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M Bevers

Publications and source records attributed to M Bevers.

5 recordsLinked to original sources

Numerically exploring habitat fragmentation effects on populations using cell-based coupled map lattices.

We examine habitat size, shape, and arrangement effects on populations using a discrete reaction-diffusion model. Diffusion is modeled passively and applied to a cellular grid of territories forming a coupled map lattice. Dispersal mortality is proportional to the amount of nonhabitat and fully occupied habitat surrounding a given cell, with distance decay. After verifying that our model produces the results expected for single patches of uniform habitat, we investigate heterogeneous and fragmented model landscapes. In heterogeneous single-patch systems near critical patch size, populations approach Gaussian spatial distributions with total population constrained by the capacity of the most limiting cell. In fragmented habitat landscapes, threshold effects are more complex and parametrically sensitive. The results from our experiments suggest the following: the ability to achieve persistence in hyperdispersed patchy habitats by adding similarly fragmented patches requires meeting threshold reproduction rates; persistent metapopulations in which no local population is individually persistent appear when dispersal distances and reproduction rates are both high, but only within narrow parameter ranges that are close to extinction thresholds; successful use of stepping-stone patches to support metapopulation systems appears unlikely for passively diffusing species; elongated patches offer early colonization advantages, but blocky patches offer greater population resilience near extinction thresholds. A common theme running through our findings is that population viability estimates may depend on our ability to determine when population and habitat systems are approaching extinction threshold conditions.

Animals↗

PGFM response to exogenous oxytocin and determination of the half-life of oxytocin in nonpregnant mares.

We investigated the half-life of oxytocin in reproductively normal mares and the prostaglandin response after oxytocin administrations. Mares were given oxytocin, 10 or 25 iu, i.v., on the day of, or 2 days after, ovulation, and frequent jugular blood samples were collected for analysis of oxytocin and Prostaglandin F metabolite (PGFM) by RIA. Neither dose of oxytocin nor day of treatment affected the half-life of the exogenous oxytocin, which was determined to be 6.8 min. A significant increase in PGFM was observed within 6 min of oxytocin administration and peak values were observed within 10 min. PGFM response after oxytocin administration on the day of ovulation appeared elevated compared to the response 2 days after ovulation.

Animals↗

Influence of linoleic/linolenic acid ratio in the diet of periparturient cattle on plasma concentrations of PGF2 alpha metabolite and placental expulsion rate.

Forty-eight cows Holstein Friesian x Dutch Friesian (HF x DF) were randomly assigned to 2 groups fed 1 of 2 diets (isocaloric and isonitrogenous but different in linoleic/linolenic acid ratio) from 4 wk before expected parturition until 7 d after calving. Effects of the diet on plasma linoleic/linolenic acid ratio, plasma PGFM levels and placental explusion rate were studied. Dietary treatment resulted in significant differences in linoleic/linolenic acid ratio in blood plasma (1.00 +/- .22 vs 4.41 +/- .53). The placental expulsion rate was not significantly different between the 2 treatment groups. Plasma PGFM levels, as analyzed for 28 cows from 30 d before parturition until 1.5 d after parturition, were similar for the diets. Cows with a longer placental expulsion rate had lower PGFM levels at parturition (for instance, placental expulsion rate shorter (n = 11) and longer (n = 17) than 6 h, 1248 vs 2965 pg/ml, residual standard deviation 1185 pg/ml, P < 0.01). The results show that the dietary linoleic/linolenic acid ratio can influence the plasma linoleic/linolenic acid ratio without affecting the placental expulsion rate or plasma PGFM levels around parturition.

Animals↗

Absence of direct effects of GnRH on testicular steroid secretion in the ram.

Effects of GnRH, administered via the testicular artery, on testicular steroidogenesis were studied in rams during the non-breeding season. Concentrations of testosterone and 17-hydroxyprogesterone in testicular venous blood showed similar profiles which were identical for GnRH-treated (0.5 ng infused over 60 min or 25 ng injected) and control testes. Increases of testicular venous concentration of both hormones were only marginally reflected in peripheral venous concentrations. Peripheral administration of hCG (200 i.u., i.v.) stimulated testosterone secretion to a larger extent than 17-hydroxyprogesterone secretion in 10/11 rams, GnRH-treated and control testes showing identical responses. High testicular venous concentrations of both hormones after administration of GnRH were paralleled by increased concentrations of endogenous LH. These LH peaks were evoked by 25 ng GnRH in 7/8 rams. The observed effects of GnRH treatment on testicular steroid secretion thus cannot be considered to be the result of direct stimulation of steroidogenesis by GnRH.

Animals↗

Plasma concentrations of prolactin, progesterone, relaxin and oestradiol-17 beta in sows treated with progesterone, bromocriptine or indomethacin during late pregnancy.

Pregnant gilts (3/group) were given no treatment, 10 mg bromocriptine twice daily by mouth, from Day 111 of pregnancy to 1 day post partum, 25 mg progesterone s.c. at 6-h intervals from Days 111 to 116 inclusive or 400 mg indomethacin by mouth at 6-h intervals from Day 111 to 116 inclusive. Before spontaneous delivery maternal plasma prolactin and relaxin concentrations started to rise almost simultaneously between 58 and 47 h before the first piglet and both hormones reached peak values when the plasma progesterone concentration had started to decline rapidly (approximately 21-23 h). Suppression of prolactin levels by bromocriptine prevented the onset of lactation completely but had no obvious influence on changes of the other hormone concentrations and the course of parturition. Progesterone treatment delayed the onset of expulsion of the piglets but did not delay the simultaneous increase in prolactin and relaxin concentrations. These changes in hormone levels were prevented by indomethacin treatment but occurred essentially unchanged when the treatment was ended. The results support the concept that parturition in the pig is preceded by a biphasic increase of plasma prostaglandin levels.

Animals↗