(-)-Epigallocatechin gallate (EGCG), a catechin polyphenol component, is the main ingredient of green tea extract. Although the anti-carcinogenic and cancer inhibitory effects of EGCG have been widely reported, its genotoxicity is not clear and seldom reported. In this study, we examined the effects of EGCG on DNA strand breaks in the isolated lymphocytes and whole blood lymphocytes obtained from two smoking subjects and a nonsmoking healthy subject using a single-cell gel electrophoresis (SCG) assay. The results showed that after 2 hrs of treating the isolated lymphocytes from the smokers, EGCG induced a significant increase in DNA strand breaks at concentrations from 2.5 × 10-5 M to 2.0 × 10-4 M, while after 2 hrs of treating the whole blood obtained from the same smokers, EGCG suppressed the DNA strand breaks in the lymphocytes at concentrations of 1.0 × 10-4 M and 2.0 × 10-4 M. A similar suppressive result was also shown in the whole blood lymphocytes from the nonsmoker at nearly the same concentrations, while at concentrations of 1.0 × 10-3 M or 2.0 × 10-3 M, EGCG induced a significant increase in DNA strand breaks in the whole blood lymphocytes from the nonsmoker. This result suggests that EGCG is not only inhibitory against DNA strand breaks in whole blood, but also genotoxic to the isolated or whole blood lymphocytes at high concentrations. Thus, more research is needed to comprehensively assess the effects of EGCG on genetic materials.
Lymphocytes ; Upper case emm ; In Blood ; DNA strand break ; seconds

Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) is a new surgical management which brings hopes of cure to patients with primary or metastatic liver tumor who do not have sufficient future liver remnant (FLR).This review summarizes the current research on the development,indication,surgical procedures and safety of ALPPS.It also discusses the major concerns and unanswered doubts of ALPPS,such as the comparison with selective portal vein embolization (PVE) and the long-term oncological progression.

OBJECTIVETo investigate the changes in serum amylase (AMY) and lipase (LPS) and their clinical significance in patients with acute paraquat poisoning (APP).

METHODSThe clinical data of 62 APP. patients who were admitted to Guangzhou 12th People's Hospital in 2014 were retrospectively analyzed. With clinical death being regarded as the end point of observation, the 62 patients were divided into survival group (n=32) and death group (n=30). The fasting venous blood of the patients on the 1st, 3rd, and 7th day after admission were collected, and the AMY and LPS levels were determined; the obtained data were compared between the two groups and analyzed statistically.

RESULTSThe AMY and LPS levels of the survival group on the 1st, 3rd, and 7th day after admission were significantly lower than those of the death group (P<0.05); the AMY and LPS levels of the death group on the 3rd day were significantly higher than those on the 1st day after admission (P<0.05); the survival group demonstrated no significant changes in AMY and LPS levels (P>0.05).

CONCLUSIONChanges in AMY and LPS levels in APP patients are reliable indicators for the determination of poisoning severity and prognosis.

Amylases ; blood ; Humans ; Lipase ; blood ; Paraquat ; poisoning ; Poisoning ; blood ; mortality ; Prognosis ; Retrospective Studies

Objective To analyze the clinical characteristics of hospital acquired mycotic pneumonia in elderly patients (aged≥ 80 years).Methods The clinical data were reviewed on 64 cases of elderly patients aged 80-93 years with hospital-acquired infection of mycotic pneumonia from June 2007 to July 2011.According to the results of sputum culture,therapy plan was made and antibiotic drugs were selected.Results Among these 64 patients,Candida mycoderma (62.5 ％,40 cases) occupied the first place and C.glabrata (20.3％,13 cases) was the second place (x2 =127.50,P＜0.01).Their chest x-ray or CT films were not characteristic,but lamellar shadows (68.8％,44cases) and cotton-like shadows (40.6 ％,26 cases) were found in the majority.60 cases (93.8 ％ ) of these patients had more than 3 complications,and 58 cases (90.6％) of them took over 2 kinds of antibiotics.The improvement rate of these patients was 81.3％ (52 cases)and mortality rate was 18.8％(12 cases).Conclusions Elderly patients (aged≥ 80 years) with hospital acquired infection of mycotic pneumonia have high incidence and mortality rate.The key point to cure is to make an early diagnosis and treat them as early as possible.

To elucidate arsenic-induced oxidative DNA damage, the genotoxicity of arsenic in human cells was comparatively studied with single cell gel electrophoresis (SCGE) assay in combination with the observation of the protective effects of dimethyl sulfoxide (DMSO) and catalase. Arsenic, at the concentration of 2.4 μM by coincubation for 24 hours, significantly induced DNA damage in HL60, a human promyelocytic leukemia cell line. In contrast, significant DNA damage was found in human mononucleocytes at the concentration of 4.8 μM or above. The cells were incubated separately with DMSO (12 mM/l), a well-known hydroxyl radical (OH-) scavenger, and catalase (1,300 U/ml), a hydrogen peroxide (H2O2) scavenger, for 6 hours and then further coincubated with various concentrations of arsenic for 24 hours at 37°C and 5% CO2. The findings showed that both DMSO and catalase significantly reduced the arsenic-induced tail moment, a parameter of total damaged DNA, in HL60 and mononucleocytes. Hence our findings indicate that arsenic, with micromolar concentrations, induces typical and various extents of DNA damage in human cells via reactive oxygen species in a dose-dependent manner.
Human ; DNA Damage ; Arsenic ; Dimethyl Sulfoxide ; Arsenic measurement

Objective To evaluate the alterations of thromboxane (TXB_2)、 prostacyclin (PGI_2)in murine acute pancreatitis (AP) and the therapeutic effect of calcium channel bocker-verapamil. MethodsA rat AP model was established to observe the alterations of plasma levels of TXB_2, 6-keto-PGF_ 1? and TXB_2/6-keto-PGF_ 1? ratio and the effect of verapamil. Pancreatic histology was examined by light and electron microscopy. ResultsAt 16 and 24 hours after induction of AP, the plasma levels of TXB_2[(1112?235)pg/ml、(1265?162)pg/ml] and TXB_2/6-keto-PGF_ 1? ratio(9.9?0.9,10.2?1.3)increased significantly. With varapamil therapy, the plasma levels of TXB_2[(671?102)pg/ml、(697?93)pg/ml] and TXB_2/6-keto-PGF_ 1? ratio (6.9?2.2)、(6.4?0.7) were dramatically lower than those in control group (P

OBJECTIVETo confirm that arsenic (As) induces oxidative DNA damage in phytohemagglutinin (PHA)-stimulated and unstimulated human lymphocytes.

METHODSThe alkaline comet assay combined with specific enzyme (Formamidopyrimidine-DNA glycosylase, FPG) digestion was used to measure As-induced base damage.

RESULTSThe enzyme-sensitive sites were readily detected with the alkaline comet assay after the cells were treated with 10 micromol As for 2 hours. The repair patterns observed for FPG-created DNA single strand breaks (SSBs) in As-treated cells were comparable to those in hydrogen peroxide (H(2)O(2))-treated cells. The enzyme-created SSBs, As-induced base damage, were more significantly revealed in PHA-stimulated lymphocytes. About 63% and 68% of SSBs induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes by 2-hour repair incubation, but about 34% and 43%, respectively, were repaired in unstimulated cells. About 40% and 49% of base damage induced by As and H(2)O(2), respectively, were repaired in PHA-stimulated lymphocytes, but about 19% and 21 %, respectively, were repaired in unstimulated cells.

CONCLUSIONSAs induces oxidative DNA damage in human lymphocytes within micromolar concentrations. Like the damage induced by H(2)O(2), As-induced DNA damage was more slowly repaired in unstimulated lymphocytes.

Adult ; Arsenic ; pharmacology ; DNA Damage ; DNA Repair ; DNA, Single-Stranded ; drug effects ; DNA-Formamidopyrimidine Glycosylase ; Electrophoresis ; methods ; Humans ; Hydrogen Peroxide ; pharmacology ; Lymphocytes ; drug effects ; N-Glycosyl Hydrolases ; Oxidation-Reduction ; Phytohemagglutinins ; pharmacology

Congenital heart disease（CHD）is a common congenital anomaly that is the leading cause of death among children under the age of five years with birth defects in both developed and developing countries. With the increasing prevalence of CHD，the importance of early diagnosis and intervention of CHD is well accepted. Prenatal ultrasonography is routinely applied for the screening of CHD but many factors influence its diagnostic accuracy. Biomarker testing is a simple and rapid method that can be used as an adjunct to prenatal screening for CHD. This review aims to provide new ideas for the early diagnosis of children with CHD by exploring the pathogenesis of biomarkers in CHD. In recent years，many studies have been devoted to the exploration of biomarkers related to CHD，and the studies on biomarkers in CHD are summarized from three aspects：epigenetics，proteomics and environmental factors.

After the preparation of cationic liposomes composed of DDAB/DOPE, cationic liposome-DNA complexes and lipid-polycation-DNA (LPD) complexes were formulated, respectively. Gel retardation assay was employed to select appropriate ratios of cationic liposomes to DNA of the liposome-DNA complexes. The morphology of LPD and liposome-DNA complexes was observed by transmission electron microscopy. The diameter and surface charge of LPD and liposome-DNA complexes were measured by photon correlation spectroscopy (PCS). Their transfection efficiencies in Chang cells and HepG2 cells were evaluated by beta-gal assay kit. It was found that LPD and liposome-DNA complexes had a regular spherical surface. However, compared with liposome-DNA complexes, LPD had rather smaller particle size and much higher transfection efficiency in Chang cells and HepG2 cells in vitro. LPD could be prepared easily with small particle sizes and high transfection activities. LPD may be a good non-viral gene delivery vehicle for applications in gene delivery.
Cations ; DNA ; genetics ; Genetic Therapy ; Genetic Vectors ; Humans ; Lipids ; chemistry ; Liposomes ; chemistry ; Liver Neoplasms ; metabolism ; pathology ; Protamines ; chemistry ; Transfection ; Tumor Cells, Cultured

Objective To study the hematopoietic stem cell injury(HSC)induced by busulfan. Methods C57BL/6 mice were treated with i.p. injection of 20 mg/kg or 40 mg/kg busulfan. All mice were euthanized at 15 days and 30 days after busulfan treatment for analysis of the peripheral blood cell counts, bone marrow cellularity and HPC (LKS-, lineage-sca1 -c-kit+), HSC(LSK, lineage-sca1 +c-kit+)and long-term HSC(CD34 - LSK, CD34 - lineage-sca1 +c-kit+)frequency. The colony-forming unit-granulocyte and macrophage(CFU-GM)ability of HPC was measured by colony-forming cell(CFC)assay,and the HSC self-renewal capacity was analyzed by single-cell colony-forming assay. Results The busulfan administration decreased the WBC,RBC and PLT compared with control mice. The HPC function (CFU-GM)was impaired(P < 0.05), and the HSC colony forming ability was decreased at 15 days after busulfan treatment(P < 0.05), whereas the body weight of the mice didn't change significantly after busulfan treatment. Conclusions Our findings suggest that busulfan can induce hematopoietic stem cell injury,and provide a support for the study of hematopoietic stem cell injury mechanism.