BACKGROUND:Nanohydroxyapatite/colagen basal bone materials have a porous structure which is very close to natural bone. After implanting to the human body, it can be gradualy degraded and absorbed over time to play a strongly guiding and bridging role. OBJECTIVE:To investigate the clinical effect of nanohydroxyapatite/colagen basal bone materials on lumbar posterolateral bone graft fusion. METHODS: Fifty-eight patients with lumbar disease, including 28 males and 30 females, aged 47to81 years were included and were performed lumbar laminectomyvia posterior midline approach, or simultaneously performed discectomy and lumbar posterolateral bone graft fusion between transverse process. The bone graft material was nanohydroxyapatite/colagen basal bone repair material. Pedicle screw system was used to make the internal fixation. Patients were folowed up for 18 months after treatment. Pain relief and bone graft fusion condition were observed. RESULTS AND CONCLUSION: Fifty-eight patients had successfuly completed the treatment. The incisions healed by first intention. The clinical symptoms and signs were significantly improved compared with before treatment. The complications such as infection, screws shifting and loosening, spondylolisthesis and displacement of adjacent vertebral in fixed segments, and the adverse reactions associated with bone graft material were not occurred during the folow-up. At the 1st, 6th, 12th and 18th months after implanting nanohydroxyapatite/colagen basal bone materials, the visual analog scale scores of the lower limbs and waist were al lower than those before implantation (P < 0.05). At the 12thand 18th months of folow-up, the bone graft rates were 84% and 90%, respectively. These results demonstrate that the application of nanohydroxyapatite/colagen basal bone materials in the process of lumbar posterolateral bone graft fusion can ease the symptoms of lower limb pain and lower back pain, which is conducive to bone graft fusion.

BACKGROUND:Nano-hydroxyapatite/polyamide 66 composite has good material-cel interface and three-dimensional porous network structure, and it can also be gradualy degraded over time after implantation in the human body. OBJECTIVE:To explore the effect of nano-hydroxyapatite/polyamide 66 in early repair of femoral head necrosis. METHODS:A retrospective analysis was performed on clinical data of 62 cases of early osteonecrosis of the femoral head, including 32 males and 30 females, aged 34-51 years. These patients were divided into control group (31 cases) and observation group (31 cases) according to treatment methods. Core decompression with nano-hydroxyapatite/polyamide 66 implantation and core decompression with bone graft were respectively performed in the observation and control groups. Incidence of pain in the two groups was compared at 1 day after treatmen; and during the 12-month folow-up, the Harris score of the hip function in the two groups was compared. RESULTS AND CONCLUSION:There was no significant difference in the visual analog scale scores between two groups at 1 day after treatment. The Harris scores in the observation group were significantly higher than those in the control group at 3 and 12 months after treatment (P < 0.05). There was no adverse reaction in the two groups. These findings indicate that nano-hydroxyapatite/polyamide 66 material for repair of early femoral head necrosis has good biocompatibility, and can obtain good effects on limb function recovery.

Objective To investigate the effect of exogenous murine interleukin-18 (IL-18) on early mouse collagen Ⅱ -induced arthritis (CIA). Methods Mice were injected intraperitoneallg IL-18 (0.2 μg/d) combination with IL-10 (0.1 μg/d), IL-4 (0.1 μg/d) and IL-12 (0.1 μg/d) daily for five days before the onset of CIA. The arthritis response was monitored visually by macroscopic scoring. Reverse transcription -polymerase chain reaction (RT-PCR) was employed to determine the mRNA expression of cytokine in patella with adjacent synovium in CIA mouse. Histology of knee was examined to assess the occurrence of cartilage destruction and bone erosion. Wilcoxon rank test was selected. Results IL-18/IL-4 treatment could slightly suppress the macroscopic score of arthritis, but a more pronounced amelioration was found in mice treated with the combination of IL-18 and IL-10 during early treatment. On 38 days after immunizatian macroscopic score in treated group (0.12±0.20) was significantly improves than in the control group (0.29±0.19, P<0.05). This resulted in both the suppression of macroscopic signs of inflammation and the reduction of cellular infiltrates in the synovial tissue, which provided the protection against cartilage destruction. Moreover, the expression of Thl cytokines [IL-18 (0.22±0.06), IL-12 (0.14±0.05)] and inflammatory cytokine [IL-6 (0.22±0.11)] was greatly inhibited both in the synovial tissue and in the articular cartilage in the treatment groups compared with those in the control groups (P<0.05). However, the mRNA levels of Th2 cytokines [IL-10 (6.35±0.12), IL-4 (3.57±0.13)] were up-regulated after IL-18/IL-10 treatment (P<0.05). Moreover, IL-18R (0.40±0.15) levels were down-regulated compared with those in the control group (P<0.05). T-bet mRNA levels were decreased in IL-18/IL-10 compared with the control group, and GATA-3 mRNA (5.71±0.11) levels were significantly higher than those in the control group (P<0.05). Conclusion Low dose IL-18/IL-10 treatment can inhibit Th1 cytokines expression and induce Th2 cytokines expression, which may be mediated not only by inhibiting Th1 responses through IL-18/IL-18R mechanism, but also by inducing anti-inflammatory mediators such as IL-10 and IL-4 through a GATA-3-dependent mechanism.

Objective To investigate the effect of exogenous murine interlukin-18 (mIL-18) on early and established murine coUagen-induced arthritis (CIA). Methods Mice were injected intraperitoneally with IL-18 (0.2 μg/mouse) daily for 5 days before or after the onset of CIA. The response was monitored visually by macroscopic scoring. Reverse transcription-polymerase chain reaction (RT-PCR) was employed to determine the mRNA expression of cytokines in patella with adjacent synovium in CIA mouse. Histolpgy of knee synovium was used to assess the occurrence of cartilage destruction and bone erosions. Results IL-18 alone had no effect on macroscopic score, occurrence of arthritis, advancement of histology on early stage of CIA. Moreover, expression of Th 1 cytokines and Th2 cytokines in the synovial tissue and" articular cartilage remained unchanged compared with the control group, however, a pronounced progression of histology was found in mice treated with IL-18 in estabhshed CIA. Forty-three days after immunization, the macroscopic score in the treated group (0.33±0.11 ) was significantly improved than in the control group (0.25±0.09) (P<0.05). Moreover, the mRNA levels of IL-10 and IL-18BP both in the synovial tissue and in the articular cartilage in the treated groups decreased significantly than those in the control groups (P<0.05). Conclusion Low dose mIL-18 alone has no effect on early stage CIA. But pronounced exacerbation is found in mice treated with IL-18 on established arthritis, which supports that IL-18 initiates this effect by inhibiting IL-10 and IL-18 BP.

Objective To study the protective function and the mechanism of Shenqi Dihuang decoction on the kidney of type 2 diabetes melltuds rats. Methods Type 2 diabetes mellitus rat models were set up by injection of small dose of streptozotocin (STZ). The SD rats were randomized into a control group, a model group and a treatment group. The treatment group was given Shenqi Dihuang decoction. The control group and the model group were given the same amount of water. After 24 weeks, renal morphology examination and biochemical indicator were examined. The levels of Ang-Ⅱ and endothelin (ET) in senum were tested by radioimmunoassay and the level of transforming growth factorβ1 (TGF-β1) in renal cortex were determined by immunohistochemistry. Results The kidney function and kidney lesions were significantly improved in the treatment group than in the model group. Ang-Ⅱ And ET levels in serum and renal cortex was reduced, and the expression of TGF-β1 in the treatment group was decreased. Conclusion Shenqi Dihuang Decoction has protective effect on the kidney of diabetic rats, the mechanism may be related to its inhibition on the over expression of Ang- Ⅱ, ET and TGF-β1.

Objective To observe the effects of happy family cognitive training on patients with vascular cognitive impairment. Meth-ods From April, 2015 to April, 2016, 80 patients with vascular cognitive impairment were divided randomly into happy family cognitive training group (n=40) and control group (n=40). Both groups accepted routine medicine and rehabilitation exercise, while the happy family cognitive training group received happy family cognitive training additionally. They were assessed with Montreal Cognitive Assessment (MoCA) and Activities of Daily Living (ADL) before and after 12 weeks of treatment. Results The scores of MoCA and ADL improved more in the family cognitive training group than in the control group after treatment (t>5.454, P<0.001). Conclusion Happy family cogni-tive training is effective on vascular cognitive impairment, for cognitive function and activities of daily living.

Objective To observe effects of angieminⅡ(AngⅡ)and captopril on outward potassium channel currents in canine atrial myoeytes,and to study mechanisnof Ang II and capupril on atrial arrhythmia.Method Ten healthy adult mongrel dogs(general class),weighing 15 to 20 kg,male and female informality,were provided bythe service centre of Tianjin Li-qun experimental animals.Single canine atrial myotcyte was acutely isolated and whole-cell configtmtion of the patch-clamp tchnique was used to detec trapidly activating delayed reefifier outward K+ current(Ikr),slowly activating delayed recti fier outward K+ current(Iks),ultra-rapidly aetivatin delayed rectifier outward K+ current(Ikur)and transient outward potassium current(Ito)before and after An II and captopril peffion.Software of pClamp 7.0 for windows and pClampfit 7.0 Was used to measure current and data were expressed as mean±standard deviation(x±s).SPSS 10.0 statistical was used for statistical analysis.The paired t test was useel for comparison betwn before and after treatment.P<0.05 was comidered as statistical significance.Results AngII(0.5/mol/L)increased Ikr and Iks,ilfibited Ito[(19.54±2.41)pA/pF vs.(24.83±2.52)pA/pF,P=0.001;(20.69±2.29)pA/pF Vfl.(25.59±3.42)pA/pF,P:0.0003;(6.34±1.93)pA/pF vs.(3.71±1.50)pA/pF,P=0.001)],and had no effect on k[(19.78±1.22 pA/pr Vs.(20.39±1.50)pA/pF,P=0.258)].Captopril(5tot/L)had no significant effect on Ikr.,b.k and[(19.11 4-4.91)pA/pF vs.(18.99 4-4.04)-∥pF,P=0.808;(20.76 4-2.89)pA/pF vs.(20.27 a-3.46)pA/pF,P=0.305;(18.50 4-3.78)pA/pF vs.(18.25 4-4.02)pA/pF,P=0.704;(7.31±1.99)pA/pF vs.(6.89±2.12)pA/pF,P=0.136)].Conclusioas AngⅡmay promote atrial electrical remocof atrial fibrillation through outward potassium currents.As angiotemin-eonverting enzy/ne inhibitor.captioruk can prevent atrial electrical rodding of atrial fibrillation by inhibiting renin-angiotensin-system.

AIM: To investigate the effects of fluvas-tatin on expression of intercellular adhesion molecule-1 after myocardial ischemia-reperfusion in rabbits with hyper-lipidemia. METHODS: 30 rabbits which were gastric perfusion administered intralipid were randomly divided into 3 groups ( n - 10 in each) : IR ( ischemia-reperfusion) group, S (sham-operation) group and F (fluvastatin 10 mg?kg-1 ) group. Electrocardiography and cardiac function were recorded during the experiment. At the end of reperfusion, ischemic area and infarct size were defined by Evans blue and triphenyltetrazolium chloride staining. The expression of ICAM-1 in myocardium was measuredby RT-PCR. RESULTS: After ischemia-reperfusion, the expression of ICAM-1 mRNA in myocardial and infarct size decreased and cardiac function significantly improved in F group compared with IR group. CONCLUSION: The increase of expression of ICAM-1 mRNA in myocardial may be one of the important factors in inducing myocardial ischemia-reperfusion injury. The myocardial protective mechanism of fluvastatin maybe attribute to its effect on decreasing the expression of ICAM-1 mRNA in myocardial .

Objective To investigate the effects and mechanism of different dosage of fluvastatin on the prevention of heart muscle ischemia reperfusion injury in rabbits.Method Thirty-five rabbits were randomly divided into 5 groups with 7 rabbits in each: sham group,myocardial ischemia reperfusion control group,low dosage of fluvastatin pretreatment group (2 mg/kg,Group F1),middle dosage of fluvastatin pretreatment group(5 mg/kg,Group F2) and large dosage of fluvastatin pretreatment group(20 mg/kg,Group F3).The left ventricular systolic pressure(LVSP),the max rate of rise of left ventricular pressure(?dp/dt_(-max)) and left ventricular end-diastolic pressure(LVEDP) were detected during the experiment.At the end of reperfusion,the infarct size and area at risk were defined by Evans blue and TTC staining,and the levels of myocardial nitrogen monoxidum(NO) and nitricoxide synthase(NOS) were measured.Result Compared with the ischemia reperfusion group,the indexes of heart function improved significantly,the level of myocardial NO was increased significantly and the myocardial infarct size was decreased significantly in the groups F2 and F3.There was no significant difference between the group F1 and ischemia reperfusion group.Conclusion Fluvastatin exerts a cardioprotective effect against myocardial ischemia reperfusion injury in rabbits.NO is likely involved in this protective mechanism.

Background The rat model of N-methyl-N-nitrosourea (MNU)-induced photoreceptor cell apoptosis is often used to study retinal degeneration.But the changes in the gene expression patterm in retinal degeneration in rats have not been reported.Objective This study was undertaken to investigate regulation of gene expression in the retina of MNU-induced retinal degeneration in rats by performing microarray analysis of retinal RNA.Methods Fifty 6-week-old SD rats were numbered and randomized into the normal group and the model group.The retinal degeneration model was established by a single hypodermic injection of 40 mg/kg of MNU,and the rats in the normal group received equivalent volume of physiological saline in the same way.The rats were sacrificed 12 hours or 24 hours after injection.Retinal sections from the right eyes were prepared for the measurement of the retinal thickness by histopathological examination,and retinas from the left eyes were used to confirm the differential gene expression as detected by microarray (normal group and 12 hours model group).Genes exhibiting changes in expression by ≥2.0 folds were further confirmed using real-time PCR.Results The whole thickness of the retina declined in the rats from the 24 hours model group compared to the normal group and 12 hours model group (t =9.926,P=0.002;t=2.736,P=0.028).The thickness of the outer nuclear layer was (26.58±2.90) μm in the 24 hours model group,showing a significant decrease in comparison with (38.11 ± 1.01) μm in the normal group and (35.07t3.03) μm in the 12 hours model group (t=6.028,P=0.009;t=6.839,P=0.006).However,there was no significant difference in retinal thickness between the normal group and the 12 hours model group (whole thickness:t=1.541,P=0.324;outer nuclear layer thickness:t=2.040,P=0.134).Microarray analysis of the rat genes showed that out of 17 000 genes,142 genes involved in biological process and 94 genes involved in molecular functions were differentially expressed,where most of them participate in the mitogen activated protein kinase signaling pathway,Tolllike receptor signaling pathway and apoptosis pathway.Real-time PCR analysis demonstrated that the expression of CCL2,IL-1b,CCL3,c-fos,c-myc,p53 and MMP3 were consistently up-regulated,conforming with the results from microarray analysis.Conclusions The changes in gene expression pattern appear in the early stage of MNUinduced retinal degeneration.These microarray results provided clues to understanding the molecular pathways underlying photoreceptor degeneration and indicating the directions for future studies.