Bootstrap methods for estimating spatial synchrony of fluctuating populations

We describe and examine methods for estimating spatial correlations used in population ecology. We base our analyses on a hypothetical example of a species that has been censured at 30 different locations for 20 years. We assume that the population fluctuations can be described by a simple linear model on logarithmic scale. Stochastic simulations is utilized to check how seven different ways of resampling perform when the goal is to find nominal 95% confidence intervals for the spatial correlation in growth rates at given distances. It turns out that resampling of locations performs badly, with true coverage level as low as 30–40%, especially for small correlations at long distances. Resampling of timepoints performs much better, with coverage varying from 80 to 90%, depending on the strength of density regulation and whether the spatial correlation is estimated for the response variable or for the error terms in the model. Assuming that the underlying model is known, the best results are achieved for parametric bootstrapping, a result that strongly emphasize the importance of defining and estimating a proper population model when studying spatial processes.     

Effect of tower base painting on willow ptarmigan collision rates with wind turbines

1. Birds colliding with turbine rotor blades is a well‐known negative consequence of wind‐power plants. However, there has been far less attention to the risk of birds colliding with the turbine towers, and how to mitigate this risk.
2. Based on data from the Smøla wind‐power plant in Central Norway, it seems highly likely that willow ptarmigan (the only gallinaceous species found on the island) is prone to collide with turbine towers. By employing a BACI‐approach, we tested if painting the lower parts of turbine towers black would reduce the collision risk.
3. Overall, there was a 48% reduction in the number of recorded ptarmigan carcasses per search at painted turbines relative to neighboring control (unpainted) ones, with significant variation both within and between years.
4. Using contrast painting to the turbine towers resulted in significantly reduced number of ptarmigan carcasses found, emphasizing the effectiveness of such a relatively simple mitigation measure.

     

Sex-hormone-binding globulin and albumin concentrations in human cerebrospinal fluid

Polyacrylamide gel electrophoresis of plasma and concentrated cerebrospinal fluid (CSF) preincubated with tritium labelled 5 alpha-dihydrotestosterone (DHT) showed identical migration of the radioactivity, indicating the presence of sex-hormone-binding globulin (SHBG) in human CSF. The concentrations of SHBG (measured as the binding capacity) and albumin were measured in concentrated CSF (12 women and 1 man) and samples of plasma of some patients (9 women). SHBG could not be detected in 6 of the CSF samples, and the mean value of the determinable samples was 42.3 +/- 13.4 pmol/l. The mean +/- SE of the SHBG concentration in plasma was 90.8 +/- 8.9 nmol/l and the mean albumin concentrations in CSF and plasma were 3.4 +/- 0.6 mumol/l and 670 +/- 107 mumol/l respectively. The distribution ratio for SHBG over the blood-CSF barrier was 10 times higher than for albumin. It was concluded that the SHBG-binding in the CSF is negligible but that the albumin-binding may contribute to the CSF concentrations of testosterone and estradiol, which are 10-25% above the plasma unbound concentrations.     

Genetic evidence that the putative receptor binding domain of apolipoprotein B (residues 3130 to 3630) is not the only region of the protein involved in interaction with the low density lipoprotein receptor

We have searched for sequence differences in the region of the apolipoprotein B (apo B) gene encoding amino acids 3130-3630 in eight individuals with reduced affinity of low density lipoprotein (LDL) for the normal LDL-receptor. All individuals were hypercholesterolaemic and were selected either on the basis of reduced fractional catabolic rate (FCR) of autologous LDL or substantially reduced binding of their LDL to normal LDL-receptors determined by an in vitro cell growth assay using the U937 macrophage-like cell line. Segments of the apo B gene were amplified by the polymerase chain reaction. Using a combination of cloning and sequencing the amplified fragment, together with chemical cleavage mismatch analysis, no sequence differences were identified in this region of the gene. We therefore conclude that variation outside the region of the apo B gene that codes for amino acids 3130-3630 must be responsible for the reduced LDL clearance in these patients.     

mTORC1 Down-Regulates Cyclin-Dependent Kinase 8 (CDK8) and Cyclin C (CycC)

In non-alcoholic fatty liver disease (NAFLD) and insulin resistance, hepatic de novo lipogenesis is often elevated, but the underlying mechanisms remain poorly understood. Recently, we show that CDK8 functions to suppress de novo lipogenesis. Here, we identify the mammalian target of rapamycin complex 1 (mTORC1) as a critical regulator of CDK8 and its activating partner CycC. Using pharmacologic and genetic approaches, we show that increased mTORC1 activation causes the reduction of the CDK8-CycC complex in vitro and in mouse liver in vivo. In addition, mTORC1 is more active in three mouse models of NAFLD, correlated with the lower abundance of the CDK8-CycC complex. Consistent with the inhibitory role of CDK8 on de novo lipogenesis, nuclear SREBP-1c proteins and lipogenic enzymes are accumulated in NAFLD models. Thus, our results suggest that mTORC1 activation in NAFLD and insulin resistance results in down-regulation of the CDK8-CycC complex and elevation of lipogenic protein expression.