Growth of ectomycorrhizal fungi stimulated by lipids from a pine root exudate

Summary The content of fatty acids was analysed in an exudate from roots of pine seedlings grown axenically in vermiculite with a synthetic nutrient medium. The dominating fatty acdis were fewer in the exudate than in the roots. Unsaturated fatty acids were predominant. The total lipid fraction of the exudate promoted mycelial growth in two of the three ectomycorrhizal fungi tested.     

Protein synthesis by microsomal particles from regenerating rat liver

1. Washed microsome particles from regenerating liver were shown to incorporate [(14)C]leucine into protein more actively than similar preparations from normal liver. 2. The total incorporation in the preparations from regenerating liver increased linearly with the amount of protein incubated, whereas this was not so with preparations from normal liver. 3. The greater activity of regenerating-liver microsomes appeared to be associated with the bound polysomes. 4. The size distribution of polysomes obtained after removal of membrane with deoxycholate was the same in normal and regenerating liver. 5. In general the activity of polysome preparations from normal and regenerating liver was similar. 6. It is concluded that the greater activity of the particles in the microsome fraction from regenerating liver is to be attributed to the ribosomes bound to membrane and that their activity is controlled by factors present in the membrane.     

Distinct regulation of glucose transport and GLUT1/GLUT3 transporters by glucose deprivation and IGF-I in chromaffin cells

Effects of prolonged metabolic (glucose deprivation) and hormonal [insulin-like growth factor I (IGF-I)] challenge on regulation of glucose transporter (GLUT) expression, glucose transport rate and possible signaling pathways involved were studied in the neuroendocrine chromaffin cell. The results show that bovine chromaffin cells express both GLUT1 and GLUT3. Glucose deprivation and IGF-I activation led to an elevation of GLUT1 and GLUT3 mRNA, the strongest effect being that of IGF-I on GLUT3 mRNA. Both types of stimulus increased the GLUT1 protein content in a cycloheximide (CHX)-sensitive manner, and the glucose transport rate was elevated by 3- to 4-fold after 48 h under both experimental conditions. IGF-I-induced glucose uptake was totally suppressed by CHX. In contrast, only approximately 50% of transport activation in glucose-deprived cells was sensitive to the protein synthesis inhibitor. Specific inhibitors of mTOR/FRAP and p38 MAPK each partially blocked IGF-I-stimulated glucose transport, but had no effect on transport rate in glucose-deprived cells. The results are consistent with IGF-I-activated transport being completely dependent on new GLUT protein synthesis while the enhanced transport in glucose-deprived cells was partially achieved independent of new synthesis of proteins, suggesting a mechanism relying on preexisting transporters.     

Effects of experimental seismic shock on vasoactivity of arteries, integrity of the vascular endothelium and on primary stress hormones of the Atlantic salmon

The postulated harmful effects of underwater detonations of explosives on the vascular endothelium in farmed Atlantic salmon were assessed under controlled conditions. Acclimated salmon were exposed to a series of 10 underwater explosions over 70 min, each of ≃2 MPa in pressure amplitude, in a laboratory tank. No mortality occurred immediately or during the subsequent 7 days of observation. The response to each of the 10 detonations was cessation of swimming for a few minutes and failure to express a flight reaction.
Structurally, the vascular endothelium of the ventral aorta (VA) and the coeliaco mesenteric artery (CMA) revealed signs of injury within the first 30 min after the experimental shock. In contrast to vessels from the controls, the injury was further aggravated by the mounting procedure for tension recording. The endothelial impairment was temporary, persisting throughout the first days while being restored after 1 week.
Functionally, the cholinergic and adrenergic vasoconstrictor responses in the CMA were markedly reduced during the first day after the shock. These responses were similar to those observed in the endothelium probed CMA of controls. The loss of structural integrity and the reduced functional responses indicated a temporary impairment of the vascular endothelium in response to this experimental simulation of a seismic shock.
The primary stress hormones, adrenaline and cortisol, were not immediately elevated in plasma, but revealed different patterns of delayed increases. The head kidney content of catecholamines was not altered by the acoustic shock, while the atrial uptake of both calecholamines declined progressively during the 48 h of observation. Plasma chloride was not affected.     

Chromogranin A-derived peptides: interaction with the rat posterior cerebral artery

Chromogranin A (CgA), an acidic granule protein of the regulated secretory pathway in the diffuse neuroendocrine system, is postulated to serve as a prohormone for regulatory peptides. Betagranin (rCgA(1-128)), the first N-terminal cleavage product of rat CgA, is 87% homologous to the bovine vasostatin I (bCgA(1-76)), previously shown to be vasoinhibitory in bovine resistance arteries. In this study the vasoactivity of homologous rat and bovine peptides was investigated in the rat posterior cerebral artery. Firstly, we examined the interaction of rhodamine (Rh)-labelled bCgA(7-40) and bCgA(47-70) with elements of the arterial wall by fluorescence microscopy. Secondly, rCgA(7-57), bCgA(1-40), bCgA(7-40) and bCgA(47-66) (chromofungin) were studied for effects on arterial tone and intracellular calcium as function of pressure in an arteriograph. Although without dilator or constrictor responses at 60-150 mm Hg, the rat peptide (rCgA(7-57)) evoked a significant delay in the onset of forced dilatation at 170 mm Hg, in contrast to the bovine peptides bCgA(1-40), bCgA(7-40) and bCgA(47-66) (chromofungin). Neither Rh-bCgA(7-40) nor Rh-bCgA(47-70) stained the endothelial layer, while Rh-bCgA(47-70) but not Rh-bCgA(7-40) stained the smooth muscle compartment. Analogously, bCgA(47-66) but not bCgA(7-40) reduced intracellular calcium, however without modifying the myogenic response. Thus, the betagranin peptide rCgA(7-57) and the two bovine chromofungin-containing peptides, highly homologous to the corresponding sequence (rCgA(47-66)), affected the rat cerebral artery without vasodilator effects, indicating significant species differences in vasoactivity of the N-terminal domain of CgA.     

The chromogranin A peptide vasostatin-I inhibits gap formation and signal transduction mediated by inflammatory agents in cultured bovine pulmonary and coronary arterial endothelial cells

The proinflammatory agent tumour necrosis factor alpha (TNFalpha) is one of several agents causing vascular leakage. The N-terminal domain of CgA, vasostatin-I (CgA1-76), has recently been reported to inhibit TNFalpha induced gap formation in human umbilical venous endothelial cells. Here we report on the effect of recombinant human CgA1-78, vasostatin-I, on TNFalpha induced gap formation in two model systems of vascular leakage in arterial endothelial cells of bovine pulmonary (BPAEC) and coronary (BCAEC) origin. Vasostatin-I inhibited the TNFalpha induced gap formation in both models, being inactive in the unstimulated cells. The phosphorylation of p38MAP kinase in TNFalpha activated BPAEC was markedly attenuated in the presence of vasostatin-I and the inhibitory effect corresponded to that of the specific p38MAPK inhibitor SB203580. Vasostatin-I also inhibited the phosphorylation of p38MAPK induced by both thrombin and pertussis toxin in these cells. The results demonstrate that vasostatin-I has inhibitory effects on TNFalpha-induced disruption of confluent layers of cultured pulmonary and coronary arterial endothelial cells. This suggests that vasostatin-I may affect endothelial barrier dysfunction also in arterial vascular beds. Furthermore, the inhibitory activity of vasostatin-I may be associated with the p38MAPK signalling cascade via a pertussis toxin sensitive, presumably Galphai coupled mechanism.     

The biology and life history of arctic populations of the littoral mite Ameronothrus lineatus (Acari, Oribatida)

The present study attempts to elucidate possible microevolutionary adaptations of life-history traits of high-latitude populations of the holarctic, littoral oribatid mite Ameronothrus lineatus by comparing arctic and temperate populations. Additionally, the paper provides an overview of the limited research on general ecology and population biology of arctic populations. In the Arctic the larviparous A. lineatus has a 5-year life cycle (larva-to-larva), and adults survive a further 2–3 years. High survival to maturity is consistent with a low lifetime reproductive output of ca. 20 larvae. The life history can be regarded as an extreme version of the typical oribatid life history. However, several life-history features suggest specific adaptations of arctic populations. In particular, the pre-moult resting stage is synchronized with the warmest part of the arctic summer, which shortens this vulnerable part of development. High reproductive investment by females at relatively low temperatures may represent a physiological adaptation to the cool arctic summer. Finally, prolonged cold exposure positively affects reproduction and survival the following summer, suggesting adaptation of the species to the highly seasonal arctic environment. On the other hand, the ability of all life-cycle stages to overwinter, and a flexible life history with the species being able to take advantage of favourable climatic conditions to accelerate development and larviposition, seem to be ancestral features. Thus, the success of A. lineatus in arctic habitats is probably attributable to a combination of derived and ancestral life-history traits. Studies of conspecific temperate populations are required to elucidate further local adaptations of arctic populations.     

The fluorescent cationic dye rhodamine 6G as a probe for membrane potential in bovine aortic endothelial cells.

The membrane potential of cultured bovine aortic endothelial cells was assessed by a fluorescent probe as an alternative to direct methods. We used the fluorescent cationic dye rhodamine 6G, a lipophilic probe with high permeability in cell membranes. A linear relationship was obtained between fluorescence intensity (F.I.) and membrane potential (Em) as a function of the extracellular Na(+) concentration in the presence of the ionophore gramicidin. From the equation derived from the linear relationship F.I. = -0.004 Em + 0. 03 (P < 0.001), the fluorescence measurements could be converted to membrane potential. The resting plasma membrane potential obtained was -65 +/- 7 mV. Nigericin (27 microM), ouabain (1 mM), and bradykinin (20 nM) induced a decrease in F.I. (depolarization), while ATP (25-100 microM) induced an increase in F.I. (hyperpolarization). Mitochondrial membrane potential inhibitors myxothiazol (3 microM) and oligomycin (4 microM) did not influence F. I. measured in the cultured bovine aortic endothelial cells. The results indicate that rhodamine 6G can be used as a sensitive and specific dye in studies of substances that affect the membrane potential of endothelial cells.