The decentralization of a sales support department in a medium-large company : A quantitative assessment based on ideas of Thomas L. Saaty and Stafford Beer

In this paper we discuss an integration of the Beer cybernetic oriented management theory and Saaty's hierarchical approach to assess management problems in a more quantitative way

Non-Equilibrium Fractionation Factors for D/H and 18O/16O During Oceanic Evaporation in the North-West Atlantic Region

Ocean isotopic evaporation models, such as the Craig-Gordon model, rely on the description of nonequilibrium fractionation factors that are, in general, poorly constrained. To date, only a few gradient-diffusion type measurements have been performed in ocean settings to test the validity of the commonly used parametrization of nonequilibrium isotopic fractionation during ocean evaporation. In this work, we present 6 months of water vapor isotopic observations collected from a meteorological tower located in the northwest Atlantic Ocean (Bermuda) with the objective of estimating nonequilibrium fractionation factors (k, ‰) for ocean evaporation and their wind speed dependency. The Keeling Plot method and Craig-Gordon model combination were sensitive enough to resolve nonequilibrium fractionation factors during evaporation resulting into mean values of k18 = 5.2 ± 0.6‰ and k2 = 4.3 ± 3.4‰. Furthermore, we evaluate the relationship between k and 10-m wind speed over the ocean. Such a relationship is expected from current evaporation theory and from laboratory experiments made in the 1970s, but observational evidence is lacking. We show that (a) in the observed wind speed range [0–10 m s−1], the sensitivity of k to wind speed is small, in the order of −0.2‰ m−1 s for k18, and (b) there is no empirical evidence for the presence of a discontinuity between smooth and rough wind speed regime during isotopic fractionation, as proposed in earlier studies. The water vapor d-excess variability predicted under the closure assumption using the k values estimated in this study is in agreement with observations over the Atlantic Ocean.publishedVersio

Never let it go: Stopping key mechanisms underlying metastasis to fight pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive neoplasm, predicted to become the second leading cause of cancer-related deaths before 2030. This dismal trend is mainly due to lack of effective treatments against its metastatic behavior. Therefore, a better understanding of the key mechanisms underlying metastasis should provide new opportunities for therapeutic purposes. Genomic analyses revealed that aberrations that fuel PDAC tumorigenesis and progression, such as SMAD4 loss, are also implicated in metastasis. Recently, microRNAs have been shown to play a regulatory role in the metastatic behavior of many tumors, including PDAC. In particular, miR-10 and miR-21 have appeared as master regulators of the metastatic program, while members of the miR-200 family are involved in the epithelial-to-mesenchymal switch, favoring cell migration and invasiveness. Several studies have also found a close relationship between cancer stem cells (CSCs) and biological features of metastasis, and the CSC markers ALDH1, ABCG2 and c-Met are expressed at high levels in metastatic PDAC cells. Emerging evidence reveals that exosomes are involved in the modulation of the tumor microenvironment and can initiate PDAC pre-metastatic niche formation in the liver and lungs. In this review, we provide an overview of the role of all these pivotal factors in the metastatic behavior of PDAC, and discuss their potential exploitation in the clinic to improve current therapeutics and identify new drug targets

Age at menarche and risk of major cardiovascular diseases: Evidence of birth cohort effects from a prospective study of 300,000 Chinese women

AbstractBackgroundPrevious studies of mostly Western women have reported inconsistent findings on the association between age at menarche and risk of cardiovascular disease (CVD). Little is known about the association in China where there has been a large intergenerational decrease in women's mean age at menarche.MethodsThe China Kadoorie Biobank recruited 302,632 women aged 30–79 (mean 50.5)years in 2004–8 from 10 diverse regional sites across China. During 7years follow-up, 14,111 incident cases of stroke, 14,093 of coronary heart disease (CHD), and 3200 CVD deaths were reported among 281,491 women who had no prior history of CVD at baseline. Cox regression yielded adjusted hazard ratios (HRs) relating age at menarche to CVD risks.ResultsThe mean (SD) age of menarche was 15.4 (1.9)years, decreasing from 16.2 (2.0) among women born before 1940 to 14.7 (1.6) for those born during the 1960s–1970s. The patterns of association between age at menarche and CVD risk appeared to differ between different birth cohorts, with null associations in older generations but U-shaped or weak positive associations in younger women, especially those born after the 1960s. After minimizing the potential confounding effects from major CVD risk factors, both early and late menarche, compared with menarche at age 13years, were associated with increased risk of CVD morbidity and mortality, which was more pronounced in younger generations.ConclusionAmong Chinese women the associations between age at menarche and risk of CVD differed by birth cohort, suggesting other factors may underpin the association

Rheumatoid arthritis versus diabetes as a risk factor for cardiovascular disease: a cross-sectional study, the CARRE Investigation.

Objectives: Patients with rheumatoid arthritis (RA) have an increased cardiovascular risk, but the magnitude of this risk is not known precisely. A study was undertaken to investigate the associations between RA and type 2 diabetes (DM2), a well-established cardiovascular risk factor, on the one hand, and cardiovascular disease (CVD) on the other. Methods: The prevalence of CVD (coronary, cerebral and peripheral arterial disease) was determined in 353 randomly selected outpatients with RA (diagnosed between 1989 and 2001, aged 50-75 years; the CARRÉ study) and in participants of a population-based cohort study on diabetes and CVD (the Hoorn study). Patients with RA with normal fasting glucose levels from the CARRÉ study (RA, n = 294) were compared with individuals from the Hoorn study with normal glucose metabolism (non-diabetic, n = 258) and individuals with DM2 (DM2, n = 194). Results: The prevalence of CVD was 5.0% (95% CI 2.3% to 7.7%) in the non-diabetic group, 12.4% (95% CI 7.5% to 17.3%) in the DM2 group and 12.9% (95% CI 8.8% to 17.0%) in those with RA. With non-diabetic individuals as the reference category, the age- and gender-adjusted prevalence odds ratio (OR) for CVD was 2.3 (95% CI 1.1 to 4.7) for individuals with DM2 and 3.1 (95% CI 1.6 to 6.1) for those with RA. There was an attenuation of the prevalences after adjustment for conventional cardiovascular risk factors (OR 2.0 (95% CI 0.9 to 4.5) and 2.7 (95% CI 1.2 to 5.9), respectively). Conclusions: The prevalence of CVD in RA is increased to an extent that is at least comparable to that of DM2. This should have implications for primary cardiovascular prevention strategies in RA