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Biomedical subjects

A Cockburn

Publications and source records attributed to A Cockburn.

At least 19 recordsLinked to original sources
PubMed2006

Cryptic gentes revealed in pallid cuckoos Cuculus pallidus using reflectance spectrophotometry.

Many cuckoo species lay eggs that match those of their hosts, which can significantly reduce rejection of their eggs by the host species. However, egg mimicry is problematic for generalist cuckoos that parasitize several host species with different egg types. Some generalist cuckoos have overcome this problem by evolving several host-specific races (gentes), each with its own, host-specific egg type. It is unknown how generalist cuckoos lacking gentes are able to avoid egg rejection by hosts. Here we use reflectance spectrophotometry (300-700 nm) on museum egg collections to test for host-specific egg types in an Australian generalist cuckoo reported to have a single egg type. We show that the colour of pallid cuckoo (Cuculus pallidus) eggs differed between four host species, and that their eggs closely mimicked the eggs of the host they parasitized. These results reveal that pallid cuckoos have host-specific egg types that have not been detected by human observation, and indicate that gentes could be more common than previously realized.

Adaptation, Physiological↗
PubMed2005

Dispersal, philopatry, and infidelity: dissecting local genetic structure in superb fairy-wrens (Malurus cyaneus).

Dispersal influences evolution, demography, and social characteristics but is generally difficult to study. Here we combine long-term demographic data from an intensively studied population of superb fairy-wrens (Malurus cyaneus) and multivariate spatial autocorrelation analyses of microsatellite genotypes to describe dispersal behavior in this species. The demographic data revealed: (1) sex-biased dispersal: almost all individuals that dispersed into the study area over an eight-year period were female (93%; n = 153); (2) high rates of extragroup infidelity (66% of offspring), which also facilitated local gene dispersal; and (3) skewed lifetime reproductive success in both males and females. These data led to three expectations concerning the patterns of fine-scale genetic structure: (1) little or no spatial genetic autocorrelation among females, (2) positive spatial genetic autocorrelation among males, and (3) a heterogeneous genetic landscape. Global autocorrelation analysis of the genotypes present in the study population confirmed the first two expectations. A novel two-dimensional local autocorrelation analysis confirmed the third and provided new insight into the patterns of genetic structure across the two-dimensional landscape. We highlight the potential of autocorrelation analysis to infer evolutionary processes but also emphasize that genetic patterns in space cannot be fully understood without an appropriate and intensive sampling regime and detailed knowledge of the individuals genotyped.

Animals↗
PubMed2004

Assessment of the safety of foods derived from genetically modified (GM) crops.

This paper provides guidance on how to assess the safety of foods derived from genetically modified crops (GM crops); it summarises conclusions and recommendations of Working Group 1 of the ENTRANSFOOD project. The paper provides an approach for adapting the test strategy to the characteristics of the modified crop and the introduced trait, and assessing potential unintended effects from the genetic modification. The proposed approach to safety assessment starts with the comparison of the new GM crop with a traditional counterpart that is generally accepted as safe based on a history of human food use (the concept of substantial equivalence). This case-focused approach ensures that foods derived from GM crops that have passed this extensive test-regime are as safe and nutritious as currently consumed plant-derived foods. The approach is suitable for current and future GM crops with more complex modifications. First, the paper reviews test methods developed for the risk assessment of chemicals, including food additives and pesticides, discussing which of these methods are suitable for the assessment of recombinant proteins and whole foods. Second, the paper presents a systematic approach to combine test methods for the safety assessment of foods derived from a specific GM crop. Third, the paper provides an overview on developments in this area that may prove of use in the safety assessment of GM crops, and recommendations for research priorities. It is concluded that the combination of existing test methods provides a sound test-regime to assess the safety of GM crops. Advances in our understanding of molecular biology, biochemistry, and nutrition may in future allow further improvement of test methods that will over time render the safety assessment of foods even more effective and informative.

Animals↗
PubMed2001

Semelparity in a large marsupial.

Complete mortality of males after mating is known in several small dasyurid and didelphid species (up to 300g) and has previously been suggested to be a consequence of their small size and their inability to sequester sufficient fat reserves for an intense rut in the winter. Males of these species use increased corticosteroid levels to allow protein catabolism, enabling them to support their mating effort with other body reserves. However, increased corticosteroid levels have negative consequences such as anaemia, gastrointestinal ulceration, immune suppression and disease. The Australian dasyurid Dasyurus hallucatus shows complete male die off after mating in tropical savannah, yet males of this species may weigh as much as 1120 g and continue to eat during the rut. Die off in D. hallucatus shows many similarities to that in the smaller species including weight loss, fur loss, parasite infestation, increased testosterone levels and anaemia. However, in contrast to smaller species, there is no evidence of elevated corticosteroid levels or gastrointestinal ulceration. Consequently, the phenomenon of male die off after mating lacks a universal explanation.

Animals↗
PubMed2000

Pre-dawn infidelity: females control extra-pair mating in superb fairy-wrens.

Despite great interest in the use of extra-pair mating as a tool for examining female choice and intersexual selection, the underlying assumption of female control has proved difficult to verify empirically. We combined microsatellite genotyping and radiotelemetry of fertile females in order to investigate mate choice in superb fairy-wrens Malurus cyaneus, the bird with the highest known rate of extra-pair fertilization. All five females radio tracked during the peak of fertility, two to four days before the first egg is laid, undertook pre-dawn forays. All extra-pair young produced by the female were sired by a male visited during their forays, indicating that females control extra-pair fertilizations. In a larger sample of paternity data, some broods were sired by two extra-group males. In virtually all the cases the territory of the two sires were on an identical linear trajectory from the female's territory. This again suggests that extra-group paternity in superb fairy-wrens is directly linked to female extra-territorial forays. In other species mixed paternity has been taken to indicate that females attempt to insure against infertile pairings or try to maximize the genetic diversity of their brood. However, in fairy-wrens the likelihood of multiple extra-group paternity increased greatly as females traversed more territories in order to mate, perhaps suggesting that females which foray further are more likely to have difficulties locating the preferred male.

Animals↗
PubMed1999

The politics of "natural" disaster: who made Mitch so bad?

The devastation in Central America following the 1998 hurricane (Hurricane Mitch) resulted more from economic and political policies than from "natural" disaster. Over the last 30 or 40 years, huge numbers of poor people in these countries have been forced off good, stable agricultural land onto degraded hillsides and into shanty towns constructed on floodplains--areas known to pose serious hazards of flooding and mudslides. This, together with the failure of impoverished countries to anticipate disaster through mass evacuations or to respond effectively to the hurricane's widespread damage--ensured the loss of thousands of lives.

Central America↗
PubMed1997

Effect of piperonyl butoxide on cell replication and xenobiotic metabolism in the livers of CD-1 mice and F344 rats.

Male CD- 1 mice were fed diets containing 0 (control), 10, 30, 100, and 300 mg/kg/day piperonyl butoxide (PBO) and 0.05% sodium phenobarbital (NaPB) and male F344 rats were fed diets containing 0 (control), 100, 550, 1050, and 1850 mg/kg/day PBO and 0.5% NaPB for periods of 7 and 42 days. In both species PBO and NaPB increased relative liver weight and whereas PBO produced a midzonal (mouse) or periportal/midzonal (rat) hypertrophy, NaPB produced a centrilobular hypertrophy. In the rat, individual cell necrosis was also observed at 42 days after high doses of PBO. Replicative DNA synthesis, assessed as the hepatocyte labeling index following implantation of 7-day osmotic pumps containing 5-bromo-2'-deoxyuridine during Study Days 0-7 and 35-42, was increased in mice given 300 mg/kg/day PBO and NaPB for 7 days and in rats given 550 and 1050 mg/kg/day PBO and NaPB for 7 days and 1050 mg/kg/day PBO for 42 days. While PBO had no effect on body weights in mice, the body weights of rats given 550, 1050, and 1850 mg/kg/day PBO for 42 days were reduced to 92, 89, and 70% of control, respectively. PBO induced microsomal cytochrome P450 content and mixed function oxidase activities in the mouse and rat, although the effects were less marked than those produced by NaPB. In summary, this data demonstrates that PBO can produce liver enlargement in the mouse and the rat which is associated with induction of xenobiotic metabolism, hypertrophy, and hyperplasia. The hepatic effects of PBO in the mouse were similar to but less marked than those produced by NaPB. In the rat high doses of PBO were hepatotoxic and resulted in a marked reduction in body weight. Thus while the reported formation of eosinophilic nodules in mouse liver by PBO may occur by a mechanism(s) similar to that of NaPB and other nongenotoxic enzyme inducers, the reported tumor formation in rats at greater than the maximum tolerated dose is most likely associated with marked enzyme induction in conjunction with a regenerative hyperplasia resulting from PBO-induced hepatotoxicity.

Administration, Oral↗
PubMed1995

Glucocorticoid amelioration of nephrotoxicity: a study of cephaloridine-methylprednisolone interaction in the rat.

Groups of ten male rats were treated with a high challenge dose of cephaloridine (CPH, 3750 mg kg-1), with methylprednisolone (MP, 100 mg kg-1) or with cephaloridine and methylprednisolone (CPH + MP) by single subcutaneous injection. A control group received the injection vehicles only. Urine was collected from all animals daily over 18-h collection periods, up to 96 h after treatment. Blood was collected at 24, 48, 72 and 96 h after treatment. At necropsy, kidneys were weighed, processed and examined histopathologically. Results show that methylprednisolone significantly ameliorated the nephrotoxicity of the challenge dose of cephaloridine. CPH-only treated rats had severe toxic nephrosis characterised by acute tubular necrosis, and elevated blood urea and creatinine. By contrast, the majority of CPH + MP treated rats had only a slight or moderate toxic nephrosis, and had lower blood urea and creatinine levels compared with rats treated with CPH only, indicating preservation of kidney function. Interestingly, rats treated with CPH + MP had higher urinary enzymes (alkaline phosphatase, lactate dehydrogenase, gamma glutamyltransferase and N-acetyl-beta-glucosaminidase) as well as protein and glucose, compared with rats treated with CPH only. This is taken to indicate that rats treated with CPH only had such marked kidney damage and necrosis that the population of cells able to produce these marker enzymes was significantly and rapidly depleted, but the protection afforded by methylprednisolone allowed CPH + MP treated rats to sustain urinary enzyme output. Effects on urinary glucose and other parameters such as body weight and kidney weight demonstrate interactions between glucocorticoid pharmacology and cephaloridine nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effect of urinary alkalinisation and acidification on the tissue distribution of hexachlorophene in rats.

1. Urinary alkalinisation may be helpful in treating acute poisoning with uncouplers of oxidative phosphorylation containing a phenolic hydroxyl (pKa 4-6) or other acidic moiety. 2. We studied the effects of urine alkalinisation and acidification on the tissue distribution of hexachlorophene (HCP, pKa 5.7) in male Sprague Dawley rats (10 rats/group). 3. Ammonium chloride (10 mL kg-1, 2% m/v) or sodium bicarbonate (10 mL kg-1, 2% m/v) were administered by gavage on three occasions over 24 h, prior to a single gavage dose of HCP (180 mg kg-1). Controls received aqueous sodium chloride (10 mL kg-1, 0.9% m/v) followed by either HCP (180 mg kg-1) or vehicle alone. 4. Urine pH, body mass and body temperature were monitored during the study and, at the conclusion of the experiment (12 h post-HCP dose), organ mass (liver, kidney, brain), and plasma, urine and tissue HCP concentrations were measured. 5. No clinical features of toxicity were observed in any group. However, sodium bicarbonate significantly reduced median HCP in liver--median plasma and kidney HCP concentrations were also reduced but not significantly. Conversely, ammonium chloride significantly increased median HCP concentrations in liver and kidney--median plasma HCP was also increased but not significantly. 6. The results provide some support for the hypothesis that blood pH influences the tissue distribution of uncouplers of oxidative phosphorylation containing an acidic moiety. Urinary alkalinisation may be useful in treating acute poisoning with these compounds.

Ammonium Chloride↗
PubMed1994

Sequence analysis of the ribosomal DNA internal transcribed spacer 2 from populations of Anopheles nuneztovari (Diptera: Culicidae).

Sequence variation of the ribosomal DNA internal transcribed spacer 2 (ITS2) was examined for populations of the malaria vector Anopheles nuneztovari collected in Colombia, Venezuela, Bolivia, Suriname, and Brazil. Mosquitoes from Colombia and Venezuela had identical ITS2 sequences and were distinguished from sequences in other populations by three insertion/deletion events (indels) and by one transversion. The length of the ITS2 was 363-369 bp, and it had a G+C content of 55.3%-55.7%. Variation in the length of the ITS2 between and within populations was due to indels in simple repeats. ITS2 consensus sequences were similar or identical for samples from the following three groups: (1) Colombia, Bolivia, and Venezuela; (2) Suriname and northern Brazil; and (3) eastern and central Brazil. The presence of two different consensus sequences from a single location near Manaus, Brazil, suggests that populations from eastern Brazil and those from Suriname converge in this region of the Amazon Basin. These data show that putative cryptic species of An. nuneztovari are distinguished by very minor differences in DNA sequence of the ITS2 region.

Animals↗
PubMed1994

A critical review of the optimum duration of chronic rodent testing for the determination of non-tumourigenic toxic potential: a report by the BTS Working Party on Duration of Toxicity Testing.

This review indicates that for the detection of non-neoplastic toxic effects: 1. Four decades of accumulated literature provide no lead as to the optimum duration of repeat dose toxicity testing required for all classes of chemicals, although 6 months repeated administration appears adequate for pharmaceuticals. 2. Three month studies predicted the 2 year outcome for 70% of the compounds evaluated in this pilot study using data published by the US National Toxicology Program. 3. In spite of the limitations of this pilot study, this finding is considered encouraging as it is close to that generated previously on more detailed confidential pharmaceutical data. This suggests that the exercise should now be expanded using confidential surveys of industrial data to determine the concordance resulting from the evaluation of a larger group of chemicals.

Animals↗
PubMed1994

Glucocorticosteroid interactions with natural toxins: a mini review.

A growing area of research in pharmacology and toxicology is concerned with the role of adrenal glucocorticosteroids (predominantly corticosterone in rats and mice, and cortisol in humans) in modulating toxicological responses. These steroids are secreted from the adrenal cortex, and in laboratory rodents secretion occurs particularly in response to stressful environmental change or noxious challenge, which can include a toxic insult. Glucocorticoids have profound biochemical effects in diverse tissues (e.g., inhibition of DNA and RNA synthesis; effects on carbohydrate metabolism, protein catabolism, and immunosuppression, and anti-inflammatory effects). Given this range of pharmacological actions of glucocorticoids, effects on the response and tolerance to a toxic insult can be hypothesised. Indeed, it is now becoming clear that the toxicological response to a toxin can be modulated by pretreatment with, or coadministration of, natural glucocorticosteroids or their synthetic analogues. As achieving the maximum tolerated dose (MTD) in an experimental animal, whether via a natural toxin or a synthetic chemical, can be stressful, the implications of these findings are far reaching. This review is intended to illustrate the principle that the toxicological responses to natural toxins (e.g., kainic acid, aflatoxin B1, trichothecenes) can be modulated by corticosterone and other natural and synthetic glucocorticosteroids. Particular emphasis is given to neurotoxicity and hepatotoxicity in laboratory rodent models, but nephrotoxicity and cardiotoxicity, of which there are fewer studies, are also covered. Glucocorticoids can both enhance toxicity or protect against toxicity, and the direction of the effect depends on the target organ, the particular steroid, the properties of the toxin, and the temporal relationship of the coadministration regime.

Animals↗
PubMed1992

Corticosterone does not cause testicular toxicopathology in the rat: relevance to methylxanthines, ACTH and stress.

1. Methylxanthines, ACTH and stress are well known to produce testicular pathology (e.g. seminiferous tubule atrophy). Methylxanthines, ACTH and stress alter hormone secretion, particularly from the pituitary-adrenocortical system. Consequently, it has recently been suggested that there may be a causal relationship between changes in endogenous physiological adrenocortical secretions, particularly corticosterone, and testicular pathology. 2. This study tested the hypothesis that corticosterone mediates the testicular effects of both methylxanthine treatment and stress. Corticosterone was administered daily by subcutaneous injection to groups of 10 male rats at dose levels of 2 or 20 mg kg-1 in propylene glycol (1 ml kg-1) for 1 month (the shortest duration of methylxanthine or ACTH exposure known to produce testicular pathology). The highest dose of corticosterone resulted in plasma concentrations that closely matched values resulting from stress (200-700 ng ml-1) compared with controls (< 25 ng ml-1). 3. The highest dose of corticosterone caused reduced body weight gain, lower thymus, adrenal, seminal vesicle and prostate weights, but did not induce any testicular pathology. 4. That a high, but physiologically relevant, dose of corticosterone did not cause testicular pathology in this experiment excludes this steroid in the direct aetiology of methylxanthine, ACTH and stress-induced testicular pathology. Other steroids secreted from the adrenal, in combination with corticosterone, may be involved.

Adrenocorticotropic Hormone↗
PubMed1987

The preclinical toxicology of anisoylated plasminogen streptokinase activator complex.

The preclinical toxicological evaluation of anisoylated plasminogen streptokinase activator complex (APSAC) was designed with specific regard to the potential for immunogenic effects in animals arising from the high molecular weight of the complex. Animals were treated with multiples of the human dose by use of a dose regimen spanning that proposed clinically and in conventional repeat dose toxicity studies employing the maximum practicable dose level and duration. Few adverse effects were noted, despite the large doses administered with respect to the clinical dose. The thrombolytic activity of APSAC resulted in pronounced acute effects on blood coagulation times and fibrinogen levels in rats and dogs but there was little evidence of clinically relevant systemic toxicity in either species. Evidence of a possible effect on the liver was seen 24 hours after single doses much higher than the proposed human dose in the rat (40-fold higher) and dog (9-fold higher). No hepatic effects were apparent following repeated administration. The main adverse effect was focal acute myocarditis, which was seen only in rats of the Sprague Dawley strain. Administration of human plasminogen alone or in combination with streptokinase also produced this lesion, suggesting that plasminogen may play a central role in its appearance. Experiments in anaesthetised dogs showed APSAC to be devoid of undesirable haemodynamic effects. An intravenous acute toxicity study in rats with p-anisic acid, which is released on deacylation of APSAC, showed the levels of p-anisic acid which occur in humans to be of no toxicological significance. Finally, in a series of tests designed to investigate potential genetic toxicity, no mutagenic activity was detected.

Animals↗