Morphological Traits of Two Seed-Feeding Beetle Species and the Relationship to Resource Traits.

Morphological traits are useful to investigate insect sex-related differences in body size and to reveal differences in resource use. It has been suggested that as the resource increases, so does the body size of organisms interacting with the resource, highlighting the crucial role of resource quality and quantity in determining the morphological traits of organisms interacting with the resource. Here, we describe morphological traits of two species of Bruchinae, Merobruchus terani (Kingsolver 1980) and Stator maculatopygus (Pic 1930), consuming seeds of Senegalia tenuifolia (Fabaceae: Mimosoideae). We evaluated the influence of monthly sample and sampling sites on tibia and femur length and biomass. In addition, we tested two predictions in which body size related to resource amount and body size related to longevity. Males of M. terani were heavier than females, whereas the two sexes of S. maculatopygus did not differ in biomass. Both species had larger body sizes in the late ripe-fruit stage. With respect to sampling sites, biomass of M. terani did not differ, whereas S. maculatopygus did differ in biomass. Merobruchus terani showed a positive relationship with seed traits, whereas S. maculatopygus showed no relationship. At the same time, fruit traits showed a negative effect on morphological traits for both beetle species. The longevity experiment, performed using only M. terani, showed an equal longevity and seed consumption rate for both sexes. Our study indicates that different species, interacting in the same system and performing similar functional behaviors, respond differently to the same resource.

Intranasal DDAVP induced increases in plasma von Willebrand factor alter the pharmacokinetics of high-purity factor VIII concentrates in severe haemophilia A patients.

Because native circulating factor VIII (FVIII) is maximally stabilized when it is bound to von Willebrand factor (vWf), increased plasma vWf levels may enhance the infused FVIII concentrate intravascular survival and efficacy in severe haemophiliacs. To assess whether the kinetic characteristics and recovery of high purity, plasma-derived (Monoclate-P, Centeon) and recombinant (Bioclate , Centeon) FVIII concentrates are enhanced by increased plasma vWf concentrations, we compared the pharmacokinetic response to a bolus of FVIII infused alone with the response to a bolus infused 2 h after the intranasal delivery of 300 microg of desmopressin acetate (DDAVP) High Concentration Nasal Spray (Stimate, Centeon) in 10 adult severe haemophiliacs. FVIII activity was determined using a one-stage clotting assay on cryopreserved plasma specimens obtained at baseline and at 14 distinct time points (0.25-48 h) following the FVIII infusions. Ristocetin co-factor activity (RCoFA) and vWf antigen levels were assayed at baseline and 2 h after Stimate. FVIII kinetic parameters were calculated using standard, noncompartmental kinetic methods. Statistical analysis was performed using a paired t-test with 95% confidence limits. The mean rises in RCoFA (0.65+/-0.44 IU mL(-1)) and vWf antigen (0.19+/-0.07 IU mL-1) induced by Stimate were significant (P<0.01 and P<0.0001, respectively). The mean increases in the volume of distribution at steady state (Vss) (13.2+/-9.3 dL) and mean residence time (MRT) (4.4+/-3.9 h) between the FVIII-only arm and the FVIII plus Stimate arm were highly significant (P = 0.0015 and P = 0. 0059, respectively). The mean differences in recovery, area under the curve (AUC), half-life, and clearance (Cl) were not significantly altered. Subgroup analysis revealed statistically significant increases in Vss and MRT (P = 0.025 and P = 0.012, respectively) following the administration of intranasal DDAVP in the Monoclate-P cohort, but not in the Bioclate group. These data suggest that even modest pharmacologically induced increases in plasma vWf can favourably affect the kinetics of high-purity, plasma-derived FVIII concentrates in severe haemophiliacs.

Effect of intermediate- and high-purity factor VIII concentrates on immune function in HIV-seropositive haemophiliacs as assessed by quantitative CD 4 counts.

Intermediate-purity factor VIII (FVIII) concentrates are believed to adversely influence cellular immune function and accelerate HIV progression in haemophiliac patients. There are reports that cellular immunity, as measured by serial CD4 lymphocyte counts, is better preserved in HIV-infected haemophiliacs who receive high-purity concentrates compared with those receiving intermediate- or low-purity products. We retrospectively evaluated the rate of CD4 cell count decrease in 44 asymptomatic HIV-seropositive severe haemophilia A patients whose purity of prescribed FVIII concentrate was primarily determined by State of residence. Prior to January 1989 all study subjects received treatment with intermediate- or low-purity products. In January 1989 the patients from Mississippi (n = 15) began to exclusively receive a high-purity, monoclonal antibody purified, plasma-derived product from their State Department of Health. The Mississippi cohort was subsequently converted to a high-purity, recombinant FVIII product in May 1993. Patients from Tennessee and Arkansas (n = 29) received intermediate-purity factor during the entire analysis period. Patients were monitored for an average of 68 months with an average of 11 CD4 cell count measurements. The rate of CD4 cell count decrease was derived from the calculated slope of a simple regression in order to account for large individual CD4 count fluctuations during the study period. There was no statistically significant difference in starting CD4 cell count between the 2 study groups. The rate of CD4 cell count decrease was 21.8 ± 52.9 cells µL(-1) year(-1) and 17.0 ± 32.6 cells µL(-1) year(-1) in the high-purity FVIII group and inter-mediate-purity FVIII group, respectively (P = 0.83). The difference in rate of CD4:CD8 ratio decrease between the two groups was also not statistically significant (P = 0.41). These data suggest that the use of the more costly, high-purity monoclonal antibody purified and recombinant FVIII concentrates does not influence the rate of decrease in CD4 cell count in HIV-seropositive haemophiliacs compared with concentrates of lower specific activity obtained using standard chromatographic techniques.

Stimulation of mouse lymphocytes by a mitogen derived from Mycoplasma arthritidis. VI. Detection of a non-MHC gene(s) in the E alpha-bearing RIIIS mouse strain that is associated with a specific lack of T cell responses to the M. arthritidis soluble mitogen.

Previous work using inbred, congenic and recombinant mouse strains showed a positive association with expression of E alpha and the ability of splenic cells to bind to and undergo proliferation in response to a T cell mitogen present in culture supernatants of Mycoplasma arthritidis (MAS). Studies described in the present manuscript confirm this association because lymphocytes from mice expressing H-2a, H-2d, H-2j, H-2k, H-2p, H-2u, and H-2v all of which possess E alpha responded to MAS, whereas those expressing H-2b, H-2f, H-2q, and H-2s, which lack E alpha, failed to respond. One exception was noted in that the inbred RIIIS mouse (H-2r) that expresses E alpha failed to respond to MAS but responded normally to concanavalin A, and phytohemagglutinin. In contrast, the congenic B10.RIII (H-2r) mouse did respond to MAS, suggesting the presence of an MAS nonresponsive, non-major histocompatibility complex (MHC) gene(s) in the RIIIS mouse. MAS nonresponsiveness in the RIIIS mouse was recessive because the lymphocytes from F1 crosses with responder B10.RIII (H2r) and C3H (H2k) mice responded to MAS. Analysis of (RIIIS X B10.RIII)F1 X RIIIS or B10.RIII parental test cross progeny confirmed that nonresponsiveness to MAS was associated with a recessive, non-MHC gene(s). Evidence was also found that a non-MHC, MAS-nonresponsive gene(s) is also present in the inbred SWR (H-2q) and SJL (H-2s) strains, because lymphocytes from F1 crosses between these strains and the RIIIS mouse failed to respond to MAS. Both RIIIS and B10.RIII splenic cells bound the mitogen in MAS to a similar degree, confirming the presence of the binding site in both mice. In contrast, C3H.SW (H-2b) splenic cells that do not express E alpha failed to bind the mitogen. The nonresponsiveness of RIIIS lymphocytes to MAS was exercised at the level of the T cell rather than the accessory cell. Thus RIIIS T cells failed to respond to MAS presented by RIIIS, B10.RIII, or (RIIIS X B10.RIII)F1 accessory cells. In contrast, B10.RIII and (RIIIS X B10.RIII)F1 T cells responded to MAS when presented by RIIIS, B10.RIII, or F1 accessory cells. Similar observations were made using SWR and SJL T cells, which failed to respond to MAS irrespective of the source of accessory cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Variant von Willebrand's disease and pregnancy.

The clinical course and coagulation profile of a pregnant patient with variant von Willebrand's disease were followed from the second trimester through puerperium. The clinical course was characterized by a normal delivery and absence of abnormal bleeding or need for replacement therapy. The coagulation profile demonstrated an increase in factor VIII procoagulant activity, factor-VIII-related antigen, and platelet aggregation activity in response to ristocetin prior to delivery. Postpartum, these factors decreased to prepregnancy values with distinctly different patterns. Factor VIII procoagulant activity continued to rise for 5 days after delivery and then decreased with a half-life of approximately 6 days. Factor-VIII-related antigen began to decrease just prior to delivery, displaying a half-life or approximately 6 days. Ristocetin cofactor activity, however, dropped immediately postpartum and displayed a half-life of approximately 6 hr. The ristocetin cofactor activity was associated with factor-VIII-related antigen, which displayed a significantly smaller molecular weight than does normal factor-VIII-related antigen. Larger aggregates of factor-VIII-related antigen. Larger aggregates of factor-VIII-related antigen did not appear during the pregnancy, and ristocetin cofactor activity could not be demonstrated in fragments of less than 0,8 x 10(6).