Background: At present there is no simple, accurate blood test that may be used to determine the severity of stroke or to predict mortality and morbidity in stroke patients presenting to emergency departments. Methods: Patients with stroke-like symptoms who presented to an emergency department of a university hospital in Hong Kong were recruited for the study. DNA extracted from patients' plasma was analyzed for the ␤-globin gene with a fluorescent-based PCR test. The primary outcome measures were in-hospital and 6-month mortality and morbidity using the post-stroke modified Rankin Score. Results: Among the 88 consecutive patients recruited to the study, 70 (80%) had ischemic stroke, 11 (13%) had intracerebral hemorrhage, and 7 (8%) had transient ischemic attacks. Median plasma DNA concentrations taken within 3 h of symptom onset were higher in patients who died compared with those who survived at discharge (6205 vs 1334 kilogenome-equivalents/L; P ‫؍‬ 0.03). Among patients with NIH Stroke Scale scores >8, median plasma DNA concentrations were higher in patients who died compared with those who survived to 6 months (2273 vs 968 kilogenome-equivalents/L; P ‫؍‬ 0.002). Plasma DNA concentrations correlated with the volume of cerebral hematoma (r ‫؍‬ 0.66; P ‫؍‬ 0.03). Plasma DNA concentrations >1400 kilogenome-equivalents/L had a sensitivity of 100% and a specificity of 74.4% for predicting hospital mortality after stroke, and the area under the ROC curve was 0.89 (95% confidence interval, 0.80 -0.94). The adjusted odds ratio for plasma DNA concentrations predicting 6-month mortality was

Background: Cell-free DNA concentrations increase in the circulation of patients after trauma and may have prognostic potential, but little is know concerning the temporal changes or clearance of the DNA or its relationships with posttraumatic complications. We investigated temporal changes in plasma DNA concentrations in patients after trauma with use of real-time quantitative PCR. Methods: Serial plasma samples were taken from two trauma populations. In the first study, samples were collected every 20 min from 25 patients within the first 3 h of trauma. In the second study, samples were collected every day from 36 other trauma patients admitted to the intensive care unit (ICU). Results: In the first study, plasma DNA was increased within 20 min of injury and was significantly higher in patients with severe injury and in patients who went on to develop organ failure. In patients with less severe injuries, plasma DNA concentrations decreased toward reference values within 3 h. In the second study, plasma DNA concentrations were higher in patients who developed multiple organ dysfunction syndrome between the second and fourth days of admission than in patients who did not develop the syndrome. In patients who remained in the ICU with continuing organ dysfunction, plasma DNA remained higher than in healthy controls even at 28 days after injury. Most survivors with multiple organ dysfunction syndrome showed an initial very high peak followed by a prolonged smaller increase. Conclusions: Plasma DNA concentrations increase early after injury and are higher in patients with severe injuries and in those who develop organ failure. In-

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Apurinic/apyrimidinic endonuclease 1 (APE1) is an essential enzyme in the base excision repair pathway, which is the primary mechanism for the repair of DNA damage caused by oxidation and alkylation. We hypothesized that polymorphisms of APE1 are associated with risk for lung cancer. In the hospital-based matched case-control study, a total of 730 lung cancer cases and 730 cancer-free controls were genotyped for four APE1 haplotype-tagging polymorphisms (that is, -656T>G, 400A>G, 630T>C, and 1350T>G). Among them, the single-nucleotide polymorphism -656T>G located in the promoter region of APE1 was significantly associated with risk for lung cancer. We found that, compared with -656 TT homozygotes, the variant genotypes were associated with a significantly decreased risk [adjusted odds ratio, 0.51; 95% confidence interval (95% CI), 0.33-0.79 for -656 TG; adjusted odds ratio, 0.43; 95% CI, 0.25-0.76 for -656 GG, respectively]. Furthermore, we found a statistically significant reduced risk of -656T>G variants among heavy smokers (adjusted odds ratio, 0.52; 95% CI, 0.30-0.93 for -656 TG; adjusted odds ratio, 0.27; 95% CI, 0.13-0.57 for -656 GG, respectively), with a significant gene-smoking interaction (P = 0.013). A similar gene-smoking interaction in the context of APE1 haplotypes was also observed. The in vitro promoter assay revealed that the -656 G allele had a significantly higher transcriptional activity than that of the -656 T allele. Together, our results suggest that polymorphisms of the APE1 gene possibly interact with smoking and may contribute to the development of lung cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(1):223 -9)