Dermoid cysts occur in the maxillary sinus mucosa were rare. Patient's CT showed: maxillary sinuses Sinus cavity expansion, sinus wall thinning. The inside of the sinus wall disappeared, the maxillary sinus filled with soft tissue mass shadow. Bacterial culture: Staphylococcus aureus. Pathological report: a very small a mount of scattered broken squamous epithelium and keratosis, no atypia cells. Lesions consistent with epidermoid cyst. Patients with epidermoid cysts, formated probably in the process of embryonic development, the reasons of rapid growth may be considered for inflammatory stimulation.
Epidermal Cyst ; Humans ; Male ; Maxillary Sinus ; Young Adult

One alkaline protease from Actinomucor elegans AS3.2778 was purified protein. The enzyme was purified using ammonium sulfate precipitation, ion exchange chromatography, hydrophobic chromatography and size exclusion chromatography method, and its properties were also investigated. The molecular weight of this enzyme is 32 kDa with SDS-PAGE method, optimum temperature is 60℃, optimum pH is 8.5 to 10.5, it is stable in the pH range of 6.0 to 9.0 at < 40℃ temperature, and being completely inhibited by the serine protease inhibitor, PMSF, indicated that it belongs to the serine protease family. Specificity test indicated this protease has extensive selectivity to peptide bones, especially to peptide bones composed of Leucine residue.

Objective To summarize the experience of using anastomotic apparatus and ring in the reconstruction of alimentary tract after gastrectomy. Methods Anastomotic apparatus or anastomotic ring was used to reconstruct alimentary tract after total or partial gastrectomy including esophagojejunostomy, esophagogastrostomy, gastroduodenostomy, gastrojejunostomy and jejunojejunostomy. Results The reconstruction of alimentary tract after gastrectomy using anastomotic apparatus and ring was successfully completed once in 182 cases. There were not anastomotic leakage, bleeding and infection after operation. During the follow-up period of 3～12 months, gastroscope or barium meal examinations showed that only 3 cases had the stricture of anastomotic entrance, and the other patients recovered well. Conclusion Compared with using traditional manual anastomosis to reconstruct alimentary tract after gastrectomy, anastomotic apparatus and ring had the advantages of convenience, simplicity, rapidity and reliability, and could raise operative efficiency greatly, shorten operative time and prevent the complications of post-operation such as the leakage and striture of anastomotic entrance. Using anastomotic apparatus and ring was recommended in the reconstruction of alimentary tract.

OBJECTIVE:To optimize the ratio of glycerol in Chloramphenicol and Ephedrine Nasal Drops included in China's Hospitals Agents Norms.METHODS:By formula optimization and observation on clinical trials,the ratio of glycerol in Chloramphenicol and Ephedrine Nasal Drops was reduced from 300mL to 50mL.RESULTS & CONCLUSION:The Chloramphenicol and Ephedrine Nose Drops prepared in an optimized ratio of glycerol is of much less irritability,good transparency,good compliance in patients,more reliable efficacy,thus deserving to be popularized.

Objective To investigate the effects of IGFBP-3,RXR? and STAT-1 on A?_ 1-42 induced apoptosis in rat hippocampus neurons.Methods Apoptosis was induced by fibrillar A?_ 1-42.The percentage of neurons apoptosis was evaluated by microscopy after staining with TUNEL/DAPI.IGFBP-3 and RXR? positive neurons were observed by immunofluorescence.The expression of RXR? and STAT-1 protein were detected by Western blotting.Results After treatment with 20?mol/L A?_ 1-42 for 24 hours,the apoptotic hippocampus neurons were shown by TUNEL/DAPI assay.The percentage of apoptotic neurons was increased in a time-dependent manner.During the development of apoptosis,both the percentage of IGFBP-3/RXR? positive neurons and the expression of RXR? protein increased markedly after 3-6hours(P

Immunological alterations and changes in neurotransmission are considered to be crucial in the pathological process of depression. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in depression, which shines a clue for new anti-depression therapy. Immune activation will lead to depression through serotonin and glutamate systems. This paper is attempted to review the immune mediated alterations on serotonin and glutamate systems.

Objective To systematically assess the efficacy of memantine on moderate to severe Alzheimer's disease (AD).Methods With the evaluation method of the Cochrane system,searches were made in the Cochrane Library,MEDLINE,Embase,Forest Laboratories,CNKI,Wanfang Data,and VIP Data up to February 2013 for double blind,randomized,and placebo-controlled trials (RCTs) evaluating the efficacy of memantine for moderate to severe AD.A meta-analysis of included clinical trials was conducted using the Revman 5.2 software to evaluate the efficacy of memantine on overall clinical status,cognitive function activities of daily living,and behavioral and psychological disturbances.Results A total of 8 RCTs were included (2 527 patients with moderate to severe AD).Results of the meta-analysis showed that,for patients with moderate to severe AD,memantine had better efficacy than placebo on overall clinical status,cognitive function,and activities of daily living (MD=-0.24,95％CI:0.340.15;SMD=-0.26,95％CI:-0.340.18;SMD=-0.13,95％CI:-0.21-0.05),but there was no significant difference in efficacy on behavioral and psychological function between memantine and placebo (P =0.08).Analysis of subgroups showed that memantine had better efficacy than placebo on cognitive function in moderate AD patients (SMD =-0.22,95％CI:-0.37 0.06) and on overall clinical status,cognitive function,and activities of daily living in severe AD patients (MD-0.29,95％CI:-0.40 0.18;SMD=-0.31,95％CI:0.46-0.15;SMD=-0.16,95％ CI:-0.25 0.06;MD=-3.13,95％ CI:-4.88-1.39;respectively).Conclusions Memantine has efficacy on overall clinical status,cognitive function and activities of daily living in patients with moderate to severe AD,especially in patients with severe AD.

OBJECTIVE To investigate the effect of asiaticoside (AS) on endothelial-to-mesenchymal transition (EndoMT) in hypoxia pulmonary hypertension (HPH). METHODS Male Sprague-Dawley (SD) rats were divided into normoxia control group, hypoxia model group, and AS 25 and 50 mg · kg-1 group. Hypoxia model group and AS group were subjected to intermittent hypoxia exposure. Control group and model group received 1-1.5 mL saline daily, and AS groups were ig administrated with AS 25 and 50 mg·kg-1 for 4 weeks. Human pulmonary artery endothelial cells (HPAECs) were divided into normoxia control group and hypoxia AS groups. Hypoxia groups were cultured with AS 0, 25, 50, 100 and 200 mg·L-1 for 72 h under hypoxic (5%O2, 5%CO2) conditions. Anti-proliferation effect of AS was investigated by CCK-8 assay. Then, HPAECs were divided into normoxia control group, normoxia AS 100 mg · L-1 group, hypoxia model group, and hypoxia AS 100 mg · L-1 group. After five days of culture, migration ability of cells was detected by Transwell test. Expression of CD31 andα-SMA was detected by immunofluorescence and Western blotting in both in vivo and in vitro experiments. RESULTS In both in vivo and in vitro experiments, compared with normoxia control group, expression of CD31 was reduced (P<0.01) andα-smooth muscle actin (α-SMA) was increased (P<0.01) in hypoxia model group in both immunofluorescent analysis and Western blotting. Compared with hypoxia model group, expression of CD31 was increased andα-SMA was decreased (P<0.05, P<0.01) in AS treatment groups. Compared with normoxia control group, proliferation and migration ability of HPAEC were elevated in hypoxia model group (P<0.05). Compared with hypoxia group, AS 100 mg · L-1 depressed proliferation and migration of HPAEC under hypoxia exposure up to 72 h (P<0.05). CONCLUSION EndoMT might be involved in HPH and could be partly inhibited by AS.

Objective To investigate the relationship between activation of gliacytes , mitogen-activated protein kinase (p38MAPK) and neuronal apoptosis after microinjecting aggregated Aβ25-35 into hippocampus.Methods The model was established by using stereotaxic technique to inject 10μg aggregated Aβ25-35 into dorsal hippocampus in rats .The rats were grouped as the control , vehicle and model groups .Immunohistochemistry and Western blotting were used for detection of activation of microglia(MG), atrocytes (AS) and expression of p-p38MAPK in the hippocampus.ELISA was used to evaluate the level of TNF-αand IL-1β.The survival neurons were observed by Nissl staining and the apoptotic neurons were identified by tunnel staining .Results Expression of ox-42, GFAP, p-p38MAPK were up-regulated in hippocampus, as well as TNF-α、IL-1β, which reached a highest value on the 7th day after injection of Aβ25-35.However, the number of neuron with Nissl positive decreased gradually , and the tunnel positive neurons increased highly and reached a peak value on the 7th day.There were significant differences between the control and vehicle group ( P <0.01). Conclusion Apoptosis of the neuron caused by Aβ25-35 injection may result from activation of gliacytes , p38 MAPK and increase of TNF-αand IL-1βlevel.

This study is to explore whether the Wnt/beta-catenin signaling pathway is involved in the process of tripchlorolide (T4) protecting against oligomeric Abeta(1-42)-induced neuronal apoptosis. Primary cultured cortical neurons were used for the experiments on day 6 or 7. The oligomeric Abeta(1-42) (5 micromol x L(-1) for 24 h) was applied to induce neuronal apoptosis. Prior to treatment with Abeta(1-42) for 24 h, the cultured neurons were pre-incubated with T4 (2.5, 10, and 40 nmol x L(-1)), Wnt3a (Wnt signaling agonists) and Dkk1 (inhibitors) for indicated time. Then the cell viability, neuronal apoptosis, and protein levels of Wnt, glycogen synthase kinase 3beta (GSK3beta), beta-catenin and phospho-beta-catenin were measured by MTT assay, TUNEL staining and Western blotting, respectively. The result demonstrated that oligomeric Abeta(1-42) induced apoptotic neuronal cell death in a time- and dose-dependent manner. Pretreatment with T4 significantly increased the neuronal cell survival and attenuated neuronal apoptosis. Moreover, oligomeric Abeta(1-42)-induced phosphorylation of beta-catenin and GSK3beta was markedly inhibited by T4. Additionally, T4 stabilized cytoplasmic beta-catenin. These results indicate that tripchlorolide protects against the neurotoxicity of Abeta by regulating Wnt/beta-catenin signaling pathway. This may provide insight into the clinical application of tripchlorolide to Alzheimer's disease.