Purpose:To study the malignant probability of a solitary thyroid nodule,probable risk factor,the status of B-mode ultrasonography,computed tomography,fine needle aspiration and frozen section in the operation and other adjuvant examination in the diagnosis.Methods:In the retrospective analysis of 902 cases of solitary thyroid nodule treated by surger- y and diagnosed by pathology in the Cancer Hospital of Fudan University from March 1998 to May 2001,we analyzed the value of B-mode ultrasonography,computed tomography,fine needle aspiration and frozen section in the operation and com- pared them with the final pathological conclusion.Results:This disease occurred mostly in 20～50 years old women,while the malignant nodules occurred more frequently in men(P50 years) (P50 years) is a risk factor.B-mode ultrasonography can be used as routine preoperative examination.CT is valuable in the cases with metastasis to neck lymph nodules.With FNA the pathological diagnosis of the nodule suspected to be malignant can be made preoperatively.

Integrative Medicine ; Medicine, Chinese Traditional

Adult ; Bronchoalveolar Lavage ; methods ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; therapy ; Respiration, Artificial ; methods ; Ventilators, Mechanical

Child, Preschool ; Dwarfism ; congenital ; diagnosis ; Humans ; Male ; Osteochondrodysplasias ; congenital

Accidents, Occupational ; statistics & numerical data ; Adolescent ; Adult ; Aged ; Female ; Follow-Up Studies ; Hand Injuries ; epidemiology ; etiology ; Humans ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Young Adult

Objective To investigate the effect and mechanism of phosphorylated protein kinase R-like ER kinase(p-PERK) and C/EBP homologous protein(CHOP) after hypoxic-ischemic brain damage ( HIBD) . Methods Neonatal 7-day-old Sprague Dawley rats were divided into sham-operation control group and HIBD group( n=30 per group) . Each group was divided into 0 h,6 h and 24 h subgroup after operation ( n=10 per group) . The ratio of apoptosis of brain cell was measured by flow cytometer and the expression of p-PERK and CHOP were detected by Western blot. Results (1)Apoptosis cell appeared at 6 h in HIBD group,the ratio of cell apoptosis was(2. 17 ± 0. 19)%. The apoptosis cell obvious increased at 24 h,the ratio of cell apoptosis was(13. 42 ± 0. 83)%. There was a significant increase in the ratio of apoptosis after HIBD 6 h and 24 h, as compared with sham-operation control group [ ( 0. 57 ± 0. 06 )%( P <0. 01 ) ] . ( 2 ) The expression of both p-PERK and CHOP was very low in sham-operation control group. In the HIBD group,the expression of both p-PERK and CHOP began to increase at 6 h and increased furthermore at HIBD 24 h. The differences in the expression levels of p-PERK and CHOP in HIBD group among different time points were significant( P<0. 01 ) . ( 3 ) The expression of p-PERK positively correlated with the expression of CHOP (r=0. 997,P< 0. 05). Conclusion With the emerging of apoptosis after HIBD,the expression of both p-PERK and CHOP increases. The imbalance in the expression of PERK induces the apoptosis of brain cells in the HIBD of neonatal rats by regulation of CHOP expression.

Aim: To study the effects of astragaloside IV on experimental ventricular remodeling in mice and its mechanism from matrix metalloproteinase aspect.Method: Ventricular remodeling in mice was induced by con-secutively subcutaneous injection of isoproterenol for 14 days.Astragaloside IV(40,80 mg/kg)and propranolol(40 mg/kg,positive control)were administered by gavage to mice.Echocardiography was used to observe the left ventricular end diastolic diameter(LVIDd),left ventricular end systolic diameter(LVIDs),fractional shortening(FS)and ejection fraction(EF).The myocardial pathological pattern was detected by HE staining.Expressions of matrix metalloproteinases(MMP2,MMP9)and tissue inhibitor of metalloproteinases(TIMP1,TIMP2)mRNA in myocardium were detected by RT-PCR.Activities of MMP2 and MMP9 were assayed by zymography.Results:Compared with those of control mice,LVIDd and LVIDs were increased,FS and EF were decreased in the model group.Myocardial injury and fibrosis existed in histop at hological slices of the model group.In addition,the mRNA expressions and activities of MMP2 and MMP9 were increased in the model group.However,there were no markable changes to TIMP1 and TIMP2.Treatment with astragaloside IV reduced LVIDd and LVIDs,increased FS and EF,attenuated myocardial injury,and down-regulated mRNA expressions and activities of MMP2 and MMP9 compared with the model group.Conclusion: Astragaloside IV can greatly improve ventricular remodeling and dysfunction via decreasing MMP2 and MMP9 mRNA expression and activities in cardiac ventricles.

0.05);there were significant decrease in FPG,PPG and HbA1c in the DM+INS+RSG group after 1 and 3 months treatment(P

OBJECTIVE:To study the anti-oxidative effects of spirulina kinase (SPK) in vitro. METHODS:The methods of phenanthroine-Fe2+ oxidation method,DPPH and auto-oxidation of pyrogallol were used to measure the effects of different concen-trations of SPK on scavenging hydroxyl (OH-) free radical,DPPH free radical and superoxide anion (O2-) free radical;IC50 of SPK was calculated. Prussian blue reaction was used to determine total reducing ability(by absorbance)of different concentrations of SPK to Fe3+. Vitamin C(VC)was used as positive control in above trials. RESULTS:SPK could eliminate the OH-free radical, DPPH free radical and O2- free radical in concentration-dependant manner,and the maximum elimination rate of SPK to OH- free radical and DPPH free radical were 86.82% and 78.98%(IC50 were 54.31,0.636 g/L),which were higher than VC (64.77%, 73.49%). The maximum elimination rate of SPK to O2- free radical was 78.31%(IC50 was 3.918 g/L),which was lower than VC (94.14%). In reducing ability test,SPK improved absorbance in reducing ability test system,and maximum absorbance was simi-lar to VC in concentration-dependant manner. CONCLUSIONS:SPK has obvious anti-oxidant activities in vitro.

Background Proliferation of the human Tenon capsule fibroblasts(HTFs) is a main cause of failure of filtering surgery.To search the drug of inhibiting the growth of the HTFs is essential for the improvement of successful rate of filtering surgery.Objective The aim of this study was to investigate the inhibitory effect of apigenin on HTFs and its mechanism.Methods Human Tenon capsular tissue was obtained during the strabismus correction surgery.HTFs was primarily cultured using explant method and identified using vimentin by immunochemistry.The 3-5 generation of cells were incubated to 96-well plate.Apigenin of 0,20,40,80,160 μmol/L was added into the medium,respectively,for 24,48,72 hours,and the proliferation of HTFs was detected by sulfonyl chloride (SRB) at the wavelength of 560 nm (A560).Bromodeoxyuridine (BrdU) of 10 μg/L was added to culture the cells for 48 hours to calculate the labeling rate of BrdU.The morphology of the cells was observed using Hoechst 33258 staining,and apoptosis and cells cycle were evaluated by flow cytometry.Results Cultured cells grew well with the positive response for vimentin,showing the green fluorescence in cytoplasm.SRB assay showed that the A560 value was gradually declined with the increase of the dosage of apigenin and prolong of time (Fgroup =480.306,P =0.000 ; Ftime =555.144,P =0.000).The labeling rate after 0,40,80 μmol/L apigenin acted for 48 hours was (87.860 ±0.632)％,(61.520±4.306)％ and (23.480±4.472)％,showing a significant difference among the three groups (F =299.347,P =0.000).The labeling rate of HTFs for BrdU was significantly decreased in the 40 and 80 μmol/L apigenin groups compared with the 0 μmol/L apigenin group (P＜0.05).Hoechse 33258 staining found that the number of the HTFs was gradually decreased and the cell number of karyopyknosis and nuclear deformation was increased with the increase of apigenin dosage.Percentage of cells in G0/G1 phase were raised and that in S and G2/M phase were declined in the higher dosage apigenin group,with a significant difference among the different groups (FG0/G1 =58.621,P=0.000;Fs =32.357,P=0.001 ;FG2/M =83.998,P=0.000).In the 72nd hour after acted by 0,40,80,160 μmol/L apigenin,the apoptosis rate of HTFs was (4.77±0.21) ％,(13.24±1.35)％,(18.33±1.86) ％,(31.58 ± 2.77) ％,respectively,with a statistically significant difference among the four groups (F =204.791,P＜0.05).Conclusions Apigenin restrains the growth of HTFs by evoking G0/G1 cell cycle arrest and inducing apoptosis in a dosage-and time-dependent manner.