OBJECTIVETo study the effects of sacral nerve root electrostimulation (SNS) on the colon function and its mechanisms in rats with spinal cord injury (SCI).

METHODSOne hundred and four Wistar rats were divided into three groups: A, B and C. A group ( n = 24) was divided into three subgroups (n = 8) for studying the bioelectricity: Normal group (NG), SCI group (SCI) and SCI group with SNS(SNS); B group( n = 24) was divided into three subgroups( n = 8) for studying the colon motility: NG, SCI and SNS. C group( n = 56) were divided into three groups for studying the change of morphology and neurotransmitters(SP and VIP): NG (n = 8), SCI (n = 24), and SNS (n = 24) . In SCI and SNS, included of three subgroups: 24, 48, 72 h after spinal cord injury (n = 8).

RESULTSIn SCI group, the activity of bioelectricity in proximal and distal colon was reduced; the colon motility was lessened, and colon mucosa appeared different degree of damage; cell-cell connections between intestinal epithelial cells were destroyed. The expressions of substance P(SP) and vasoactive intestinal peptide (VIP) in colon were decreased obviously. SNS was found to activate the bioelectricity, promote the colon motility, improve the intestinal mucosal, and increase the expressions of SP and VIP. Conclusion: SNS can activate the peristalsis, rehabilitate the motility of denervated colon, protection of the intestinal mechanical barrier between intestinal epithelial cells and tight junction, rebuild the colon function through activating the bioelectricity and increase the expressions of SP and VIP.

Animals ; Colon ; physiopathology ; Electric Stimulation Therapy ; Epithelial Cells ; drug effects ; Intestinal Mucosa ; drug effects ; Lumbosacral Region ; innervation ; Neurotransmitter Agents ; metabolism ; Rats ; Rats, Wistar ; Spinal Cord Injuries ; therapy ; Substance P ; metabolism ; Vasoactive Intestinal Peptide ; metabolism

OBJECTIVETo observe the ultrastructural change of the route of gut bacterial translocation in a rat with spinal cord injury (SCI).

METHODSForty Wistar rats were divided into the following groups: control group and 3 SCI groups (10 in each group). The rats in the SCI groups were established SCI model at 24 h, 48 h, and 72 h after SCI. Small intestine mucous membrane tissue was identified and assayed by transmission electron microscope, scanning electron microscope and immunofluorescence microscopy.

RESULTSSmall intestine mucous membrane tissue in control group was not damaged significantly, but those in SCI groups were damaged significantly. Proliferation bacteria in gut lumen attached on microvilli. The extracellular bacteria torn the intestinal barrier and perforated into the small intestinal mucosal epithelial cell. The bacteria and a lot of particles of the seriously damaged region penetrated into the lymphatic system and the blood system directly. Some bacteria were internalized into the goblet cell through the apical granule. Some bacteria and particles perforated into the submucosa of the M cell running the long axis of M cells through the tight junctions. In the microcirculation of mucosa, the bacteria that had already broken through the microvilli into blood circulation swim accompanying with erythrocytes.

CONCLUSIONThe routes of bacterial translocation interact and format a vicious circle. At early step, the transcellular pathway of bacterial translocation is major. Following with the destroyed small intestine mucous, the routes of bacterial translocation through the lymphatic system and the blood system become direct pathways. The goblet cell-dendritic cell and M cell pathway also play an important role in the bacterial translocation.

Animals ; Bacteria ; Bacterial Translocation ; Epithelial Cells ; microbiology ; Goblet Cells ; microbiology ; Intestinal Mucosa ; microbiology ; pathology ; ultrastructure ; Intestine, Small ; microbiology ; pathology ; ultrastructure ; Microvilli ; microbiology ; Rats ; Rats, Wistar ; Spinal Cord Injuries ; microbiology

Objective: Under the microstrain environment, to investigate the impact and mechanisms of osteoblast differentiation of the naringin monomer on marrow stem cells (MSCs) in vitro. Methods: The cyclical stretch microstrain was loaded on silicone rubber membrane with cultured rabbit MSCs using EF3200 mechanical tester with the system of BioDynamic biological reaction tank. The experiment was divided into eight groups, A: the blank control group in conventional cultured environment; B: the group of alone microstrain loading; C: the group cultured in environment containing naringin and the naringin concentrations, respectively were 2, 20, and 200 ng/mL; D: under microstrain environment, the joint application with naringin at concentration of 2, 20, and 200 ng/mL. Flow cytometry was used to test the proliferation index (PI) of MSCs after microstrain loading. The gene expression of the cells in osteocalcin (OCN), osteoblast specific transcription factor (Runx2) and collagen type I (Col I) were assayed by RT-PCR. Results: Under the microstrain environment combined with naringin, MSCs showed obvious polarity and the long axis of cells parallel to the direction of mechanical stimulus direction. The combination of naringin and microstrain stimulation can significantly improve the MSCs proliferation activity. Naringin (200 ng/mL) could improve the gene expression of OCN under the stimulation of 50000 microstrain. Under 50000 microstrain stimulation, naringin at different concentration could significantly enhance the Runx2 gene expression and the effect between the enhancement and the naringin concentration was positive. Under the microstrain stimulation, naringin at low concentration could promote the Col I gene expression, on the contrary, naringin at high concentration could inhibit the Col I gene expression. Conclusion: Under the microstrain environment, naringin monomer could enhance the proliferation of MSCs and promote the osteogenetic differentiation of MSCs.

Adult ; Humans ; Male ; Patellar Dislocation ; congenital ; diagnosis ; therapy

Objective To investigate the mechanism of an inhibitor of NADPH oxidases,diphenylene iodonium (DPI),in preventing radiation-induced lung injury.Methods Totally 48 adult SD male rats were randomly classified into 4 groups:control group (C),radiation group (R),radiation plus DPI group (R + D) and DPI group (D).The radiation induced pulmonary injury model was preformed by using 6 MV X-rays to deliver 8 Gy per day for 5 consecutive days with 40 Gy in total to the thorax of each animal.Rats in R + D group were subcutaneously administered with 0.02％ DPI (1 mg/kg) at 1 h prior to radiation while rats in D group received the same dose of DPI without radiation.DPI was given from 3 d before radiation to 30 d after the first radiation.Rats in C and D groups received the same dose of saline.Animals were sacrificed at 1 month and 6 months after radiation,respectively.The lungs were removed and processed for HE and Masson staining,hydroxyproline content measurement,and TGF-β1 immunohistochemical detection.Results At 1 month post-radiation,rats in R group showed typical alveolitis,the level of hydroxyproline was (0.69 ± 0.05) μg/mg,and the positive area of TGF-β1 expression was (39.97 ± 0.90) ％,while the level of hydroxyproline in R + D group was (0.55 ± 0.03) μg/mg and the positive area of TGF-β1 expression was(33.83 ± 1.55) ％,rats in R + D group showed less severe alveolitis compared with R group(t =5.32,5.93,P ＜0.05).At 6 months post-radiation,rats in R group showed typical lung fibrosis with hydroxyproline level of (1.04 ±-0.02) μg/mg and TGF-β1 expression of (37.80 ± 0.85) ％,whereas the hydroxyproline level in R + D group was (0.85 ± 0.02) μg/ mg,the TGF-β1 expression was(23.93 ± 1.16)％,rats in R + D group showed moderate lung fibrosis(t =15.77,16.68,P ＜ 0.05),rats in C and D group had no noticeable changes.Conclusions Diphenylene iodonium could prevent radiation-induced lung injury by reducing the level of hydroxyproline and the expression of TGF-β1.

BACKGROUND:There are various therapies for children limb fractures involving the epiphysis or the metaphysis. According to the different methods, studies on the growth of the epiphyseal plate are a lot, most of which focus on the effects of Kirschner wires with different diameters or holow screw internal fixation on the development of epiphyseal plate. However, there are rare studies on the influence of cross-epiphyseal plate internal fixation on the growth of epiphyseal plate as wel as the influence level. OBJECTIVE:To prepare a peri-epiphyseal fracture model in young rabbits and to observe the effects of cross-epiphyseal plate implantation and removal on the growth of epiphyseal plate. METHODS: Traverse fracture models were made 5 mm above the right femoral distal epiphyseal plate of 60 young rabbits, and then fixed with suitable “L” steel plate and four screws across the epiphyseal plate and peri-epiphyseal fracture line. The left side served as control. Eight rabbits were kiled and observed at 2, 4, 8, 12 weeks after modeling, respectively, to take out the femoral specimens for measurement of femoral length, thickness of the epiphyseal plate, and number of mastocytes per unit column. Histopathology observation was done and changes in mastocytes and thickness of the epiphyseal plate were detected. Another seven rabbits were selected to remove the metal plate, continued to feed for 2 weeks and finaly executed to observe the above-mentioned indexes. RESULTS AND CONCLUSION: (1) There were significant differences in the above indexes between the plate and control groups at 4, 8, 12 weeks after modeling (P < 0.05 orP< 0.001) but not at 2 weeks after modeling (P> 0.05). These findings indicate that within 2 weeks after cross-epiphyseal plate internal fixation, proper pressue has no remarkable influence on the growth of epiphyseal plate; but after persistent internal fixation (> 4 weeks), the growth of epiphyseal plate can be partialy or completed retarded. (2) At 2 and 4 weeks after modeling, the plate was removed, and 2 weeks later, the femoral length, thickness of the epiphyseal plate and mastocyte counting per unit column were improved to different extents, and there were no differences between the plate and control group (P > 0.05). At 8 and 12 weeks after modeling, the plate was removed, and 2 weeks later, the femoral length and thickness of the epiphyseal plate were shortened, and the number of mastocytes per unit column was decreased obviously, which significantly differed from the control group (P < 0.001). These findings indicate that the chondrocytes in the proliferative and hypertrophy layers lose the differentiation and proliferation abilities, and the femoral length and epiphyseal plate thickness are difficult to recover.

OBJECTIVETo discuss the effect of Drynariae Rhizoma's naringin on osteoclasts induced by mouse monocyte RAW264.7.

METHODRAW264.7 cells were induced by 100 μg x L(-1) nuclear factor-κB receptor activator ligand (RANKL) and became mature osteoclasts, which were identified through TRAP specific staining and bone resorption. MTT method was sued to screen and inhibit and the highest concentration of osteoclasts. After being cultured with the screened medium containing naringin for 5 days, positive TRAP cell counting and bone absorption area analysis were adopted to observe the effect of naringin on the formation of osteoclast sells and the bone absorption function. The osteoclast proliferation was measured by flow cytometry. The effects of RANK, TRAP, MMP-9, NFATc1 and C-fos mRNA expressions on nuclear factor-κB were detected by RT-PCR.

RESULTNaringin could inhibit osteoclast differentiation, bone absorption function and proliferation activity of osteoclasts, significantly down-regulate RANK, TRAP, MMP-9 and NFATc1 mRNA expressions in the osteoclast differentiation process, and up-regulate the C-fos mRNA expression.

CONCLUSIONNaringin could inhibit osteoclast differentiation, proliferation and bone absorption function. Its mechanism may be achieved by inhibiting the specific gene expression during the osteoclast differentiation process.

Acid Phosphatase ; metabolism ; Animals ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Flavanones ; pharmacology ; Isoenzymes ; metabolism ; Matrix Metalloproteinase 9 ; genetics ; Mice ; NFATC Transcription Factors ; genetics ; Osteoclasts ; cytology ; drug effects ; Tartrate-Resistant Acid Phosphatase

Objective To investigate the relationship between platelet-activating factor acetylhydrolase gene Arg92His(4, 275; G→A), Ile198Thr(7, 593; T→C) and Val279Phe(9, 994; G→T) mutation and cerebral artery athero-sclerosis stenosis. Methods Six hundred forty-twopatients with cerebral infarction underwent cerebral digital subtrac-tion angiography (DSA).The patients were then divided into cerebral artery atherosclerosis stenosis (CAAS) group(n=477) and control group(n=81) accroding to the site and severity of their cerebral artery stenosis. Furthermore, the CAAS group were divided into intracranial artery stenosis(ICAS) subgroup(n=251), extracranial artery stenosis(ECAS) subgroup (n=115) and extracranial-intracerebral artery stenosis(ECAS) subgroup(n=111). The distributions of genotype and allele frequencies of Arg92His,Ile198Thr and Val279Phe mutation of platelet-activating factor acetylhydrolase gene were ex-amined and comparied in different groups. Results There were significant differences in the distributions of genotype and allele of Arg92His mutation between ICAS subgroup and control group(42.6% vs. 30.3%;23.3% vs. 16.4%, P <0.05). These associations were not detected in ECAS and IECAS subgroups. There was no significant association be-tween Ile198Thr and Val279Phe and stenosis at any site(P>0.05). The distributions of genotype and allele of Arg92His, Ile198Thr and Val279Phe mutation were no significantly difference between CAAS group and control group (P >0.05). Conclusions Arg92His mutation may be associated with intracranial artery atherosclerotic stenosis.

BACKGROUND:Severe spinal angular kyphosis aggravated spinal cord injury and early degeneration, even caused incomplete paralysis or complete paralysis. Surgical treatment is the only solving approaches and method, but it is difficult, exhibits high risk, and easily affects postoperative complications. OBJECTIVE:To analyze the science and effectiveness of posterior vertebral column resection osteotomy combined with step correction in treatment of stiff angular kyphosis based on biomechanical principle. METHODS:A total of 90 cases underwent posterior vertebral column resection osteotomy combined with bilateral pedicle screw spinal cord gradual y shortening echelon tight closure and orthopedic fixation were selected, including 37 males and 52 females, at the average age of 47 years. Kyphotic angle, spinal sagittal imbalance, trunk side offset rate, operation time, intraoperative blood loss were compared and analyzed before and after treatment. RESULTS AND CONCLUSION:The kyphotic angles were 31°-138° (averagely 90.1°) preoperatively and 10°-90° (averagely 41.6°) postoperatively, with an improvement rate of 65%. The distance from C 7 plumb line to the S 1 upper edge was averagely 5.2 mm, with a correction rate of 73%. Intraoperative blood loss was 1 200-6 000 mL, averagely 2 089 mL. Operation time was 212-470 minutes, averagely 326 minutes. The patients were fol owed up for 20 to 35 months after the surgery. Osteotomy segments had achieved bone fusion in al patients, and no complications of spinal cord injury or orthopedic angle loss appeared. These data verified that in the accordance with cellbiomechanics and spinal biomechanical principles, bilateral pedicle screw spinal cord gradual y shortening echelon tight closure and orthopedic fixation protected utmost spinal cord cells against injury in the correction of thoracolumbar angular kyphosis. There is sufficient basis for cellphysiology and it accorded biomechanical and physiological characteristics. During the surgery, we should pay attention to protection and release of nerve root and avoid postoperative corresponding nerve root irritation. Ful fusion ensures kyphosis correction and avoids spine lateral offset, is an effective safeguard for the recovery of spinal function and postoperative orthopedic effect.

Objective To study the effect of intranasal(IN)delivery of nerve growth factor(NGF) on pyriform cortex of satin-poisoned rats.Methods Sprague-Dawley rats were treated with satin and atropine sulphate, pralidoxime to establish satin-poisoned rat model.Then NGF or saline was administered via the olfactory pathway.24 hours later, damaged and residual healthy neurons were estimated and quantified on pyriform cortex using hematoxylin-eosin(HE)staining and neuronal nuclei antigen(NeuN) immunohistochemistry.Results A massive quantity of degenerating neurons were seen in the pyriform cortex of rats with intranasal saline.And compared to the normal rats, the number of neurons of rats with intranasal saline was significantly reduced by 39.44% [(404.75?25.17)/mm~2].But the number of neurons in rats with intranasal NGF [(651.94?36.02)/mm~2] didn't change significantly compared to the normal rats.Conclusion Intranasal delivery of NGF, reducing the degenerating neurons on pyriform cortex of satin-exposure rats, is a potential treatment for satin intoxication.