Humans ; Facial Injuries/etiology* ; Wound Healing

Objective To establish the animal model with stress ulcer(SU) and probe the relationship between the gastric mucosal injury and lasting stress time,the dynamic structural changes of pH of gastric juice.Methods Twenty-four SD young rats were randomly divided into 4 groups:control group,45 min(groupⅠ),90 min(groupⅡ),3 h(groupⅢ)groups under water immersion restraint stress(WRS).The change of gastric mucosal ulcer index(UI),pH of gastric juice were observed.Results Acute gastric mucosal damage was induced by WRS,with the WRS time prolonged,UI increased gradually and pH of gastric juice remarkably decreased in experimental rats.UI was positively rela-ted with stress time(r=0.957 P

Objective:To investigate the effect of mycophenolate mofetil(MMF)on proliferation and apoptosis of cyst-lining epithelial cells in patients with autosomal dominant polycystic kidney disease(ADPKD),and to compare its effect with that of rapamycin(RAPA)in vitro.Methods: Primary cultured cyst-lining epithelial cells were treated with MMF and RAPA at different concentrations(0,0.005,0.05,0.5,5 ?g/ml)for 48 h or 72 h.The inhibitory effects of them on the cells were evaluated by MTT assay;the cell cycle distribution and apoptotic ratio were determined by flow cytometry.The morphological changes of cyst-lining epithelial cells were observed under transmission electron microscope.Results: Both MMF and RAPA significantly inhibited the proliferation of cyst-lining epithelial cells in a dose-and time-dependent manner.After 48 h treatment,the cells were blocked at S phase by MMF and at G0/G1 phase by RAPA.Both drugs induced cell apoptosis,with the maximal apoptotic rate being(5.53?0.27)% for MMF and(4.36?0.10)% for PAPA.Typical morphological changes of apoptotic cells were observed under electron microscope.Conclusion: MMF can effectively inhibit proliferation and induce apoptosis of cyst-lining epithelial cells,but its inhibitory effect is weaker than that of RAPA.

Cancer is one of the main causes of death for human beings. Clinical oncologists increasingly rely upon imaging for diagnosis, stage, response assessment, and follow-up in cancer patient. However, 18F-FDG is not a tumor specific agent, inflammation and infection also have intensive uptake of 18F-FDG, resulting in false positive diagnosis, and some tumors have low uptake of 18F-FDG or even do not uptake 18F-FDG, leading to false negative diagnosis. So it is urgent to develop non-18F-FDG novel tumor targeting agent. Recently, a large number of researches in vitro have demonstrated that berberine has anti-tumor activity against a variety of tumor cells by inducing tumor cell apoptosis through inhibition of mitochondrial respiratory chain etc. So far, there is no credible evidence of berberine targeting in tumor in vivo. We proposed a hypothesis that berberine has the characteristics of tumor targeting biodistribution in vivo, and verified the proposal by 18F-berberine PET/CT imaging in VX2 muscle tumor-bearing rabbit model. In this review, we intend to give an overview of the progress of berberine anticancer, the structural bases of berberine anticancer and the uderlying molecular mechanisms of berberine anticancer indentified so far. We also introduce the first visualization of 18F labeled berberine derivatives targeting tumor in VX2 muscle tumor-bearing rabbit model by PET/CT. These breakthrough findings suggest that 18F-berberine derivatives as a potential PET/CT tumor targeted molecular imaging agent may have important implications for cancer targeting therapy, molecular imaging and modernization of Traditional Chinese Medicine.
Berberine ; chemistry ; Fluorodeoxyglucose F18 ; chemistry ; Humans ; Molecular Imaging ; Neoplasms ; diagnosis ; Positron-Emission Tomography ; Tissue Distribution ; Tomography, X-Ray Computed

Environmental Monitoring ; methods ; Inhalation Exposure ; Occupational Exposure ; analysis ; Workplace

Adolescent ; Humans ; Kearns-Sayre Syndrome ; Male

It is important to pay more attention to students’ basic skills training and their comprehensive abilities cultivating in microbiology experiment teaching. Explorations and reforms in enforcing the students’ base and cultivating their abilities were carried out in order to improve teaching quality and train specialized talents with high quality.

A set of teaching methods have been explored and practiced in this paper, which include paying attention to knowledge originating process teaching, enhancing thought training, constructing microbiology knowledge system, concerning reality, following the advanced achievement during the microbiology class teaching process, in order to improve teaching quality overall, cultivate students’ innovative ability.

Objective To understand the dynamics of DC subsets in chronic HIV-infected patients during antiretroviral therapy (ART).Methods Seventeen treatment-naive chronic HIV-infected patients were enrolled in our study,and blood was collected at week 0,4,12,24,48 and 60 of ART.Additional 15 HIV-uninfected age-matched healthy adults and 15 long term non-progressors(LTNP) were recruited as controls.CD4+T cell counts and viral loads were examined routinely.The counts of DC subsets were measured by flow cytometry and IFN-α plasma levels were measured by ELISA.Data analysis was performed using SPSS version 16.0.Results ( 1 ) Before ART,mDC ( percentage and absolute count) in ⅢⅤ-infected group were significantly lower than those in healthy group and LTNP group,P＜0.001 in both groups.After 60 weeks of ART,mDC in HIV-infeeted group were significantly increased,and there were no significant differences compared with healthy controls and LTNP group.(2) pDC and IFN-α plasma levels remained relatively stable during ART,and similar to those in healthy controls and LTNP group.(3)Significant associations were found for DC subsets and CD4+ T cell counts before ART.mDC subsets at week 12,24,60 post ART were positively correlated with CD4+ T cell counts,and negntively correlated with virus load.Changes in mDC at week 8 post ART positively correlated with the changes in CD4+T cells at week 60 post ART,and negatively correlated with the changes in virus load at week 60 post ART.Conclusion The counts of mDC significantly reduced in HIV-infected patients,increased after ART,and positively correlated with CD4+ T cell counts.The findings suggest that mDC may play an important role in controlling HIV infection,mDC may serve as an early predictor for immune reconstitution in the initiation of ART.

Objective To study the effect of mild brain hyothermia on cerebral ischemic injury. Methods Global cerebral ischemia was established by modified Pulsinelli 4-vessel occlusion model. Forty-eight Sprague-Dawley rats were divided into 4 group: a sham-operated group, a normothermia (37～38℃) ischemic group and a mild is-chemic hypothermia (31～32℃) group; the mild ischemic hypothermia was subdivided into 4 groups with the hypo-thermia lasting for 30 min, 60 min, 120 min and 240 min, respectively. After 240 rain of reperfusion following 20 min cerebral ischemia, the levels of nitric oxide products nitrite (NO2) ,endothelin-1 (ET1) , tumor necrosis fac-tor alpha (TNFα) and interleukin-1 beta (IL-1β) in brain tissue and the lactate dehydrogenase (LDH), aspartate aminotransferase(AST) , creatine kinase(CK) and its brain band isoenzyme (CK-BB) in plasma were measured. Results The levels of IL-1β,TNFα, ET1 and NO2. in brain tissue, and the amounts of LDH, AST, CK and CK-BB in serum were higher in normothermia ischemic group than those in sham-operated group (P <0.05). Mild hypother-mia lasting for 60 min to 240 min markedly decreased the levels of IL-1β, TNF-α, ET1 and NO2 in brain tissue, and the amounts of LDH, AST, CK and CK-BB in serum in normothermia ischemic group, when compared with normo-thermia ischemic group (P < 0.05 or P < 0.01). Mild hypothermia lasting for 30 min did not influence the content of IL-1β, TNF-α, ET1 and NO2 in brain tissue when compared with normothermia isehemia group (P > 0.05). Con-clusion Mild brain hypothermia post-ischemia can significantly suppress the inflammation response in ischemic brain tissue and stabilize the function of cell membrane. The best neuroprotection of mild brain hypothermia must be carried out immediately and last for more than 60 minutes.