Antidiabetes drugs correlate with decreased risk of lung cancer: a population-based observation in Taiwan.

Background: The risk of some forms of cancer has been found to be higher in patients with diabetes mellitus (DM) than in the general population. The aim of this study was to examine, with sufficient statistical power, the association between DM and lung cancer and the impact of antidiabetes drugs on lung cancer risk in Taiwan.

Materials And Methods: From a randomly selected data set of 1 million National Health Insurance (NHI) claims in Taiwan from 2000-2005, 19,624 cases (patients ≥ 20 years of age) of newly diagnosed DM were identified.

Polypharmacy increases the risk of Parkinson's disease in older people in Taiwan: a population-based study.

Background: Little is known about the relationship between polypharmacy and Parkinson's disease (PD). In the present study, we tested the hypothesis that polypharmacy increases the risk of PD in older people in Taiwan.

Methods: From a randomly sampled cohort of one million health insurance enrollees, we identified 2827 new cases of PD over the period 2000-2008 aged ≥ 65 years and selected 11 308 age-matched controls without PD.

Correlation between the urine profile of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone metabolites and N7-methylguanine in urothelial carcinoma patients.

A major carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is present in cigarette smoke and its metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), is used as an exposure biomarker for environmental tobacco smoke (ETS). This metabolite (NNAL) can be either detoxified into glucuronidated NNAL (NNAL-Gluc) or activated into an unstable reactive metabolite that methylates DNA along with formation of 4-hydroxy-4-(3-pyridyl)-butyric acid [hydroxy acid (HA)]. Therefore, the carcinogenic risk associated with ETS exposure is greatly modulated by individual variations in metabolic activation and detoxification capabilities.

Enhancements of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) metabolism and carcinogenic risk via NNK/arsenic interaction.

Epidemiological studies indicated an enhancement of cigarette smoke-induced carcinogenicity, including hepatocellular carcinoma, by arsenic. We believe that arsenic will enhance the expression of hepatic CYP2A enzyme and NNK metabolism (a cigarette smoke component), thus its metabolites, and carcinogenic DNA adducts. Male ICR mice were exposed to NNK (0.

Liquid chromatography/tandem mass spectrometric method for the simultaneous determination of tobacco-specific nitrosamine NNK and its five metabolites.

A sensitive and robust high-performance liquid chromatography-electrospray ionization tandem mass spectrometry method to analyze 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and its five metabolites in one passage was developed and validated. The method achieved excellent reproducibility and accuracy. Linearity was observed for all six compounds (R(2)=0.

An enhanced LC-MS/MS method for microcystin-LR in lake water.

A LC-MS/MS method with enhanced sensitivity and specificity was established for monitoring microcystin-LR (MC-LR) in drinking water supplies in southern Taiwan. The enhanced sensitivity was achieved by the selection of a doubly charged MC-LR as the precursor ion to result in an multiple reaction monitoring (MRM) pair ions of m/z 498.6 --> 135.

Identification and characterization of a "biomarker of toxicity" from the proteome of the paralytic shellfish toxin-producing dinoflagellate Alexandrium tamarense (Dinophyceae).

The objective of this study was to identify and characterize a "biomarker of toxicity" from the proteome of Alexandrium tamarense, a paralytic shellfish toxin (PST)-producing dinoflagellate. A combination of 2-DE and MS approaches was employed to identify proteins of interest in the vegetative cells of several strains of A. tamarense with different toxin compositions and from different geographical locations.

In vitro aflatoxin B1-induced p53 mutations.

The tumor suppressor gene p53 is commonly mutated with high frequencies at certain hot spots in human cancers. In liver cancers there is an especially high frequency of mutations at codon 249. To study the impact of carcinogen targeting and the role of cytosine methylation on the mutation spectrum, a common liver cancer carcinogen aflatoxin B1 (AFB1), was studied using the p53 cDNA template to examine mutation induction.