BACKGROUND:In treatment of lumbar diseases, lumbar fusion therapy fails in 20%of cases and may lead to a series of complications such as pain, intervertebral space col apse, and delayed kyphosis deformity.
OBJECTIVE:To observe the effect of nucleus pulposus on interbody fusion after removing the anterior column disc of rabbit lumbar vertebra.
METHODS:A total of 36 healthy Japanese white rabbits were randomly and equal y divided into three groups, with 12 rabbits in each group. (1) Group of anterior longitudinal ligament+bone grafting:The L3 intercalated disc were wel exposed and anterior longitudinal ligament was stripped, obtaining a space to L3 intercalated disc, then the iliac bone was implanted. (2) Group of excising anterior 1/3 disc+bone grafting:After the anterior 1/3 disc tissue was excised, the iliac bone was implanted and sutured as Group of anterior longitudinal ligament+bone grafting. (3) Group of excising anterior 1/3 disc+fixation:After the anterior 1/3 disc tissue was excised, the iliac bone was implanted and the anterior column fixation was performed.
RESULTS AND CONCLUSION:Biomechanical testing showed that, at 12 weeks, the verticality tensile force in the group of anterior longitudinal ligament+bone grafting was obviously higher than other two groups, and have better fusion rate and could bear stronger force. Lateral position lumbar radiography showed that, the bone graft was absorbed and no new bone grew into the intervertebral space in the group of excising anterior 1/3 disc+bone grafting at 12 weeks;the formation of osseous bridge was found in the group of excising anterior 1/3 disc+fixation;complete bony fusion was found in the group of anterior longitudinal ligament+bone grafting. Histological examinations showed that, at 12 weeks, no bone tissue formed in the group of excising anterior 1/3 disc+bone grafting;a smal amount of bone trabecula and osteocytes were observed in the group of excising anterior 1/3 disc+fixation;a great quantity of newborn bone trabecula and osteocytes, remodeling lamel ar bone and canalis haversi structure were observed in the group of anterior longitudinal ligament+bone grafting. The stability of anterior column has notable effect on interbody fusion, after the anterior column disc is destroyed, the free nucleus pulposus may affect spinal fusion, so restoring the stability of the anterior column may promote interbody fusion, but stil cannot get solid spinal fusion.

Coal Mining ; Humans ; Occupational Diseases ; prevention & control ; Occupational Health ; Tuberculosis ; prevention & control

Objective To explore the effects of TNF-α on the expression of IP33R1 mRNA and protein in human mesangial cells (HMCs) and elucidate the mechnism of TNF-α indnces the IP3R1 expression in the occurrence of hepatorenal syndrome (HRS).Methods HMCs was stimulated by tumor (TNF-α) with 100 ng/mL for different hours (2,4,8,24 hours).The expression change of IP3R1 mRNA and protein were detected by quantitative real-time polymerase chain reaction and immunoblot assay.Several inhibitors including D609,U73122,PP1,Safingol,Rottlerin and non-radioactive PKC assay to examine the mechanism of signal transduction of TNF-α-regulated IP3R1 in HMCs.Results The levels of IP3R1 mRNA at 2 h post-TNF-α exposure were significantly enhanced and reached peak at 8 h in HMCs (P ＜ 0.01),then descened at 24 h (P ＜ 0.01).The levels of IP3R1 protein at 4 h post-TNF-α exposure were obviously increased and reached peak at 24 h post-TNF-α exposure (P ＜ 0.01).Compared with the control group,safingol (PKC-α inhibitor) and D609 (PC-PLC inhibitor) each significantly suppressed TNF-α-induced expression of IP3R1 mRNA (3.30 ± 0.81) vs.(1.95 ± 0.130,P ＜ 0.05 ; (2.10 ± 0.49),P ＜ 0.01 andIP3R1 protein (3.09±0.13) vs.(1.86+0.39),P＜0.01; (1.98±0.02),P＜0.01.TNF-αpromoted autophosphorylation,and hence the activation,of PKC-α with maximal phosphorylation that occurred 8 h post-stimulation measured by non-radioactive PKC assay,and the effect was marked attenuated by pretreated with D609 or safingol.Conclusions TNF-α increased the expression of IP3R1 and this was mediated,at least in part,through the PC-PLC/PKC-α signaling pathways in HMCs.

Objective To explore the effects of TNF-α on the expression of IP3 R1 mRNA and protein in human mesangial cells (HMCs) and elucidate the role of protein kinase C (PKC) in this signal pathway.Methods Quantitative real-time polymerase chain reaction and immunoblot assay were used to examine the effects of TNF-α on IP3R1 mRNA and protein expression.Depletion PKC,the selective inhibitor of PKCα Safingol and inhibitor of PKCδ Rottlerin,overexpression of dominant negative mutant of PKC to examine the mechanism of signal transduction of TNF-α-regulated IP3 R1 in HMCs.PKCα activation was assayed by Western blot.Results TNF-α increased IP3R1 mRNA and protein expression in HMCs,effects that were blocked by prolonged incubted chronic PMA,Safingol and also by domain negative PKCα construct.TNF-α promoted PKCα activation with maximal PKCα phosphorylation that occurred 8 h post-stimulation.Conclusion TNF-α increased the expression of IP3 R1 and this was mediated through the PKCα activation signaling pathways in HMCs.

BACKGROUND: Studies have shown that adipose derived mesenchymal stem cells are involved in the skin repair after scald, but the hydrogel made of the excreta by adipose derived mesenchymal stem cells is rarely reported in the treatment of skin scald. OBJECTIVE: To analyze the therapeutic effect of human adipose derived mesenchymal stem cell conditioned medium hydrogel in a mouse model of skin scald. METHODS: Adipose derived mesenchymal stem cells were obtained from adipose tissues by enzyme digestion combined with adherent culture method. Morphological and flow cytometry were used to identify phenotype and induce differentiation. Secondly, the stable proliferative phase cells were harvested to obtain the conditioned medium, and chitosan, mannitol, beta-glycerol phosphate sodium and hyaluronic acid were added to prepare the thermosensitive hydrogel. Then the 95 ℃ aluminum block was used to rapidly establish a model of degree III skin scald on the left (experimental group) and right (control group) sides of the back of 24 C57BL/6 mice. In the experimental group, adipose derived stem cell conditioned medium hydrogel was applied twice a day on the right side of the mouse back, and in the control group, fresh medium hydrogel was applied twice a day on the left side of the mouse back. The treatment period lasted for 7 days. Healing time and healing process were observed to calculate the healing rate. Histopathological changes were observed by hematoxylin-eosin staining at paraffin sections at 4, 14, 28 days after skin scald. RESULTS AND CONCLUSION: (1) The human adipose derived mesenchymal stem cells had fibroblast-like morphology and proliferated vigorously, and the average doubling time was 55 hours. These cells could be induced to differentiate into osteoblasts, chondrocytes and adipocytes. High expression of CD29, CD44, CD90 and CD105 were observed on these cells with low expression of CD31 and CD34, which met the standard of mesenchymal stem cells. (2) Thethermosensitive hydrogel prepared by the conditioned medium was cool and transparent viscous liquid at 4-20 ℃, and was changed into semi-solid gel at( 37 ℃ after 15 minutes. (3) The normal structure) subcutaneous fat and muscle tissue (of 95 ℃ aluminum block scalded mice wer) standards of degree III burns. The wound area was roughly 3 cm2. (4) In the repair process, shorter wound healing time, less scar and better dermis structure were observed in the experimental group compared with the control group. (5) Inflammatory infiltration, thickness of granulation tissue, epidermal thickness, fibroblasts and vascular density were significantly improved in the experimental group as compared with the control group (P < 0.05). To conclude, human adipose derived mesenchymal stem cells conditioned medium hydrogel can promote the wound healing and promote the quality of regenerated skin after skin scald.

ObjectiveTo detect the expression level of programmed cell death (PDCD) 5 and tumor necrosis factor(TNF)-α in serum and joint fluid from rheumatoid arthritis (RA) and osteoarthritis (OA)patients,and analyze the correlation between PDCD5 and TNF-α in order to study the role of PDCD5 in the pathogenesis of RA.MethodsFiftypatients(including 26 RA,24 OA) between December 2009 and August 2010 were selected to this study.ELISA was used to detect the concentration of PDCD5 and TNF-α in the serum and joint fluid.Two-independent sample t-test and Pearson's correlation analysis were used for statistics.ResultsIn both serum and joint fluid,the concentration of PDCD5 from RA patients [(37±33) vs (37±26) pg/ml ] was significantly higher than that of OA patients [ ( 13± 14) vs ( 11 ±7 ) pg/ml ] (P＜0.05).The concentration of TNF-α in the serum from RA and OA patients did not differ significantly(P=0.122),but its concentration in joint fluid of RA patients was significantly higher than that of OA patients (P=0.037).In the serum,there was significant correlation between PDCD5 and TNF-α (r=-0.55,P=0.004; r=-0.51,P=0.012)in both RA and OA patients.The correlation between PDCD5 and TNF-α in joint fluid of RA patients was statistically significant(r=-0.49,P=0.012),but no correlation could be found in joint fluid between PDCD5and TNF-α of OA patients(r=-0.353,P=0.09).ConclusionThis study suggests that PDCD5 and TNF-αare important apoptosis-regulatory factors in RA,and play important roles in the occurrence and development of RA.

Objective To observe the effects of berberine on neuralogical function,serum oxidized low density lipoprotein(ox-LDL),and matrix metalloproteinases-9(MMP-9) in patients with acute cerebral infarction.Methods Ninety-two patients with acute cerebral infarction were randomly divided into treatment group and control group (n=46).Control group received routine treatment,while treatment group was given 0.3 g of berberine three times a day besides routine treatment for 14 days.In both groups,decubitus venous blood was harvested before,7 and 14 days after treatment.Serum ox-LDL and MMP-9 were determined with enzyme-linked immunosorbent assay (ELISA).Before and 7 and 14 days after treatment,the neural function defect was graded by the US National Institutes of health stroke scale (NIHSS) and the modified Rankin scale (mRS).Results The neurological function was improved significantly in 7 and 14 days after the treatment for both two groups according to NIHSS and mRS,and the difference between treatment group and control group was statistically significant (P<0.05).After treatment,ox-LDL and MMP-9 declined significantly in both groups,and were lower in treatment group than in control group (all P<0.05).Conclusion Berberine significantly reduces ox-LDL and MMP-9 levels in patients with acute cerebral infarction and improves the degree of neurological function deficit.

Objective To evaluate the effectiveness of suberselective uterine arterial embolization for uterine fibroids.Methods Uterine arterial embolization with golyvimylalcohol(PVA) particles or Iodized oil and Gelfoam or Pingyangmycin lipiodol and Gelfoam was performed in 182 patients with uterine fibroids.Results Bilateral and unilateral superselective uterine arterial embolization were performed in 173 cases and 9 cases respectively. 6～28 months (mean 11 months) after the procedure, complete disappearance of tumor(16 cases), an average shinkage of 67% in tumor volume(152 cases) and a mean 42% reduction of uterine volume were obtained in 168 followed-up cases. The clinical symptoms were relieved significantly.The main side effets were hypogastic pain(135/182).Conclusion Superselection uterine arterial embolization is an effective and microinvasive method in treating uterine fibroids.

Aim To explore the role of endoplasmic re-ticulum stress( ERS) in Astragaloside Ⅳ-induced car-dioprotection against ischemia/reperfusion injury in rats. Methods A model of myocardial ischemia 30 min followed by 120 min reperfusion was made by liga-ting coronary artery in male Wistar rats. Rats were di-vided randomly into 4 groups: sham group, ischemia/reperfusion group, ERS inhibitor TUDCA group, As-tragaloside Ⅳgroup. Myocardial samples were collect-ed from the risk zones during ischemia and reperfu-sion, ERS was determined by measuring levels of glu-cose regulated protein 78 ( GRP78 ) , an established marker of ERS with Western blot. Immunofluorescence study was used to test GRP78 intensity with laser scan-ning confocal microscopy, TTC method was used to measure the infarct size,hematoxylin-eosin staining was used to observe the changes of morphological changes of myocardium. Results There was no statistical difference in GRP78 expression during ischemia com-pared to the sham group, but was markedly increased upon reperfusion. Astragaloside Ⅳ could mimic TUD-CA and significantly decreased the GRP78 expression, reduced infarct size and improved the morphology of myocardial tissue with a significant statistical difference compared with the control group ( P<0. 05 ) . Conclu-sions ERS is induced upon reperfusion but not during ischemia in isolated rat hearts. Astragaloside Ⅳ pre-vents myocardial reperfusion injury presumably by the inhibition of ERS.

BACKGROUND: This study aimed to explore the effects of TNF-α on the expression of IP3R1 mRNA and protein in human mesangial cells (HMCs), and to elucidate the mechanism of TNF-α relating to IP3R1 expression in the occurrence of hepatorenal syndrome (HRS). METHODS: HMCs were stimulated by tumor (TNF-α) with 100 ng/mL for different hours (2, 4, 8, and 24 hours). The expression changes of IP3R1 mRNA and protein were detected by quantitative real-time polymerase chain reaction and immunoblotting. Several inhibitors including D609, U73122, PP1, safingol, rottlerin and non-radioactive protein kinase C (PKC) were used to examine the mechanism of signal transduction of TNF-α-regulated IP3R1 in HMCs. RESULTS: The levels of IP3R1 mRNA at 2 hours after TNF-α exposure were significantly enhanced and peaked at 8 hours in HMCs (P<0.01), then descended at 24 hours (P<0.01). The levels of IP3R1 protein at 4 hours after TNF-α exposure were obviously increased and peaked at 24 hours after TNF-α exposure (P<0.01). Compared to the control group, safingol (PKCα inhibitor) and D609 (phosphatidylcholine-specific phospholipase C inhibitor) significantly blocked the TNF-α-induced expression of IP3R1 mRNA (3.30±0.81 vs. 1.95±0.13,P<0.05; 2.10±0.49,P<0.01) and IP3R1 protein (3.09±0.13 vs. 1.86+0.39,P<0.01; 1.98±0.02,P<0.01). TNF-α promoted PKCα activation with maximal PKCα phosphorylation that occurred 8 hours after stimulation measured by non-radioactive PKC assay, and the effect was markedly attenuated by pretreatment with D609 or safingol. CONCLUSION: TNF-α increased the expression of IP3R1 and this was mediated, at least in part, through the PC-PLC/PKCα signaling pathways in HMCs.