The Evolution of Work

The division of labor first increased during industrialization and then decreased again after 1970 as job roles have expanded. We explain these trends in the organization of work through a simple model where (a) machines require standardization to exploit economies of scale and (b) more customized products are subject to trends and fashions which make production tasks less predictable and a strict division of labor impractical. At the onset of industrialization, the market supports only a small number of generic varieties which can be mass-produced under a strict division of labor. Thanks to productivity growth, niche markets gradually expand, producers eventually move into customized production and the division of labor decreases again. The model predicts capital-skill substitutability during industrialization and capital skill complementarity in the maturing industrial economy. Moreover, conventional calculations of the factor content of trade underestimate the impact of globalization because they do not take into account changes in product market competition induced by trade. We test our model by exploiting the time-lags in the introduction of bar-coding in three-digit SIC manufacturing industries in the US. We find that both increases in investments in computers and bar-coding have led to skill-upgrading. However, consistent with our model bar-coding has affected mainly the center of the skill distribution by shifting demand away from the high-school educated to the less-than-college educated.

Multiproduct firms and price-setting: theory and evidence from U.S. producer prices

In this paper, we establish three new facts about price-setting by multiproduct firms and contribute a model that can explain our findings. Our findings have important implications for real effects of nominal shocks and provide guidance for how to model pricing decisions of firms. On the empirical side, using micro-data on U.S. producer prices, we first show that firms selling more goods adjust their prices more frequently but on average by smaller amounts. Moreover, the higher the number of goods, the lower is the fraction of positive price changes and the more dispersed the distribution of price changes. Second, we document substantial synchronization of price changes within firms across products and show that synchronization plays a dominant role in explaining pricing dynamics. Third, we find that within-firm synchronization of price changes increases as the number of goods increases. On the theoretical side, we present a state-dependent pricing model where multiproduct firms face both aggregate and idiosyncratic shocks. When we allow for firm-specific menu costs and trend inflation, the model matches the empirical findings.Price levels ; Productivity

Losing the error related negativity (ERN): an indicator for willed action

When people make errors in a discrimination task, a negative-going waveform can be observed in scalp-recorded EEG that has been coined the error-related negativity (ERN). We hypothesized that the ERN only occurs with slips, that is unwilled action errors, but not if an error is committed willingly and intentionally. We investigated the occurrence of the ERN in a choice reaction time task that has been shown to produce an ERN and in an error simulation task where subjects had to fake errors while the EEG was recorded. We observed a loss of the ERN when errors were committed in willed actions but not in unwilled actions thus supporting the idea that the production of the ERN is tied to slips in unwilled actions but not mistakes in willed actions

Improved glucose tolerance in mice receiving intraperitoneal transplantation of normal fat tissue

Aims/hypothesis: The association between increased (visceral) fat mass, insulin resistance and type 2 diabetes mellitus is well known. Yet, it is unclear whether the mere increase in intra-abdominal fat mass, or rather functional alterations in fat tissue in obesity contribute to the development of insulin resistance in obese patients. Here we attempted to isolate the metabolic effect of increased fat mass by fat tissue transplantation. Methods: Epididymal fat pads were removed from male C57Bl6/J mice and transplanted intraperitoneally into male littermates (recipients), increasing the combined perigonadal fat mass by 50% (p < 0.005). At 4 and 8weeks post-transplantation, glucose and insulin tolerance tests were performed, and insulin, NEFA and adipokines measured. Results: Circulating levels of NEFA, adiponectin and leptin were not significantly different between transplanted and sham-operated control mice, while results of the postprandial insulin tolerance test were similar between the two groups. In contrast, under fasting conditions, the mere increase in intra-abdominal fat mass resulted in decreased plasma glucose levels (6.9 ± 0.4 vs 8.1 ± 0.3mmol/l, p = 0.03) and a ∼20% lower AUC in the glucose tolerance test (p = 0.02) in transplanted mice. Homeostasis model assessment of insulin resistance (HOMA-IR) was 4.1 ± 0.4 in transplanted mice (vs 6.2 ± 0.7 in sham-operated controls) (p = 0.02), suggesting improved insulin sensitivity. Linear regression modelling revealed that while total body weight positively correlated, as expected, with HOMA-IR (β: 0.728, p = 0.006), higher transplanted fat mass correlated with lower HOMA-IR (β: −0.505, p = 0.031). Conclusions/interpretation: Increasing intra-abdominal fat mass by transplantation of fat from normal mice improved, rather than impaired, fasting glucose tolerance and insulin sensitivity, achieving an effect opposite to the expected metabolic consequence of increased visceral fat in obesit

Clock gene expression patterns in the calanoid copepod Calanus finmarchicus during eraly and late diapause

During winter the temperate/subpolar calanoid copepod Calanus finmarchicus enters seasonal diapause, a type of dormancy, to overcome this period of low food availability. Daily and seasonal rhythms of zooplankton might be under the control of an endogenous circadian clock ensuring optimal synchronizatzion of physiological, biochemical and behavioral processes to prevailing local environmental conditions. Photoperiod (daylength) is supposed to be the most reliable entrainment cue of an animals seasonal cycle for synchronization with the environment. A small timing mismatch between biological processes and the environment such as temporal shifts of the onset of phytoplankton blooms caused by climate change could potentially have severe consequences for the entire Calanus-based ecosystem. Nevertheless, limited knowledge is available concerning the synchronization of C. finmarchicus and marine organisms inhabiting polar regions with their environment. This study aimed to investigate the performance of the clock at distinct times during diapause to gain knowledge concerning the role of the clock in seasonal diapause of C. finmarchicus. Thus, diurnal clock gene expression patterns in C. finmarchicus being in early (September 2014, 10 h L: 14 h D) and late (January 2015, DD) diapause. Copepods have been collected by 24 h in situ sampling from Kongsfjorden, Svalbard (78.6°N, 11.6°E). Primers were designed for recently described potential clock genes (cry1, cry2, clk, cyc, per1, tim, dbt2, vri) in C. finmarchicus. Clock gene expression patterns were analyzed with Real-Time quantitative PCR. We could show that most clock genes showed a diel rhythmic oscillation during early diapause (LD), whereas in late diapause (DD) a significant rhythmic oscillations was not detectable for most of the investigated genes. Comparison of early and late diapause between each diel time point revealed significant differences. Overall, copepods caught in early diapause had higher relative mRNA levels compared to copepods sampled in January. These findings indicate a diurnal clock in C. finmarchicus. This might be the first sign of a circadian clock in C. fi•nmarchicus and the potential involvement of the clock in seasonal diapause. Further studies need to investigate diurnal protein levels and clock-associated genes to get an understanding of the interplay of clock genes, photoperiod sensing and diapause in C. finmarchicu

Basal lipolysis, not the degree of insulin resistance, differentiates large from small isolated adipocytes in high-fat fed mice

Aims/hypothesis: Adipocytes in obesity are characterised by increased cell size and insulin resistance compared with adipocytes isolated from lean patients. However, it is not clear at present whether hypertrophy actually does drive adipocyte insulin resistance. Thus, the aim of the present study was to metabolically characterise small and large adipocytes isolated from epididymal fat pads of mice fed a high-fat diet (HFD). Methods: C57BL/6J mice were fed normal chow or HFD for 8weeks. Adipocytes from epididymal fat pads were isolated by collagenase digestion and, in HFD-fed mice, separated into two fractions according to their size by filtration through a nylon mesh. Viability was assessed by lactate dehydrogenase and 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium assays. Basal and insulin-stimulated d-[U-14C]glucose incorporation and lipolysis were measured. Protein levels and mRNA expression were determined by western blot and real-time RT-PCR, respectively. Results: Insulin-stimulated D-[U-14C]glucose incorporation into adipocytes isolated from HFD-fed mice was reduced by 50% compared with adipocytes from chow-fed mice. However, it was similar between small (average diameter 60.9 ± 3.1μm) and large (average diameter 83.0 ± 6.6μm) adipocytes. Similarly, insulin-stimulated phosphorylation of protein kinase B and AS160 were reduced to the same extent in small and large adipocytes isolated from HFD-mice. In addition, insulin failed to inhibit lipolysis in both adipocyte fractions, whereas it decreased lipolysis by 30% in adipocytes of chow-fed mice. In contrast, large and small adipocytes differed in basal lipolysis rate, which was twofold higher in the larger cells. The latter finding was associated with higher mRNA expression levels of Atgl (also known as Pnpla2) and Hsl (also known as Lipe) in larger adipocytes. Viability was not different between small and large adipocytes. Conclusions/interpretation: Rate of basal lipolysis but not insulin responsiveness is different between small and large adipocytes isolated from epididymal fat pads of HFD-fed mic

The Portal Theory Supported by Venous Drainage–Selective Fat Transplantation

OBJECTIVE The "portal hypothesis" proposes that the liver is directly exposed to free fatty acids and cytokines increasingly released from visceral fat tissue into the portal vein of obese subjects, thus rendering visceral fat accumulation particularly hazardous for the development of hepatic insulin resistance and type 2 diabetes. In the present study, we used a fat transplantation paradigm to (artificially) increase intra-abdominal fat mass to test the hypothesis that venous drainage of fat tissue determines its impact on glucose homeostasis. RESEARCH DESIGN AND METHODS Epididymal fat pads of C57Bl6/J donor mice were transplanted into littermates, either to the parietal peritoneum (caval/systemic venous drainage) or, by using a novel approach, to the mesenterium, which confers portal venous drainage. RESULTS Only mice receiving the portal drained fat transplant developed impaired glucose tolerance and hepatic insulin resistance. mRNA expression of proinflammatory cytokines was increased in both portally and systemically transplanted fat pads. However, portal vein (but not systemic) plasma levels of interleukin (IL)-6 were elevated only in mice receiving a portal fat transplant. Intriguingly, mice receiving portal drained transplants from IL-6 knockout mice showed normal glucose tolerance. CONCLUSIONS These results demonstrate that the metabolic fate of intra-abdominal fat tissue transplantation is determined by the delivery of inflammatory cytokines to the liver specifically via the portal system, providing direct evidence in support of the portal hypothesis