The nature and causes of annual fluctuations in numbers of Aphis fabae Scop. on field beans (Vicia faba)

Experiments for nine successive years showed that Aphis fabae Scop. populations on mid-March-sown field beans were either large with peak densities between late June and mid-July or very small with peak densities in early August. It is concluded that the largest populations develop when many plants have been colonized by primary migrants from Euonymus europaeus and temperature and radiation are above average during June and early July, as in the year 1957. Cold, dull weather slows multiplication and decreases the size of the peak population even when there is a large initial colonization, as in 1954. The peak population may also be less than predicted from the initial colonization when natural enemies are exceptionally abundant in early June, as in the year 1960. Yield losses of mid-March-sown crops in years of large A. fabae populations ranged from 53 % in 1954 (peak population of 1260 aphids per plant) to 100% in 1957 (6920 aphids per plant). Small summer populations with peak densities of about 0·2–85 aphids per plant developed on mid-March-sown plots in years when fewer than about 6% of the plants were colonized by primary migrants. Yield losses ranged from 6·3–13·6%. Three years' experiments indicated that crops sown in late April or May are relatively lightly infested in years when large populations develop on mid-March-sown crops. Conversely, they may be relatively heavily infested when the populations on these crops are small, as in 1955 when temperatures and sunshine during July and early August were above average. Small and large early summer populations tend to alternate in successive years. The alternation is upset by hot, sunny weather during July and August, and perhaps September and October, which compresses the population cycle Thus the large and small populations expected from this alternation in 1956 and 1960 developed instead during exceptionally fine weather in late summer 1955 and 1959, converting 1956 and 1960 to years of small and large populations respectively.     

Intra-specific mechanisms in relation to the natural regulation of numbers of Aphis fabae Scop

Parthenogenetic virginoparous apterae of Aphis fabae Scop. on field beans (Vicia faba) reproduced faster initially in populations of eight colonizing apterae than in those with 2–4 or 16–32 per plant. The aphids were at first mutually benefited but were quickly affected by competition as numbers rose above the critical density represented by about eight apterae and their first progeny. This is because the aphids remained densely aggregated and seemingly created a local shortage despite abundant food and space elsewhere on the plant. Such self-induced competition provides the basis for self-regulation of numbers of A. fabae in relation to (1) food and space provided by the growing plant and (2) mortality from natural enemies and from other causes including insecticides. As competition increased, the multiplication of A. fabae populations slowed, newly formed adult apterae emigrated and increasing numbers of alatae were formed. The mean weights of apterae decreased from about 1·8 mg. to 0·3 mg. and of alatae from 0·9 to 0·2 mg. Such decrease probably favours production of many adults that might otherwise fail to mature. Experiments in a glasshouse and in field cages indicated the success with which an A. fabae population adapts to and exploits a growing plant. Field bean plants sown in mid-March and infested as in the field produced an average of 15,000–17,000 A. fabae emigrants per plant of which 78–84% were adults (mostly alatae). This is equivalent to about 1600 million alate emigrants from 1 acre (0·4 hectare) of an infested field bean crop.     

Effects of low-chloride solutions on action potentials of sheep cadiac purkinje fibers

The rapid repolarization during phase 1 of the action potential of sheep cardiac purkinje fibers has been attributed to a time- and voltage-dependent chloride current. In part, this conclusion was based on experiments that showed a substantial slowing of phase 1 when larger, presumably impermeant, anions were substituted for chloride in tyrode’s solution. We have re- examined the electrical effects of low-chloride solutions. We recorded action potentials of sheep cardiac purkinje fibers in normal tyrode’s solution and in low-chloride solutions made by substituting sodium propionate, acetylglycinate, methylsulfate, or methanesulfonate for the NaCl of Tyrode’s solution. Total calcium was adjusted to keep calcium ion activity of test solutions equal to that of control solutions. Propionate gave qualitatively variable results in preliminary experiments; it was not tested further. Low-chloride solutions made with the other anions gave much more consistent results: phase 1 and the notch that often occurs between phases 1 and 2 were usually unaffected, and the action potential duration usually increased. The only apparent change in the resting potential was a transient 3-6 mV depolarization when low-chloride solution was first admitted to the chamber, and a symmetrical transient hyperpolarization when chloride was returned to normal. If a time- and voltage-dependent chloride current exists in sheep cardiac purkinje fibers, our results suggest that it plays little role in generating phase 1 of the action potential.     

Plasminogen activator and collagenase production by cultured capillary endothelial cells

Cultured bovine capillary endothelial (BCE) cells produce low levels of collagenolytic activity and significant amounts of the serine protease plasminogen activator (PA). When grown in the presence of nanomolar quantities of the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), BCE cells produced 5-15 times more collagenolytic activity and 2-10 times more PA than untreated cells. The enhanced production of these enzymes was dependent on the dose of TPA used, with maximal response at 10(-7) to 10(-8) M. Phorbol didecanoate (PDD), an analog of TPA which is an active tumor promoter, also increased protease production. 4-O-methyl-TPA and 4α-PDD, two analogs of TPA which are inactive as tumor promoters, had no effect on protease production. Increased PA and collagenase activities were detected within 7.5 and 19 h, respectively, after the addition of TPA. The TPA-stimulated BCE cells synthesized a urokinase-type PA and a typical vertebrate collagenase. BCE cells were compared with bovine aortic endothelial (BAE) cells and bovine embryonic skin (BES) fibroblasts with respect to their production of protease in response to TPA. Under normal growth conditions, low levels of collagenolyic activity were detected in the culture fluids from BCE, BAE, and BES cells. BCE cells produced 5-13 times the basal levels of collagenolytic activity in response to TPA, whereas BAE cells and BES fibroblasts showed a minimal response to TPA. Both BCE and BAE cells exhibited relatively high basal levels of PA, the production of which was stimulated approximately threefold by the addition of TPA. The observation that BCE cells and not BAE cells produced high levels of both PA and collagenase activities in response to TPA demonstrates a significant difference between these two types of endothelial cells and suggests that the enhanced detectable activities are a property unique to bovine capillary and microvessel and endothelial cells.     

Dissociation of intracellular lysosomal rupture from the cell death caused by silica

The relationship between intracellular lysosomal rupture and cell death caused by silica was studied in P388d(1) macrophages. After 3 h of exposure to 150 μg silica in medium containing 1.8 mM Ca(2+), 60 percent of the cells were unable to exclude trypan blue. In the absence of extracellular Ca(2+), however, all of the cells remained viable. Phagocytosis of silica particles occurred to the same extent in the presence or absence of Ca(2+). The percentage of P388D(1) cells killed by silica depended on the dose and the concentration of Ca(2+) in the medium. Intracellular lyosomal rupture after exposure to silica was measured by acridine orange fluorescence or histochemical assay of horseradish peroxidase. With either assay, 60 percent of the cells exposed to 150 μg silica for 3 h in the presence of Ca(2+) showed intracellular lysosomal rupture, was not associated with measureable degradation of total DNA, RNA, protein, or phospholipids or accelerated turnover of exogenous horseradish peroxidase. Pretreatment with promethazine (20 μg/ml) protected 80 percent of P388D(1) macrophages against silica toxicity although lysosomal rupture occurred in 60-70 percent of the cells. Intracellular lysosomal rupture was prevented in 80 percent of the cells by pretreatment with indomethacin (5 x 10(-5)M), yet 40-50 percent of the cells died after 3 h of exposure to 150 μg silica in 1.8 mM extracellular Ca(2+). The calcium ionophore A23187 also caused intracellular lysosomal rupture in 90-98 percent of the cells treated for 1 h in either the presence or absence of extracellular Ca(2+). With the addition of 1.8 mM Ca(2+), 80 percent of the cells was killed after 3 h, whereas all of the cells remained viable in the absence of Ca(2+). These experiments suggest that intracellular lysosomal rupture is not causally related to the cell death cause by silica or {"type":"entrez-nucleotide","attrs":{"text":"A23187","term_id":"833253","term_text":"A23187"}}A23187. Cell death is dependent on extracellular Ca(2+) and may be mediated by an influx of these ions across the plasma membrane permeability barrier damaged directly by exposure to these toxins.