The Temporary Staffing Industry in Protected Employment Economies: Germany, Japan and the Netherlands

The paper addresses how the temporary staffing industry secures social security and a degree of employment stability in three non-liberal market economies with a well developed temp work sector and several decades of industry regulation. Until the 1980s unions in Germany, Japan and the Netherlands effectively opposed the deregulation of the staffing industry. Restrictions placed on the temporary staffing industry institutionalized an “employment-type” alternative to the US-style form of “registered” and “on-call” temp staffing. In the face of high unemployment in the 1990s unions participated in de-regulatory drives aimed at expanding the role of the industry in troubled national labor markets. In most cases, de-regulation dismantled key dimensions of the “employment type” of staffing, and unions shifted their efforts to securing equal treatment of temporary staff. To date, legislation has fallen short of mandating equal treatment, and in the best cases (Germany and the Netherlands) collective bargaining has taken on the role of securing equal wages for temporary staff. Japan, Germany and the Netherlands represent three different degrees of industry de-regulation, with the best case of equal treatment of temps in the Netherlands, and the deepest segmentation of temporary and regular workers in Japan. In comparison to Germany and Japan, Dutch unions early on engaged in regulating temporary staffing services. The early experience of regulating rather than rejecting contingent labor and the density of neo-corporatist institutions for social bargaining in the Netherlands means that Dutch unions have developed stronger capacities for regulating contingent employment despite the weak organization of contingent workers. Unions in Japan and Germany have only recently developed capacities for representing contingent labour, but the significant weakening of social bargaining in both countries is associated with growing labor market segmentation between temporary and regular employees

Meal size is a critical driver of weight gain in early childhood

Larger serving sizes and more frequent eating episodes have been implicated in the rising prevalence of obesity at a population level. This study examines the relative contributions of meal size and frequency to weight gain in a large sample of British children. Using 3-day diet diaries from 1939 children aged 21 months from the Gemini twin cohort, we assessed prospective associations between meal size, meal frequency and weight gain from two to five years. Separate longitudinal analyses demonstrated that every 10 kcal increase in meal size was associated with 1.5 g/wk or 4% (p = 0.005) faster growth rate, while meal frequency was not independently associated with growth (β = 0.3 g/wk p = 0.20). Including both meal parameters in the model strengthened associations (meal size: β = 2.6 g/wk, p < 0.001; meal frequency: β = 1.0 g/wk, p = 0.001). Taken together, the implication is that meal size promotes faster growth regardless of frequency, but meal frequency has a significant effect only if meal size is assumed to be held constant. Clearer advice on meal size and frequency, especially advice on appropriate meal size, may help prevent excess weight gain

Parental Reports of Infant and Child Eating Behaviors are not Affected by Their Beliefs About Their Twins’ Zygosity

Parental perception of zygosity might bias heritability estimates derived from parent rated twin data. This is the first study to examine if similarities in parental reports of their young twins’ behavior were biased by beliefs about their zygosity. Data were from Gemini, a British birth cohort of 2402 twins born in 2007. Zygosity was assessed twice, using both DNA and a validated parent report questionnaire at 8 (SD = 2.1) and 29 months (SD = 3.3). 220/731 (8 months) and 119/453 (29 months) monozygotic (MZ) pairs were misclassified as dizygotic (DZ) by parents; whereas only 6/797 (8 months) and 2/445 (29 months) DZ pairs were misclassified as MZ. Intraclass correlations for parent reported eating behaviors (four measured at 8 months; five at 16 months) were of the same magnitude for correctly classified and misclassified MZ pairs, suggesting that parental zygosity perception does not influence reporting on eating behaviors of their young twins

Cell-type-specific role of CHK2 in mediating DNA damage-induced G2 cell cycle arrest

Cancer is a life-threatening disease that affects one in three people. Although most cases are sporadic, cancer risk can be increased by genetic factors. It remains unknown why certain genes predispose for specific forms of cancer only, such as checkpoint protein 2 (CHK2), in which gene mutations convey up to twofold higher risk for breast cancer but do not increase lung cancer risk. We have investigated the role of CHK2 and the related kinase checkpoint protein 1 (CHK1) in cell cycle regulation in primary breast and lung primary epithelial cells. At the molecular level, CHK1 activity was higher in lung cells, whereas CHK2 was more active in breast cells. Inhibition of CHK1 profoundly disrupted the cell cycle profile in both lung and breast cells, whereas breast cells were more sensitive toward inhibition of CHK2. Finally, we provide evidence that breast cells require CHK2 to induce a G2–M cell cycle arrest in response of DNA damage, whereas lung cells can partially compensate for the loss of CHK2. Our results provide an explanation as to why CHK2 germline mutations predispose for breast cancer but not for lung cancer

Fatty acid 16:4(n-3) stimulates a GPR120-induced signaling cascade in splenic macrophages to promote chemotherapy resistance

Although chemotherapy is designed to eradicate tumor cells, it also has significant effects on normal tissues. The platinum-induced fatty acid 16:4(n-3) (hexadeca-4,7,10,13-tetraenoic acid) induces systemic resistance to a broad range of DNA-damaging chemotherapeutics. We show that 16:4(n-3) exerts its effect by activating splenic F4/80+/CD11blow macrophages, which results in production of chemoprotective lysophosphatidylcholines (LPCs). Pharmacologic studies, together with analysis of expression patterns, identified GPR120 on F4/80+/CD11blow macrophages as the relevant receptor for 16:4(n-3). Studies that used splenocytes from GPR120-deficient mice have confirmed this conclusion. Activation of the 16:4(n-3)-GPR120 axis led to enhanced cPLA2 activity in these splenic macrophages and secretion of the resistance-inducing lipid mediator, lysophosphatidylcholine(24:1). These studies identify a novel and unexpected function for GPR120 and suggest that antagonists of this receptor might be effective agents to limit development of chemotherapy resistance.—Houthuijzen, J. M., Oosterom, I., Hudson, B. D., Hirasawa, A., Daenen, L. G. M., McLean, C. M., Hansen, S. V. F., van Jaarsveld, M. T. M., Peeper, D. S., Jafari Sadatmand, S., Roodhart, J. M. L., van de Lest, C. H. A., Ulven, T., Ishihara, K., Milligan, G., Voest, E. E. Fatty acid 16:4(n-3) stimulates a GPR120-induced signaling cascade in splenic macrophages to promote chemotherapy resistance

Characterisation of agro-morphological traits of corchorus accessions

http://www.tandfonline.com/loi/sagb202019-09-03hj2018Plant Production and Soil Scienc

Spatially explicit poisoning risk affects survival rates of an obligate scavenger

Obligate scavengers such as vultures provide critical ecosystem services and their populations have undergone severe declines in Asia and Africa. Intentional poisoning is a major threat to vultures in Africa, yet the impact on vulture populations of where poisoned carcasses are positioned is not known. We used re-sightings of 183 African white-backed vultures captured and tagged in two regions of South Africa, some 200 km apart, to estimate spatial differences in relative survival rates across life stages. Juvenile survival rates were similar in the two regions, whilst subadult and adult survival rates differed significantly. Using agent-based modelling, we show that this pattern of relative survival rates is consistent between regions that differ in intensity of poisoning, despite the proximity of the two regions. This may have important consequences for vulture conservation and the targeting of conservation efforts, particularly with regard to the efficacy of “vulture safe zones” around vulture breeding populations

Renal artery stenosis-when to screen, what to stent?

Renal artery stensosis (RAS) continues to be a problem for clinicians, with no clear consensus on how to investigate and assess the clinical significance of stenotic lesions and manage the findings. RAS caused by fibromuscular dysplasia is probably commoner than previously appreciated, should be actively looked for in younger hypertensive patients and can be managed successfully with angioplasty. Atheromatous RAS is associated with increased incidence of cardiovascular events and increased cardiovascular mortality, and is likely to be seen with increasing frequency. Evidence from large clinical trials has led clinicians away from recommending interventional revascularisation towards aggressive medical management. There is now interest in looking more closely at patient selection for intervention, with focus on intervening only in patients with the highest-risk presentations such as flash pulmonary oedema, rapidly declining renal function and severe resistant hypertension. The potential benefits in terms of improving hard cardiovascular outcomes may outweigh the risks of intervention in this group, and further research is needed