Objective To discuss the degenerative factors, the spinal segment distribution, and the mechanism in hyperextension injury of cervical spine. Method Eighty-nine patients with hyperextension injury of cervical spine were retrospectively analyzed by observing the degenerativelesion, the spinal cord segment with high signal in T2WI, and the location of facial trauma. Results Fifty-eight cases showed the disc hemiation which was the most common lesion, followed by 8 cases showing the calcification of the posterior longitudinal ligament. Besides, 7 cases presented the developmental stenosis of spinal canal, and also, 6 cases showed disc hemiation combined with the yellow ligament hypertrophy. The intervertebral level of the spinal cord with high signal in T2WI were distributed as follows:4 cases were at C2/3, of which onesuffered the forehead trauma; 12 cases were at C3/ 4, of which 10 had the forehead trauma, and one had the zygomatic trauma; 12 cases were at C4/5, of which 5 had the forehead trauma, one had both the zygomatic and the forehead trauma, and one had both the forehead and with the lower jaw trauma; 11 cases were at CS/6,of which 3 had the forehead trauma, 3 had the zygomatic trauma, and 2 had the lower jaw trauma. The location of the spinal cord with single high signal in T2WI did not correspond with the intervertebral disc level in 4 cases. For 10 cases the high signal in T2WI was found at two discontinuous segments. For 2 cases the 1 high signal in T2WI was found at over two segments. For 6 cases the high signal in T2WI was found at over three segments. Conclusions Disc hemiation is the most common underlyding factor in cervical hyperextension injury. The spinal level with high signal in T2WI was correlative to the impacted facial site. The shear force at the inflection point with or without the anterior-posterior compression force accounted for the cervical hyperextension injury.

To investigate the effect of the localization of oligonucleotides decoy (ODNs decoy) on the activation of nuclear factor-kappaB (NF-kappaB) in TNF-alpha induced HeLa cells. The mercapto group-modified nuclear localization signal (NLS) peptide was covalently conjugated to amino group-modified NF-kappaB ODNs decoy by Sulfo-SMCC cross-linker. The NLS-ODNs decoy was transfected into HeLa cells by TransME transfection reagent. The intracellular distribution of fluorescent labeled NLS-ODNs decoy was detected with a microscope. The cell viability was detected by MTT assay, and then the activity of NF-kappaB in cell nuclear extract was assayed by electrophoretic mobility shift assay (EMSA). The results showed that NLS peptide was successfully conjugated to ODNs decoy by Sulfo-SMCC cross-linker. The NLS-ODNs decoy effectively entered into nucleus with high rate of 17.9%. It was observed that the cell viability of HeLa cell was not significantly affected by the transfection of NLS-ODNs decoy, while NLS-ODNs decoy significantly inhibited the activation of NF-kappaB in TNF-alpha induced HeLa cells nuclear extracts. This experiment can provide a new covalent conjugation of NLS peptide to ODNs can effectively drive decoy into nucleus, and thus improve its inhibitory effects on the activation a transcription factor.
Base Sequence ; Cell Nucleus ; metabolism ; HeLa Cells ; Humans ; Molecular Sequence Data ; NF-kappa B ; genetics ; metabolism ; Nuclear Localization Signals ; genetics ; Oligonucleotides ; genetics ; metabolism ; Transfection

Plasticity in the glutamatergic synapses on striatal medium spiny neurons (MSNs) is not only essential for behavioral adaptation but also extremely vulnerable to drugs of abuse. Modulation on these synapses by even a single exposure to an addictive drug may interfere with the plasticity required by behavioral learning and thus produce impairment. In the present work, we found that the negative reinforcement learning, escaping mild foot-shocks by correct nose-poking, was impaired by a single in vivo exposure to 20 mg/kg cocaine 24 h before the learning in mice. Either a single exposure to cocaine or reinforcement learning potentiates the glutamatergic synapses on MSNs expressing the striatal dopamine 1 (D1) receptor (D1-MSNs). However, 24 h after the cocaine exposure, the potentiation required for reinforcement learning was disrupted. Specific manipulation of the activity of striatal D1-MSNs in D1-cre mice demonstrated that activation of these MSNs impaired reinforcement learning in normal D1-cre mice, but inhibition of these neurons reversed the reinforcement learning impairment induced by cocaine. The results suggest that cocaine potentiates the activity of direct pathway neurons in the dorsomedial striatum and this potentiation might disrupt the potentiation produced during and required for reinforcement learning.