No elevated plasma catecholamine levels during sleep in newly diagnosed, untreated hypertensives

The sympatho-adrenergic system is highly involved in regulating sleep, wake and arousal states, and abnormalities in this system are regarded as a key factor in the development and progression of arterial hypertension. While hypertension is associated with a hyperadrenergic state during wakefulness, the effect of hypertension on plasma-catecholamine levels during sleep is not yet known. Twelve young participants with newly diagnosed, untreated hypertension and twelve healthy controls slept for 7 hours in the sleep laboratory. Before and after sleep, subjects rested in a supine position for 3-h periods of wakefulness. We sampled blood at a fast rate (1/10 min) and monitored blood pressure and heart rate continuously. We show that plasma NE and E levels did not differ between hypertensives and normotensive during sleep as well as before and after sleep. Blood pressure was higher in hypertensives, reaching the largest group difference in the morning after sleep. Unlike in the normotensives, in the hypertensive participants the morning rise in blood pressure did not correlate with the rise in catecholamine levels at awakening. Our results suggest that hypertension in its early stages is not associated with a strong hyperadrenergic state during sleep. In showing a diminished control of blood pressure through sympatho-adrenergic signals in hypertensive participants, our data point towards a possible involvement of dysfunctional sleep-related blood pressure regulation in the development of hypertension.     

Robustness of Selection Procedures

In the article Bechhofers Indifference-zone formulation for selecting the t populations with the t highest means is considered in a set of non-normal distributions. Selection rules based on the sample mean, the 10% and the 20% trimmed means, two estimators proposed by Tiku (1981) for valuating the smallest and highest accepted sample values higher, the sample median and a linear combination of quantile estimators, two adaptive procedures and a ranksum procedure are investigated in a large scale simulation experiment in respect of their robustness against deviations from an assumed distribution. Robustness is understood as a small percentage of the difference β_A-β between the actual probability of incorrect selection β_A and the nominal β-value. We obtained a relatively good robustness for the classical sample mean selection rule and useful derivations for the employment of other selection rules in an area of practical importance.     

The determination of genome size in male and female germ cells of Drosophila melanogaster by DNA-Feulgen cytophotometry

The amounts of DNA in haploid and diploid cells of Drosophila melanogaster have been determined by DNA-Feulgen cytophotometry, using Xenopus laevis erythrocyte nuclei as a reference standard. The haploid male genome is estimated to be 0.18 pg DNA and the haploid female genome, 0.20 pg DNA.     

Antibody-mediated targeting of the urokinase-type plasminogen activator proteolytic function neutralizes fibrinolysis in vivo

Urokinase-type plasminogen activator (uPA) plays a central role in tissue remodeling processes. Most of our understanding of the role of uPA in vivo is derived from studies using gene-targeted uPA-deficient mice. To enable in vivo studies on the specific interference with uPA functionality in mouse models, we have now developed murine monoclonal antibodies (mAbs) directed against murine uPA by immunization of uPA-deficient mice with the recombinant protein. Guided by enzyme-linked immunosorbent assay, Western blotting, surface plasmon resonance, and enzyme kinetic analyses, we have selected two highly potent and inhibitory anti-uPA mAbs (mU1 and mU3). Both mAbs recognize epitopes located on the B-chain of uPA that encompasses the catalytic site. In enzyme activity assays in vitro, mU1 blocked uPA-catalyzed plasminogen activation as well as plasmin-mediated pro-uPA activation, whereas mU3 only was directed against the first of these reactions. We additionally provide evidence that mU1, but not mU3, successfully targets uPA-dependent processes in vivo. Hence, systemic administration of mU1 (i) rescued mice treated with a uPA-activable anthrax protoxin and (ii) impaired uPA-mediated hepatic fibrinolysis in tissue-type plasminogen activator (tPA)-deficient mice, resulting in a phenotype mimicking that of uPA;tPA double deficient mice. Importantly, this is the first report demonstrating specific antagonist-directed targeting of mouse uPA at the enzyme activity level in a normal physiological process in vivo.     

A method to estimate pollen viability from pollen size variation

The mean diameter of viable pollen grains is approximately 13 μm greater than the mean diameter of inviable grains in Mimulus guttatus. We show that this difference is large enough to be detected by particle counters and that these machines can be used to obtain a rapid estimate of pollen viability. While requiring a separate calibration, a size-based statistic is also strongly correlated with pollen viability in Collinsia verna. These results suggest that statistics derived from the size distribution of pollen grains may provide an alternative to more labor-intensive methods for estimating pollen viability, particularly in cases where inviability results from inbreeding depression or hybrid failure.     

Application of a multiphase microreactor chemostat for the determination of reaction kinetics of Staphylococcus carnosus

Bioprocess and Biosystems Engineering - Bioreactors at the microliter scale offer a promising approach to accelerate bioprocess development. Advantages of such microbioreactors include a reduction...     

The DNA content of sperm of Drosophila melanogaster

Karyotypes are described of diploid and tetraploid R. ficaria with particular reference to the variation in structure and size of their SAT-chromosomes. In four wild populations of tetraploid R. ficaria an excessive enlargement of the satellite region is present on the short arm of one of the four SAT-chromosomes and is described in detail. The unusual and irregular behaviour of this body in the form of bridges and fragments at mitotic anaphase is outlined and an attempt is made to explain it in terms of delayed or incomplete replication in heterochromatic segments. The whole process is discussed with reference to allocycly, subchromatids, a breakage fusion cycle, and B-chromosomes