Objective To study whether intranasally administered transforming growth factor beta1(TGF-?1)can reach central nervous system(CNS)through the trigeminal nerve pathway.Methods Nineteen healthy male SD rats were randomly assigned into control group(n=6)and administration(IN)0.5h group(n=3),1h group(n=4),2h group(n=3)and 6h group(n=3).Rats in IN groups were given 50?l(20?g)recombinant human TGF-?1(rhTGF-?1)intranasally and were sacrificed at 0.5,1,2 or 6h after IN following blood sample collection.The cerebellum,midbrain,pon,medulla and trigeminal nerve were separated quickly and the concentration of TGF-?1 was analyzed by ELISA.Results Compared with the control group(15.01?1.50pg/mg),TGF-?1 was significantly elevated in the trigeminal nerve in all the IN groups(P0.05).TGF-?1 concentrations in plasma and other caudal CNS regions,such as cerebellum,midbrain and cervical spinal cord,were not significantly changed compared with that in control group.Conclusion TGF-?1 is likely to be absorbed by the trigeminal nerve following intranasal administration,and is subsequently delivered to some brain regions through the trigeminal nerve pathway,which may provide a potential treatment strategy for trigeminal nerve and CNS disorders.

Objective To investigate the clinical characteristics and therapy methods of dorsolateral medullary syndrome.Methods The clinical data of 36 cases of dorsolateral medullary syndrome were analyzed retrospectively.Results The palients presented with acute or sub-acute oneset.Vertigo(83.3%),dysarthria(61.1%),dysphagia(52.8%),Horner's syndrome(80.6%),ataxia(72.2%) and crossed sensory disturbance(50%) were the most common symptoms and signs.MRI examination demonstrated dorsolateral medullary infarction in 32 of 36 patients.13 patients received DSA examination and the results showed 6 patients with different degree disease of vertebral arery,2 patients with isolated posterior inferior cerebellar artery occlusion,1 patient with vertebral occlusion and ipsilateral posterior inferior cerebellar artery stenosis.In 33 patients who received anticoagulation,antiplatelet and activating blood circulation to dissipate blood stasis therapies,26 patients improved 7~10 days after treatments and the symptoms almost disappeared during 1～2 months.6 cases remained different degree sensory disturbance and ataxia 1 case died.3 patients were treated with percutaneous transluminal angioplasty and stenting.The symptoms relieved at the day of operation and recovered completely 1 week after operation.Conclusions Dorsolateral medullary syndrome is a clinical syndrome because of insufficient blood-supply in local blood vessel.MRI is sensitive for the diagnosis of dorsolateral medullary syndrome.The location and degree of the disease can be identified by DSA.Intervention treatment is an effective method in the therapy of dorsolateral medullary syndrome.

Endovascular treatment is becoming a novel technique in the treatment of carotid stenosis. Since this technique is in its infancy, there are many controversies on this technique and theory now. This paper briefly reviews the most recent advances in endovascular treatment of carotid stenosis.

Antiplatelet therapy is commonly used for the secondary prevention of embolic stroke of undetermined source (ESUS). However, the embolic source of ESUS is extremely heterogeneous, and the effect of antithrombotic therapy is different. This article describes the etiology and secondary prevention research progress of ESUS, in order to provide reference for clinical diagnosis and treatment.

Aim To evaluate the effects of ferulic acid ( FA ) on lipopolysaccharide ( LPS )-induced neuroin-flammation in microglia cells and its potential mecha-nisms. Methods Microglial activation was induced by stimulation with LPS, and the effects of FA pretreat-ment on microglial activation and production of proin-flammatory mediators, nitric oxide/iNOS were investi-gated. The role of the mitogen-activated protein kinases in the antiinflammatory actions of FA in LPS-stimulated microglia was further elucidated. Results Cell viabil-ity experiments revealed that FA did not produce cyto-toxicity in microglia. FA significantly inhibited LPS-in-duced production of tumour necrosis factor-alpha ( TNF-α) , interleukin-6 ( IL-6 ) , interleukin-1 beta ( IL-1β) , and nitric oxide ( NO ) . Protein and mRNA levels of COX-2 and inducible nitric oxide synthase ( iNOS) were also attenuated by FA. Further experi-ments on intracellular signalling mechanisms showed that inhibition of extracellular regulated kinase ( ERK) contributed to the anti-neuroinflammatory actions of FA. Conclusion The results suggest that FA inhibits LPS-induced microglial inflammation by partial targe-ting of ERK signalling and attenuation of ERK.

Community Health Committee (CHC), an innovative public participation mechanism of grassroots health service management, established a bottom-up communication channel between the public and government to communicate health related problems and opinions, and set up a grassroots community health services supervision system. The rural residents were endowed with opportunities to take part in grassroots health care decision making and management by CHC. CHC changed the top-down model of traditional health management, improved the grassroots medical services, and increased governance capability of local government We introduced the CHC practice in Zhejiang project counties, exhibited the primary effects and experience of this pilot program, and explored new mechanism and model for rural community residents to participate in grassroots health service management

Objective To investigate the relationship between serum levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) and Suzuki' s grading system in adult moyamoya disease (MMD).Methods Fifty-two adult patients with MMD,who were diagnosed in Jinling hospital between April 2009 and January 2010,were retrieved from the Nanjing Stroke Registry Program (NSRP).Sixteen sex- and age-matched healthy individuals with MMD patients consisted of the control group.Using enzyme-linked immunosorbent assay,serum concentrations of VEGF and MMP-9 were compared between adult MMD patients and healthy individuals.By Suzuki' s six-grading system,patients were divided into different subgroups,and the correlation of serum levels of VEGF and MMP-9 corresponding to different subgroup and Suzuki's grading was respectively analyzed.In addition,the correlation of serum levels of VEGF and MMP-9 was also evaluated.Results Serum VEGF concentrations in ischemic and hemorrhagic MMD patients was respectively ( 289.4 + 69.2 ) pg/ml and ( 324.3 ± 95.6 ) pg/ml and were significantly higher compared to those in healthy controls ( ( 63.5 ± 7.6 ) pg/ml; F =69.43,P ＜ 0.01 ).Similar findings were observed for MMP-9 ( ( 499.4 ± 76.2 ) ng/ml and ( 531.2 + 100.2 ) ng/ml versus (257.1 ±30.7) ng/ml; F =66.023,P ＜0.01 ).With the increase of Suzuki' s grading,serum levels of VEGF and MMP-9 respectively showed a high trend ( r =0.879,P ＜ 0.01:r =0.838,P ＜ 0.01 ).In addition,a positive correlation between serum levels of VEGF and MMP-9 was found in the MMD group( r =0.590,P ＜0.01 ).Conclusion The results show that serum levels of VEGF and MMP-9 in adult MMD are higher than those in healthy controls,which may play a role in neovascularization in MMD,and moreover,serum levels of VEGF and MMP-9 show a high trend with the progression of MMD,which suggest that serum levels of VEGF and MMP-9 can reflect the severity of MMD.

Objective Neuroinflammation following traumatic brain injury (TBI) may give rise to neurodisorder.This study aimed to investigate the effect of intranasal delivery of nerve growth factor ( NGF) on neuroinflammation following TBI and its action mechanism in rats. Methods Thirty-six male adult Sprague-Dawley rats were equally divided into a sham , a TBI, and a TBI+NGF group.The rats in the TBI +NGF group were treated with NGF intranasally at 12 and 24 hours after TBI.The levels of IL-1βand TNF-αin the injured cerebral cortex were detected by ELISA , the DNA-binding activity of NF-κB evaluated by EMSA , and the expres-sion of amyloid-β( Aβ42 ) determined by Western blot . Results NGF attenuated the inflammation following TBI .Compared with the TBI group, the level of IL-1βwas obviously decreased in the TBI +NGF group at 12 hours (70.65 ±3.10 vs 37.51 ±1.92) and 24 hours (68.85 ±8.10 vs 36.23 ±2.99, P<0.05), and so was that of TNF-α(47.12 ±7.38 vs 27.63 ±5.77 and 56.15 ±11.20 vs 29.94 ±8.62, P<0.05).The DNA-binding activity of NF-κB was reduced to 111.62 ±0.49 and 131.52 ±0.88, and the expression of Aβ42 to 0.23 ±0.008 and 0.52 ±0.004 at 12 and 24 hours respectively after treatment with NGF , both with statistically significant differences from the TBI group (P<0.05). Conclusion Intranasal administration of NGF attenuates TBI-induced neuroinflamma-tion in rats, which may be associated with its regulatory effect on the Aβ42/NF-κB signaling pathway .

Objective Survivin is overexpressed in gastric cancer. However it not expressed in normal gastric mucosa. The expression of survivin is tightly related to the prognosis of gastric cancer.By gene reconstruction we generated pcDNA3 survivin mutant(Cys84Ala) plasmid, and observed its effect on the gastric carcinoma cell lines. Methods The survivin mRNA and protein expression levels were determined by reverse transcription polymerase chain reaction(RT PCR) analysis,Western blot and immunohistochemical staining respectively . Flowcytometry and acridine orange staning were employed to detect apoptosis. Results Overexpression of survivin mRNA and protein were detected in the gastric cancer cell lines. Inhibition of survivin by survivin mutant cDNA induced apoptosis,activated caspase 3 activity,cleaved PARP and promoted cytochrome C releasing in gastric cancer cells,and effectively sensitized gastric cancer cells to chemotherapeutic agents. Conclusion Inhibition of survivin may induce apoptosis in gastic cancer and sensitize gastric cancer cells to chemotherapeutic agents.Survivin targeted therapeutic protocol may potentially benefit gastric cancer therapy.

Objective To investigate the possible signal pathway of the apoptosis in gastric cancer cell lines(SGC 7901 and MKN 45)induced by arsenic trioxide. Methods TUNEL method was used to observe the influence of calcium antagonist, inhibitors of protein kinase C (PKC) and protein tyrosine kinase(PTK) on the apoptosis of gastric cancer cells induced by arsenic trioxide. Levels of cAMP, PKC and PTK were detected before and after the treatment with arsenic trioxide. Results Both PKC and PTK inhibitors could induce apoptosis of gastric cancer cell lines, also both of them had a cooperative action with arsenic trioxide in inducing apoptosis of gastric cancer cells, while calcium antagonist had no any effect on the apoptosis of gastric cancer cell lines. PKC and PTK levels decreased but cAMP level increased during the apoptosis of gastric cancer cells induced by arsenic trioxide ( P