Search PubMed⌕ Search

Biomedical subjects

S Barron

Publications and source records attributed to S Barron.

At least 19 recordsLinked to original sources
PubMed2006

Adult persons with intellectual disabilities on the island of Ireland.

BACKGROUND: Information on the numbers of adult persons (aged 20 years and over) with intellectual disability (ID) is rarely collated at a national level. This is an impediment to service planning especially for a changing population. METHODS: A database of all persons in receipt of ID services has been operating in the Republic of Ireland since 1995. In Northern Ireland, regional databases can be used to provide similar information. RESULTS: A total of 25,134 persons were known to services in 2002; an overall prevalence for the island of 6.34 per 1,000. However this rate varied for different age groupings and across the two parts of the island. General population characteristics, as well as service factors, appear to account for this. Significantly more people lived with family carers in Northern Ireland. By 2021, it was estimated that the population would increase by over 20% with around one-third of persons aged over 50 years. CONCLUSIONS: These data illustrate the variations that exist in the numbers of adult persons with ID known to services across and within regions of a country. Hence caution must be exercised in extrapolating prevalence rates derived in one area to another. The availability of comparative national data highlights issues around the equitable funding and delivery of services.

Adult↗
PubMed2004

A preliminary audit investigating remedy reactions including adverse events in routine homeopathic practice.

UNLABELLED: Homeopathic medicines are regarded as safe but practitioners report several types of healing or remedy reactions including aggravations, new symptoms and recurrence of old symptoms, some of which could be regarded as side effects or unwanted effects. Some remedy reactions may be regarded as adverse events. AUDIT QUESTIONS: Do such reactions occur within our unit, and if so, how frequently? Do patients regard these events as "adverse"? METHODS: The audit was carried out in the Bristol Homeopathic Hospital Outpatient Department. All patients were given a questionnaire to complete when at their first follow-up consultation approx 6-10 weeks after their first appointment. One hundred and sixteen patients were sampled over a 2-month period. RESULTS: Reactions were frequent: 28 out of the 116 (24%) patients, experienced an aggravation. Thirteen patients (11%) reported an adverse event even though 5 of those were patients who also reported an aggravation followed by an overall improvement of their symptoms. Thirty-one patients described new symptoms (27%) and 21(18%), a return of old symptoms. Those experiencing the latter appeared to have better outcomes. CONCLUSIONS: Remedy reactions are common in clinical practice; some patients experience them as adverse events. Systematically recording side effects would facilitate our understanding of these reactions and would enable standards to be set for audit of information and patient care.

Adult↗
PubMed2002

Oligodendroglial expression of Edg-2 receptor: developmental analysis and pharmacological responses to lysophosphatidic acid.

Edg-2 is a member of the G-protein-coupled seven-transmembrane receptor family recently identified in oligodendrocytes. Here we show that both in vitro and in vivo, Edg-2 transcripts are not detected during early stages of oligodendroglial development, but are expressed only in mature oligodendrocytes, shortly before the onset of myelination. Lysophosphatidic acid (LPA) has been reported to be a ligand of Edg-2 receptor in different cell types. However, in oligodendroglial cultures, LPA had no effect on survival, maturation, or cytoskeleton organization. In myelinating oligodendrocyte-neuron cocultures, LPA did not influence myelinogenesis. In addition, LPA failed to induce Ca2+ mobilization and had no effect on forskolin-induced cAMP accumulation. Phosphorylation of the ERK1/ERK2 MAP kinases was the only response elicited by LPA in oligodendrocytes. Therefore, in contrast to other cell types, in which LPA exerts pleiotropic effects, Edg-2-positive postmitotic oligodendrocytes display a restricted responsiveness to LPA.

Animals↗
PubMed2001

Role of polyamines and NMDA receptors in ethanol dependence and withdrawal.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chair was John M. Littleton. The presentations were (1) Examination of ethanol spermine and acamprosate actions on native and recombinant NMDA receptors, by David Lovinger; (2) Ethanol inhibition of NMDA neurotoxicity on the polyamine site in cerebellar granule cells, by Sture Liljequist; (3) Alterations in expression of NMDA receptor subunits during ethanol exposure and withdrawal, by Raj Ticku; (4) Alterations in polyamine synthesis and release as a potential mechanism for ethanol dependence and withdrawal, by Izuru Matsumoto; (5) The role of polyamines in neurotoxicity induced by alcohol withdrawal in vitro, by John Littleton; and (6) Agmatine reduces some of the effects of "third trimester" alcohol exposure using a rodent model, by Susan Barron.

Alcoholism↗
PubMed2000

Neural grafting reverses prenatal drug-induced alterations in hippocampal PKC and related behavioral deficits.

Administration of heroin or phenobarbital to pregnant mice evokes neurochemical and behavioral deficits consequent to disruption of septohippocampal cholinergic innervation. The present study evaluates the relationship between the drug-induced biochemical changes and the behavioral deficits, applying two different approaches: neural grafting and within-individual correlations of biochemistry and behavior. Mice were exposed transplacentally to phenobarbital or heroin on gestational days 9-18 and tested in adulthood. Drug-exposed mice displayed impaired radial arm maze performance, increases in presynaptic choline transporter sites (monitored with [(3)H]hemicholinium-3 binding), upregulation of membrane-associated protein kinase C (PKC) activity, and desensitization of the PKC response to a cholinergic agonist, carbachol. Grafting of cholinergic cells to the impaired hippocampus reversed the behavioral deficits nearly completely and restored basal PKC activity and the PKC response to carbachol to normal; the drug effects on hemicholinium-3 binding were also slightly obtunded by neural grafting, but nevertheless remained significantly elevated. There were significant correlations between the performance in the eight-arm maze and both basal PKC activity and PKC desensitization, and to a lesser extent, between behavioral performance and hemicholinium-3 binding. Taken together, these findings indicate an inextricable link between the biochemical effects of prenatal drug exposure on the PKC signaling cascade and adverse behavioral outcomes. The ability of neural grafting to reverse both the drug-induced changes in PKC and behaviors linked to septohippocampal cholinergic function suggest a mechanistic link between this signaling pathway and neurobehavioral teratology caused by heroin or phenobarbital.

Animals↗
PubMed2000

Effects of chronic ethanol administration on expression of BDNF and trkB mRNAs in rat hippocampus after experimental brain injury.

Previous evidence indicates that both chronic alcohol treatment and traumatic brain injury modulate expression of certain neurotrophins and neurotrophin receptors in cortical tissue. However, the combined effects of chronic alcohol and brain trauma on expression of neurotrophins and their receptors have not been investigated. In the present study, we examined the effects of 6 weeks of chronic ethanol administration on lateral fluid percussion (FP) brain injury-induced alterations in expression of mRNAs for the neurotrophin brain-derived neurotrophic factor (BDNF) and its high affinity receptor, trkB, in rat hippocampus. In both the control- (pair-fed isocaloric sucrose) diet and the chronic ethanol-diet groups, unilateral FP brain injury induced a bilateral increase in levels of both BDNF and trkB mRNAs in the dentate gyrus granule cell layer, and of BDNF mRNA in hippocampal region CA3. However, no significant differences in expression were found between the control-diet and ethanol-diet groups, in either the sham-injured or FP-injured animals. These findings suggest that 6 weeks of chronic ethanol administration does not alter the plasticity of hippocampal BDNF/trkB expression in response to experimental brain injury.

Alcohol-Related Disorders↗
PubMed2000

The effects of neonatal ethanol and/or cocaine exposure on isolation-induced ultrasonic vocalizations.

Isolation-induced ultrasonic vocalizations (USVs) are emitted by young rat pups when isolated from their dam and conspecifics. These USVs play an important role in maternal/offspring interactions, and have been used as an indicator of response to stress and isolation. This study examined the effects of neonatal ethanol and/or cocaine exposure on USVs in neonatal rats. The neonatal exposure paradigm serves as a model for the "human third trimester of pregnancy" in terms of CNS development. There were five treatment groups including an artificially reared (AR) ethanol-exposed group (6 g/kg/day), an AR cocaine-exposed group (60 mg/kg/day), an AR ethanol- and cocaine-exposed group (6 g/kg/day+60 mg/kg/day), an AR isocaloric control, and a normally reared control. Both groups that received ethanol took longer to vocalize, and displayed fewer vocalizations than non-ethanol-exposed pups when tested on clean bedding (Experiment 1) or on chips from the nest of a lactating dam (Experiment 2). These results suggest that neonatal ethanol exposure alters the pup's immediate response to isolation. This could have direct effects on maternal/infant interactions, and might help explain some of the long-term effects of ethanol exposure on social behaviors.

Animals↗
PubMed2000

Three months of chronic ethanol administration and the behavioral outcome of rats after lateral fluid percussion brain injury.

This study examined the effects of 3 months of chronic ethanol administration (CEAn) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were given either an ethanol liquid diet (ethanol diet groups) or a pair-fed isocaloric sucrose control diet (control diet groups) for 3 months. Then, rats from both diet groups were subjected to either lateral FP brain injury of moderate severity (1.8 atm) or to sham operation. Postinjury behavioral measurements revealed that brain injury caused significant spatial learning disability in both diet groups. There were no significant differences in spatial learning ability in the sham or brain-injured animals between the control and ethanol diets. However, a trend towards cognitive impairment in the sham animals and a trend towards reduced deficits in the brain-injured animals were observed in the ethanol diet group. Histologic analysis of injured animals from both diet groups revealed similar extents of ipsilateral cortical and hippocampal CA3 damage. These results, in general, suggest that 3 months of CEAn does not significantly alter the behavioral and morphologic outcome of experimental brain injury.

Alcohol Drinking↗
PubMed1999

Edg-2 in myelin-forming cells: isoforms, genomic mapping, and exclusion in Charcot-Marie-Tooth disease.

Edg-2 is an heptahelical receptor whose spatio-temporal distribution during rat brain development is consistent with a role in the control of myelination. We have now identified two splice variants of Edg-2 mRNA in rat brain that encode two receptor isoforms differing by a stretch of 18 amino acids in the NH2-terminal extracellular tail of the receptor. Prenatally (i.e., before oligodendrocyte myelination), the two variants detected by selective in situ hybridization are equally abundant, vary in parallel, and remain restricted to proliferative zones in the brain. Postnatally, the long isoform becomes predominant in myelinating structures, where its abundance increases sharply during the period of myelination. In the adult human brain, only the long variant was detected, while in situ hybridization showed it selectively expressed in the white matter and in clusters of cells showing features of oligodendrocytes of the temporal cerebral cortex. Consequently, the human Edg-2 gene was studied to assess its possible contribution in inherited neuropathies. The coding sequence was found to be contained in three exons and to map to chromosome 9q31.3-32 by using radiation hybrid panel and Yeast-Artificial Chromosomes. Two intragenic bi-allelic polymorphisms and a rare mutation were identified. As a first application to molecular genetic studies, they were used to exclude the Edg-2 gene in six families with phenotype of demyelinating Charcot-Marie-Tooth disease of unknown origin.

Adult↗
PubMed1999

The effects of neonatal cocaine exposure on a play-rewarded spatial discrimination task in juvenile rats.

This study examined the effects of neonatal cocaine exposure on the rewarding properties of play in a modified T-maze. Animals were artificially reared from postnatal day (PND) 4-9 with drug concentrated in four daily feeds. There were four treatment groups, 40 mg/kg/day cocaine, 20 mg/kg/day cocaine, an artificially reared control and a surgery control. From PND 38-42, subjects were tested with a food reward (EXP 1) or a play reward (EXP 2). No deficits in learning were seen when the reward was food. The 20 mg/kg/day cocaine group, however, showed impaired learning and altered play behavior when the reward was access to a play partner. Neonatal cocaine exposure thus appears to differentially affect learning based on the type of reward presented.

Animals↗
PubMed1999

Effects of six weeks of chronic ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury.

This study examined the effects of 6 weeks of chronic ethanol administration on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were given either an ethanol liquid diet (ethanol diet-groups) or a pair-fed isocaloric sucrose control diet (control diet groups) for 6 weeks. After 6 weeks, the ethanol diet was discontinued for the ethanol diet rats and they were then given the control sucrose diet for 2 days. During those 2 days, the rats were trained to perform a beam-walking task and subjected to either lateral FP brain injury of low to moderate severity (1.8 atm) or to sham operation. In both the control diet and the ethanol diet groups, lateral FP brain injury caused beam-walking impairment on days 1 and 2 and spatial learning disability on days 7 and 8 after brain injury. There were no significant differences in beam-walking performance and spatial learning disability between brain injured animals from the control and ethanol diet groups. However, a trend towards greater behavioral deficits was observed in brain injured animals in the ethanol diet group. Histologic analysis of both diet groups after behavioral assessment revealed comparable ipsilateral cortical damage and observable CA3 neuronal loss in the ipsilateral hippocampus. These results only suggest that chronic ethanol administration, longer than six weeks of administration, may worsen behavioral outcome following lateral FP brain injury. For more significant behavioral and/or morphological change to occur, we would suggest that the duration of chronic ethanol administration must be increased.

Animals↗
PubMed1999

Acquisition of a fixed ratio schedule in adult male rats neonatally exposed to ethanol and/or cocaine.

Acquisition of an operant learning task for sucrose reinforcement was examined in rats after neonatal exposure to ethanol and/or cocaine. Subjects were raised using an artificial rearing procedure from postnatal days 4 to 11 and were intragastrically fed a milk diet containing either ethanol (6 g/kg/day), cocaine (60 mg/kg/day), the combination (6 g/kg/day + 60 mg/kg/day), or an isocaloric control diet. There was also a suckled sham control. Adult male offspring (postnatal day 65 to postnatal day 68) were shaped to lever press for sucrose reinforcement and then began daily 15-min sessions of fixed ratio (FR) training. The number of days to acquire an FR 20 was measured. Neonatal exposure to the ethanol/cocaine combination significantly increased the number of days to reach the FR 20. There was also a trend for fewer of these subjects to reach the FR 20, although this difference was not statistically significant. These results suggest that subjects neonatally exposed to the ethanol/cocaine combination have difficulty learning an operant task. This impairment was unique to the ethanol/cocaine combination group and suggests that polydrug exposure during development may have a more adverse outcome than exposure to ethanol or cocaine alone.

Age Factors↗
PubMed1999

The behavioral response to novelty is altered in rats neonatally exposed to cocaine.

It has recently been suggested that the effects of in utero cocaine exposure may result in subtle deficits related to a challenging environment, including exposure to novelty or stress. This study used a neonatal drug-exposure model to examine the behavioral response to a novel environment in rodents. Subjects were artificially reared (AR) from postnatal Days 4-10. There were four treatment groups; AR 40 mg/kg/day cocaine, AR 20 mg/kg/day cocaine, AR control group receiving no drug, and a normally reared control. In Experiment 1, subjects were tested for their preference of maternal home-cage or clean wood-chip odors in a T-maze on postnatal Day 15. Subjects from all treatment groups preferred the maternal odor. In Experiment 2, subjects were habituated to four familiar odors and tested with a novel odor in an open field (postnatal Days 16-21). Neonatal exposure to 20 mg/kg/day cocaine led to an overall increase in exploratory behavior during testing, whereas 40 mg/kg/day did not, supporting the hypothesis that developmental exposure to cocaine at some doses may alter the offspring's response to a changing environment.

Animals↗
PubMed1998

Brain opioid receptor adaptation and expression after prenatal exposure to buprenorphine.

Previous in vivo studies revealed that buprenorphine can down-regulate mu and up-regulate delta2 and kappa1 opioid receptors in adult and neonatal rat brain. To assess gestational effects of buprenorphine on offspring, pregnant rats were also administered this drug and opioid receptor binding parameters (Kd and Bmax values) were measured by homologous binding assays of postnatal day 1 (P1) brain membranes. Buprenorphine concentrations of 2.5 mg/kg injected into dams elicited an up-regulation of kappa1 opioid receptors as detected with the kappa1-selective agonist 3H-U69593. Parallel studies with the mu-selective agonist [D-ala2, mephe4,gly-ol5] enkephalin revealed a buprenorphine-induced down-regulation in receptor density at 0.3, 0.6 or 2.5 mg/kg drug treatment. A greater down-regulation of mu receptors for P1 males than for their female counterparts was observed. Buprenorphine did not cause a reduction in binding affinity in these experiments. Changes in opioid receptor adaptation induced by buprenorphine were further supported by data from cross-linking of 125I-beta-endorphin to brain membrane preparations. RT-PCR analysis of opioid receptor expression was also estimated in P1 brains. However, significant changes in neither mu nor kappa receptor message were detected in P1 brains as a result of prenatal buprenorphine treatment under the conditions of these experiments. Since buprenorphine is being evaluated in clinical trials for the treatment of heroin abuse, the in utero actions of the drug have ramifications for its use in the treatment of maternal drug abuse.

Adaptation, Physiological↗
PubMed1997

Prenatal buprenorphine exposure and sexually dimorphic nonreproductive behaviors in rats.

This set of experiments examined the effects of prenatal buprenorphine (BUP) exposure on three measures of sexual differentiation in rats. Pregnant female rats were divided into four treatment groups: 0.6 mg/kg BUP, 0.3 mg/kg BUP, a pair-fed control (PFC), and an untreated control (UTC). Drugs were injected starting on gestation day (GD) 6 and continuing through GD 20 with a 48-h interval between drug administrations. Three variables were examined in the offspring: anogenital (AG) distance on postnatal day (PND) 1, spontaneous parental behavior on PNDs 23-28, and saccharin consumption on PNDs 42-55. Whereas prenatal BUP exposure had no effect on AG distance, spontaneous parental behavior was impaired in the 0.6-mg/kg-exposed offspring on two measures: pup-retrieval latencies and pup-directed behaviors. Furthermore, although both control groups and the 0.3-mg/kg-exposed offspring showed the expected sex difference in consumption of a 0.25% saccharin solution, this difference was not displayed by the 0.6-mg/kg-exposed offspring. These findings suggest that exposure to relatively high doses of buprenorphine during development may have long-term effects on behavior.

Animals↗
PubMed1997

Effects of six weeks of chronic ethanol administration on lactic acid accumulation and high energy phosphate levels after experimental brain injury in rats.

The effects of 6 weeks of chronic ethanol administration on the lateral fluid percussion (FP) brain injury-induced regional accumulation of lactate and on the levels of total high-energy phosphates were examined in rats. In both the chronic ethanol diet (ethanol diet) and pair-fed isocaloric sucrose control diet (control diet) groups, tissue concentrations of lactate were elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres at 5 min after brain injury. In both diet groups, concentrations of lactate were elevated only in the injured left cortex and the ipsilateral hippocampus at 20 min after FP brain injury. No significant differences were found in the levels of lactate in the cortices and hippocampi of sham animals and brain-injured animals between the ethanol and control diet groups at 5 min and 20 min after injury. In the ethanol and control diet groups, tissue concentrations of total high-energy phosphates (ATP + PCr) were not affected in the cortices and hippocampi at 5 min and 20 min after lateral FP brain injury. No significant differences were found in the levels of total high-energy phosphates in the cortices and hippocampi of the sham and brain-injured animals between the ethanol and control diet groups at 5 min and 20 min after injury. Histologic studies revealed a similar extent of damage in the cortex and in the CA3 region of the ipsilateral hippocampus in both diet groups at 14 days after lateral FP brain injury. These findings suggest that 6 weeks of chronic ethanol administration does not alter brain injury-induced accumulation of lactate, levels of total high energy phosphates, and extent of morphological damage.

Adenosine Triphosphate↗
PubMed1996

Problem solving following neonatal exposure to cocaine, ethanol, or cocaine/ethanol in combination in rats.

This study examined the effects of neonatal drug exposure on performance in a digging maze. Subjects were Sprague-Dawley rats, artificially reared (AR) and fed through a gastrostomy tube from postnatal days (PND) 4-10. The AR groups included a cocaine group (20 mg/kg/day cocaine hydrochloride), an ethanol group (4 g/kg/day ethanol), a cocaine/ethanol group (20 mg/kg/day cocaine and 4 g/kg/day ethanol), and an AR control group. A suckled control raised by its dam was also included. At approximately PND 55, subjects were tested in a digging maze paradigm. The digging maze required subjects to use a species typical behavior (digging) to solve a novel problem (gaining access to water). While neonatal treatment had no effect on acquisition of a simple runway task for water reward, neonatal exposure to cocaine and ethanol in combination resulted in impaired performance on the digging maze task. None of the other neonatal treatment groups showed impairments on this task. These findings suggest that exposure to these doses of cocaine and ethanol during neonatal development may have more serious effects on problem solving tasks in rats than exposure to either drug alone.

Animals↗