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The observed motoneuron death was completely prevented by hemoglobin.
2
We hypothesized that additional variants could be found in these and novel motoneuron and related diseases.
3
Because motoneuron targets in the larva are continuously growing, synaptic contacts are structurally plastic, undergoing continuous expansion.
4
Genetic analyses indicate that the muscle is the BMP-sending cell and the motoneuron is the BMP-receiving cell.
5
It is frequently encountered after traumatic brain injury or spinal cord injury, rather than lower motoneuron disease.
6
However, evaluation of spinal tissue from Pompe patients and animal models indicates glycogen accumulation and lower motoneuron pathology.
7
Thus these findings, all together, suggest that a state of early neuronal hyperexcitability may be a major contributor of motoneuron vulnerability.
8
Therefore, we analyzed our database of 1024 whole exome sequencing samples of motoneuron and related diseases for novel single nucleotide variations.
9
These results indicate that motoneuron excitability changes are observed in the soleus muscle with mechanical conditioning but not with electrocutaneous conditioning.
10
These findings suggest that the current MUNIX definition is most suitable for motoneuron diseases that demonstrate secondary evidence of muscle fiber reinnervation.
11
In contrast, bath application of 50 microM serotonin produced either depolarizing or hyperpolarizing responses depending on the developmental age of the motoneuron.
12
The voxel-based analysis demonstrated varying extents of white matter involvement in different phenotypes of motoneuron disease, albeit in quite similar anatomical locations.
13
While motoneuron death is the defining characteristic of ALS, the events that underlie its pathology are not restricted to the nervous system.
14
Motor unit number index (MUNIX) measurement has recently achieved increasing attention as a tool to evaluate the progression of motoneuron diseases.
15
Three years ago it was reported that reduced levels of vascular endothelial growth factor (VEGF) caused ALS-like motoneuron degeneration in mice.
16
In vitro motoneuron-muscle co-cultures are powerful tools to study the role of different growth factors, hormones and cellular structures involved in NMJ formation.