Performance of Two Fruit Fly (Diptera: Tephritidae) Pupal Parasitoids (Coptera haywardi [Hymenoptera: Diapriidae] and Pachycrepoideus vindemiae [Hymenoptera: Pteromalidae]) under Different Environmental Soil Conditions

We evaluated the performance of Coptera haywardi (Ogloblin) (Diapriidae) and Pachycrepoideus vindemiae (Rondani) (Pteromalidae), both hymenopteran pupal parasitoids of Anastrepha spp. (Diptera: Tephritidae). Performance was studied by manipulating the following environmental conditions in the laboratory: (1) soil type, (2) soil moisture content, (3) soil compaction, and (4) depth at which pupae were buried in the soil. There were two experiments: in the first, exposure time of pupae was held constant and in the second, it varied. In the first experiment, C. haywardi was significantly more effective than P. vindemiae in parasitizing fly pupae. With exposure time held constant (36 h), only soil type and pupal burial depth were significantly related to parasitism rates. While P. vindemiae only parasitized pupae located on the soil surface, C. haywardi attacked pupae that were buried up to 5 cm deep, performing better in clayey than in loamy soil. In the second experiment, exposure time (24, 36, 48, and 72 h) had no significant effect on parasitism rates, but soil type did. P. vindemiae again only attacked pupae on the soil surface while C. haywardi was also able to parasitize pupae that were buried up to 5 cm deep. We conclude that C. haywardi represents a viable candidate to replace the environmentally unfriendly P. vindemiae in augmentative biological control programs against fruit flies.     

Altered fatty acid membrane composition modifies lymphocyte localization in vivo

In the present paper, we report the results of a study on the in vivo localization of 51Cr-labeled lymphocytes with an altered lipid bilayer. In vitro treatment of lymphocytes with fatty acids (arachidic and linolenic acids) modifies the relative composition of plasma membrane fatty acids. Phospholipids of the plasma membrane of lymphocytes incubated with arachidic acid show a preferential increase of fatty acids with chain length between C:12 and C:16. Cells incubated with linolenic acid show an increase percentage of fatty acids C:16 to C:20 and the relative amount of the fatty acids with chain length superior to C:20 is higher in cells treated with linolenic than with arachidic acid. We have found that these alterations in plasma membrane fatty acid composition can modify the normal pattern of lymphocyte localization in vivo after iv transfer into syngeneic hosts. The possible role of factors such as cell to cell adhesion and/or fluidity of plasma membranes in the control of lymphocyte migration are discussed.     

Hemorrhage in mice produces alterations in B cell repertoires

Multiple organ system failure secondary to infection is the major cause of late deaths after trauma and hemorrhage. The production by B cells of antibodies directed against bacterial antigens is an important component of host defenses. In order to determine the effects of hemorrhage on B cell function, we examined hemorrhage-induced alterations in available (clonal precursors) and actual (plasma cells) B cell repertoires in the course of an immune response toward bacterial antigens. Hemorrhage produced greater than twofold decreases in the absolute frequency and number of clonal precursors specific for the bacterial antigens dextran, levan, and pneumococcal polysaccharide type II. After blood loss, there were decreases in absolute frequency, but not in numbers, of clonal precursors capable of producing antibodies against the nonbacterial antigens ovalbumin and mouse transferrin. Immunization with the bacterial antigen levan within 24 hr of hemorrhage resulted in approximately 50% fewer levan-specific plasma cells than that seen in normal, unhemorrhaged mice. These results demonstrate that hemorrhage produces marked alterations in B cell repertoires, which may contribute to postinjury abnormalities in host defenses.     

Two major classes of mitogen-reactive B lymphocytes defined by life span

The relative numbers of short- and long-lived mitogen-reactive B cells in the peripheral pool were evaluated by studying the decay of lipopolysaccharide (LPS)-reactive B lymphocytes in LPS nonresponder, histocompatible hosts for periods of up to 3 wk after cell transfer. The results obtained demonstrate the existence of two major classes of mitogen-reactive B cells defined by life span. The "short-lived" cell component comprises about 80 to 90% of the reactive cells and decays with a life expectancy of 18 to 24 hr. The long-lived cell component, with life expectancies of 10 to 20 days, comprises about 10 to 20% of the reactive cells and is preferentially enriched in circulating B cells. The present ratio for short- and long-lived B cells implies a highly dynamic state for the immune system which must be advantageous in the selection of available repertoires.     

Life span of B lymphocytes: the experimental basis for conflicting results

Recent claims have challenged the view that most peripheral, mature B cells are long-lived, and propose rates of peripheral decay that are compatible with bone marrow production. This disagreement can only reflect differences in the protocols and methods used to measure peripheral lymphocyte life spans. We have now assessed toxic or other nonselective effects of hydroxyurea treatment on the survival and migration of peripheral, noncycling cells, as well as possible reasons for exaggerated decays of LPS-reactive B cells transferred to LPS nonresponder hosts, the two methods leading to conclusions of short life spans. We also studied general effects on cell survival introduced by either repeated [3H]thymidine injections or the stress associated with surgery, thoracic duct cannulation in particular--methods with which the notion of long life spans had been established. The results failed to show toxic or nonselective effects of hydroxyurea treatments and artificial decays of LPS-reactive cells in adoptive hosts. In contrast, the present experiments demonstrate that both the stress associated with surgery and repeated [3H] thymidine administration profoundly deplete a pool of short-lived B cells, consequently selecting for an apparent higher proportion of long-lived cells.     

Glutamate agonists from marine algae

The occurrence of three glutamate agonists — glutamic acid, D-homocysteic acid and kainic acid — in a spontaneous mutant of Palmaria palmata is reported. Glutamic acid and D-homocysteic acid, but not kainic acid, were found in the wild-type plant. The closely related glutamate agonist, domoic acid, was found in the red alga Chondria baileyana and in the diatom Nitzschia pungens forma multiseries. In the diatom, domoic acid can build up to high levels in excess of 3% (dry wt.), making N. pungens a potential commercial source of this neuroactive amino acid. Information is also presented on the distribution, chemistry and biological activity of neuroactive amino acids from algae, and a possible biogenic relationship among kainoid metabolites is discussed. author for correspondence     

Effects of brain ischemia on intermediate filaments of rat hippocampus

Neurofilaments subunits (NF-H, NF-M, NF-L) and glial fibrillary acidic protein (GFAP) were investigated in the hippocampus of rats after distinct periods of reperfusion (1 to 15 days) following 20 min of transient global forebrain ischemia in the rat. In vitro [¹⁴Ca]leucine incorporation was not altered until 48 h after the ischemic insult, however concentration of intermediate filament subunits significantly decreased in this period. Three days after the insult, leucine incorporation significantly increased while the concentration NF-H, NF-M, and NF-L were still diminished after 15 days of reperfusion. In vitro incorporation of³²P into NF-M and NF-L suffered immediately after ischemia, but returned to control values after two days of reperfusion. GFAP levels decreased immediately after ischemia but quickly recovered and significantly peaked from 7 to 10 days after the insult. These results suggest that transient ischemia followed by reperfusion causes proteolysis of intermediate filaments in the hippocampus, and that proteolysis could be facilitated by diminished phosphorylation levels of NF-M and NF-L.