Search

Aims: To investigate the difference between Lancefield group C Streptococcus dysgalactiae (GCSD) strains isolated from diseased fish and animals by sequencing and phylogenetic analysis of the sodA gene. Methods and Results: The sodA gene of S trep. dysgalactiae strains isolated from fish and animals were amplified and its nucleotide sequences were determined. Although 100% sequence identity was observed among fish GCSD strains, the determined sequences from animal isolates showed variations against fish isolate sequences. Thus, all fish GCSD strains were clearly separated from the GCSD strains of other origin by using phylogenetic tree analysis. In addition, the original primer set was designed based on the determined sequences for specifically amplify the sodA gene of fish GCSD strains. The primer set yield amplification products from only fish GCSD strains. Conclusions: By sequencing analysis of the sodA gene, the genetic divergence between S trep. dysgalactiae strains isolated from fish and mammals was demonstrated. Moreover, an original oligonucletide primer set, which could simply detect the genotype of fish GCSD strains was designed. Significance and Impact of the Study: This study shows that S trep. dysgalactiae isolated from diseased fish could be distinguished from conventional GCSD strains by the difference in the sequence of the sodA gene. [ABSTRACT FROM AUTHOR]

Artificial reproduction and subsequent improved culture of the Japanese eel Anguilla japonica have not yet been achieved, but are expected in the near future. To allow the development of aquaculture activities, chromosome manipulation techniques are necessary for the genetic improvement of the eel. In the present paper suitable conditions were determined for heat shock treatment for the induction of triploidy. This was done using fertilized eggs obtained from gametes of cultured eels that were induced to mature by repeated injections of salmon pituitary extract, followed by an injection of 17α,20β-dihydroxy-4-pregnen-3-one to induce ovulation in the female eels and by repeated injections of human chorionic gonadotropin in the male eels. Three variables (i.e. timing after fertilization, temperature, and duration of the shock) were varied to maximize the yield of triploid larvae by examining hatching and triploid rates of treated groups. Ploidy was determined by DNA content flow cytometry and/or chromosome counting. The triploid yield was the highest (70%), when a 37°C heat shock was applied for 3 min, 10 min after fertilization. Under such conditions the rate of triploidy reached 70–100% and the rate of hatching was 5.2–24.6% when the control hatching rate was 28.5% on average. [ABSTRACT FROM AUTHOR]

STUDY DESIGN:: Cross-sectional study comparing trained spinal cord injured (SCI) subjects (lesion level: L1∼T6) with healthy young subjects (CONT). OBJECTIVE:: To investigate the kinetics of response in oxygen uptake (&Vdot;O2) in human upper-body skeletal muscles, nine trained SCI subjects underwent submaximal supine arm exercises. METHOD:: The SCI subjects underwent an incremental arm exercise test until exhaustion. The days after this first round of testing, breath-by-breath &Vdot;O2 and beat-by-beat heart rate (HR) on- and off-kinetics were determined during three repetitions of constant exercise at 50% of &Vdot;O2peak. The overall time course of response was determined from the half time (t1/2). Increased capillary blood lactate production (Δ[La]b) at the onset of exercise was defined as the difference between at rest and at the end of exercise. Cardiac output () was measured using the acetylene rebreathing method during the steady state of exercise. In accordance with the Fick principle, the difference in arterial-venous O2 content (Ca-vO2) was defined as &Vdot;O2/. RESULTS:: During the steady state of the submaximal arm exercise, a more significant increase in the steady state of was obtained in the CONT subjects than in the trained SCI subjects: respectively, 14.9±1.4 l/min versus (12.7±0.8 l/min). There was no difference in the steady state of &Vdot;O2 between the two groups; as a result, SCI subjects had the greater Ca-v2. Meanwhile,&Vdot;O2 on- and off-kinetics became much faster in the trained SCI subjects than in the CONT subjects. In addition, t1/2 HR on-kinetics was not significantly different between the SCI and CONT groups. Increased Δ[La]b was closely related to larger t1/2 &Vdot;O2 on-kinetics (r=0.624, P<0.05). CONCLUSION:: It is concluded that the acceleration of &Vdot... [ABSTRACT FROM AUTHOR]

We investigated the association of beta 2-glycoprotein I and P-selectin with platelet-derived microparticles in 48 patients with immune thrombocytopenic purpura and 20 normal controls using two-color flow cytometric analysis. In addition, anticardiolipin antibodies were detected by an enzyme-linked immunosorbent assay. Platelet microparticles from the patients showed a higher positivity for beta 2-glycoprotein I than those from the normal controls (23.1 +/- 15.4% vs. 5.3 +/- 3.1%, p < 0.01), but this positivity was not related to the presence of platelet-associated IgG or to the severity of thrombocytopenia. In the 18 patients with more than 20% P-selectin-positive microparticles, beta 2-glycoprotein I positivity was significantly higher than in the 30 patients with less than 20% P-selectin-positive microparticles (37.1 +/- 20.5% vs. 21.5 +/- 17.3%, p < 0.01). In addition, anticardiolipin antibodies were detected in eight patients, and they had a significantly higher level of beta 2-glycoprotein I-positive microparticles than the patients without such antibodies (42.0 +/- 22.9% vs. 22.6 +/- 18.9%, p < 0.05). Our results suggest that anticardiolipin antibodies activate platelets in immune thrombocytopenic purpura and cause the generation of microparticles rich in beta 2-glycoprotein I and P-selectin. These microparticles may then act to regulate coagulation abnormalities in patients with anticardiolipin antibodies. [ABSTRACT FROM AUTHOR]

We investigated the association of β-glycoprotein I and P-selectin with platelet-derived microparticles in 48 patients with immune thrombocytopenic purpura and 20 normal controls using two-color flow cytometric analysis. In addition, anticardiolipin antibodies were detected by an enzyme-linked immunosorbent assay. Platelet microparticles from the patients showed a higher positivity for β-glycoprotein I than those from the normal controls (23.1±15.4% vs. 5.3±3.1%, p<0.01), but this positivity was not related to the presence of platelet-associated IgG or to the severity of thrombocytopenia. In the 18 patients with more than 20% P-selectin-positive microparticles, β-glycoprotein I positivity was significantly higher than in the 30 patients with less than 20% P-selectin-positive microparticles (37.1±20.5% vs. 21.5±17.3%, p<0.01). In addition, anticardiolipin antibodies were detected in eight patients, and they had a significantly higher level of β-glycoprotein I-positive microparticles than the patients without such antibodies (42.0±22.9% vs. 22.6±18.9%, p<0.05). Our results suggest that anticardiolipin antibodies activate platelets in immune throm bocytopenic purpura and cause the generation of microparticles rich in β-glycoprotein I and P-selectin. These microparticles may then act to regulate coagulation abnormalities in patients with anticardiolipin antibodies. [ABSTRACT FROM AUTHOR]

In a river reservoir, the Ishitegawa Dam Reservoir in Japan, sites of abundant phytoplankton growth were investigated in connection with the water movement in the reservoir from January 1982 to January 1984 by comparing the distributions of chlorophyll a, water temperature, and coliform bacteria (Project A). The results distinguished three types of phytoplankton growth, of which one type, the abundant surface growth at the head of the reservoir, was most frequently observed. This case was considered to be caused by mixing of the surface lake water with the inflowing nutrient-rich river water at the shallow lake-head. Subsequently the effects of dissolved calcium and magnesium on the chlorophyll a and phytoplanktonic particulate phosphorus concentrations at the head of the reservoir were investigated until December 1987 (Project B). A trophic index, named the Ca-Mg index, was found which correlated positively with the chlorophyll a and phytoplanktonic particulate phosphorus concentrations in a logarithmic scale and varied in relation to the changes in the same index of the inflowing river water. Based on the ecological results of these two projects, two proposals are presented for inhibiting abundant phytoplankton growth at the head of a river reservoir. Proposal A: make the head deep and, in addition, create a strong near-bottom underflow of the inflowing river water. Proposal B: make a bypass in order to cut off the inflow of river water in the case of a high Ca-Mg index. [ABSTRACT FROM AUTHOR]

We investigated the increase of platelet-associated IgG and complement component, ³CO caused by the in vitro action of anti-platelet MoAbs, and the effect of mouse and human IgG on these events, Anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib MoAbs caused a slight increase of C3, but not of platelet-associated IgG. In contrast, anti-CD9 and anti-Fey II receptor MoAbs caused an increase of both platelet-associated C3 and IgG. In particular, three MoAbs which activated the complement system caused a marked increase of C3. When platelet-rich plasma was treated with aspirin and prostaglandin, before incubation with antibodies, the increase of platelet-associated IgG was inhibited in all cases. In contrast, the increase of platelet-associated C3 was scarcely influenced. These results suggest that the binding to platelets of platelet-activating antibodies caused the increased expression of IgG molecules on the platelet surface and a possible increase of platelet-associated IgG, However, the increase of platelet-associated C3 appeared to depend on specific characteristics of the antibodies tested, such as a complement-activating effect. In addition, intact mouse or human IgG inhibited the increase of platelet-associated C3 caused by complement-activating antibodies, white F(ab') 2 mouse or human IgG had no such effect. This suggested that the Fc portion of IgG may block the increase of C3 mediated by anti-platelet antibodies. [ABSTRACT FROM AUTHOR]

The ultrastructural localization of the enzyme Δ-3 β-hydroxysteroid dehydrogenase (3 β-HSD) was studied in the goldfish interrenal cells by using the potassium ferricyanide method. Immersion fixation in a mixture of 1 % paraformaldehyde and 0.25% glutaraldehyde results in a consistently good ultrastructural preservation and enzyme localization. A precipitate of copper ferrocyanide indicating the localization of 3 β-HSD activity was observed in close vicinity to the smooth endoplasmic reticulum or in contact with the outer surface of its membrane. A small number of precipitated grains were also found in the lumen of mitochondrial cristae. Addition of phenazine methosulfate increased the intensity of the reaction without changing the localization of the copper ferrocyanide grains. These findings suggest that the outer surface of the smooth endoplasmic reticulum is the major site of 3 β-HSD activity in goldfish interrenal cells. [ABSTRACT FROM AUTHOR]