Objective To determine chloramphenicol and metronidazolel in honey by isotope-labelled internal standards ultra performance liquid chromatography-mass spectrometry.Methods Samples were extracted with ethyl acetate solution,and cleaned up on a MCS cartridge.The target analytes were separated on a ZORBAX SB-C18column with gradient elution using a mobile phase made up of methanol and 5 mmol/L ammonium acetate solution (containing 0.05％ formic acid).Detection was carried out using positive and negative electrospray ionization and multiple reaction monitoring (MRM),and quantified with isotope internal standardmethod.Results The chloramphenicol and metronidazolel showed good linearity in the range of 0.05-5.00 ng/ml.The recovery at three spiked levels of 0.5,2.0 and 5.0 μg/kg were in the range of 79.3％-96.7％.The relative standard deviation (RSD) was 5.5％-14.8％.The limits of quantitation were 0.15 μg/kg,the limits of detection were 0.05 μg/kg.Conclusion The method is sensitive and accurate.It could be applied to the high-throughput analysis of chloramphenicol and metronidazolel.

Objective To investigated the expression of scavenger receptor A(SR-A) and lipopolysaccharide(LPS) receptor CD14 in endotoxin-induced acute liver injury.Methods Ninety Wistar rats were randomly divided into endotoxaemia group(LPS group) and normal saline group(NS group).The model of endotoxaemia and acute endotoxin-induced liver injury was established by injection of endotoxin(5mg/kg) via tail veins in LPS group,while the rats in NS group received injection of 0.2ml normal saline as control.At 0,1.5,3,6,12h after injection,the levels of endotoxin,TNF-?,IL-1,alanine transaminase(ALT) and total bilirubin(TB) in plasma,SR-A and CD14 expressions in liver tissues were determined,pathological changes of liver tissues and ultrastructural changes of Kupffer cells(KCs) were observed by light and electron microscopy respectively,while the phagocytosis of KCs was determined too.Results Compared with NS group,KCs were activated on morphology and functions(proliferated diffusely,enlarged in size and increased in phagocytosis function),levels of TNF-? and IL-1 increased markedly,the pathological changes of cell degeneration and necrosis and the liver function were gradually aggravated,while SR-A expression decreased and CD14 expression increased obviously(P

Aim To explore whether 5-lipoxygenase inhibitor zileuton attenuates neuroinflammation and brain damage via modulating ERK1/2 signaling path-way in rats of cerebral ischemia, and further investigate the possible mechanisms. Methods Sprague-Dawley rats underwent the cerebral ischemic injury by the su-ture occlusion model, and were randomly divided into sham operation, MCAO, zileuton-treated and PD98059 groups. Neurological deficit scores, cerebral infarct volume, and cerebral water content were measured, myeloperoxidase ( MPO ) activities in rat brain were measured as an index of neutrophil infiltration;content of TNF-α in blood was determined by the method of ELISA;expression of p-ERK1/2 and t-ERK1/2 in rat brain were detected by Western blot. Results Zileu-ton reduced neurological deficit scores, cerebral infarct volume, cerebral water content, MPO activity and TNF-α content, all of which were abolished by PD98059 administration. Zileuton up-regulated the ex-pression of p-ERK1/2 , which was inhibited by PD98059 administration. Conclusions Zileuton at-tenuates neuroinflammation and ischemic brain damage through the activation of ERK1/2 signaling pathway.

Objective To compare the efficacy and the side-effect of three different ways in treating the patients with malignant pleural effusion. Methods 98 patients histologically proved malignant pleural effusion were randomly divided into three groups, bleomycin group(BLM), bleomycin with mycobacterium group( BLM + UTL) and blemycin with intertleukino2 ( BLM +IL). 31 patients were treated with bleomycin intrapleural injection in BLM group,32 patients were treated with bleomycin and Utilin's(mycobacterium) intrapleural injection in BLM + ULL group and 35 patients were treated with bleomycin and intertleukin-2 intrapleural injection in BLM + IL group. The therapeutic efficacy, change of performance and side effects were compared among the three groups after one period of treatment. The changes of CEA and TNF in the pleural effusion were examined before and after treatment. Results The therapeutic efficacy and performance improvement were higher in BLM+UTL and BLM+IL group than that of BLM group(P＜0. 05) ,the pleural CEA of post-treatment in three groups were lower than that of pre-treatment(P＜0.01) ,the CEA after treatment in BLM+UTL group and BLM+IL group was lower than that of BLM group(P＜0. 01,respectively). The pleural TNF of post-treatment in BLM+UTL and BLM+IL groups was higher than that of pre-treatment(P＜0. 01 ) in BLM group. The pleural TNF of post-treatment in BLM+UTL and BLM+IL group was higher than that of BLM group ( P＜0. 01 ). Conclusion Intrapleural injection of mycobacterium with bleomycin or interlekin-2 with bleomycin has better efficacy than using bleomycin only in treating malignant pleural effusion.

Objective To construct double expression retroviral vectors targeting chronic myeloid leukemia (CML) b3a2-type mRNA and investigate its effect on the phenotype of K562 cells. Methods The eGFP coding sequence was inserted into the retroviral vector pMSCV-neo to construct pMSCV/GFP, then H1-RNA pol III-based transcription cassettes was subcloned into it to form pMSCV/GFP-H1-BCR/ABL40AS. Two control vectors pMSCV/GFP-H1-BCR/ABL40S & pMSCV/GFP-H1-BCR/ABL80AS were constructed in addition. All these constructions were identified by restriction enzyme analysis and DNA sequencing. After that, the recombinant vectors were transferred into retrovirus packaging cell line PT67 by using lipofectamine2000, and G418 were used to select stable virus-producing cell lines. Viral titer was determined by infection of NIH3T3 cells sequentially. The cell-growth curve was assayed, cell apoptosis was checked with Annexin V-PE/7AAD double staining and flow cytometry analysis after 24-hour infection, the PKR phosphorylation was assayed by Western blotting. Results The plasmids were successfully constructed. Four cell lines, named as PT67-MSCV/GFP, PT67-40as, PT67-40s and PT67-80as were gained by G418 selection, and virus titers were 6.2?10~ 5 , 5.6?10~ 5 , 4.6?10~ 5 and 6.0?10~ 5 CFU/ml respectively. PT67-40as suspensions could induce K562 cell apoptosis by (22.54?3.19)%, significantly different from PT67-MSCV/GFP or PT67-40s (P

Objective To investigate the effects of circadian clock gene Period2(Per2)on the proliferation,differentiation and apoptosis of K562 cells and its probable molecular mechanism.Methods The Per2 expression plasmid pcDNA3.1-Per2 and empty control plasmid were respectively transfected into K562 cells with cationic liposome,and the resistant cells stably expressing Per2 gene were obtained by G418 selection.Their morphological changes were observed under light microscope following Wright-Giemsa staining.Trypan blue excluding staining and MTT assay were employed to evaluate cell proliferation.Flow cytometry was performed to analyze cell cycle distribution and cell apoptosis,and electron microscopy was used to detect cell apoptosis.Meanwhile,the expressions of proliferation and apoptosis associated proteins,such as P53,Cyclin B1 and C-Myc,were respectively detected by RT-PCR and Western blot analysis at mRNA and protein level.Results The K562/Per2 cell line stably expressing Per2 gene was screened out.As compared with either the empty plasmid transfected group(K562/empty)or the untreated group(K562/untreated),K562/Per2 cells was smaller in volume and showed no obvious cellular differentiation.Circadian clock gene Per2 could significantly inhibit both growth and proliferation of K562 cells.The percentage of K562 cells in G2/M phase increased [K562/Per2 group(36.1?5.5)%,K562/empty group(12.5?2.9)%,untreated group(9.7?2.3)%,P

Betulinic acid (BA), a pentacyclic lupane-type triterpene, has a wide range of bioactivities. The main objective of this work was to evaluate the hepatoprotective activity of BA and the potential mechanism underlying the ability of this compound to prevent liver damage induced by alcohol in vivo. Mice were given oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and induced liver injury by feeding 50% alcohol orally at the dosage of 10 ml/kg after 1 h last administration of BA. BA pretreatment significantly reduced the serum levels of alanine transaminase, aspartate transaminase, total cholesterol, and triacylglycerides in a dose-dependent manner in the mice administered alcohol. Hepatic levels of glutathione, superoxide dismutase, glutathione peroxidase, and catalase were remarkably increased, while malondialdehyde contents and microvesicular steatosis in the liver were decreased by BA in a dose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying the hepatoprotective effects of BA might be due to increased antioxidant capacity, mainly through improvement of the tissue redox system, maintenance of the antioxidant system, and decreased lipid peroxidation in the liver.
Animals ; Antioxidants/pharmacology ; Blood Chemical Analysis ; Enzymes/blood ; Ethanol/*toxicity ; Lipid Peroxidation/drug effects ; Liver/*drug effects/enzymology/metabolism/pathology ; Male ; Mice ; Random Allocation ; Triterpenes/*pharmacology

OBJECTIVES: This study is aimed at developing a set of data groups (DGs) to be employed as reusable building blocks for the construction of the eight most common clinical documents used in China's general hospitals in order to achieve their structural and semantic standardization. METHODS: The Diagnostics knowledge framework, the related approaches taken from the Health Level Seven (HL7), the Integrating the Healthcare Enterprise (IHE), and the Healthcare Information Technology Standards Panel (HITSP) and 1,487 original clinical records were considered together to form the DG architecture and data sets. The internal structure, content, and semantics of each DG were then defined by mapping each DG data set to a corresponding Clinical Document Architecture data element and matching each DG data set to the metadata in the Chinese National Health Data Dictionary. By using the DGs as reusable building blocks, standardized structures and semantics regarding the clinical documents for semantic interoperability were able to be constructed. RESULTS: Altogether, 5 header DGs, 48 section DGs, and 17 entry DGs were developed. Several issues regarding the DGs, including their internal structure, identifiers, data set names, definitions, length and format, data types, and value sets, were further defined. Standardized structures and semantics regarding the eight clinical documents were structured by the DGs. CONCLUSIONS: This approach of constructing clinical document standards using DGs is a feasible standard-driven solution useful in preparing documents possessing semantic interoperability among the disparate information systems in China. These standards need to be validated and refined through further study.
Asian Continental Ancestry Group ; China ; Delivery of Health Care ; Electronic Health Records ; Health Level Seven ; Hospitals, General ; Humans ; Information Systems ; Semantics

Pancreatic cancer (PC) is often asymptomatic in the early stage and most patients have progressed to the advance stage at the time of diagnosis.At present,chemotherapy is mainly used in patients with advanced PC,but PC patients have poor response to chemotherapy,which brings great challenges to the treatment of PC.Oxidative stress-induced reactive oxygen species (ROS) can cause damages in DNA,proteins,and lipids and produce the toxic and mutagenic metabolites that alter the biological behavior of tumor and transform the tumor into a malignant phenotype.Antioxidants have an antitumor effect and provide a basis for the design of anti-oxidative stress drugs for the treatment of PC.This article summarizes the research advances in the molecular pathways associated with oxidative stress and PC,in order to explore new ROS-targeted methods for the treatment of PC.

AIM:To investigate the RNA oxidative damage in human gastric cancer tissue and para-carcinoma tissue for exploring the role of RNA oxidation in the occurrence of gastric cancer .METHODS:Immunohistochemical ob-servation and LC-MS/MS analysis were performed in 61 cases of gastric carcinoma .The position and concentration of 8-oxoguanosine ( 8-oxoGsn ) were detected , respectively . RESULTS: The results of immunohistochemical observation showed that 8-oxoGsn was obviously up-regulated in the gastric cancer .The positive staining mainly accumulated in the cy-toplasm of the tumor cells .The results of mass spectrometry showed that the level of 8-oxoGsn in the gastric cancer tissues was higher than that in the para-carcinoma tissues (P<0.05).CONCLUSION:8-oxoGsn is up-regulated in gastric canc-er.RNA oxidative damage may play important roles in the occurrence of gastric cancer .