ABSTRACT
Spinal cord ischemia and reperfusion (SCIR) injury is the major cause of a wide range of complications, including neural degeneration and devastating paraplegia. Decrease of inhibitory neurotransmitters and increase of excitory neurotransmitters are the major cause for the excitotoxicity of neurons. However, no study has reported the temporal loss of motor neuron in the ventral horn of spinal cord area following SCIR-induced spastic paralysis, not even the mechanism under it. In the present study, we found that the rabbits were mainly spastic paralyzed after spinal cord ischemia-reperfusion injury. And the ischemia 60 min group is the optimal treating condition, because of the higher rate of spastic paralysis and lower mortality. Motor neurons in the ventral horn of spinal cord were significant degeneration at 3 h following spastic paralysis and only 12.5% motor neurons were observed at 72 h post-operation, compared with control group. ELISA results indicated that Glycine and GABA were both downregulated following spastic paralysis. But Glycine immediately decreased at 10 min post-operation and lasted for the whole process (at least 72 h). Meanwhile GABA only significantly decreased at 72 h. Furthermore, Glutamic expression was significant upregulation at 3 hours post-operation, and the upregulation back to the base level at 72 h post-operation. Glutamic receptor-(NR1) and Glycine α1 receptor upregulated accordingly, whereas GABBR2 didn't upregulate significantly until at 72 h post-operation. Abundant extracellular Ca2+ influxed into cytoplasm in neurons following spastic paralysis. The type of paraplegia is mainly spastic paraplegia after SCIR (ischemia 60 min treatment). Following spastic paraplegia, motor neuron in the ventral horn of spinal cord area was significant degeneration at early stage and last for the whole process. It may contribute to the decrease of Glycine at early stage and followed exitotoxicity, which caused intracellular calcium overload to make neurons dead. It would lay the foundation for better understanding the motor neuron degeneration and mechanism following spastic paralysis. And it would supply a novel and effective target for spastic paralysis prevention and therapy.
ABSTRACT
To investigate the genetic polymorphism of Y-chromosomal short tandem repeats (STR) loci in Jing, Yi, Yao, and Zhuang minority populations from Guangxi Province, China. 17 Y-STR loci were co-amplified using AmpFlSTR(R) Yfiler PCR Amplification Kit System, and the PCR products were analyzed by genetic analyzer. Cluster and phylogenic tree analyses were conducted to show the genetic distance among the populations. There were 61 different haplotypes in 100 unrelated Yao males, 67 in 105 unrelated Yi males, 79 in 103 unrelated Jing males, and 91 in 107 unrelated Zhuang males. The haplotype diversities of Jing, Yi, Yao and Zhuang were determined as 0.9784, 0.9866, 0.9911, and 0.9956, respectively. Among these 4 minority populations, the genetic distance between Jing and Zhuang was the smallest (0.0391), while the genetic distance between Yi and Yao was the largest (0.3376). The 17 Y-STR loci in the 4 minority populations from Guangxi Province revealed a highly polymorphic genetic distribution, which show a high potential for population genetics and forensic practice.
