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Biomedical subjects

M L Ross

Publications and source records attributed to M L Ross.

10 recordsLinked to original sources
PubMed1992

Adrenocorticotrophic hormone fails to alter plasma fibrinogen and fibronectin values in calves but does so in rabbits.

The intramuscular administration of adrenocorticotrophic hormone (ACTH) to calves, in either a short-acting form (cosyntrophin) or a longer-acting form (ACTHAR Gel), failed to induce any alteration in circulating fibrinogen or fibronectin values, despite marked elevations in plasma cortisol concentrations. With the longer-acting ACTH, plasma cortisol was elevated for at least 12 h following treatment and induced the expected physiological response of an elevation in blood glucose. In contrast, both forms of ACTH induced marked increases (p < 0.01) in plasma fibrinogen and fibronectin when administered to rabbits. The elevation in the circulating levels of these proteins was first observed 24 h after ACTH administration, by which time plasma corticosteroid values had returned to pre-treatment values. With both ACTH preparations the increases in the circulating levels of these proteins were sustained for at least 96 h. The results suggest that, in cattle, the well-recognized increases in plasma fibrinogen values following stress are not associated with the concomitant increase in plasma cortisol. Further, the results clearly illustrate the marked species differences in the response of acute-phase reactant proteins to elevated glucocorticoids.

Adrenocorticotropic Hormone↗
PubMed1989

Platelet aggregation in the Asian elephant is not dependent on thromboxane B2 production.

1. The platelet aggregation response to several known platelet agonists was evaluated in four Asian elephants. The platelets were highly responsive to stimulation with platelet-activating factor (PAF) and collagen, less responsive to adenosine diphosphate (ADP) and non-responsive to arachidonic acid, serotonin and epinephrine. 2. Arachidonic acid (1 x 10(-4) M), while inducing no aggregation, caused the release of 1248 +/- 1147 pg/ul (mean +/- SD) of thromboxane B2 (TXB2), the stable metabolite of thromboxane A2 from stimulated platelet. The addition of 1 x 10(-4) M ADP to platelets caused suboptimal aggregation and the release of only 25 +/- 10 pg TXB2/microliters. 3. The calcium channel blocker, verapamil, produced a dose-dependent inhibition of PAF-induced but not collagen-induced aggregation. The cyclooxygenase inhibitor, acetylsalicylic acid, produced no inhibition of either collagen- or PAF-induced aggregation.

Adenosine Diphosphate↗
PubMed1989

Failure of aspirin to impair bovine platelet function.

The effect of aspirin on bovine platelet function and thromboxane A2 (TXA2) production in stimulated platelets was evaluated. A single dose of aspirin (100 mg/kg of body weight) was administered orally to Holstein cows, and blood samples were obtained before and at regular intervals for 7 days after treatment. The production of TXA2 was assessed by measuring the stable metabolite thromboxane B2, using a specific radioimmunoassay. Within 4 hours of aspirin administration, the production of TXA2 was significantly (P less than 0.05) decreased, irrespective of whether collagen, adenosine diphosphate, or platelet activating factor was used to initiate platelet aggregation. Despite the inhibition of TXA2 release from the stimulated platelets, platelet function, assessed by initial rate of aggregate formation and extent of aggregation, was unaffected by aspirin administration. The extent of aggregate formation in response to collagen, adenosine diphosphate, or platelet activating factor was independent of the amount of TXA2 released from platelets before and after aspirin treatment. The results suggested that TXA2 formation is not the primary biochemical pathway involved in the aggregation of stimulated bovine platelets.

Animals↗
PubMed1988

Ten electrophoretic methods compared with a selected method for quantifying lactate dehydrogenase isoenzymes in serum.

Using the Selected Method of McKenzie and Henderson (Selected Methods Clin Chem 1983;10:59-67) as a reference method, we compared the performance of 10 commercially available methods for determination of lactate dehydrogenase (LD, EC 1.1.1.27) isoenzymes. Results were expressed as percentage of total LD activity, as determined with two different types of densitometers shown to have an average difference less than 1.4% for each isoenzyme. All methods gave generally comparable results, as judged by Bland-Altman plots and correlation analyses. However, in general, estimates by the commercial methods for LD-1, LD-2, and LD-3 were lower, and for LD-4 and LD-5 were higher than with the Selected Method. The overall CV was less than 20% for all methods and isoenzymes, except for LD-4 and LD-5 by the Beckman Paragon, Helena LD-VIS, Gel LDH, Gel PC, and Iso Dot, Gelman LDH Isozyme, and Sebia Hydragel assays, for which it was greater than 20%. Overall, accuracy was best with the Helena Iso Dot and LD-VIS assays, followed by the Corning LD Flur assay; accuracy was poorest with the Gelman LDH Isozyme, Sebia Hydragel, and Beckman Paragon assays.

Electrophoresis↗
PubMed1987

Ovine platelet function and its inhibition by T-2 toxin.

Ovine platelets suspended in homologous plasma aggregated effectively in response to adenosine-diphosphate, acid-soluble collagen and aggregated moderately to serotonin and arachidonic acid. Ovine platelet aggregation, in response to each agent, was inhibited in a concentration dependent fashion by T-2 toxin. The platelet aggregates which formed in the presence of T-2 toxin appeared to be less stable than aggregates in comparable control platelet suspensions.

Adenosine Diphosphate↗
PubMed1987

Inhibitory effect of trichothecene mycotoxins on bovine platelets stimulated by platelet activating factor.

Several species of fungi, which infect cereals and grains, can produce a class of compounds, known as trichothecene mycotoxins, which is characterized by a substituted epoxy-trichothecene ring structure. Cattle are susceptible to intoxication from feeds contaminated with T-2 toxin, one of the more potent trichothecene mycotoxins, while swine refuse to ingest feed contaminated with T-2 toxin. The bovine platelet has been used as a model cell system to evaluate the effects of T-2 toxin and its natural metabolites, HT-2 toxin and T-2 tetraol, on cell function in vitro. Due to the lipophilic nature of these mycotoxins, a biologically active phospholipid was used to stimulate the platelets in the presence and absence of the toxins. The mycotoxin T-2 toxin and its major metabolite HT-2 toxin inhibited platelet activating factor-stimulated bovine platelets, suspended in homologous plasma, in a concentration but not time dependent manner. Significant inhibition of platelet function (p less than 0.01) occurred with 135 ng T-2 toxin per 10(6) platelets and with 77 ng HT-2 toxin per 10(6) platelets. These mycotoxins exerted an additive inhibitory effect on the platelet aggregation response. In contrast, the minor metabolite T-2 tetraol had no inhibitory effect on platelet function and had no influence on the responses of T-2 toxin or HT-2 toxin when the mycotoxins were present together in the platelet suspensions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗