99 research outputs found
Effects of TemperatureâClimate Patterns on the Production of Some Competitive Species on Grounds of Modelling
Climate change has serious effects on the setting
up and the operation of natural ecosystems. Small increase
in temperature could cause rise in the amount of some
species or potential disappearance of others. During our
researches, the dispersion of the species and biomass
production of a theoretical ecosystem were examined on
the effect of the temperatureâclimate change. The answers
of the ecosystems which are given to the climate change
could be described by means of global climate modelling
and dynamic vegetation models. The examination of the
operation of the ecosystems is only possible in huge centres
on supercomputers because of the number and the
complexity of the calculation. The number of the calculation
could be decreased to the level of a PC by considering
the temperature and the reproduction during modelling a
theoretical ecosystem, and several important theoretical
questions could be answered
Effect of low-dose zearalenone exposure on luteal function, follicular activity and uterine oedema in cycling mares
The effect of 10-day zearalenone administration starting 10 days after ovulation was studied in 6 cycling trotter mares in the summer period. After an entire oestrous cycle (Cycle 1), mares were given 7 mg purified zearalenone per os daily (1 mg/ml in ethyl alcohol) beginning on Day 10 of Cycle 2. Toxin exposure was continued until the subsequent ovulation. Luteal function and follicular activity were monitored daily by rectal palpation, ultrasonography and blood sampling for progesterone. During toxin exposure, all animals were in good physical condition. The toxin had no effect on the length of the interovulatory intervals, luteal and follicular phases. It did not influence significantly the plasma progesterone profiles (logistic curve parameters A1 to A6), the follicular activity (growth rate, maximum size of the ovulatory follicles, maximum number and the time of first increase in the number of large follicles) and the uterine oedema. It is concluded that in cyclic mares the methods used in this study could not detect any adverse effect of zearalenone (administered at a low dose similar to natural exposure) on reproduction
Coronary metabolic adaptation restricted by endothelin in the dog heart
Endothelin elicits long-lasting vasoconstriction in the coronary bed. This remarkable spastic response raises the question whether or not the metabolic adaptive mechanisms of the coronaries are activated under endothelin effect. The role of the compensatory mediators adenosine and inosine was investigated before and after intracoronary (ic.) administration of endothelin-1 (ET-1, 1.0 nmol) using 1-min reactive hyperemia (RH) tests on in situ dog hearts (n=15) with or without blocking the ATP-sensitive potassium (K +ATP) channels by glibenclamide (GLIB, 1.0 mmol min â1, ic.). The release of adenosine and inosine via the coronary sinus was measured by HPLC during the first minute of RH. Endothelin-1 reduced baseline coronary blood flow (CBF) and RH response (hyperemic excess flow (EF) control vs. ET-1: 81.7±13.6 vs. 43.4±10.9 ml, P<0.01), while it increased the net nucleoside release (adenosine, control vs. ET-1: 58.9±20.4 vs. 113.7±39.4 nmol, P<0.05; inosine: 242.1±81.8 vs. 786.9±190.8 nmol, P<0.05). GLIB treatment alone did not change baseline CBF but also reduced RH significantly and increased nucleoside release (EF control vs. GLIB: 72.1±11.7 vs. 31.9±5.5 ml, P<0.01; adenosine: 18.8±4.6 vs. 63.0±24.8 nmol, P<0.05; inosine: 113.0±37.2 vs. 328.2±127.5 nmol, P<0.05). Endothelin-1 on GLIB-treated coronaries further diminished RH and increased nucleoside release (EF: 21.5±8.0 ml, P<0.05 vs. GLIB; adenosine: 75.3±28.1 nmol, NS; inosine: 801.9±196.6 nmol, P<0.05 vs. GLIB). The data show that ET-1 reduces metabolic adaptive capacity of the coronaries, and this phenomenon is due to decreased vascular responsiveness and not to the blockade of ischemic mediator release from the myocardium. The coronary effect of ET-1 may partially be dependent on K +ATP channels
- âŠ