Purification and partial characterisation of and α-tocopherol-binding protein from rabbit heart cytosol

An -tocopherol-binding protein has been isolated and purified from rabbit heart cytosol. The purified protein had an apparent molecular mass of 14,200, as derived from SDS-PAGE. The content of the protein in rabbit heart was around 11.8 g per g of tissue. The binding of -tocopherol to the purified protein was rapid, reversible, and saturable. Neither nor tocopherol could displace the bound -tocopherol from the protein, suggesting a high specificity for -tocopherol. -Tocopherol-binding protein did not bind oleate. Transfer of -tocopherol from liposomes to mitochodria was stimulated 8-fold in the presence of the binding protein, suggesting that this protein may be involved in the intracellular transport of -tocopherol in the heart.     

Pulmonary gas exchange kinetics during exercise: physiological inferences of model order and parameters

1. 1. The ventilatory and pulmonary gas exchange responses during moderate exercise can be appropriately modelled with first-order dynamics.

2. 2. A delay term, reflecting tissue-to-lung transit time, is needed for accurate characterization, however.

3. 3. The O₂ uptake time constant ( reflects the enzymatically controlled tissue O₂ utilization.

4. 4. is appreciably longer than , consequent to the tissue CO₂ capacitance.

5. 5. As typically longer than , transient errors in alveolar and arterial blood gas tensions are predicted: small for P_CO2 but much larger for P_O2.

6. 6. At work rates above the lactate threshold, a slow and delayed component of V̇_O2 induces an additional V̇ component (“excess” V̇_O2), leading to more rapid fatigue.

7. 7. The ventilatory compensation for the metabolic acidemia at these work rates is slow, with compensation being poor for rapid-incremental exercise.

8. 8. A justifiable control model of the coupling of ventilation to metabolism must cohere with these demonstrable physiological characteristics.

Multiple origins of self-fertilization in tristylous Eichhornia paniculata (Pontederiaceae): Inferences from style morph and isozyme variation

Populations of Eichhornia paniculata (Pontederiaceae) exhibit a wide range of mating systems, from predominant outcrossing to high levels of self-fertilization. The origin of self-fertilization in this tristylous species is associated with the loss of style-length morphs from populations and the spread of self-pollinating, floral variants. We examined geographic variation in style morph and allozyme frequencies to determine whether the loss of style morphs and transition to selfing could have multiple origins in E. paniculata. Surveys of floral variation in 167 populations from six states in northeastern Brazil revealed that at least one style morph was absent from 29.3%. Non-trimorphic populations occurred in all states and ranged in frequency from 9% in Ceará to 68% in Alagoas. Selfing variants occurred in 8.5% and 55% of trimorphic and non-trimorphic populations, respectively, and were distributed among five of six states with primary concentrations in Alagoas and Pernambuco. A comparison of electrophoretic variation at 24 isozyme loci in 28 trimorphic, 13 dimorphic and 3 monomorphic populations indicated that non-trimorphic populations contained 84% of the allelic variation present in trimorphic populations and were markedly differentiated from one another. Analyses of genetic distance and the distribution of rare alleles indicated that non-trimorphic populations were often more similar to neighbouring trimorphic populations than to one another. Populations with selfing variants occurred at low frequency in three genetically distinct parts of the range. These results, in combination with genetic and morphological evidence suggest that style morphs are lost repeatedly from populations of E. paniculata and that selfing variants may have originated on at least three separate occasions in northeastern Brazil.     

The evolution and ecology of multiple antipredator defences

Prey seldom rely on a single type of antipredator defence, often using multiple defences to avoid predation. In many cases, selection in different contexts may favour the evolution of multiple defences in a prey. However, a prey may use multiple defences to protect itself during a single predator encounter. Such “defence portfolios” that defend prey against a single instance of predation are distributed across and within successive stages of the predation sequence (encounter, detection, identification, approach (attack), subjugation and consumption). We contend that at present, our understanding of defence portfolio evolution is incomplete, and seen from the fragmentary perspective of specific sensory systems (e.g., visual) or specific types of defences (especially aposematism). In this review, we aim to build a comprehensive framework for conceptualizing the evolution of multiple prey defences, beginning with hypotheses for the evolution of multiple defences in general, and defence portfolios in particular. We then examine idealized models of resource trade-offs and functional interactions between traits, along with evidence supporting them. We find that defence portfolios are constrained by resource allocation to other aspects of life history, as well as functional incompatibilities between different defences. We also find that selection is likely to favour combinations of defences that have synergistic effects on predator behaviour and prey survival. Next, we examine specific aspects of prey ecology, genetics and development, and predator cognition that modify the predictions of current hypotheses or introduce competing hypotheses. We outline schema for gathering data on the distribution of prey defences across species and geography, determining how multiple defences are produced, and testing the proximate mechanisms by which multiple prey defences impact predator behaviour. Adopting these approaches will strengthen our understanding of multiple defensive strategies.     

The stimulatory effect of chronic lithium treatment on basal thyrotropin secretion in rats: In vivo antagonism by methylparaben

Chronic treatment of rats with lithium chloride was examined in order to determine its effect on hypothalamic monoamine and metabolite content, basal thyrotropin (TSH) secretion and thyroid function. The hypothalamic concentrations of noradrenaline (NA), dopamine (DA) and its metabolites, dihydroxyphenylacetic acid. (DOPAC) and homovanillic acid (HVA) in the lithium treated rats remained unaltered when compared to control levels. NA turnover and the NA metabolite, 3-methoxy-4-hydroxyphenylglycol (total MHPG), were significantly lower (p<0.01), whereas both serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), were significantly higher (p<0.01 and p<0.02, respectively) in the lithium treated rat hypothalami than in controls. Chronic lithium treatment significantly elevated basal TSH levels (p<0.05). This effect was antagonized by methylp-hydroxybenzoate (methylparaben, p<0.01), which did not itself affect basal TSH levels. Free serum T₃ and T₄ levels were not significantly affected by chronic lithium treatment, although T₄ tended to be slightly lower than control levels. The monoamine changes observed in the hypothalamus of lithium treated rats did not appear to account for the elevated TSH levels observed in these rats since NA activity which is generally regarded as stimulatory was decreased and 5-HT which has an inhibitory effect on TSH secretion, was increased. The elevated TSH levels may have been due to a reduced negative feedback inhibition of TSH release by the mildly reduced circulating T₄ levels caused by chronic lithium treatment. A further possibility is that the pituitary cGMP (and hence TSH) response to TRH may have been enhanced by chronic lithium treatment and methylparaben may have antagonized this effect.     

Absence of an effect of the lithium-induced increase in cyclic GMP on the cyclic GMP-stimulated phosphodiesterase (PDE II). Evidence for cyclic AMP-specific hydrolysis

Chronic treatment of rats with LiCl is known to induce a decrease in cAMP, while this decrease has also been found to occur together with both a simultaneous increase in total cortical phosphodiesterase (PDE; EC 3.1.4.17) activity and a concomitant increase in cGMP. These studies have implicated an involvement of PDE in lithium (Li⁺) action and it has been suggested that cGMP and the cGMP-stimulated PDE may be instrumental in the observed effects of Li⁺ on cAMP. In this study, three isozymes of PDE were isolated and identified from rat cortex and their activity determined, together with simultaneous measurement of cAMP and cGMP, after chronic treatment with oral LiCl (0.35% m/m). Li⁺ treatment exerted profound effects on cyclic nucleotides in the cortex, inducing significant suppression of cAMP while increasing cGMP levels. However, the ion only induced a slight but insignificant increase in the activities of the three PDE isozymes. To confirm these observations, methylparaben (MPB), a drug demonstrating both an ability to induce a selective stimulation of cAMP-specific PDE and also to lower intracellular levels of cGMP, was co-administration orally (0.4% m/m) with Li⁺ over the same period. This combination emphasized certain actions of Li⁺ not noted with Li⁺ alone. MPB inhibited the Li⁺-induced increase in cGMP, yet did not prevent the ion from decreasing cAMP. However, the combination of Li⁺ and MPB engendered a synergistic 100% increase in the activity of the membrane-bound, cAMP-specific PDE, PDE IV. This combination also produced a significant suppression of cAMP, while no reduction in cGMP was observed. The data is indicative that Li⁺-induced suppression of cAMP does not appear to be related to an effect on the cGMP-dependent PDE II, and that the increases in cGMP and PDE induced by Li⁺ observed previously and in the present study are two unrelated events. Instead, the synergistic response of Li⁺ plus MPB on PDE IV, and the associated reduction of cAMP, indicate that Li⁺ may promote selective cAMP hydrolysis via an effect on membrane-bound forms of PDE. This effect of Li⁺ on PDE IV, as well as the reciprocal effects on cyclic nucleotide balance, may have important implications in explaining the antipsychotic actions of the ion.     

Deletion analysis of the essentiality of penicillin-binding proteins 1A, 2B and 2X of Streptococcus pneumoniae

Abstract An internal fragment from each of the penicillinebinding protein (PBP) 1A, 2B and 2X genes of Streptococcus pneumoniae , which included the region encoding the active-site serine residue, was replaced by a fragment encoding spectinomycin resistance. The resulting constructs were tested for their ability to transform S. pneumoniae strain R6 to spectinomycin resistance. Spectinomycin-resistant transformants could not be obtained using either the inactivated PBP 2X or 2B genes, suggesting that deletion of either of these genes was a lethal event, but they were readily obtained using the inactivated PBP 1A gene. Analysis using the polymerase chain reaction confirmed that the latter transformants had replaced their chromosomal copy of the PBP 1A gene with the inactivated copy of the gene. Deletion of the PBP 1A gene was therefore tolerated under laboratory conditions and appeared to have little effect on growth or susceptibility to benzylpenicillin.     

Planktivory in benthic nototheniid fish in McMurdo Sound,Antarctica

Synopsis Four species of nototheniid fish were sampled from below the sea ice near Cape Armitage, McMurdo Sound:Pagothenia borchgrevinki from just below the ice 1.5 km offshore,Trematomus bernacchii, Trematomus hansoni andTrematomus centronotus from off the bottom in about 20 m of water near the shore. Scale worms and isopods were conspicuous non-planktonic prey, and present in the three benthic fish species. The planktonic pteropod molluscLimacina helicina was numerically common in all four species of fish. The planktonic hyperiid amphipodHyperiella dilatata was also found in all fish species. WhereasP. borchgrevinki is planktivorous in accord with its pelagic habit, theTrematomus spp. clearly also feed on plankton from the water column.T. hansoni is particularly planktivorous, taking smaller copepods thanP. borchgrevinki.     

ThechlL (frxC) gene: Phylogenetic distribution in vascular plants and DNA sequence fromPolystichum acrostichoides (Pteridophyta) andSynechococcus sp. 7002 (Cyanobacteria)

We examinedchlL (frxC) gene evolution using several approaches. Sequences from the chloroplast genome of the fernPolystichum acrostichoides and from the cyanobacteriumSynechococcus sp. 7002 were determined and found to be highly conserved. A complete physical map of the fern chloroplast genome and partial maps of other vascular plant taxa show thatchlL is located primarily in the small single copy region as inMarchantia polymorpha. A survey of a wide variety of non-angiospermous vascular plant DNAs shows thatchlL is widely distributed but has been lost in the pteridophytePsilotum and (presumably independently) within the Gnetalean gymnosperms.The namefrxC was originally used to denote a gene encoding a product with probable Fe : S cluster binding activity. This activity was postulated due to the amino acid sequence similarity between this product and the Fe : S-binding nitrogenase iron proteinnifH. Fe : S-binding is a property shared by ferredoxins, which are denoted by the prefix frx. However, this gene does not encode a ferredoxin. It is much larger than any known ferredoxin, it binds its Fe : S cluster between two halves of a homodimer (Fujita & al. 1989,Burke & al. 1993 a, c) instead of within a single subunit, and it lacks the pattern of clustered cysteines present in all ferredoxins (Meyer 1988). Therefore, we use the namechlL to recognize the sequence and functional similarities to the bacterial PChlide reductase subunit,bchL. Similar usage has been adopted for this (Suzuki & Bauer 1992) and other (Choquet & al. 1992,Burke & al. 1993b) PChlide reductase subunits.