Prey choice and search speed:Why simple optimality fails to explain the prey choice of Oystercatchers <i>Haematopus ostralegus</i> feeding on <i>Nereis diversicolor</i> and <i>Macoma balthica</i>

Oystercatchers breeding on the saltmarsh of Schiermonnikoog rely on two staple foods during the breeding season: the bivalve Macoma balthica and the worm Nereis diversicolor. Both prey are highly profitable, yet individual birds tend to specialize on either of the two prey species for prolonged periods of time, contradicting the simple or 'classic' optimal prey choice model. Although male Oystercatchers often specialize on Macoma, while females often specialize on Nereis, none of the intensively studied individuals was so inefficient at handling either prey that this could have been the reason for excluding one of the prey from the diet. Furthermore, the two prey did not have different distributions in space, nor could short-term fluctuations in prey availability explain the specialization of individuals. It appears that Oystercatchers hunting for Macoma search at a slower speed and make more pecks per distance searched than do birds hunting for Nereis. This accords with the suggestion that, from the point of view of the Oystercatcher, buried Macoma are more cryptic than Nereis which emerge from their burrows to feed on the surrounding substrate. The incompatibility of searching for the two prey at the same time explains why the simple optimal prey choice model does not apply in this and probably many other cases. As argued by Gendron &amp; Staddon (1983), the problem of search speed and the problem of prey choice cannot be treated independently.</p

PRMT4 inhibitor TP-064 inhibits the pro-inflammatory macrophage lipopolysaccharide response in vitro and ex vivo and induces peritonitis-associated neutrophilia in vivo

Previous in vitro studies have shown that protein arginine N-methyltransferase 4 (PRMT4) is a co-activator for an array of cellular activities, including NF-κB-regulated pro-inflammatory responses. Here we investigated the effect of PRMT4 inhibitor TP-064 treatment on macrophage inflammation in vitro and in vivo. Exposure of RAW 264.7 monocyte/macrophages to TP-064 was associated with a significant decrease in the production of pro-inflammatory cytokines upon a lipopolysaccharide challenge. Similarly, thioglycollate-elicited peritoneal cells isolated from wildtype mice treated with TP-064 showed lowered mRNA expression levels and cytokine production of pro-inflammatory mediators interleukin (IL)-1β, IL-6, IL-12p40, and tumor necrosis factor-α in response to lipopolysaccharide exposure. However, TP-064-treated mice exhibited an ongoing pro-inflammatory peritonitis after 5 days of thioglycollate exposure, as evident from a shift in the peritoneal macrophage polarization state from an anti-inflammatory LY6ClowCD206hi to a pro-inflammatory LY6ChiCD206low phenotype. In addition, TP-064-treated mice accumulated (activated) neutrophils within the peritoneum as well as in the blood (7-fold higher; P Biopharmaceutic

Hypocholesterolemic phospholipid transfer protein knockout mice exhibit a normal glucocorticoid response to food deprivation

Objectives: Glucocorticoids, adrenal-derived steroid hormones, facilitate the physiological response to stress. High-density lipoproteins (HDL) are considered the primary source of cholesterol used for glucocorticoid synthesis in mice. Phospholipid transfer protein (PLTP) is a key player in HDL formation. In the current study we tested the hypothesis that HDL deficiency associated with genetic lack of PLTP negatively impacts the adrenal steroid function. Methods: We determined the glucocorticoid response to overnight food deprivation stress and the adrenal lipid and genetic phenotype of wild-type and PLTP knockout mice. Results: Basal plasma corticosterone levels, adrenal weights, and adrenocortical neutral lipid stores were not different between wild-type and PLTP knockout mice. Strikingly, plasma corticosterone levels were also equally high in the two groups of mice under fasting conditions (twoway ANOVA genotype effect: P>0.05). However, compensatory mechanisms were active to overcome adrenal lipid depletion, since gene expression levels of cholesterol synthesis, acquisition and mobilization proteins were similar to 2-fold higher in PLTP knockout adrenals versus wild-type adrenals. In support of an overall similar glucocorticoid stress response, hepatic relative mRNA expression levels of the glucocorticoid receptor target/glucocorticoid-sensitive genes PEPCK, ANGPTL4, FGF21, TDO2 and HMGCS2 were also not different. Conclusions: We have shown that hypocholesterolemic PLTP knockout mice exhibit a normal glucocorticoid response to food deprivation. These novel data (1) highlight that the effect of HDL deficiency on adrenal glucocorticoid output in mice is model dependent and (2) imply that other (lipoprotein) cholesterol sources than HDL can also generate the pool utilized by adrenocortical cells to synthesize glucocorticoids.Toxicolog

The formation of cupper transition nano-layer in polytetrafluoroethylene surface by means of ion beam assisting deposition

The deposition of Cu on polytetrafluoroethylene surface assisted by the Ar ion beam with the temperature of 1 keV is investigated numerically. Ar ions provide the kinematic mixing of Cu atoms and atoms of substrate forming the connecting 10 nm layer of mixed material. This layer can ensure a good adhesion of Cu films deposited on polytetrafluoroethylene.Осаждение медного покрытия на поверхность политетрафторэтилена, стимулированное пучком ионов аргона с температурой 1 кэВ, изучалось методами численного моделирования. Ионы аргона обеспечивали смешивание атомов меди и поверхности, что позволило сформировать переходной слой шириной 10 нм. Такой слой может обеспечить хорошие адгезионные свойства металлической пленки, осажденной на поверхность политетрафторэтилена.Осадження мідного покриття на поверхню політетрафторетилену, стимульоване пучком іонів аргону з температурою 1 кеВ, вивчалось методами чисельного моделювання. Іони аргону забезпечували змішування атомів міді і поверхні, що дозволило сформувати перехідний шар шириною 10 нм. Такий шар може забезпечити гарні адгезійні властивості металевої плівки, обложеної на поверхню політетрафторетилену

Apolipoprotein A1 deficiency in mice primes bone marrow stem cells for T cell lymphopoiesis

The bone marrow has emerged as a potentially important target in cardiovascular disease as it generates all leukocytes involved in atherogenesis. In the current study, we evaluated whether a change in bone marrow functionality underlies the increased atherosclerosis susceptibility associated with high-density lipoprotein (HDL) deficiency. We found that HDL deficiency in mice due to the genetic lack of hepatocyte-derived apolipoprotein A1 (APOA1) was associated with an increase in the Lin-Sca-1+Kit+ (LSK) bone marrow stem cell population and lymphoid-primed multipotent progenitor numbers, which translated into a higher production and systemic flux of T cell subsets. In accordance with APOA1 deficiency-associated priming of stem cells to increase T lymphocyte production, atherogenic diet-fed low-density lipoprotein receptor knockout mice transplanted with bone marrow from APOA1-knockout mice displayed marked lymphocytosis as compared to wild-type bone marrow recipients. However, atherosclerotic lesion sizes and collagen contents were similar in the two groups of bone marrow recipients. In conclusion, systemic lack of APOA1 primes bone marrow stem cells for T cell lymphopoiesis. Our data provide novel evidence for a regulatory role of HDL in bone marrow functioning in normolipidemic mice.Biopharmaceutic