Comparing the 2007 and 2011 GOLD Classifications as Predictors of all-Cause Mortality and Morbidity in COPD.

To better classify patients with chronic obstructive pulmonary disease (COPD) for prognostic purposes and to tailor treatment, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2007 classification was revised in 2011. The primary aim of the current data analyses was to evaluate the accuracy of the GOLD 2007 and 2011 GOLD classifications to predict all-cause mortality and morbidity in a well-described COPD cohort. The prognostic values of both GOLD classifications, expressed as the C-statistic, were assessed in the Cohort of Mortality and Inflammation in COPD (COMIC) study of 795 COPD patients, with a follow-up of 3 years. Outcomes were all-cause mortality and morbidity. Morbidity was defined as time until first COPD-related hospitalisation and time until first community-acquired pneumonia (CAP). The prognostic value of the GOLD 2011 classification was compared between symptom classification based on the modified Medical Research Council (mMRC) score and the Clinical COPD Questionnaire (CCQ) scores with two different thresholds. Although the GOLD 2011 CCQ classification had the highest accuracy to predict mortality and morbidity in our study, the C-statistics differed only numerically. Furthermore, our study showed that the instrument used to determine the level of symptoms in the GOLD 2011 classification has not only important consequences on the mortality prognosis, but also affects the morbidity prognosis in COPD. Therefore, patients' estimated prognosis could alter when different types of tools are used to evaluate the prognosis.

DNA damage processing and aberration formation in plants.

Various types of DNA damage, induced by endo- and exogenous genotoxic impacts, may become processed into structural chromosome changes such as sister chromatid exchanges (SCEs) and chromosomal aberrations. Chromosomal aberrations occur preferentially within heterochromatic regions composed mainly of repetitive sequences. Most of the preclastogenic damage is correctly repaired by different repair mechanisms. For instance, after N-methyl-N-nitrosourea treatment one SCE is formed per >40,000 and one chromatid-type aberration per approximately 25 million primarily induced O6-methylguanine residues in Vicia faba. Double-strand breaks (DSBs) apparently represent the critical lesions for the generation of chromosome structural changes by erroneous reciprocal recombination repair. Usually two DSBs have to interact in cis or trans to form a chromosomal aberration. Indirect evidence is at hand for plants indicating that chromatid-type aberrations mediated by S phase-dependent mutagens are generated by post-replication (mis)repair of DSBs resulting from (rare) interference of repair and replication processes at the sites of lesions, mainly within repetitive sequences of heterochromatic regions. The proportion of DSBs yielding structural changes via misrepair has still to be established when DSBs, induced at predetermined positions, can be quantified and related to the number of SCEs and chromosomal aberrations that appear at these loci after DSB induction. Recording the degree of association of homologous chromosome territories (by chromosome painting) and of punctual homologous pairing frequency along these territories during and after mutagen treatment of wild-type versus hyperrecombination mutants of Arabidopsis thaliana, it will be elucidated as to what extent the interphase arrangement of chromosome territories becomes modified by critical lesions and contributes to homologous reciprocal recombination. This paper reviews the state of the art with respect to DNA damage processing in the course of aberration formation and the interphase arrangement of homologous chromosome territories as a structural prerequisite for homologous rearrangements in plants.