p.s) could be recorded from the longitudinal muscle layer of earthworm in sodium-free solution. 2. The amplitude and frequency of the m.e.j.p.s indicated the diffuse innervation and random release of the chemical transmitter from the nerve terminals. 3. Generation of the m.e.j.p.s was prevented by treatment with D-tubocurarine, but not by atropine and picrotoxin. 4. Hyperpolarizations of the membrane by applications of inward current increased the frequency and amplitude of the m.e.j.p.s in sodium-free solution. 5. The reversal potential level for the m.e.j.p.s in sodium-free solution was -;20 mV., and this value was 20 mV. negative to that measured in physiological solution. Low-potassium solution shifted the reversal potential levels in a more negative and high-calcium in a less negative direction. 6. The change of the reversal potential produced by a tenfold change of the external potassium concentration was 24.5 mV., and that by change of the external calcium concentration was 17 mV.


Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 617-626 ◽  
Author(s):  
R. Baker ◽  
G. Schubiger

The Notch (N) gene encodes a cell signaling protein that mediates neuronal and epidermal determination in Drosophila embryos. N also regulates several aspects of myogenic development; embryos lacking N function have too many muscle founder cells and fail to properly differentiate somatic muscle. To identify cell-autonomous requirements for Notch function during muscle development, we expressed a Notch minigene in the mesoderm, but not in the ectoderm, of amorphic N-embryos. In these embryos, muscle founder hypertrophy is rescued, indicating that Notch is autonomously required by mesoderm cells to regulate the proper number of muscle founders. However, somatic muscle differentiation is only partially normalized, suggesting that Notch is also required in the ectoderm for proper muscle development. Additionally, mesodermal expression of Notch partially rescues epidermal development in overlying neurogenic ectoderm. This is unexpected, since previous studies suggest that Notch is autonomously required by proneural ectoderm cells for epidermal development. Mesodermal expression of a truncated Notch protein lacking the extracellular domain does not rescue ventral epidermis, suggesting that the extra-cellular domain of Notch can non-autonomously rescue epidermal development across germ layers.


Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4525-4535 ◽  
Author(s):  
S. Knirr ◽  
N. Azpiazu ◽  
M. Frasch

In the Drosophila embryo, a distinct class of myoblasts, designated as muscle founders, prefigures the mature pattern of somatic body wall muscles. Each founder cell appears to be instrumental in generating a single larval muscle with a defined identity. The NK homeobox gene S59 was the first of a growing number of proposed ‘identity genes’ that have been found to be expressed in stereotyped patterns in specific subsets of muscle founders and their progenitor cells and are thought to control their developmental fates. In the present study, we describe the effects of gain- and loss-of-function experiments with S59. We find that a null mutation in the gene encoding S59, which we have named slouch (slou), disrupts the development of all muscles that are derived from S59-expressing founder cells. The observed phenotypes upon mutation and ectopic expression of slouch include transformations of founder cell fates, thus confirming that slouch (S59) functions as an identity gene in muscle development. These fate transformations occur between sibling founder cells as well as between neighboring founders that are not lineage-related. In the latter case, we show that slouch (S59) activity is required cell-autonomously to repress the expression of ladybird (lb) homeobox genes, thereby preventing specification along the lb pathway. Together, these findings provide new insights into the regulatory interactions that establish the somatic muscle pattern.


Parasitology ◽  
1993 ◽  
Vol 106 (4) ◽  
pp. 421-427 ◽  
Author(s):  
H. R. Parri ◽  
M. B. A. Djamgoz ◽  
L. Holden-Dye ◽  
R. J. Walker

SUMMARYIvermectin has been shown to increase chloride conductances of invertebrate cells. On the muscle cells of the parasitic nematode Ascaris, ivermectin acts as both a GABA receptor antagonist and a chloride channel opener. In this study, ion-sensitive microelectrodes were used to investigate the effect of ivermectin on intracellular C1− concentration of the somatic muscle bag cells of Ascaris suum. Incubation of muscle cells with ivermectin (10 μM in 1% dimethyl sulphoxide vehicle for 60 min) increased intracellular C1− by 2·9 mM or 15% compared to controls (P > 0·01, n = 6).


1997 ◽  
Vol 181 (2) ◽  
pp. 197-212 ◽  
Author(s):  
Cheryl A. Keller ◽  
MaryRuth S. Erickson ◽  
Susan M. Abmayr
Keyword(s):  

Sign in / Sign up

Export Citation Format

Share Document