Objective To analyze the MRI features of intracranial ectopic germinomas compared with pathologic findings.Methods MRI manifestations of intracranial ectopic germinomas in 24 cases verified by operation and pathology were retrospectively analyzed.Results Tumors were located at suprasellar region in 5 cases,basal nucleus region in 6 cases,round lateral ventriculus in 2 cases,pellucid septum and lateral ventriculus in 1 case,3 cases suprasellar and pineal region in 3 cases,basal nucleus and pineal region in 3 cases,pineal region and round lateral ventriculus in 2 cases,lateral ventriculus,and third ventricles as well as pineal region in 2 cases.Lesions were showed marked enhancement in 22 cases and 10 cases had cystic degeneration on MRI.Pathologically,18 of 24 cases were seen clear border,cystic degeneration 11 cases,hemorrhage 2 cases and calcification 2 cases.Conclusion Intracranial ectopic germinomas are common in male children and are of MR characteristics,its MRI findings are correlated with pathology.

Objective To assess the carotid elasticity using wave intensity(WI) in subjects with different plasma glucose level.Methods 107 subjects were enrolled in this study,according to their plasma glucose levels,subjects were categorized as normal plasma glucose group (group A),normal plasma glucose in higher level group (group B) and pre-diabetes group (group C).Carotid WI examination was performed and analyzed.The parameters included magnitude of the peak during late systole (W2),negative area during the mid-ejection (NA),and stiffness parameter (β),pressure strain elasticity modulus (Ep),arterial compliance(AC),augmentation index(AI),one point pulse wave velocity(PWVβ).Results Compared to group A,W2,β,Ep,PWVβ increased significantly while AC decreased in group C(P ＜0.05),but there was no obvious difference of NA between two groups.Furthermore,this statistically difference was not found in group B(P ＞0.05).Conclusions Carotid elasticity have been altered in pre-diabetes group which can be evaluated by WI,but no marked change is observed in normal plasma glucose of higher level group.

Objective To investigate the mechanisms of the protective effects of dexmedetomidine against the propofol-induced neuroapoptosis in primary cultured cortical neurons.Methods The neurons were cultured 7days and then divided into four groups: vehicle-control group (treated with equal volume of intralipid), propofoltreated group (treated with 500 μmol/L propofol), propofol plus dexmedetomidine treated group (treated with 500 μmol/L propofol and 0.1 μmol/L dexmedetomidine), and LY294002 pretreated group (treated with 500 μmol/L propofol ,0.1 μ mol/L dexmedetomidine and 10 μmol/L LY294002).12 hours after different treatments, neuron viability was measured by MTT assay,neuroapoptosis was detected by Hoechst33258 staining, and the levels of pAkt and Bcl-2 protein were detected by Western blot.Results Compared with the vehicle-reduced group,propofol reduced neuron viability greatly((53.4±4.2)％ vs (99.9±6.3)％;P＜0.01), but increased neuroapoptosis greatly((44.6±4.3)％ vs (5.8±0.4)％;P＜0.01).The levels of pAkt((0.41±0.03) vs (0.86±0.07))and Bcl-2 ((0.15±0.02) vs (0.72±0.03)) were decreased greatly (both P＜0.01).Compared with propofol treatment group, the neuron viability of propofol plus dexmedetomidine group were increased greatly((86.4±5.3) ％ , P＜0.01) ,the neu roapoptosis was decreased greatly ((23.1 ± 3.5) ％, P＜ 0.01), and the levels of pA kt (0.8 ± 0.03) and Bc1-2 (0.52 ±0.05) were increased greatly (both P＜0.01).Compared with propofol plus dexmedetomidine treated group,LY294002 inhibited the protective effects of dexmedetomidine, decreased neuron viability greatly ((64.3±5.1) ％ ,P＜0.01), increased the number of apoptotic neurons((38.8±4.9) ％, P＜0.01), and reduced the levels of pAkt (0.52±0.04) and Bcl-2(0.31±0.02) significantly (P＜0.01).Conclusion Dexmedetomidine exerts the neuroprotective effects against propofol-induced neuroapoptosis by activating the PI3K-Akt-Bcl-2 signalling pathway.

Objective To observe the effect of simvastatin on bone metastasis of breast cancer in nude mice model.Methods Sixty mice were divided into three groups randomly with 20 in each group.Mice were inoculated with MDA-MB-231 cells into the left cardiac ventricle.After 7 days,mice were treated with either simvastatin,saline,or nothing twice per week for 19 days.The area of osteolytic metastases was subsequently measured in long bones of all mice using an image analysis system.After sacrifice,parathyroid hormone-related protein (PTHrP) concentrations in bone marrow from all mice were determined using a two-site immunoradiometric assay.Osteoclast number expressed per millimeter of tumor/bone interface was assessed using an OsteoMeasure System.Measured data were compared with analysis of variance,and P ＜ 0.05 for the difference was statistically significant.Results The area of osteolytic lesions was significantly lower in mice treated with simvastatin compared with mice receiving saline and no treatment (0.51 ±0.18 mm2 vs 2.13 ± 1.24 mm2 vs 2.29 ± 1.22 mm2 ; F =15.600,P =0.002 ; F =15.673,P =0.001).In addition,treatment with simvastatin decreased the concentrations of PTHrP in bone marrow plasma (0.98 ±0.20 pmol/L vs 2.11 ±0.31 pmoL/L vs 1.99 ± 0.29 pmol/L; F =61.469,P ＜ 0.001 ; F =58.274,P ＜ 0.001) and the osteoclast numbers per millimeter of tumor/bone interface (4.00 ± 1.73 vs 11.40 ±4.93 vs 10.91 ± 3.87 ; F =17.820,P =0.001 ; F =17.184,P =0.002) compared with controls.Conclusion Simvastatin may reduce the production of PTHrP of breast cancer cells,which suppresses the development of destructive bone lesions as well as the growth of breast cancer cells in bone.

Objective To investigate the effect of propofol exposure on neuroapoptosis in pri-mary cultured cortical neurons and its mechanisms.Methods Cortical neurons were primarily cultured for seven days,then divided into two groups:control group (treated with equal volume of 20% in-tralipid),propofol-treated group (treated with 500 μmol/L propofol).The neurons were treated for 12 h.The neuron viability was determined by MTT.Neuroapoptosis was identified by Hoechest 33 258 dying.Mitochondrial membrane potential was measured by the fluorescent dye rhodamine 123 (Rh123).Western blot was performed to detect the level of cyt-c and cleaved-caspase-3.Results Neu-rons survival rate (54.4%±6.4%)in the propofol group was significantly lower than that of control group (99.8% ± 4.1%) (P < 0.05 ), the rate of neuronal apoptosis (46.5% ± 5.3%) was significantly higher than that of control group (7.2%±0.9%)(P <0.05),mitochondrial membrane potential (59.6%±4.3%)was significantly lower than that of the control group (99.9% ± 5.7%) (P <0.05 ),cyt-C protein level (0.38 ± 0.03 )was significantly higher than that of control group (0.1 5±0.02)(P < 0.05 ),level of cleaved-caspase-3 protein level (0.46 ± 0.04)was significantly higher than that of control group (0.13±0.02)(P <0.05).Conclusion Propofol induces neuroapo-tosis in primary cultured cortical neurons,which is associated with the decreased level of MPP and the increase levels of cyt-c and cleaved-caspase-3.

Objective To investigate the protective effect and the mechanisms of 17β-estradiol on ketamine-induced apoptosis on primary cultured rat cortical neurons. Methods Cortical neurons were primarily cultured for seven days,then divided into four groups :control group ( treated with equal valume of DMSO ),estradiol-treated group ( treated with 0.1 μmol·L-1 17β-estradiol),ketamine-treated group(treated with 100 μmol·L-1 ketamine),ketamine plus 17β-estradiol-treated group( treated with 0. 1 μmol·L-1 17β-estradiol+100μmol·L-1 ketamine). The neurons were treated for 24 hours. The neuron viability was determined by MTT. Neuroapoptosis was measured by nuclear morphometry after Hoechest 33258 dying. Western blotting was performed to detect the expression levels of cleaved-caspase-3 and Bcl-2protein. Results The neuron viability in the ketamine group was(54. 02±7. 78)%,significantly decreased from the control group,whereas ketamine plus 17β-estradiol increased the cell viability to(88. 09±6. 54)%,significantly higher than the ketamine group. The neuroapoptosis rate in the ketamine group was(49. 50±4. 34)%,significantly increased from the control group,while that in the drug combination group was(15. 74 ± 3. 40)%,significantly lower compared with the ketamine group. Meanwhile,the cleaved-caspase-3 expression increased,and Bcl-2 expression decreased remarkably after ketamine treatment,while which was reversed in the drug combination group. Conclusion 17β-estradiol can protect against ketamine-induced injury by inhibiting neuron apoptosis.

Objective The goal of this study was to investigate the correlation between the level of serum vitamin D and bone metabolism and disease activity in ankylosing spondylitis(AS) patients,and thus to explore the role of vitamin D in bone metabolism in AS patients.Methods The serum levels of BALP,TRACP-5b,25-(OH)D3 and blood lymphocytes VDR of 80 AS patients were measured by enzyme-linked immunosorbent assay (ELISA) and compared with those of the control group.Bone mineral density (BMD)was measured by dual-energy X-ray absorptiometry (DEXA).The ESR and CRP level of AS patients were also measured.The correlation between those parameters was analyzed and evaluated.Patients were divided into normal,insufficient and deficient subgroups according to the serum 25-(OH)D3 levels for further comparison.Indepondent saimple t test,t'test andx2 test were used for statistical analysis.Results The 25-(OH)D3 of AS patients [(11.9±2.7) μg/L] was significantly lower than that of the control groups [(22.3±7.9) μg/L] (P＜0.05),while the serum levels of BALP [(3.9±2.7) μg/L] and TRACP-5b [(46±25) ng/L] of AS patients were significantly higher than those of the control group [(2.4±1.0) μg/L] (P＜0.05).According to linear correlation analysis,25-(OH)D3 was negatively correlated with CRP (r=0.324,P=0.003).The ESR,BALP,TRACP-5b in the deficient subgroup were higher than those in the normal and insufficient subgroups(P＜0.05).Conclusion The plasma 25-(OH)D3 may decrease in AS patients,and this may activate bone metabolism,results in increased morbidity of osteoporo-sis,and negatively affect disease activity.

Background and purpose:RASSF10 acts as a kind of tumor suppressor in various tumor tissues, but researches in cardiac adenocarcinoma has not been reported. This study aimed to detect the methylation status and expression ofRas-association domain family 10 (RASSF10) in gastric cardia adenocarcinoma (GCA), and explore its role in occurrence and development of GCA.Methods:Methylation speciifc polymerase chain reaction (MSP), reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry method were respectively used to detect methylation status, mRNA expression and protein expression ofRASSF10 in 81 GCA tissues and corresponding normal tissues.Results:The promoter methylation frequency ofRASSF10 in GCA tissues (64.20%, 52/81) was signiifcantly higher than that in corresponding normal tissues (20.99%, 17/81,P<0.05), and was closely correlated with TNM stages, differential degree and lymph node metastasis (P<0.05). RASSF10 mRNA expression in GCA tissues (0.57±0.05) was significantly lower than that in corresponding normal tissues (0.78±0.02,P<0.05), and was closely correlated with TNM stages and lymph node metastasis (P<0.05). Protein expression of RASSF10 in GCA tissues (31.10%, 26/81) was signiifcantly lower than that in corresponding normal tissues (71.60%, 58/81,P<0.05), and was closely correlated with TNM stages, differential degree and lymph node metastasis (P<0.05). The promoter methylation frequency ofRASSF10 in GCA tissues was inversely related to its protein expression.Conclusion:Inactivation of RASSF10 caused by aberrantmethylation in the promoter region may be closely correlated with the GCA tumorgenesis.

Objective To investigate the protective effects and the mechanisms of 17β-estradiol on the propofol-induced neuroapoptosis in primary cultured rat cortical neurons.Methods The neurons were cultured for 7 days and then divided into three groups: vehicle-control group ( treated with equal volume of 20% intralipid ) , propofol-treated group ( treated with 500μmol/L propofol) , and propofol plus 17β-estradiol treated group ( treated with 500μmol/L propofol and 0.1 μmol/L 17β-estradiol).12 hours after the treatment, neuroapoptosis was detected by Hoechst 33258 staining and TUNEL assay, and the levels of Bcl-2, Bax and cleaved caspase-3 proteins were detected by Western blot.Results Compared with the vehicle-control group, the neuroapoptosis increased greatly ( P<0.01 ) , Bcl-2 level reduced ( P <0.01), Bax and cleaved caspase-3 levels increased greatly (P<0.01), and Bcl-2/Bax ratio reduced significantly (P<0.01).Compared with the propofol-treatment group, the neuroapoptosis decreased greatly ( P <0.01), Bcl-2 level increased ( P<0.01 ) , Bax and cleaved caspase-3 levels reduced greatly ( P <0.01 ) , and Bcl-2/Bax ratio increased greatly ( P <0.01 ) . Conclusions 17β-estradiol can protect cortical neurons against propofol-induced cortical neuroapoptosis by regulating the expression of Bcl-2 and Bax.

Objective To investigate the effect of 17β-estradiol on ketamine-induced long-term cognitive deficits in neonatal rats.Methods 80 SD male rats aged 7 days were randomly divided into group C,V,E,K and K+E,and 16 per group.Group C was intraperitoneally injected with same volume of saline for three consecutive days,Group V was subcutaneously injected with same volume of sesame oil for three consecutive days,Group E was subcutaneously injected with 600 μg · kg-1 17β-estradiol for three consecutive days,group K was intraperitoneally injected with 75 mg · kg-1 ketamine for three consecutive days,group K+E was intraperitoneally injected with 75 mg · kg-1 ketamine in combination with 600 μg · kg-1 17β-estradiol injected subcutaneously for three consecutive days.At 2 months of age,learning and memory abilities were tested with the Mortis water maze.After Morris water naze test,ten rats from each group were decapitated and the prefrontal cortex (PFC) was isolated to detect acetylcholine esterase(AchE) activity with ELISA assay and to measure acetylcholine(Ach) level by hydroxylammonium chloride method.Results The escape latency ((40.26±2.36) s,(30.25±2.20) s,(21.55±2.42) s) and path length((1019.35±58.13) cm,(811.16±27.58) cm,(598.34±34.74) cm) of group K were more than those of group C on the third,fourth aud fifth training days (all P＜0.05),while escape latency ((29.46±2.20) s,(24.86± 2.14) s,(17.20±1.91) s) and path length((913.90±41.89) cm,(729.42±31.36) cm,(487.64±18.61)cm) of group K+E were significantly lower than those of group K(all P＜0.05).On test day 6,rats were subjected to a probe trial,ratio of time spent in the target quadrant ((24.5±2.7) ％) and the number of crossings over previous platform locations (1.9±0.5) in group K were fewer than those of group C (all P＜0.05),while ratio of time spent iu the target quadrant((42.3±3.0) ％) and the number of crossings over previous platform locations(3.5±0.5) of group K+E were more than those of group K (all P＜0.05).The AchE activity((0.69±0.04) U · mg pro-1) in rats PFC of group K was significantly higher than that of group C ((0.52±0.06) U · mg pro-1) (P＜0.05).The AchE activity of group K +E ((0.58±0.12)U · mg pro-1) was lower than that of group K(P＜0.05).The Ach level ((2.59±0.34)mg · g-1) in rats PFC of group K was significantly lower than that of group C ((4.35±0.56) mg · g-1) (P＜0.05).The Ach level of group K+E((3.88±0.61) mg · g-1) was higher than that of group K(P＜0.05).Conclusions These results indicate that ketamine impairs learning and memory abilities as rat matures,while 17β-estradiol treatment improves these impairments by inhibiting AchE activity and increasing Ach level.