A cold saponification method for determination of 5 lutein stereoisomers in dairy products by high performance liquid chromatography ( HPLC ) was developed. Samples were cold-saponified at room temperature and extracted by n-hexane/petroleum/dichloromethane ( 2: 2: 1 , V/V/V ) . Then 5 lutein stereoisomers were separated on a YMC C30 column with gradient elution using methanol/methyl tert-butyl ether as the mobile phase, and data were acquired by a photodiode array detector at wavelength of 445 nm. The calibration curve was linear in the range of 0 . 127-5 . 082 mg/L with correlation coefficient of 0 . 9999 , and the recoveries were from 96 . 7% to 102 . 2% with the RSDs in the range of 4 . 1%-5 . 4% ( n=6 ) . The limit of detection was 0 . 010 μg/g ( S/N=3 ) , and the limit of quantification was 0 . 030 μg/g ( S/N=10 ) . By presenting results of good accuracy, precision and sensitivity, this method validates its suitability for routine analysis of 5 lutein stereoisomers in dairy products.

Objective: To study the characteristics of P300 and topographic dist ribution mapping in obsessive-compulsive patients. Methods: The P300 and topog raphic distribution mapping were recorded in 36 patients, using a Bneuro Galileoinstrument. Results: Compared with normal subjects, the wa ve patterns of obsessi ve-compulsive patients were unstable; the frontal wave variation and dissymmetry between the two sides was 63.9%; the N2 and P3 latency was prolonged; the P2 an d P3 amplitude was decreased; the P3 topographic distribution mapping was uneven ly distributed, the normal high amplitude in the parietal region was absent. For the patient group, energy levels below grade 5 in the left brain area, the fron tal area, and for both were 42.3%, 30.3%, 15.15% respectively. Conclu sion: P300 and topographic distribution might be served as an objective index for reflectin g cognitive activity in obsessive-compulsive patients.

Objective To investigate the patent technological domain distribution of shanghai health system,and comparative analysis of patent technological hotspots between shanghai health system and enterprises.Methods The study used IPC classification method to conduct quantitative analysis of the distribution of patent technology,co-words analysis and visualization of social network establishment method were adopted to analyze patent technological hot spots.Results Within the A61 category,numbers of authorized patents of shanghai health system in orders are A61B、A61K、A61M and A61F.Further analysis of the highest authorized A61B17 group patent in the highest class A61B found that,compare to enterprises,the degree of coincidence with the high-frequency keywords of the technology hotspots is small,the technical hotspots are scattered,and lack of overall technical arrangement.Conclusions Shanghai health system mainly focused on medical device development.It is lower than that of enterprises regarding to the patent technology market demand matching,technical arrangement of the enterprise is relatively better than the health system,thus,the study suggested enhancing market demand survey,adjusting patent distribution,and broadening the scope of market promotion.

OBJECTIVETo investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro.

METHODSEca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry.

RESULTSCompared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5 µmol/L PTX and 0.625 µmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone.

CONCLUSION17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Apoptosis ; Benzoquinones ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Cycle Checkpoints ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Esophageal Neoplasms ; pathology ; Humans ; Lactams, Macrocyclic ; pharmacology ; Paclitaxel ; pharmacology

Objective:To review the imaging characteristics and evaluate the diagnostic value of Doppler echocardiography for congenital pseudoaneurysm of the mitral-aortic intervalvular fibrosa (PMAIVF).Methods:Between June 2008 and January 2020, 4 patients with PMAIVF were diagnosed by CTA, MRI and operative findings in Shanghai Children′s Medical Center and Children′s Hospital of Soochow University. The echocardiographic characteristics were analyzed retrospectively in these children.Results:PMAIVF was characterized by a pulsatile echo-free sac that expanded in systole and collapsed in diastole with to-and-fro blood flow on color and pulsed-wave Doppler echocardiography between the mitral leaflet and the aortic annulus. Three cases were diagnosed correctly, and 1 case was misdiagnosed as left atrial mass.Conclusions:PMAIVF can be diagnosed accurately by Doppler echocardiography, but it is prone to be misdiagnosed and must be distinguished from aortic root abscess, atrial mass and coronary artery fistula.

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.