Objective:To explore therapeutic effect of Fasudil combined Salmeterol Xinafoate and fluticasone propio‐nate powder for inhalation (Seretide) on patients with chronic obstructive pulmonary disease (COPD) combined pul‐monary arterial hypertension (PAH ) .Methods :A total of 120 patients ,who hospitalized in our department from Jan 2013 to Oct 2014 and conformed to diagnostic standards of COPD and PAH ,were selected .According to ran‐dom number table ,they were equally divided into routine treatment group (received routine therapeutic measures ) , Fasudil group (received Fasudil based on routine treatment group ) and combined treatment group (received Fasudil combined Seretide based on routine treatment ) . Pulmonary function indexes , mean pulmonary arterial pressure (mPAP) ,pulmonary arterial systolic pressure (PASP) ,6min walking distance (6MWD) and blood gas indexes were observed and compared among three groups before and after treatment .Results:Compared with routine treatment group after treatment ,there were significant reductions in mPAP [(54.1 ± 10.3) mmHg vs .(51.3 ± 9.5) mmHg vs . (48.5 ± 10.5) mmHg] and PASP [ (72.4 ± 9.7) mmHg vs .(63.4 ± 9.3) mmHg vs .(61.6 ± 9.1) mmHg] ,and sig‐nificant rise in 6MWD [ (259.4 ± 37.0) m vs .(274.2 ± 36.5) m vs .(288.3 ± 47.5) m] ,forced expiratory volume in one second [FEV1 ,(1.44 ± 0.32) L vs .(1.59 ± 0.38) L vs .(1.87 ± 0.34) L] and FEV1/forced vital capacity (FVC) [ (47.2 ± 11.9)% vs .(50.3 ± 12.1)% vs .(54.6 ± 11.7)% ];significant rise in partial pressure of oxygen in artery [PO2 ,(64.3 ± 9.8) mmHg vs .(68.9 ± 8.2) mmHg vs .(76.9 ± 9.5) mmHg] and saturation of arterial blood oxygen [SaO2 ,(65.0 ± 8.2)% vs .(71.0 ± 9.8)% vs .(76.8 ± 9.4)% ] ,and significant reduction in partial pressure of carbon dioxide in artery [PCO2 ,(63.6 ± 9.5) mmHg vs .(58.5 ± 9.6) mmHg vs .(51.3 ± 7.9) mmHg] in Fasud‐il group and combined treatment group ,and those of combined treatment group were significantly improved com‐pared to those of Fasudil group , P<0.05 or <0.01. Actual base excess of combined treatment group was signifi‐cantly higher than the other two groups , P<0. 01 both . Conclusion:Fasudil combined Seretide can significantly im‐prove pulmonary function reduction ,improve PAH ,quality of life and prognosis in COPD + PAH patients .

Objective: To explore mechanism of fasudil combined salmeterol and fluticasone propionate powder for inhalation (Seretide) in treating chronic obstructive pulmonary disease (COPD) complicated pulmonary artery hypertension (PAH).Methods: A total of 120 patients accorded with diagnostic standards of COPD and PAH, who hospitalized in our department from Jan 2013 to Oct 2014, were selected.According to random number table method, patients were randomly and equally divided into routine treatment group, fasudil group (received intravenous drip of fasudil based on routine treatment group) and combined treatment group (received additional Seretide therapy based on fasudil group).Levels of nitric oxide (NO), endothelin-1 (ET-1), C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured and compared among three groups before and after treatment.Results: Compared with before treatment, after two-week treatment, there were significant reductions in levels of CRP, ESR and ET-1, and significant rise in NO level in three groups, P<0.05 or<0.01;compared with routine treatment group after treatment, there were significant reductions in levels of CRP[(14.8±3.3) mg/L vs.(12.9±3.6) mg/L vs.(11.4±3.4) mg/L], ESR[(37.3±8.9) mm/h vs.(32.9±8.8) mm/h vs.(29.3±5.6) mm/h]and ET-1[(63.1±11.2) ng/L vs.(57.5±8.1) ng/L vs.(53.1±8.9) ng/L], and significant rise in NO level[(70.2±10.7) μmol/L vs.(76.0±8.0) μmol/L vs.(80.5±11.3) μmol/L]in fasudil group and combined treatment group, P<0.05 or<0.01;compared with fasudil group, there were significant reductions in levels of CRP, ESR and ET-1, and significant rise in NO level in combined treatment, P<0.05 all.Conclusion: Fasudil hydrochloride combined Seretide can significantly reduce levels of ESR, CRP and ET-1, and increase NO level in COPD + PAH patients.It may improve prognosis in these patients, which is worth extending.

BACKGROUND: Hyaluronan-methylcellulose hydrogel cannot only be conjugated with short peptide sequences and growth factors to achieve sustained release, but also has a role in blocking dural defects and reducing inflammation. It is an ideal biomaterial for the treatment of spinal cord injury. OBJECTIVE: To investigate the effect of neurotrophin-3 modified hyaluronan-methylcellulose (HAMC-NT-3) hydrogel on the recovery of neurological function in rats with spinal cord injury. METHODS: Fifty-four female Sprague-Dawley rats (provided by the Experimental Animal Center of the Academy of Military Medical Sciences in China) were randomly divided into three groups (n=18 per group) . The sham group only underwent T10 laminectomy. In the model group and the experimental group, an aneurysm clip was used to establish spinal cord injury models after T10 laminectomy. The experimental group was locally injected with HAMC-NT-3 hydrogel. The Basso Beattie Bresnahan function scoring was performed at 1 day, 1, 2, 3, 4, 5, 6, 7, and 8 weeks after surgery. The inclined plane test was performed at 4, 6 and 8 weeks after surgery to evaluate the recovery of hindlimb motor function. ELISA was used to detect the concentrations of inflammatory factors in the spinal cord at 1 week after surgery. Immunohistochemical staining was used to observe the area of syringomyelia, glial fibrillary acidic protein expression and nerve regeneration at 8 weeks after surgery. RESULTS AND CONCLUSION: (1) The Basso Beattie Bresnahan scores of the model group and the experimental group were lower than those of the sham group at various time points after surgery (P < 0.05) . The Basso Beattie Bresnahan scores of the experimental group were higher than those of the model group at 4-8 weeks after surgery (P < 0.05) . (2) In the inclined plane test, the maximum inclined angles of the model group and the experimental group at each time point after surgery were lower than that of the sham group (P < 0.05) . The maximum inclined angles of the experimental group at 6 and 8 weeks after surgery were higher than those of the sham group (P < 0.05) . (3) The concentrations of tumor necrosis factor-α, interleukin-1β, interleukin-6 and interleukin-10 in the experimental group and the model group were higher than those in the sham group (P < 0.05) . The concentrations of tumor necrosis factor-α, interleukin-1β and interleukin-6 in the experimental group were lower than those in the model group (P < 0.05) . The concentration of interleukin-10 in the experimental group was higher than that in the model group (P < 0.05) . (4) Immunohistochemical staining showed that the expression levels of glial fibrillary acidic protein in the experimental group and the model group were higher than those in the sham group, while the expression of glial fibrillary acidic protein in the experimental group was lower than that in the model group. The area of syringomyelia in the experimental group was smaller than that in the model group (P < 0.05) . These results indicate that local injection of HAMC-NT-3 hydrogel can effectively inhibit inflammation as well as astrocyte activation and proliferation, reduce fibrous scar formation, and promote the protection of nerve tissue and the recovery of hindlimb motor function after spinal cord injury.

Objective To investigate the effect and mechanism of microRNA-10b(miR-10b)on idiopathic short stature(ISS).Methods A total of 54 children with ISS and 54 healthy children were collected.The serum expression of miR-10b was detected by RT-qPCR,and the relationship between serum miR-10b expression and clinical data of children with ISS was analyzed.miR-10b inhibitor,si-TGFBR1 and their negative control transfection C28/I2 cells were used.CCK-8 experimental detection was used to detect C28/I2 cell proliferation.Western blot assay was used to detect gnome related transcription factor 2(RUNX2),collagen type X alpha 1 chain(COL10A1),transforming growth factor beta receptor 1(TGFBR1),SMAD3 and pSMAD3 protein expression.The target of miR-10b was screened in StarBase database,and the targeting relationship between miR-10b and TGFBR1 was verified by dual luciferase reporter gene assay.Results The serum expression of miR-10b was higher in the ISS group than that of the healthy control group,and the higher the miR-10b expression,the more obvious the decrease of child height,IGF-1 and alkaline phosphatase(P＜0.05).Compared with the NC group,the cell proliferation ability and RUNX2,COL10A1,TGFBR1,and pSMAD3 protein expression were up-regulated in the miR-10b inhibitor group(P＜0.05).StarBase database suggested that miR-10b had a binding site of TGFBR1,and dual luciferase reporter gene assay confirmed that TGFBR1 interacted with miR-10b(P＜0.05).Compared with the si-NC group,the expression of TGFBR1 was down-regulated and the cell proliferation ability was decreased in the si-TGFBR1 group(P＜0.05).Conclusion miR-10b inhibits chondrocyte proliferation and hypertrophy in idiopathic short stature by targeting TGFBR1/SMAD3 pathway.

Objective: To investigate the neuroprotective effect of Ghrelin on traumatic brain injury (TBI) in mice. Methods: TBI model of C57BL / 6 mice was established by electronic cortical impact instrument (eCCI). According to the random figure table method, twenty-four mice were randomly divided into sham group(Sham group), TBI group and Ghrelin intervention group(Ghrelin group) with 8 mice in each group. The model of TBI was established in TBI group and Ghrelin group.The mice in Ghrelin group was injected intraperitoneally 0.5 g/kg before and 1 h after injury respectively. And the mice Sham group and TBI group were injected with the same amount of normal saline. The changes of cerebral blood perfusion (CBP) were monitored in real time by laser speckle contrast analysis(LSCI), the changes of neuroelectrophysiology were observed by monitoring motor evoked potential (MEP), and the status of neurological deficit was evaluated by modified neurological deficit score (mNSS). Results: Compared with Sham group, the mice in TBI group had significantly lower cerebral blood perfusion(CBP) (t=-12.36, P<0.01), longer latency and lower amplitude of motor evoked potential (MEP) (t=5.03, -11.55, all P<0.01), and significantly higher mNSS scores (t=9.34, P<0.01). However, compared with the TBI group, the cerebral blood perfusion(CBP) of Ghrelin group increased significantly at 12 h after TBI((196.87±17.36) PU/mm² vs (123.62±8.04)PU/mm², t=10.45, P<0.01), while the latency of MEP decreased((5.30±0.33)ms vs (6.80±0.97)ms, t=-5.01, P<0.01), the amplitude of MEP increased((2.21±0.16)mV vs (1.27±0.27)mV, t=9.65, P<0.01). And compared with the TBI group, the neurological deficit score of Ghrelin group decreased significantly at 24 h after TBI((4.9±1.2) vs (8.4±2.6), t=-3.87, P<0.01). Conclusion Ghrelin exhibits a significant neuroprotective role by increasing cerebral blood flow perfusion, reducing the degree of neurological deficit and promoting motor function recovery in TBI mice.

Objective: To investigate the effects of Casein kinase 2-interacting protein 1 (CKIP-1) gene silencing on the proliferation of glioma cells U87-MG. Methods: The recombinant lentiviral vectors targeting CKIP-1 gene or negative control were constructed and then used to infect glioma U87-MG cell line.The effects of knock-down on the mRNA or protein expression of CKIP-1 were evaluated by real-time qPCR and western blotting.Cell cycle was detected by the flow cytometry assay, and cell proliferation changes were evaluated by cell counting, MTT, and BrdU assay, respectively.Lastly, the colony formation was used to investigate the effect of CKIP-1 knock-down on the clone formation. Results: Compared with the group of Ctrl, CKIP-1 siRNA was observed to significantly inhibit CKIP-1 expression at the mRNA levels (Ctrl (1.01±0.13) vs CKIP-1 siRNA (0.23±0.02), P<0.01) and protein levels in the U87-MG cells.Also, CKIP-1 suppression mediated by RNAi decreased the ratio of G0/G1 phase (Ctrl (69.64±0.79) vs CKIP-1 siRNA(62.64±0.66), P<0.01), increased that of G2/M phase (Ctrl (8.36±0.52) vs CKIP-1 siRNA(13.87±2.90), P<0.05), and significantly inhibited the cell proliferation and clone formation (Colony number: Ctrl (25±2) vs CKIP-1 siRNA(2±1), P<0.05) of transfected U87-MG cells. Conclusion Knocking down the expression of CKIP-1 significantly inhibit cell proliferation in human U87-MG glioma cells, indicating that CKIP-1 is involved in the development of gliomas and could promote the cell proliferation.