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Biomedical subjects

A Reeve

Publications and source records attributed to A Reeve.

At least 19 recordsLinked to original sources
PubMed2001

mGlu5 receptors and nociceptive function II. mGlu5 receptors functionally expressed on peripheral sensory neurones mediate inflammatory hyperalgesia.

Previous studies have demonstrated that the metabotropic glutamate receptor subtype 5 (mGlu5 receptor) is expressed in the cell bodies of rat primary afferent neurones. We have further investigated the function and expression of mGlu5 receptors in primary afferent neurones, and their role in inflammatory nociception. Freund's complete adjuvant-induced inflammatory hyperalgesia of the rat hind paw was significantly reduced by intraplantar, but not by intracerebroventricular or intrathecal microinjection of the selective mGlu5 receptor antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP). Pharmacological comparison in vivo of the nociceptive effects of glutamate, and ionotropic and metabotropic glutamate (mGlu) receptor agonists applied to the rat hind paw, indicated that group I mGlu receptor agonists induce a dose-dependent decrease in paw withdrawal threshold (mechanical hyperalgesia). Group I mGlu agonist-induced hyperalgesia was inhibited by co-microinjection of MPEP, but not by the mGlu1 receptor antagonist (S)-4-carboxy-phenylglycine (4-CPG). Carrageenan-induced inflammatory hyperalgesia was inhibited by pre-treatment of the inflamed hind paw with MPEP, but not following MPEP injection into the contralateral hind paw. Dorsal horn neurones receiving peripheral nociceptive and non-nociceptive afferent input were recorded in anaesthetized rats following microinjection of CHPG into their peripheral receptive fields. CHPG significantly increased the frequency and duration of firing of dorsal horn wide dynamic range (WDR) neurones and this activity was prevented by co-administration of CHPG and MPEP into their receptive fields. Immunohistochemical experiments revealed the co-expression of mGlu5 receptor protein and betaIII tubulin in skin from naive rats, indicating the constitutive expression of mGlu5 receptors on peripheral neurones. Double-labelling of adult rat DRG cells with mGlu5 receptor and vanilloid receptor subtype 1 antisera also supports the expression of mGlu5 receptors on peripheral nociceptive afferents. These results suggest that mGlu5 receptors expressed on the peripheral terminals of sensory neurones are involved in nociceptive processes and contribute to the hyperalgesia associated with inflammation.

Analgesics, Opioid↗
PubMed2001

Naming, defining, and classifying in mental retardation.

Recent discussions about changing the term mental retardation to a different term may be considered in the broader framework of three distinct but related processes: naming (terminology), defining, and classifying. The three processes are analyzed according to their purposes and functions: In naming, a term is assigned; in defining, the term is explained; and in classifying, the group is divided into subgroups according to stated principles. The current status of each process is described, especially as represented in the 1992 AAMR manual, Mental Retardation: Definition, Classification, and Systems of Supports. We suggest three sets of guiding questions that may help evaluate proposed changes in naming, defining, or classifying.

Humans↗
PubMed2000

Recognizing and treating anxiety and depression in adolescents. Normal and abnormal responses.

Recognition of depressive and anxiety disorders in adolescents reduces morbidity, mortality, and lifetime risk for psychiatric illness and maladaptive behaviors. Effective treatments for these disorders are available and are associated with minimal severe side effects. Because adolescents tend to underreport their psychologic distress, screening for these disorders in the primary care setting is incumbent on the clinician. Depression or anxiety may be a primary or a secondary condition--with each other and with other medical illness. Substance abuse, including cigarettes, should not be overlooked as an accompanying risk factor for poor health care habits and as an indicator of degree of family (lack of) support. Adolescents at risk should be screened and their symptoms taken seriously. This brief overview does not focus on the need for primary care clinicians to seek assistance and support of psychiatrists in the diagnosis and development of treatment algorithms. All clinicians should be reminded that judgments about peoples' internal mental states and function are difficult to assess objectively and with compassion. Initial assessment in the primary care setting should include a telephone consultation with a reliable psychiatric colleague and referral for more in-depth evaluation in the event of more complicated course. These disorders need to be treated comprehensively because of the lifelong implications that having a chronic disease bear on the individual and his or her physiology. Primary care clinicians are pivotal instruments in engaging adolescents to embrace appropriate therapeutic measures for their current and future health.

Adolescent↗
PubMed2000

Evidence for susceptibility genes to familial Wilms tumour in addition to WT1, FWT1 and FWT2.

Three loci have been implicated in familial Wilms tumour: WT1 located on chromosome 11p13, FWT1 on 17q12-q21, and FWT2 on 19q13. Two out of 19 Wilms tumour families evaluated showed strong evidence against linkage at all three loci. Both of these families contained at least three cases of Wilms tumour indicating that they were highly likely to be due to genetic susceptibility and therefore that one or more additional familial Wilms tumour susceptibility genes remain to be found.

Chromosomes, Human, Pair 11↗
PubMed2000

The use of herbal alternative medicines in neuropsychiatry. A report of the ANPA Committee on Research.

Growing numbers of people throughout the United States (40% in 1998) are using various forms of alternative therapies. A MEDLINE literature search of journals from the past three decades and an Internet database query were performed to determine the types and frequency of alternative therapies used, with special attention given to the herbal medicines used in neuropsychiatric disorders. Clinical effects, mechanisms of action, interactions, and adverse reactions of the herbal treatments are detailed. Objective controlled trials will be needed to establish safety and efficacy of herbal supplements. Knowledge of the properties of these therapies can improve the care of neuropsychiatric patients.

Complementary Therapies↗
PubMed1998

Neuropsychiatric correlates and treatment of lenticulostriatal diseases: a review of the literature and overview of research opportunities in Huntington's, Wilson's, and Fahr's diseases. A report of the ANPA Committee on Research. American Neuropsychiatric Association.

This report reviews clinical neuropsychiatric findings and opportunities for research in Huntington's, Wilson's, and Fahr's diseases. Consistent, systematic methodology is lacking among neuropsychiatric studies in these lenticulostriatal diseases. Systematic cross-sectional and longitudinal assessments are needed to ascertain the prevalence of psychiatric disorders as a function of disease course. Preliminary synthesis of existing data suggests the following heuristic relationships in these diseases: depression with parkinsonian states; personality changes with caudate or putamen disease; psychosis, impulsivity, and sexual disorders with caudate disease; dementia and mania with caudate and pallidal diseases; and compulsions with pallidal disease. Correlation of neuropsychiatric findings with disease stage, clinical signs, and radiologic, metabolic, physiologic, and pathologic markers of disease will add to our understanding of these conditions.

Basal Ganglia Diseases↗
PubMed1996

The opioid ketobemidone has a NMDA blocking effect.

There are clinical observations that neurogenic pain can respond well to the opioid ketobemidone, in contrast to pethidine and morphine. This has led us to the hypothesis that the analgesic effect of ketobemidone in neurogenic pain may be due to both opioid as well as additional non-opioid effects. The present study was therefore made to evaluate the effects of ketobemidone. The study consists of two parts. (1) Single unit recordings were made from dorsal horn neurones in the halothane-anaesthetised rat. Neurones were activated by transcutaneous electrical stimulation of their receptive fields at C-fibre strength and their responses quantified. The wind-up of the neurones, due to N-methyl-D-aspartate (NMDA) receptor activation, leading to marked increases in C-fibre responses and an associated post-discharge was also measured. Ketobemidone, applied to the spinal cord, equivalent to an intrathecal injection, dose-dependently and selectively reduced C-fibre evoked responses. Ketobemidone was also found to block wind-up more effectively than morphine at equieffective doses, but unlike morphine in a non-naloxone-reversible manner. (2) In a binding study ketobemidone was shown to inhibit [3H]MK-801 binding with a Ki value of 26 microM. Therefore, ketobemidone appears to possess both mu opioid agonist as well as NMDA blocking effects.

Analgesics, Opioid↗
PubMed1994

Managing sleep problems in children with special needs.

Sleep problems are common among all children, and have been shown to respond to behaviour modification techniques. Anne Reeve and Sheila Miers describe a group for mothers of children with special needs which took the same approach to solving the children's sleep problems.

Behavior Therapy↗
PubMed1993

True telomeric translocation in a baby with the Prader-Willi phenotype.

We report on a baby with a nonreciprocal de novo unbalanced translocation between chromosomes 12 and 15. Her karyotype was 45,XX, -12, -15, +der(12)t(12;15)(pter-->qter::q13-->qter). The paternal origin of the 15q11-13 region was shown by DNA marker studies and, consistent with this, the baby had the Prader-Willi (PWS) phenotype. The breakpoint on 12q was distal to D12S11 (lambda MS43) which maps to 12q24.3-qter. Fluorescent in situ hybridization using the oligonucleotides (TTAGGG)7 and (AATCCC)7 showed that the 12q telomere was still present within the translocated chromosome. Thus, the translocation was within or onto the end of the telomere of 12q. This unusual translocation is further evidence of an unexplained instability of the 15q11-13 region.

Chromosome Banding↗
PubMed1992

Apparent cleidocranial dysplasia associated with abnormalities of 8q22 in three individuals.

Cleidocranial dysplasia is an autosomal dominant, generalised skeletal disorder characterised by variable clavicular hypoplasia, frontal bossing, multiple Wormian bones, and delayed eruption of the teeth. The gene locus for this syndrome has not yet been assigned. Three individuals with manifestations of cleidocranial dysplasia associated with rearrangements of chromosome 8q22 are described. The evidence presented suggests that the gene for cleidocranial dysplasia may be located on chromosome 8q in humans in a region showing homology to mouse chromosome 3.

Adult↗
PubMed1992

Treatment of tardive dyskinesia with vitamin E.

OBJECTIVE: Vitamin E (alpha-tocopherol), a free-radical scavenger, has been reported to improve symptoms of tardive dyskinesia. The authors attempted to replicate this finding under more controlled conditions in a larger study group. METHOD: Fifteen inpatients and six outpatients with tardive dyskinesia received up to 1600 IU/day of vitamin E for 6 weeks in a double-blind, placebo-controlled crossover study. Abnormal Involuntary Movement Scale (AIMS) examinations of these patients were videotaped and rated independently by two trained raters. Levels of neuroleptic medication and vitamin E were measured during both treatment periods. Eighteen patients who demonstrated high blood levels of vitamin E were included in the data analysis. RESULTS: Vitamin E levels were significantly higher while the patients were receiving vitamin E than while they were receiving placebo. For all 18 patients, there were no significant differences between AIMS scores after receiving vitamin E and AIMS scores after receiving placebo. In agreement with previous studies, however, the nine patients who had had tardive dyskinesia for 5 years or less had significantly lower AIMS scores after receiving vitamin E than after receiving placebo. There were no changes in neuroleptic levels during vitamin E treatment. CONCLUSIONS: Vitamin E had a minor beneficial effect on tardive dyskinesia ratings in a selected group of patients who had had tardive dyskinesia for 5 years or less. This effect was not due to an increase in blood levels of neuroleptic medications.

Adolescent↗
PubMed1985

Methylphenidate therapy for aggression in a man with ring 22 chromosome. Report and literature review.

A 28-year-old mentally retarded man with ring 22 chromosome [r(22)] had deterioration of mood and behavior, decreased speech, bradykinesia, and decline of fine motor skills over a three-year period, which were further exacerbated by treatment with phenothiazines. A trial of methylphenidate hydrochloride resulted in rapid improvement of mood, behavior, and to a small extent, motor function. This finding suggests that dopamine depletion may play a role in the behavioral deterioration seen in this disorder. The possibility that genes that control dopamine metabolism may be present on chromosome 22 is raised. The phenotype of this patient is compared with the 25 reported cases of r(22).

Adult↗