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Wang X.,Chinese University of Hong Kong | Wang X.,Hubei University of Medicine | Feng Y.,Chinese University of Hong Kong | Wang N.,Chinese University of Hong Kong | And 5 more authors.
BioMed Research International | Year: 2014

Chinese medicines have long history in treating cancer. With the growing scientific evidence of biomedical researches and clinical trials in cancer therapy, they are increasingly accepted as a complementary and alternative treatment. One of the mechanisms is to induce cancer cell death. Aim. To comprehensively review the publications concerning cancer cell death induced by Chinese medicines in recent years and provide insights on anticancer drug discovery from Chinese medicines. Materials and Methods. Chinese medicines (including Chinese medicinal herbs, animal parts, and minerals) were used in the study. The key words including "cancer", "cell death", "apoptosis", "autophagy," "necrosis," and "Chinese medicine" were used in retrieval of related information from PubMed and other databases. Results. The cell death induced by Chinese medicines is described as apoptotic, autophagic, or necrotic cell death and other types with an emphasis on their mechanisms of anticancer action. The relationship among different types of cell death induced by Chinese medicines is critically reviewed and discussed. Conclusions. This review summarizes that CMs treatment could induce multiple pathways leading to cancer cell death, in which apoptosis is the dominant type. To apply these preclinical researches to clinic application will be a key issue in the future. © 2014 Xuanbin Wang et al. Source


Wolff M.S.,Mount Sinai School of Medicine | Teitelbaum S.L.,Mount Sinai School of Medicine | McGovern K.,Mount Sinai School of Medicine | Windham G.C.,850 Marina Bay Parkway | And 5 more authors.
Human Reproduction | Year: 2014

STUDY QUESTION Does phthalate exposure during early childhood alter the timing of pubertal development in girls? SUMMARY ANSWER Urinary concentrations of high-molecular weight phthalate (high-MWP) metabolites are associated with later pubarche. WHAT IS KNOWN ALREADY Phthalates are anti-Androgenic environmental agents known to alter early development, with possible effects on pubertal onset. STUDY DESIGN, SIZE, AND DURATION This multi-ethnic study included 1239 girls from New York City, greater Cincinnati, and the San Francisco Bay Area who were 6-8 years old at enrollment (2004-2007) and who were followed until 2011. PARTICIPANTS/MATERIALS, SETTING, METHODS Phthalate metabolites were measured in urine collected at enrollment from 1170 girls; concentrations ranged from <1 to >10 000 μg/l. Breast and pubic hair stages and body size were assessed one to two times annually to determine the age at transition from stage 1 to 2 for breast and pubic hair development. Associations between exposures and pubertal ages were estimated using Cox proportional hazard ratios (HR) with 95% confidence intervals (CI) and survival analyses. Associations were examined with respect to age-specific body mass-index percentile, one of the strongest predictors of pubertal onset. MAIN RESULTS AND THE ROLE OF CHANCE Urinary concentrations of high-MWP including di(2-ethylhexyl) phthalate (ΣDEHP) metabolites were associated with later pubic hair development during 7 years of observation. The relationship was linear and was stronger among normal-weight girls. Among normal-weight girls, age at pubic hair stage 2 (PH2) was 9.5 months older for girls in the fifth compared with the first quintile of urinary ΣDEHP (medians: 510 and 59 μg/g creatinine, respectively; adjusted HR 0.70, CI 0.53-0.93, P-trend 0.005. Age at first breast development was older for fifth quintile of mono-benzyl phthalate versus first (HR 0.83, CI 0.68-1.02; P-trend 0.018). No associations were observed between low-molecular weight phthalate urinary metabolite concentrations and age at pubertal transition in adjusted analyses. LIMITATIONS, REASONS FOR CAUTION While there is evidence that phthalate exposures are fairly consistent over time, the exposure measure in this study may not reflect an earlier, more susceptible window of exposure. We investigated alternative explanations that might arise from exposure misclassification or confounding. WIDER IMPLICATIONS OF THE FINDINGS Phthalates are widespread, hormonally active pollutants that may alter pubertal timing. Whether exposures delay or accelerate pubertal development may depend on age at exposure as well as other factors such as obesity and exposures earlier in life. Whether exposures act independently or as part of real life mixtures may also change their effects on maturation from birth through childhood. STUDY FUNDING/COMPETING INTEREST(S) This project was supported by the US National Institutes of Health, Environmental Protection Agency, New York State Empire Clinical Research Investigator Program and the Avon Foundation. L.H.K. is employed by Kaiser Permanente. The remaining authors declare they have no actual or potential competing financial interests. © 2014 The Author 2014. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. Source


Huang L.,Fuzhou University | Huang L.,Hong Kong Baptist University | Lai Y.,Hong Kong Baptist University | Li C.,850 Marina Bay Parkway | And 3 more authors.
Chemosphere | Year: 2015

The reactions of glutathione (GSH) with polybrominated diphenyl ethers (PBDEs) quinones with different degrees of bromination on the PBDEs ring were studied. Liquid chromatography coupled with mass spectrometric (LC-MS) analysis showed that four types of adducts were formed from the reaction of each PBDEs quinone (PBDE-Q) with GSH. The proposed reaction pathway was confirmed using ion trap-MS/MS technique. Our results demonstrate that adduct-1 was formed following the Michael Addition, a reaction of the sulfhydryl group from GSH with electron deficient carbon from PBDEs-Q ring. Compared with other carbons on the quinone ring, carbon in position 6 has a smaller steric hindrance, thus the addition reaction is likely to occur in that position. Hydrated quinone-GSH adduct-1 is easily oxidized to generate an adduct-2 in an aqueous solution. Substitution reaction from bromine atom on adduct-2 quinone ring with sulfhydryl group from GSH further generates adduct-3 that is unstable and can be readily hydrolyzed to adduct-4 in aqueous solution. Both adduct-1 and adduct-4 were unstable as well, immediately oxidized to adduct-2 and adduct-3 in the air, respectively. The results reveal that brominated quinones undergo a rapid non-enzymatic debromination upon reaction with GSH, and open a new view for our understanding on mechanism of metabolism and the toxicity of this class of compounds. © 2014 Elsevier Ltd. Source


Huang L.,Fuzhou University | Huang L.,Hong Kong Baptist University | Li C.,850 Marina Bay Parkway | Lai Y.,Hong Kong Baptist University | And 3 more authors.
Chemosphere | Year: 2015

Polybrominated diphenyl ethers (PBDEs) may be metabolized to form hydroxylated and quinone products. Study on the formation of DNA adducts altered by PBDEs quinones was conducted. Various types of DNA adducts generated from in vitro reaction of deoxyguanosine (dG), 2'-deoxyadenosine (dA), 2'-deoxycytidine (dC), thymidine (T) and DNA with a PBDE-quinone metabolite, namely 2-(2',4'-bromophenoxyl)-benzoquinone (2'4'BrPhO-BQ) were characterized. The results suggest that the quinone compound could form various DNA adducts with dG, dA and dC via Michael Addition, which was confirmed from analyses by electrospray ionization tandem mass spectrometry. Two adducts were respectively generated from the reactions of 2'4'BrPhO-BQ with dC and dG, while three adducts were produced with dA. The formation of adducts of 2'4'BrPhO-BQ-deoxynucleoside changed with different pH of reaction solution. The obtained results demonstrated that 2'4'BrPhO-BQ could covalently bind to DNA mediated by quinone group. The in vitro data of the formation of DNA adducts might be valuable to elucidate the mechanism of interaction between PBDEs and DNA in vivo. © 2014 Elsevier Ltd. Source


Kong C.J.,850 Marina Bay Parkway | Samuel M.C.,850 Marina Bay Parkway | Bauer H.M.,850 Marina Bay Parkway | Dixon P.,University of Alabama at Birmingham | Soge O.O.,University of Washington
Journal of Microbiological Methods | Year: 2013

We evaluated Neisseria gonorrhoeae Etest minimum inhibitory concentrations (MICs) relative to agar dilution MICs for 664 urethral isolates for ceftriaxone (CRO) and azithromycin (AZM), 351 isolates for cefpodoxime (CPD) and 315 isolates for cefixime (CFM). Etest accurately determined CPD, CFM and AZM MICs, but resulted in higher CRO MICs. © 2013. Source

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