AIM: To investigate the association between cycloxygenase-2 (COX-2) expression and VEGF intervention as well as the inhibitory effect of Meloxicam on the cultured human pterygium fibroblasts (HPF).METHODS: Expression of COX-2 was measured by immunohistochemistry in the cultured HPF from twenty excised pterygium cases. Expression of COX-2 in HPF was measured by Western blot following the treatment of vascular endothelial growth factor (VEGF) at the different concentrations. In addition, the effect of Meloxicam on proliferation of HPF was studied by adding the different concentrations into the cultured HPF plates by Mono-nuclear cell direct cytotoxicity (MTT) reduction assay.RESULTS: COX-2 expression was present in the cultured HPF. The level of the expression increased following VEGF treatment. The proliferation of the cultured HPF decreased following addition of the different concentrations of Meloxicam (from 75μ mol/L to 300μ mol/L) and the magnitude of the inhibition was dose-time dependent.CONCLUSION: COX-2 levels in the cultured HPF werepositively associated with VEGF stimulation and Meloxicam was inhibitory to HPF proliferation.

Objective To evaluate the outcomes of endoscopic sinus surgery (ESS) for children with chronic rhinosinusitis, who had no response to medication. Methods A total of 112 children (aged 12 to 17 years) with chronic rhinosinusitis caused by abnormal anatomy of the nose cavity were treated by ESS in our hospital. Septorhinoplasty was performed on the patients under an endoscope. Conchoplasty, adenoidectomy, or nasal polypectomy was performed simultaneously if necessary. Results The patients were followed up for 6-23 months (mean 13 months). The symptoms of rhinosinusitis disappeared in 110 patients (98.2%); whereas the other 2 patients showed no obvious improvement after the operation. Conclusions By using microinvasive ESS combined with conchoplasty, children with rhinosinusitis caused by abnormal anatomy that does not respond to medication could be cured.

OBJECTIVETo provide evidence for Chinese medical treatment of children with EB virus infection by exploring its clinical efficacy from multiple angles.

METHODSTotally 81 children patients were randomly assigned to the treatment group (46 cases) and the control group (35 cases). Patients in the treatment group took Chinese medical decoction, while those in the control received intravenous dripping of Ganciclovir and oral administration of pidotimod. The treatment period for the two groups was 2 weeks. Patients were followed-up till the 12th week. Clinical symptoms such as fever, lymphadenopathy and hepatosplenomegaly, as well as lab indices such as abnormal lymphocyte percentage, EB virus antibody, virus DNA load, T cell subsets, immunoglobulin, and so on were observed before and after treatment, at week 4 and 12 of follow-ups.

RESULTS(1) The total effective rate at week 2 was 95.6% in the treatment group, higher than that of the control group (94.3%), but there was no statistical difference between the two groups. (2) The time for defervescence, duration of pharyngeal hyperemia, duration of swollen tonsils was shorter in the treatment group than in the control group (P<0.05). The subsidence of lymphadenopathy, hepatomegaly, and abnormal lymphocytes was better in the treatment group than in the control group (P < 0.05). (3) The positive cases of peripheral blood hetero-lymphocyte was significantly reduced after treatment, at week 4 and 12 of follow-ups both in the treatment group and the control group (P < 0.01). The expression of IgA and IgM decreased after treatment in the two groups when compared with before treatment in the same group (P < 0.05, P < 0.01). IgG in the treatment group also obviously decreased after treatment, at week 4 and 12 of follow-ups (P < 0.05, P < 0.01), while it decreased only after treatment in the control group (P < 0.05). Activities of AST and ALT in the treatment group and the AST activity in the control group were markedly improved when compared with those before treatment (P < 0.05). Compared with the control group, the abnormal lymphocyte positive case number obviously decreased in the treatment group after treatment, at week 4 and 12 of follow-ups (P < 0.05). (4) After treatment, at week 4 and 12 of follow-ups, CD3+ and CD8+ significantly decreased; CD4+, CD4/CD8, and B cells significantly increased in the two groups, when compared with before treatment (P < 0.05). NK cells significantly increased more in the treatment group after treatment, at week 4 and 12 of follow-ups, higher than before treatment as well as the control group (P < 0.05). (5) EB viral DNA and EB viral CA-IgM negative conversion case numbers significantly increased in the two groups after treatment, at week 4 and 12 of follow-ups (P < 0.05). Compared with the control group, EB viral DNA and EB viral CA-IgM negative conversion case numbers significantly increased in the treatment group after treatment and at week 4 of follow-ups (P < 0.05).

CONCLUSIONSTreatment of EB virus infection by Chinese medical treatment was effective. It could promote the recovery of EB viral infection, and reduce the risk of vicious disease after EB viral infection.

Adolescent ; Child ; Child, Preschool ; Drugs, Chinese Herbal ; therapeutic use ; Epstein-Barr Virus Infections ; drug therapy ; immunology ; Female ; Herpesvirus 4, Human ; Humans ; Infant ; Male ; Phytotherapy ; T-Lymphocyte Subsets ; immunology

Objective To investigate the effects of iodine excess on spleen cell viability,lactate dehydrogenase (LDH) leakage,mitochondrial superoxide production and peroxiredoxin (Prx)3 expression in methallothionein Ⅰ / Ⅱ knockout (MT-Ⅰ / Ⅱ KO)mice.Methods Spleen cell suspensions were prepared from six to eight-week old and healthy male MT-Ⅰ / Ⅱ KO mice and wild type (WT) mice; the cell number was adjusted to 5 × 107/L and the cells were plated in 96-well plates (100 μl each well); the cells were exposed to various concentrations of KI (0,10-4,10-3,10-2 mol/L) and 10-3 mol/L H2O2,respectively,for two hours,and control group did not give KI nor H2O2.Cell viability was assayed by methyl thiazolyl tetrazolium (MTT) colorimetric method.Cell damage was detected by chemical colorimetric method.Mitochondrial superoxide production in the spleen cells was measured by flow cytometry.Western blotting technology was used to investigate the expression of Prx3.Results In both MT-Ⅰ/Ⅱ KO and WT mice,the differences of cell viability,LDH leakage,mitochondrial superoxideproduction and the expression of Prx3 of spleen cells among the treatment groups were statistically significant (F =357.92,71.03,130.36,10.36,179.58,26.92,187.43,and 7.16,all P ＜ 0.05).Compared to the control group [(100.00 ± 2.00)％,(100.00 ± 1.63)％,(3 202.22 ± 85.63),(3 161.51 ± 144.49)U/L,43.82 ± 1.56,38.60 ± 2.81,0.61 ± 0.09,0.50 ± 0.08],cell viability of 10-4,10-3,10-2 mol/L KI treatment and 10-3 mol/L H2O2 groups [(80.77 ± 1.86)％,(89.89 ± 2.90)％,(76.08 ± 1.92)％,(87.66 ± 1.74),(73.26 ± 1.86)％,(84.30 ± 2.23)％,(66.22 ± 1.71)％,(70.80 ± 1.49)％] was decreased (all P ＜ 0.05); LDH leakage [(3 880.00 ± 190.62),(3 431.17 ± 170.45),(4 178.33 ± 170.43),(3 598.63 ± 189.09),(4 388.61 ± 123.79),(3 863.72 ± 195.64),(4 615.28 ± 196.17),(4 148.12 ± 195.81)U/L] was increased significantly (all P＜ 0.05); and mitochondrial superoxide production in the spleen cells (53.83 ± 3.22,47.03 ± 1.60,58.92 ± 4.00,50.48 ± 2.59,72.72 ± 2.14,68.53 ± 2.97,80.76 ± 4.11,75.26 ± 3.41) was increased significantly (all P ＜ 0.05); Prx3 expressions in 10-3、10-2 mol/LKI and 10-3 mol/L H2O2 treatment groups (0.82 ± 0.12,0.65 ± 0.12,0.96 ± 0.15,0.73 ± 0.16,1.04 ± 0.13,0.85 ± 0.16) significantly increased (all P ＜ 0.05),the differences of Prx3 expressions between 104 mol/L KI groups (0.73 ± 0.15,0.55 ± 0.09),and control groups were not statistically significant (all P ＞ 0.05).In 104,10-3,10-2 mol/L KI and 10-3 mol/L H2O2 treatment groups,cell viability of MT-Ⅰ/Ⅱ KO mice spleen was lower than that of WT mice (t =6.47,10.93,9.30 and 4.96,all P ＜ 0.05); LDH leakage was higher than that of WT mice (t =4.30,5.58,5.56 and 4.13,all P ＜ 0.05); mitochondria superoxide production was higher than that of WT mice (t =4.64,4.33,2.80 and 2.52,all P ＜ 0.05); Prx3 expression was higher than that of WT mice (t =2.54,2.37,2.59 and 2.27,all P ＜ 0.05).Conclusions KI may decline the cell viability,increase the leakage of LDH and increase the production of mitochondrial superoxide production and Prx 3 expression,which are much more significant in MT-Ⅰ /Ⅱ KO mice,suggesting that MT Ⅰ /Ⅱ has some antioxidative effect in high concentration of iodide induced oxidative stress in the spleen.

Common mental health problems from the perspective of prevention among medical stu-dents were discussed in this activity which was learning from the concept and method of PBL. Participants had to find the solutions themselves by small-group discussion so as to improve their mental health. Results showed that most participants confirmed the innovation, interest and intellectuality of this activity. Moreover, students could not only learn knowledge related to mental health, but also improve their friendship as well as communication skills which were beneficial to medical students' mental health.

Objective:To investigate the complications of traumatic optic neuropathy and to call the surgeons' attention to precaution. Method:Retrospectively analysis of 122 cases patients with traumatic optic neuropathy and 3 cases were analyzed in detail including 1 case with purulent meningitis, another 1 case with internal carotid artery pseudoaneurysm and the other 1 case with internal carotid artery cavernous sinus fistula. Result:Most of the patients had the complications of orbital fracture, maxillofacial fracture, ocular and craniocerebral injury. A few of patients had other injuries all over the body. The case with purulent meningitis was cured with antibiotics. The case with internal carotid artery pseudoaneurysm was cured with neurosurgery. The visual acuity of the both cases were improved. The case with internal carotid artery cavernous sinus fistula died of severe hemorrhea. Conclusion: The patient with traumatic optic neuropathy has the possibility of severe cranial disorders,orbital fracture, maxillofacial fracture and injuries of viscera or limbs. It should be paid mare attention and treated accordingly.

Aim To investigate the interactions be-tween the neuroinflammation caused by lipopolysaccha-ride(LPS) and brain CYP2E1.Methods The human cholinergic neuroblastoma cell line IMR-32 was treated with LPS ( 0.1 mg · L-1 , 1.0 mg · L-1 ) , and the LDH and SOD activities were determined after 24 h in-cubation .In order to determine the roles of MAPK sig-naling pathway in the regulation of CYP 2E1 by LPS, the IMR-32 cells were treated with p38 pathway inhibi-tor SB203580 or ERK pathway inhibitor U 0126 for 45 min before the incubation with LPS .The human do-paminergic neuroblastoma cell line SH-SY5Y with CYP2 E1 over-expression was established . The LDH and SOD activities were determined in SH-SY5 Y cells over-expressed CYP2 E1 and control cells treated with LPS(0.1 mg· L-1 , 1.0 mg· L-1 ) for 24 h.Results
The levels of LDH in IMR-32 cells treated with high-dose LPS were increased by 1.38-fold ( P <0.01 ) compared with the control group , and the levels of SOD reduced by 15.0%( P <0.01 ) .Compared with the control, CYP2E1 mRNA and protein levels in IMR-32 cells treated with high-dose LPS were increased by 1.25-fold(P<0.01) and 1.19-fold(P<0.05).The up-regulation of CYP2E1 by LPS could be attenuated by SB203580 and U0126 pretreatment.Compared with the control cells, the CYP2E1 over-expression in-creased LDH levels by 1.28-fold ( P<0.01 ) and de-creased SOD levels by 3.53-fold ( P<0.01 ) after the low-dose of LPS treatment .The CYP2E1 over-expres-sion increased LDH levels by 1.54-fold ( P <0.01 ) and decreased SOD levels by 2.17-fold( P<0.01) af-ter the high-dose of LPS treatment , compared with the control cells.Conclusions LPS can induce CYP2E1 mRNA and protein levels , and the p38 and ERK sig-naling pathway may be involved in the regulation .The elevated CYP2 E1 levels aggravate the damage to neuro-nal cells caused by LPS .Brain CYP2E1 may be an im-portant contributing factor to the pathological process of neuroinflammatory injury .

Objective To investigate the expression of TLR2 in colon mucosa of ulcerative colitis (UC) and to analyze the correlation with clinical activity and endoscopic grading. Methods The biopsies from 47 UC patients and 13 healthy controls were collected, and the expression of TLR2 protein and mRNA in colonic mucosa was determined by Western Blot and semi-quantitative RT-PCR, respectively. The patients were graded according to endoscopic and clinical findings. Results The expressions of TLR2 protein and TLR2 mRNA in UC patients were significantly increased than those in healthy controls, which was correlated with the progression of the disease. Conclusion The expressions of TLR2 protein and TLR2 mRNA in colon mucosa from UC patients might be used as a marker for disease activity.

Objective:To investigate the distribution of 99Tc m-methylene diphosphonate (MDP) at different stages of bone injury repair. Methods:A total of 30 rabbit models of femur injury were established by the method of electric drill and perforation of femur. According to the different stages of bone injury repair (at 1, 2 and 3 week), rabbits were divided into group A, B and C ( n=10 each group). Femoral SPECT/CT imaging was performed on the last day of different stages of bone injury repair to obtain radioactivity counts in the region of interest (ROI) on the test side and control side and to calculate target/background ratio (T/B). The light intensity of 3 groups was analyzed by phosphor screen imaging and the distribution of 99Tc m-MDP in bone cells was observed by autoradiography. One-way analysis of variance and paired t test were used to analyze the data. Results:The T/B values of group A, B and C were 1.16±0.14, 1.39±0.23 and 1.18±0.10, respectively ( F=5.83, P<0.01). There were significant differences of the maximum radiation count between the test side (50.00±12.45, 59.50±12.83 and 55.10±9.26) and the control side (43.20±9.57, 50.00±12.30 and 44.30± 6.50) in group A, B and C ( t values: 3.24, 2.28 and 5.77, all P<0.05). There were significant differences in the light intensity of bone specimens in group A, B and C by phosphor screen imaging (37 324.67±6 481.50, 60 950.33±9 781.72 and 43 905.00±4 957.92; F=8.25, P=0.02). 99Tc m-MDP were deposited in both intracellular and extracellular during different stages of bone repair in osteocytes and osteoblasts under autoradiography. Conclusion:At different stages of bone injury repair, the concentration of 99Tc m-MDP is significantly distributed, suggesting that there are other ways of concentration mechanism of 99Tc m-MDP in bone tissue besides the chemical adsorption with hydroxyapatite.

OBJECTIVE To observe the effects of glycogen synthase 3β (GSK-3β) in the regula-tion of NLRP3 inflammasome activation after acute myocardial infarction (MI) in Sprague Dawley(SD) rats. METHODS Ligation of the left anterior descending (LAD) in SD rats was used to establish an acute myocardial infarction model. SD rats were randomly divided into 3 groups (n=10, each group):sham group,MI group,and MI+SB group:the GSK-3β inhibitor(SB216763)was given 1 h by intrave-nous injection(0.6 mg·kg-1·d-1)before surgery.The serum and heart tissue were collected to measure lactate dehydrogenase (LDH) and IL-1β content and mRNA and protein levels of NLRP3, ASC, Cas-pase-1,IL-1β and GSK-3β after 2 days and 7 days operation,respectively.RESULTS The serum levels of LDH and IL-1β in the MI group were significantly higher than those in the sham group(P<0.01),and the MI+SB group was obviously lower than the MI group(P<0.01).In addition,mRNA and protein levels of NNLRP3, ASC, Caspase-1, IL-1β and GSK-3β expressions in MI group were clearly increased (P<0.01) compared with those in sham group.These indicators were significantly decreased in SB+MI group (P<0.01). Interestingly, the indicators were all higher at 7 days than 2 days. CONCLUSION GSK-3β inhibition induces cardioprotection via attenuating the activation of NLRP3 inflammasome after the acute myocardial infarction in rats.