Chlorogenic acid (5-CQA) is one of the major components in some Chinese herbal injections. However, the metabolism of 5-CQA in rats after intravenous injection has not been determined. An ultra-high performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF MS) method was applied to identify the metabolites in bile, urine, feces and plasma after a single intravenous administration of 10 mg x kg(-1) 5-CQA to rats. Using MSE and mass defect filter techniques, a total of 35 metabolites were detected in bile, urine, feces and plasma. The predominant metabolites in bile were glutathione conjugates of O-methyl-5-CQA, accounting for approximately 80% of the metabolites excreted in bile. The major components in urine were parent drug, O-methyl-5-CQA, hydrolyzed metabolites and glucuronide conjugates. The major components in feces were O-methyl-5-CQA and its cysteine conjugates. The major component in plasma was the parent drug. The urinary and fecal excretion pathways were equally important to 5-CQA in rats. These results demonstrate that 5-CQA undergoes extensively metabolism in rats and are highly reactive to nucleophiles such as GSH. This finding indicates that attention should be paid on the injections containing 5-CQA, which may covalently bind to proteins, leading to allergenic drug reactions.

Aim To investigate the roles of intracellu-lar reactive oxygen species ( ROS ) and Nrf2 pathway in shikonin-induced A549 cell apoptosis. Methods The cytotoxicity was analyzed by MTT assay. The ap-optosis of A549 cells was analyzed by both cellular morphological and biochemical methods. The relative changes of the redox marks ( ROS/GSH) were studied by fluorescence assay in the shikonin-treated A549 cells in accompany with the changes of the intracellular redox homeostasis by GSH/GSSG ratio. ROS inhibitor was also employed in the treatment to find the role of ROS in shikonin-induced A549 cell apoptosis. Real-time PCR analysis and ELISA assay were performed as well to determine the role of Nrf2 pathway in the shiko-nin-induced A549 cell apoptosis. Results The IC50 of shikonin on A549 cells was 3. 2 mg·L-1 . The cellu-lar redox homeostasis shifted toward oxidation signifi-cantly in shikonin treatment in a time-dependent man-ner. The expression of the Nrf2 pathway related genes was up-regulated by shikonin ( 3 . 2 mg · L-1 , 8 h ) . The expression of the anti-apoptotic genes was down-regulated , and proapoptotic genes were up-regulated by shikonin (3. 2 mg·L-1, 24h). Futhermore, the inhi-bition of intracellular ROS alleviated the cytotoxicity of shikonin in A549 cells. Conclusion The critical role of shikonin-induced redox imblance in A549 cell, coped with the secondary produced ROS and Nrf2 path-way antioxidants, result in A549 cell apoptosis.

Objective To build an efficient, scientific system for full-period personnel cultivation of new nurses in Chinese medicine hospitals. Methods This article used Fink curriculum model as the research method; used Broome′s classification theory of teaching goal as the theoretical guidance; used 'the training outline for new nurse (trying out)' issued by national health and family planning commission, the book 'the core competencies of nursing for traditional Chinese medicine', and cored competencies of nurses as the framework; used Delphi method and Analytic hierarchy process as research tools, so as to help the establishment of system for full-period personnel cultivation of new nurses in Chinese medicine hospitals. Results The preliminary exploration of system for full-period personnel cultivation of new nurses in Chinese medicine hospitals based on Fink curriculum, to make the system became more scientific, reasonable and comprehensive. Conclusions The system for full-period personnel cultivation of new nurses in Chinese medicine hospitals is feasible and creative, it can help to motivate the implementation of 'the training outline for new nurse (trying out)', to improve the quality of the nursing talents, to fasten the construction of nursing talents, to promote the development of nursing career.

Objective: Nowadays, the power calibration methods of the microwave hyperthermia apparatus doesn't take the power loss of the radiator into account Aiming at this problem, the authors designed an equipment of measuring the actual output power of the microwave hyperthermia apparatus. A new method is proposed for calibration the output microwave power of microwave hyperthermia apparatus. Methods: The magnetron anode current was maintained at a default value by a control system. The microwave power generated by microwave source is coupled firstly to a low-power meter by the coaxial cable to measuring the power going through coaxial cable (P_(coaxial cable)). Then the microwave radiator is connected to the coaxial cable to make the microwave radiated by radiator. The radiator is assembled in the experimental device for the microwave completely absorbed by the water. The absorbed microwave energy of the water is calculated by measuring the water temperature change. The energy loss of the experimental device is calculated using the cooling rate. The output power of the radiator is equal to the ratio of the sum of the two aforementioned energy and the time. And the efficiency of the radiator η_(radiator), is equal to P_(radiator)/P_(coaxial cable) Results: The relationship between the actual output power of the microwave hyperthermia apparatus and the mag- netron anode current is P_(radiator) = 2η_(radiator) I. The efficiency of the radiator is η_(radiator)= (34±1)%. Conclusion: From the experimental results, the current method for calibration output power of microwave hyperthermia apparatus is defective, it dose not consider the conversion efficiency of radiator. Using the calibration method introduced in this paper, wecan accurately deter- mine the actual output power of microwave hyperthermia Apparatus.

Objective The early causes of death were analyze in 2349 patients who had undergone heart valve replacement.Methods Methods From January 1995 to December 2007,2349 patients with heart valve diseases received heart valve replacement.1109 cases were male and 1240 were female.The mean age of the patients was(41±19)years old.1962 cases had rheumatic heart valve disease,308 had congenital heart valve disease,39 had infective endocarditis,29 underwent reintervention by heart valve replacement,11 had Marfan syndrome.34 cases with coronary heart disease underwent heart valve prosthesis implantation and coronary artery bypass grafting.Mitral valve replacement(MVR)was performed in 1333 patients,aortic valve replacement(AVR)in 271,double valves replacement(DVR)in 736 and tricuspid valve replacement(TVR)in 9.There were 3075 mechanical valves and 10 bioprosthetic valves.Results From 1995 to 1999,death occurred in 16 of the 235 cases,early mortality rate was 6.81%.From 2000 to 2004,death occurred in 35 of the 1087 cases,early mortality rate was 3.22%.From 2005 to 2007,there were 29 deaths among 1027 cases,with an early mortality rate of 2.82%.Overall early mortality rate was 3.40%.The early mortality rate was 2.32%(31 in 1333 cases)in patients who underwent MVR,3.32% (9 in 271)in patients who underwent AVR,5.24%(40 in 736)in patients who underwent DVR,5.50%(7 in 127)with LVEDD≥70 mm,4.60%(14 in 304)with LVEF<0.40,2.14%(9 in 419)with NYHA class II,2.42%(37 in 1529)with NYHA class Ⅲ,and 8.48%(34 in 401)with NYHA class IV.The causes of 80 deaths were low cardiac output syndrome in 31 cases(38.8%),renal failure in 14 cases(17.5%),arrhythmia in 10 cases(12.5%),pulmonary infections in 8 cases (10.0%).cerebrovascular accidentin 5(6.3%),left ventricular rupture in 5(6.3%),multisystem and organ failure in 5(6.3%),and other cause in 2 cases(2.5%).Conclusion The causes of early death after heart valve replacement are low cardiac output syndrome,renal failure,arrhythmia,pulmonary infection,cerebrovascular accident,left ventricular rupture and multisystem and organ failure.

Objective To evaluate the effects of propofol on apoptosis in the hippocampal neurons of fetal rats in vitro.Methods The isolated hippocampal neurons were seeded into 96-well plates or 24-well plates at a density of 5 × 104 cells/ml.The cells were randomly divided into 5 groups (n =18 each) using a random number table:control group (group C),in tralipid group (group Ⅰ) and propofol 1,10,100 μmol/L groups (P1-3 groups).In group Ⅰ,10％ intralipid was added to the culture media until the final concentration reached 100 μmol/L.In groups P1-3,propofol was added to the culture media until the final concentration reached 1,10 and 100 μmol/L,respectively,and the cells were then incubated for 3 h.The cell apoptosis was assessed by flow cytometry.The expression of Bcl-2 mRNA and caspase-3 mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).The expression of Bcl-2 and actived-caspase-3 protein was determined by Western blot analysis.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,the expression of Bcl-2 mRNA and protein was down-regulated,and the expression of caspase-3 mRNA and actived-caspase-3 protein was up-regulated in P1-3 groups (P ＜ 0.05).There was no significant difference in the parameters mentioned above between group Ⅰ and group C (P ＞ 0.05).Conclusion Propofol induces apoptosis in isolated hippocampal neurons by inhibiting Bcl-2 expression and enhancing caspase-3 activity in fetal rats.

Objective To explore the correlations between Annexin A1 protein expression and clinicopathological character-istics in carcinoma of papillary thyroid.Methods The different expressions of annexin A1 in papillary thyroid tissue and para-cari-noma tissue were investigated by immunohistochemistry.Results Among 69 samples tissues of papillary thyriod carcinoma,the positive rate of annexin A1 was higher than that of 69 para-carcinoma tissues(88.41%vs .8.69%),there was a significant difference (P <0.05).Furthermore,the expression of annexin A1 was correlation with the lymph node metastasis and tumor size,which was higher in ≥1 cm diameter of tumor(P <0.05).Conclusion High AnnexinA1 positive expression in papillary thyroid cancer tissues is associated with tumor malignant progression,which might be a valuable predictor and potential target for the diagnosis and treat-ment of papillary thyroid carcinoma.

Objective To detect the expression of stem cell marker Sox2 in gastric cancer (GC). Methods The mRNA and protein expressions of Sox2 in paired primary tumor tissues and their matching, adjacent non-cancerous tissues in a series of 60 cases of human GC were examined by reverse transcription-PCR (RT-PCR) and immunohistochemistry (IHC). χ2 test was used to analyze the correlation of Sox2 expression with clinicopathological parameters of GC tissues including age, gender, tumor size, histological type, TNM stage, differentiation degree, depth of invasion and lymph node metastasis. Results RT-PCR results showed that the positive rate of Sox2 expression was significantly increased in gastric tumor tissues (53.3%, 32/60) compared with that of matching, adjacent non-cancerous tissues (20.0%, 12/60, P<0.01). Semi-quantitative analysis showed that the relative intensity of Sox2 mRNA expression was significantly higher in gastric cancer tissues (0.724±0.209) than that in tissues adjacent to carcinoma (0.256±0.065,P<0.01). The positive expression of Sox2 was significantly higher in gastric tumor tissues (50.0%, 30/60) than that of matching, adjacent non-cancerous tissues (16.7%, 10/60,P<0.01). The positive expression of Sox2 was significantly higher in gastric tumor patients with TNM stage (Ⅲ+Ⅳ) than that of TNM stage (Ⅰ+Ⅱ). The positive expression of Sox2 was significantly higher in gastric tumor patients with low differentiation and undifferentiated tumor cells than that of patients with middle and high differented cells. The positive expression of Sox2 was also significantly higher in gastric tumor patients with the depth of invasion T3-T4 than that of patients with T1-T2. The positive expression of Sox2 was significantly higher in gastric tumor patients with lymph node metastasis than that of patients without lymph node metastasis (P<0.05 or P<0.01). Conclusion The elevated expression of Sox2 is associated with the initiation, invasion, progression, and metastasis of GC. Sox2 may serve as a novel diagnostic and therapeutic marker for human GC.

Objective To explore the clinicopathological features of IgA nephrolpathy associated with malignant hypertension (IgAN-MHT) and to analyze their correlation with renal vascular lesions. Methods Twenty-nine patients of IgAN-MHT were screened from 2000 biopsy-proven eases with primary IgA nephropathy (IgAN) in our department from April 1997 to May 2007. Data of clinicopathology and follow-up of these 29 patients were collected. Semi- quantitative analysis was performed to evaluate the pathological changes. Inner lumen, outer lumen, intimal thickness, tunica media-to-internal lumen ratio of 436 arterioles, 124 interlobular arteries and 5 arcuate arteries were measured. The primary endpeint was the composite of a doubling of serum creatinine level and ESRD. Correlations of renal vascular lesions with clinical manifestation, pathological change and prognosis were examined by Spearman and Cox methods. Results 1.5% of all the IgAN patients presented malignant hypertension. The common clinical features were renal failure (100%), hyperurieacidemia (62.7%) and hypertriglyceridemia (51.7%). The average amount of urine protein excretion was 2.8 g/d. The common pathological changes were moderate mesangial proliferation, severe global sclerosis, severe interstitial inflammation and severe interstitial- tubular fibrosis. The small arteries (arcuate arteries and interlobular arteries) and arterioles (afferent arterioles) were both involved in IgAN-MHT. The characteristic lesions of intrarenal arteries included vascular occlusion, media thickening, proliferative endarteritis (onionskin lesion, musculomucoid intimal hyperplasia), hyaline arteriosclerosis, but mainly vascular occlusion (86.2%). The arteriole lesion was negatively correlated with age and total protein level; vascular occlusion was positively correlated with uric acid level. The average foUow-up period was 21.1 months. Forteen patients reached the endpoint. The arteriole lesion was the main independent risk factor for the progression of IgAN-MHT (RR=10.21, 95%CI=1.16～89.67). Conclusions The main clinical feature of IgAN-MHT is renal failure. The main histological feature of intrarenal vascular lesions is occludes arterioles. Arteriole lesion is the main independent risk factor for the progression of IgAN-MHT.

Objective To investigate the changes in plasma microRNA-126 and microRNA-1 in children with asthma exacerbation and its relationship with bronchial asthma.Methods From October 2012 to December 2013,48 children with asthma exacerbation from the Outpatient Department and the Inpatient Department in Houjie Hospital Affiliated to Guangdong Medical College were enrolled in the study (asthma group).Meanwhile,52 healthy children wcre selected as the healthy control group.The expression levels of plasma microRNA-126 and microRNA-1 were detected by real-time quantitative PCR (RT-PCR).The content of interleukin-4 (IL-4) and interferon-γ (IFN-γ) in plasma was measured by enzyme-linked immunosorbent assay (ELISA).The predictive value of microRNA-126 and microRNA-1 in plasma to bronchial asthma was evaluated by receiver operating characteristic (ROC) curve.Results The relative expression levels of plasma microRNA-126 in the asthma group were upregulated compared with those in the healthy control group [7.36 (0.96-41.21) vs 3.68 (0.75-38.91),Z =3.135,P =0.038],and microRNA-1 relative expression levels in the asthma group were lower than those of the healthy control group [2.17 (0.18-26.97) vs 5.83 (0.82-39.62),Z =2.156,P =0.045].The content of IL-4 in asthma group was higher than those of the control group [(109.98 ± 74.58) ng/L vs (78.50 ± 75.82) ng/L,t =2.122,P =0.036],and the IFN-γ level in the asthma group was lower than those of the healthy control group [(70.49 ± 12.03) ng/L vs (77.03 ± 17.16) ng/L,t =2.270,P =0.025].In the plasma of patients with asthma exacerbation,the sensitivity of microRNA-126 and microRNA-1 was 85.42％ (41/48 cases)and 79.17％ (38/48 cases),respectively.The specificity of microRNA-126 and microRNA-1 in healthy controls was 78.85％ (41/52 cases) and 73.08％ (38/52 cases),respectively.The area under ROC curve of microRNA-126 and microRNA-1 was 0.919 (95％ CI 0.866-0.973),0.867 (95％ CI 0.796-0.939).Conclusions MicroRNA-126 is significantly elevated in plasma of children with asthma exacerbation.The plasma levels of microRNA-1 were significantly downregulated.These results suggest that microRNA-126 and microRNA-1 may be potential markers for the diagnosis of bronchial asthma.