To investigate the dynamic changes in ICE mRNA expression and its relationship with IL 18 and IFN ? mRNA expression in thermal injured rats.The animals were subjected to a 30% total body surface area full thickness thermal injury,and fluid resuscitation was performed at 6 hours post burn. 54 male Wistar rats were randomly divided into three groups: normal controls,30% Ⅲ degree burn group,and selective decontamination of the digestive tract (SDD) treatment group. P1asma endotoxin was measured by limulus amebocyte lysate test,and tissue ICE,IL 18 and IFN ? mRNA expression was determined by reverse transcription po1ymerase chain reaction (RT PCR).The results showed that ICE, IL 18, and IFN ? mRNA expression significantly increased in the intestine,1ung,liver,and kidney at 2 hours,peaking at 8 hours,and a high level was maintained till 24 hours. However, treatment with SDD could lower plasma endotoxin levels,and markedly inhibit ICE, IL 18, and IFN ? mRNA expression in various organs.This study suggests that major burns can lead to a marked elevation of tissue ICE mRNA expression in vital organs,which might be associated with IL 18 and IFN ?mRNA expression induced by gut derived endotoxemia.

Objective To investigate the effects of intrathecal (IT) NaV 1.8 antisense oligonucleotide on the chronic neuropathic pain induced by chronic constrictive injury (CCI) to the sciatic nerve.Methods Twenty-four male SD rats were randomly divided into 4 groups ( n = 6 each): group Ⅰ CCI + NS 5 ?l; group Ⅱ CCI + mismatch oligonucleotide 45 ?g; group ⅢCCI + antisense oligonucleotide 45 ?g and group Ⅳ CCI + antisense oligonucleotide 90 ?g. CCI was produced by placing 4 loose ligatures on the left sciatic nerve at 1 mm interval with 4-0 chromic catgut as described by Bennett. On the 5th day after CCI IT catheter was inserted at the level of lumbar spine and identified by free flow of CSF. On the 8th day after CCI normal saline or mismatch or antisense oligonucleotide was injected IT twice a day for 5 consecutive days. Threshold to noxious thermal and mechanical stimuli was measured before CCI (baseline) and on the 1st, 3rd, 5th, 7th, 9th, 11th and 13th day after CCI. On the 14th day after CCI the lumbar segment of spinal cord was removed for determination of NaV 1.8 sodium channel expression in L4-6 dorsal root ganglion (DRG) by semi-reverse transcriptase-PCR.Results The threshold to von Frey hair stimulation and noxious thermal stimuli on the operated side was significantly lowered after CCI. On the 11th and 13th day after CCI the threshold to mechanical and thermal stimuli were significantly higher in group Ⅲand Ⅳ than in group I and H . Conclusion IT NaV 1. 8 antisense oligonucleotide can reduce the neuropathic pain by down-regulating NaV 1.8 mRNA expression.

Objective To identify the risk factors for postoperative spinal cord injury in Stanford type A aortic dissection patients.Methods 210 Stanford type A aortic dissection(TAAD) patients underwent Sun's procedure in Beijing Aortic Disease Center during July 2014 to March 2015.14 patients had spinal cord injury after surgery.Clinical data and computed tomography angiography(CTA) imaging of aorta were retrospectively analyzed and multi-logistic regression analysis was performed to identify risk factors for spinal cord injury post operation.Results 14 out of 210(6.7％) patients had transient or permanent spinal cord injury after surgery.Univariate analysis showed only false lumen derived intercostal arteries at eighth thoracic vertebral level (T8) to first lumbar vertebral level (L1) was significantly associated with post-surgery spinal cord injury (P =0.000).Multi-logistic regression analysis showed that false lumen derived intercostal arteries (P =0.000) and age (P =0.016) were significantly associated with postoperative spinal cord injury.Conclusion Major intercostal arteries derived from false lumen and rapid thrombogenesis in false lumen are the major risk factors for postoperative spinal cord injury in Stanford type A aortic dissection patients.

Objective To construct a rapid genetic DNA extraction method, with nano magnetic beads, self-designed reagents system and extracting process. Method Part I: DNA extraction from old blood cotton swab sample with self-designed DNA extraction kit, then quantiifed by UV spectrophotometer. The method was further optimized on the preliminary results. Part II: All kinds of difficult DNA sample were tested with optimized kit, to detect the applicability of the kit. Result By improving the experimental condition, the extraction effects of different DNA sample is good, meanwhile, the extraction cost is relatively low.

Neuropathic pain has been hypothesized to be the result of aberrant expression and function of sodium channels at the site of injury. To investigate the effects of NaV1.8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion (DRG) neurons in chronic neuropathic pain. 24 Sprague-Dawley rats weighing 200-260 g were anesthetized with the in of sciatic nerve trunk by 4-0 chromic gut. The mechanical and thermal pain threshold were measured before operation and 1, 3, 5, 7, 9, 11, 13 days after operation. A PE-10 catheter was implanted in subarachnoid space at lumbar region. On the 7th postoperative day the animals were randomly divided into 4 groups. The drugs were injected intrathecally twice a day for 5 consecutive days in group 2-4. The animals were decapitated 14 days after the surgery. The L4-L6 DRG of the operated side was removed and crushed, and total RNA was extracted with Trizol reagent. The contralateral side was used as control. The change of NaV1.8 sodium channel transcripts was determined by RT-PCR. Pain threshold was significantly lowered after CCI as compared with that in control group and was elevated 3 days after antisense oligonucleotide injection. Sensory neuron specific TTX-R sodium channel NaV1.8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 μg as compared with that in CCI group (P＜0.01), and it was even greater at the dosage of 90 μg. The intrathecally injected NaV1.8 antisense oligonucleotide can reduce the mechanical allodynia and thermal hyperalgesia partially by downregulating the SNS transcript expression.