Erythrocytes and age. Disintegration of erythrocytes by brilliant cresyl blue in correlation to age

The author describes changes in the disintegration of erythrocytes by brilliant cresyl blue in correlation to age, in rats aged 21, 42, 90-105, 340-360 and 690-720 days. The erythrocytes were incubated for 4 hours in an isotonic NaCl solution, in Krebs-Ringer solution and in each of these solutions plus brilliant cresyl blue. Disintegration in plain NaCl solution was found to be the greatest in the case of erythrocytes from 690- to 720-day-old rats. In the same solution plus brilliant cresyl blue, the rate of disintegration was very high in 21-day-old, 42-day-old and 690- to 720-day-old animals; at 90-105 days it was lower and at 340-360 days it was the lowest. Disintegration of erythrocytes in plain Krebs-Ringer solution was the lowest at 21 and 42 days; in the other age groups it was slightly higher. On adding brilliant cresyl blue, the rate of disintegration rose significantly in 21-, 42- and 690- to 720-day-old animals; at 90-105 days and 340-360 days it was no different from disintegration in plain Krebs-Ringer solution. It can be seen from the results that the rate of brilliant cresyl blue-induced erythrocyte disintegration is dependent on the age of the animals from which the erythrocytes are taken.     

Temporal variability of top-down forces and their role in host choice evolution of phytophagous arthropods

The role of top-down forces in host choice evolution of phytophagous arthropods is the subject of a vividly animated debate. Empirical evidence for the evolutionary role of top-down forces comes from studies showing that phytophagous arthropods prefer hosts that entail enemy-free space. The aim of this paper is to draw the attention of plant–arthropod researchers to the potentially, temporally variable nature of third trophic level effects. We show that this aspect is largely neglected in studies on enemy-free space, despite the fact that relative enemy impact varies seasonally among plants in at least some studies. We conclude that rigorous testing of the enemy-free space hypothesis can only be performed when within and between season variation in higher trophic level effects is taken into account.     

Validation of DNA methylation profiling in formalin-fixed paraffin-embedded samples using the Infinium HumanMethylation450 Microarray

A formalin-fixed paraffin-embedded (FFPE) sample usually yields highly degraded DNA, which limits the use of techniques requiring high-quality DNA, such as Infinium Methylation microarrays. To overcome this restriction, we have applied an FFPE restoration procedure consisting of DNA repair and ligation processes in a set of paired fresh-frozen (FF) and FFPE samples. We validated the FFPE results in comparison with matched FF samples, enabling us to use FFPE samples on the Infinium HumanMethylation450 Methylation array.     

"Pertussis toxin induces tachycardia and impairs the increase in blood pressure produced by alpha 2-adrenergic agonists"

Administration of purified pertussis toxin to rats induced persistent tachycardia, (observed in conscious rats but not after pithing); as little as 0.05 microgram/100 g produced a significant effect. Pertussis toxin-treatment did not affected the pressor response produced in the pithed rats by the alpha 2-adrenergic agonist methoxamine but markedly diminished the pressor effect of the alpha 2-adrenergic agonists clonidine and azepexole. A role of adenylate cyclase inhibition in the action of postsynaptic vascular alpha 2-adrenergic receptors is suggested.     

Extending the Cellulosome Paradigm: the Modular Clostridium thermocellum Cellulosomal Serpin PinA Is a Broad-Spectrum Inhibitor of Subtilisin-Like Proteases

Clostridium thermocellum encodes a cellulosomal, modular, and thermostable serine protease inhibitor (serpin), PinA. PinA stability but not inhibitory activity is affected by the Fn(III) and Doc(I) domains, and PinA is a broad inhibitor of subtilisin-like proteases and may play a key role in protecting the cellulosome from protease attack.