The impact of temperature on mortality in Tianjin, China : a case-crossover design with a distributed lag non-linear model

Background There has been increasing interest in assessing the impacts of temperature on mortality. However, few studies have used a case–crossover design to examine non-linear and distributed lag effects of temperature on mortality. Additionally, little evidence is available on the temperature-mortality relationship in China, or what temperature measure is the best predictor of mortality. Objectives To use a distributed lag non-linear model (DLNM) as a part of case–crossover design. To examine the non-linear and distributed lag effects of temperature on mortality in Tianjin, China. To explore which temperature measure is the best predictor of mortality; Methods: The DLNM was applied to a case¬−crossover design to assess the non-linear and delayed effects of temperatures (maximum, mean and minimum) on deaths (non-accidental, cardiopulmonary, cardiovascular and respiratory). Results A U-shaped relationship was consistently found between temperature and mortality. Cold effects (significantly increased mortality associated with low temperatures) were delayed by 3 days, and persisted for 10 days. Hot effects (significantly increased mortality associated with high temperatures) were acute and lasted for three days, and were followed by mortality displacement for non-accidental, cardiopulmonary, and cardiovascular deaths. Mean temperature was a better predictor of mortality (based on model fit) than maximum or minimum temperature. Conclusions In Tianjin, extreme cold and hot temperatures increased the risk of mortality. Results suggest that the effects of cold last longer than the effects of heat. It is possible to combine the case−crossover design with DLNMs. This allows the case−crossover design to flexibly estimate the non-linear and delayed effects of temperature (or air pollution) whilst controlling for season.

Nanowires of metal oxides for gas sensing applications

Nanowires of different metal oxides (SnO2, ZnO) have been grown by evaporation-condensation process. Their chemical composition has been investigated by using XPS. The standard XPS quantification through main photoelectron peaks, modified Auger parameter and valence band spectra were examined for the accurate determination of oxidation state of metals in the nanowires. Morphological investigation has been conducted by acquiring and analyzing the SEM images. For the simulation of working conditions of sensor, the samples were annealed in ultra high vacuum (UHV) up to 500°C and XPS analysis repeated after this treatment. Finally, the nanowires of SnO 2 have were used to produce a novel gas sensor based on Pt/oxide/SiC structure and operating as Schottky diode. Copyright © 2008 John Wiley & Sons, Ltd.

Investigating the development of the internal and external service tasks of non-executive directors: the case of the Netherlands (1997-2005)

During the last decade, globalisation and liberalisation of financial markets, changing societal expectations and corporate governance scandals have increased the attention for the fiduciary duties of non-executive directors. In this context, recent corporate governance reform initiatives have emphasised the control task and independence of non-executive directors. However, little attention has been paid to their impact on the external and internal service tasks of non-executive directors. Therefore, this paper investigates how the service tasks of non-executive directors have evolved in the Netherlands. Data on corporate governance at the top-100 listed companies in the Netherlands between 1997 and 2005 show that the emphasis on non-executive directors' external service task has shifted to their internal service task, i.e. from non-executive directors acting as boundary spanners to non-executive directors providing advice and counselling to executive directors. This shift in board responsibilities affects non-executive directors' ability to generate network benefits through board relationships and has implications for non-executive directors' functional requirements.

Compilation of somatic mutations of the CDKN2 gene in human cancers : non-random distribution of base substitutions

The CDKN2 gene, encoding the cyclin-dependent kinase inhibitor p16, is a tumour suppressor gene that maps to chromosome band 9p21-p22. The most common mechanism of inactivation of this gene in human cancers is through homozygous deletion; however, in a smaller proportion of tumours and tumour cell lines intragenic mutations occur. In this study we have compiled a database of over 120 published point mutations in the CDKN2 gene from a wide variety of tumour types. A further 50 deletions, insertions, and splice mutations in CDKN2 have also been compiled. Furthermore, we have standardised the numbering of all mutations according to the full-length 156 amino acid form of p16. From this study we are able to define several hot spots, some of which occur at conserved residues within the ankyrin domains of p16. While many of the hotspots are shared by a number of cancers, the relative importance of each position varies, possibly reflecting the role of different carcinogens in the development of certain tumours. As reported previously, the mutational spectrum of CDKN2 in melanomas differs from that of internal malignancies and supports the involvement of UV in melanoma tumorigenesis. Notably, 52% of all substitutions in melanoma-derived samples occurred at just six nucleotide positions. Nonsense mutations comprise a comparatively high proportion of mutations present in the CDKN2 gene, and possible explanations for this are discussed.

CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein

The CDKN2A gene encodes p16 (CDKN2A), a cell-cycle inhibitor protein which prevents inappropriate cell cycling and, hence, proliferation. Germ-line mutations in CDKN2A predispose to the familial atypical multiple-mole melanoma (FAMMM) syndrome but also have been seen in rare families in which only 1 or 2 individuals are affected by cutaneous malignant melanoma (CMM). We therefore sequenced exons 1alpha and 2 of CDKN2A using lymphocyte DNA isolated from index cases from 67 families with cancers at multiple sites, where the patterns of cancer did not resemble those attributable to known genes such as hMLH1, hMLH2, BRCA1, BRCA2, TP53 or other cancer susceptibility genes. We found one mutation, a mis-sense mutation resulting in a methionine to isoleucine change at codon 53 (M531) of exon 2. The individual tested had developed 2 CMMs but had no dysplastic nevi and lacked a family history of dysplastic nevi or CMM. Other family members had been diagnosed with oral cancer (2 persons), bladder cancer (1 person) and possibly gall-bladder cancer. While this mutation has been reported in Australian and North American melanoma kindreds, we did not observe it in 618 chromosomes from Scottish and Canadian controls. Functional studies revealed that the CDKN2A variant carrying the M531 change was unable to bind effectively to CDK4, showing that this mutation is of pathological significance. Our results have confirmed that CDKN2A mutations are not limited to FAMMM kindreds but also demonstrate that multi-site cancer families without melanoma are very unlikely to contain CDKN2A mutations.