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Biomedical subjects

S Mansfield

Publications and source records attributed to S Mansfield.

At least 19 recordsLinked to original sources
PubMed2006

Potential of selective insecticides for managing Uraba lugens (Lepidoptera: Nolidae) on Eucalypts.

The leaf skeletonizer Uraba lugens Walker (Lepidoptera: Nolidae), an Australian species, locally known as "gumleaf skeletonizer", is well established in New Zealand. This insect has the potential to become a serious pest of forestry and amenity eucalypts (Eucalyptus spp.) and is the focus of a long-term management program. The use of synthetic chemical or biological insecticides is one possible control method within an integrated control program. A series of dose-response trials were conducted using laboratory bioassays to test the efficacy of several insecticides against U. lugens: pyrethroids, spinosad, Bacillus thuringiensis kurstaki Berliner (Btk) and an insect growth regulator, Mimic. Pyrethroids and spinosad proved highly effective against U. lugens larvae, achieving 100% mortality after 3-6-d exposure. The performance of Btk was lower against gregarious skeletonizing larvae compared with solitary chewing larvae. When good coverage of the target foliage is achieved, >90% mortality is possible with Btk. Mimic performed poorly against U. lugens compared with other insecticides tested (<60% mortality). The Eucalyptus species on which larvae were feeding significantly altered insecticide efficacy. Treatments applied to Eucalyptus nitens (Deane & Maiden) Maiden had reduced efficacy compared with E. cinerea F. Muell. ex Benth. or E. fastigata Deane & Maiden. Cooler temperatures also reduced insecticide efficacy, presumably by decreasing movement and food consumption by U. lugens. Recommendations on spray applications to control U. lugens in New Zealand are given.

Animals↗
PubMed1993

Neck sprains after road traffic accidents: a modern epidemic.

This study was carried out to determine the incidence of soft tissue injuries of the cervical spine after road traffic accidents and to assess whether the incidence had changed with time. The results show that there has been a progressive increase since 1982 in the number of patients seen in accident and emergency departments with a neck sprain after road traffic accidents. The results suggest that the increase is not necessarily due to the introduction of seat belts, but that the relentless increasing epidemic may be due to other factors.

Accidents, Traffic↗
PubMed1991

Opioid binding in the rostral hypothalamus is reduced following lesion of the ventral noradrenergic tract in female rats.

Experiments were undertaken to establish whether opioid receptors exert a direct presynaptic influence on noradrenergic (NA) terminals in the preoptic/anterior hypothalamus (PO/AH) of the female rat. Thus, opioid binding studies were performed in rats with lesions of the ventral NA tract (VNAT; the main NA projection to the hypothalamus) to assess whether a loss of NA terminals may also result in a decrease in opioid binding in the PO/AH. In the first experiment, unilateral electrolytic lesions of the VNAT caused a significant reduction in both the NA content and specific [3H]-diprenorphine binding to membrane homogenates in the ipsilateral PO/AH. In the second experiment bilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the VNAT caused a significant reduction in NA levels in the PO/AH as well as significant decreases in the density of [3H]-diprenorphine binding to tissue sections of the PO/AH when compared to control animals. These results strongly suggest that the NA input to the PO/AH is regulated by endogenous opioid peptides, and provide an anatomical substrate to explain opioid-NA interactions in the control of gonadotrophin releasing hormone (GnRH) and gonadotrophin secretion.

Animals↗
PubMed1990

Facilitating care of patients with HIV infection by hospital and primary care teams.

To complement the role of primary care teams working with patients with HIV disease and AIDS within greater London and to ease the load on the special hospital units a home support team was developed. It comprises six specialist nurses, a general practitioner trained medical officer, and a receptionist and is funded from regional and district sources and charities. A nurse is available for out of hours and emergency weekend calls, with support from the patient's general practitioner or the attached medical officer. During the first 18 months 249 patients were seen; the mean duration of care was five months. Nearly a third (18/50, 30%) of patients who were terminally ill died at home. The team's activities included practical nursing care, emotional support for carers and patients, and advice and guidance to primary care teams. Problems in providing care in patients' homes included issues relating to confidentiality and 24 hour cover. With the increasing incidence of HIV infection the home support team may be a useful model for care of large numbers of patients with symptomatic HIV disease, especially in large urban areas.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Opioid peptides inhibit noradrenergic transmission in the preoptic area to block LH secretion: evidence from neonatally androgenised rats.

A series of experiments are described which show (a) that the release of noradrenaline in the preoptic area of rats is regulated by a presynaptic opioid receptor and, (b) that changes in the opioid control of preoptic noradrenaline release are associated with the anovulatory condition found in adult female rats which have been exposed to androgen neonatally. The experiments support the hypothesis that opioid-noradrenergic interaction in the preoptic area is an important component in the neural mechanism regulating gonadotrophin secretion.

Action Potentials↗
PubMed1988

Hypothalamic opioid mechanisms controlling oxytocin neurones during parturition.

The influences of opioids on oxytocin secretion and parturition were investigated in the rat. Morphine, administered centrally or peripherally, severely delays the course of established parturition. This delay is accompanied by reduced plasma oxytocin levels and is overcome by treatment either with the opioid antagonist naloxone, or by infusion of oxytocin. An endogenous opioid regulatory mechanism inhibiting oxytocin secretion becomes activated immediately prior to and during parturition. This mechanism does not operate earlier in pregnancy or during normal lactation and is not seen in nonpregnant animals. Naloxone acutely speeds up the course of established parturition, an effect accompanied by greatly elevated plasma oxytocin levels. The mechanisms underlying opioid regulation of oxytocin neurones were investigated at two sites. Precipitated withdrawal from chronic morphine treatment causes hypersecretion of oxytocin. This response is mediated by greatly enhanced electrical activity in the perikarya of oxytocin neurones indicating the presence of opioid receptors on oxytocin neurones and/or on their afferent input. Opioid receptors are also present in the neurohypophysis where they exert direct and noradrenaline mediated effects on secretion from oxytocin terminals in vitro.

Animals↗
PubMed1988

Endogenous opioid actions and effects of environmental disturbance on parturition and oxytocin secretion in rats.

Blood samples were taken from conscious, chronically-catheterized rats during parturition for measurement of oxytocin by specific radioimmunoassay. After the birth of the 3rd pup, rats were allowed to remain in their nesting cage (undisturbed rats) or were transferred for 45 min to a glass bowl (disturbed rats); at the time of transfer, rats were given an i.v. injection of the opioid antagonist naloxone or saline vehicle. Subsequent parturition was prolonged in saline-treated disturbed rats, but not in naloxone-treated disturbed rats. Parturition was significantly hastened in naloxone-treated undisturbed rats. Naloxone injections were followed by a large rise in plasma oxytocin concentrations in disturbed and undisturbed rats. We conclude, from a statistical analysis of the relationship within experimental groups between plasma oxytocin concentration and speed of parturition, that the effects of disturbance and of naloxone upon parturition may be accounted for, at least in part, by their effects upon oxytocin release. However, the effects of disturbance on parturition may not be mediated entirely by activation of opioid pathways. Naloxone did not potentiate oxytocin release in non-pregnant rats, or on Day 1 post partum, but did potentiate oxytocin release on Day 22 of pregnancy even in rats before the onset of parturition. Endogenous opioid pathways regulating oxytocin release therefore appear to be active during late pregnancy and during parturition itself.

Animals↗
PubMed1987

Effect of neonatal testosterone upon opioid receptors and the content of beta-endorphin, neuropeptide Y and neurotensin in the medial preoptic and the mediobasal hypothalamic areas of the rat brain.

The content of beta-endorphin, neuropeptide Y and neurotensin-like immunoreactivity (beta-End, NPY and NT), and the total number of opioid binding sites, were measured in the medial preoptic area (MPOA) and mediobasal hypothalamus (MBH) of ovariectomized adult rats which were oestrogen-primed. The rats had been injected neonatally with either testosterone propionate (TP) or vehicle (oil). NPY content was found to be higher in the MPOA of animals which received TP, whereas no significant difference was observed in the MBH NPY content. However, the NT concentration in the MBH of TP-treated rats was almost twice the amount detected in oil-treated rats and with this peptide no significant changes were detected in the MPOA. Finally, beta-End and the total number of opioid binding sites were reduced in both the MPOA and MBH of the rats which were exposed to TP neonatally. Since exposure to testosterone neonatally masculinises the rat hypothalamus, to the extent that female rats cannot generate oestrogen-stimulated prolactin and luteinizing hormone surges, we suggest that the neurochemical changes reported in this paper reflect some aspects of this sexual differentiation of the rat hypothalamus.

Animals↗
PubMed1987

Neonatal testosterone modifies LH secretion in the adult female rat by altering the opioid-noradrenergic interaction in the medial preoptic area.

Noradrenergic-opioid interaction in the medial preoptic area (MPOA) was examined in ovariectomised adult rats which were oestrogen-treated and had been injected neonatally with either testosterone propionate (TP) or vehicle (oil). The first experiment involved electrical stimulation of the ventral noradrenergic tract (VNAT) in anaesthetised rats. Blood samples were collected before and after the stimulation to determine plasma levels of luteinising hormone (LH). Approximately half of the animals received naloxone i.v. 15 min before the onset of stimulation. In all groups, stimulation of VNAT elicited a significant increase in plasma LH concentration. However, pretreatment with naloxone in androgenised rats, but not in oil-treated animals, almost doubled the LH increment due to stimulation. Naloxone had no effect on plasma LH concentrations in unstimulated control rats. In the second experiment hypothalamic slices containing the MPOA were preincubated with [3H]noradrenaline [( 3H]NA) and then subjected to electrical field stimulation under the conditions of (a) no drug added and (b, c) morphine superfusion without and with naloxone. The opioid agonist morphine significantly reduced the net release of [3H]NA in normal and TP-treated female rats. Addition of equimolar naloxone reversed this effect in normal females, whereas in the androgenised group it not only reversed this effect but elicited a significant increase in [3H]NA release. From these data we conclude that (1) neonatal testosterone treatment alters noradrenergic-opioid interaction regulating LH secretion in adult females and (2) the site of this change may be the presynaptic opioid input to the noradrenergic terminals in the MPOA.

Animals↗
PubMed1987

Stress-induced disruption of parturition in the rat may be mediated by endogenous opioids.

Plasma samples were obtained before and during parturition from conscious rats implanted chronically with a jugular cannula. Rats were either allowed to remain in their nesting cage throughout parturition, or were moved immediately following the birth of the second or third pup into an empty glass chamber. The time-course of parturition was prolonged for mother rats which were moved in mid-parturition to this unfamiliar environment. However, in rats given an i.v. injection of the opioid antagonist naloxone at the time of transfer, parturition followed a normal time-course, and plasma oxytocin levels were significantly higher than in animals injected with saline. Thus our hypothesis is that stress activates opioid pathways which delay parturition by inhibiting oxytocin release. Opioid-mediated mechanisms may similarly be responsible for some problems in human parturition.

Animals↗
PubMed1986

Neonatal testosterone potentiates stimulated prolactin secretion in adult oestrogen-primed rats.

Blood samples were collected from oestrogen-primed gonadectomized adult rats before and after electrical stimulation of the preoptic part of the hypothalamus. Six groups of rats were used for the experiments. These were (a) males castrated on the first day of life, (b) males castrated after puberty, (c) females ovariectomized after puberty and (d), (e) and (f) females given testosterone propionate at birth (1.25, 0.125 and 0.0125 mg/rat respectively). Neonatal exposure of the female rats to testosterone caused a dose-dependent increase in the amounts of prolactin released to levels significantly (P less than 0.01) higher than those observed in male animals and in untreated females. The results indicate that although neonatal testosterone inhibits oestrogen-stimulated prolactin secretion in adult rats, the neuroendocrine apparatus controlling secretion of the hormone is capable of being activated to greater effect after exposure to androgens at the time of birth.

Animals↗
PubMed1985

Electrical stimulation of the ventral noradrenergic tract (VNAT) releases hypothalamic noradrenaline and stimulates prolactin secretion in ovariectomized female rats treated with oestrogen.

Electrical stimulation of the ventral noradrenergic tract (VNAT) caused a significant fall in the hypothalamic content of noradrenaline in ovariectomized female rats which had been treated with oestrogen. No similar effect was observed in the cerebral cortex, which implies that the stimulation did not affect the dorsal noradrenergic tract. In parallel experiments with groups of similarly treated rats, VNAT stimulation was found to increase release of prolactin from the pituitary gland, and this increase was significantly enhanced in animals which had been stressed by fasting for 3 days.

Animals↗
PubMed1985

Fasting impairs LH secretion in female rats by activating an inhibitory opioid pathway.

Two experiments were undertaken to investigate the way that fasting impairs LH secretion and to assess whether endogenous opioid mechanisms might be responsible for the impairment. In the first experiment, pulsatile LH secretion was measured in a total of 51 chronically ovariectomized female rats. Initially 29 rats were subjected to food withdrawal for 24, 48, 72 or 120 h before the experiment. When compared with data collected from eight unfasted control rats, the 120-h fast was found to reduce significantly the mean peak and trough values of the LH pulses measured. However, in a subsequent study, the inhibition of pulsatile LH secretion by a 120-h fast was prevented in a group of eight rats given the opioid antagonist naloxone hydrochloride before the start of the blood-sampling period. Naloxone was without effect on pulsatile LH secretion in eight unfasted control rats. In the second experiment, plasma LH concentrations were measured before and after unilateral electrical stimulation of the ventral noradrenergic tract (VNAT) in ovariectomized female rats pretreated with oestradiol benzoate. In 17 rats VNAT stimulation caused a significant rise in plasma LH, but after a 72-h fast this rise was significantly less than in unfasted control rats. However, pretreatment of fasted rats with naloxone (n = 9) significantly enhanced the VNAT-stimulated release of LH to the control values. Naloxone did not potentiate VNAT-stimulated LH release in unfasted animals (n = 6) or LH release in control unstimulated rats (n = 12). The experiments indicate that both pulsatile LH secretion, and LH release caused by VNAT stimulation, are impaired by an acute fast.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗