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Biomedical subjects

B Dean

Publications and source records attributed to B Dean.

At least 37 records · Page 2Linked to original sources
PubMed2001

Quality assurance in gynecologic cytology. The value of cytotechnologist-cytopathologist discrepancy logs.

We describe a simple method for displaying and evaluating the concordance or discordance between cytotechnologists (CTs) and cytopathologists (CPs) on gynecologic cases. The provisional diagnoses made by the CTs and the final diagnoses of the CPs are captured by the laboratory information system; data generated for specified periods are displayed as a 10 x 10 matrix that classifies each possible diagnosis made by the CT and CP into 1 of 10 major categories. Matrices are generated for the entire laboratory and for individual CTs; individual CTs are evaluated based on their deviation from the laboratory average. Three statistical measures are generated: percentage of discordant diagnoses, a kappa statistic, and a weighted measure. During a 2.5-year period, approximately 4,200 cases were referred to a CP for review every 6 months. The median discordance in diagnoses increased during 2 years from 21% to 34%, and the kappa value fell from 0.69 to 0.38. This was attributed primarily to 1 CT, whose performance, as well as that of the entire laboratory, improved after remedial action. Measures of CT-CP diagnostic concordance are a useful and efficient measure of CT performance and can be incorporated into mandatory semiannual performance evaluations.

Boston↗
PubMed2001

A neuropsychology telemedicine clinic.

This article describes a neuropsychology telemedicine clinic. The clinic was established to extend the availability of a specialized service, neuropsychology, from an Army medical center to outlying Army community hospitals. Patients with neurological disorders or brain injury were seen at the medical center for a detailed cognitive and personality assessment, the neuropsychological evaluation. They were seen for follow-up feedback sessions at their local facilities via telemedicine. Referring clinicians, family members, and work supervisors were able to participate in these sessions. Screening interviews and ongoing supportive psychotherapy were also conducted via telemedicine.

Female↗
PubMed2000

Decreased muscarinic receptor binding in subjects with schizophrenia: a study of the human hippocampal formation.

BACKGROUND: Acetylcholine is important to hippocampal function, including the processes of learning and memory. Patients with schizophrenia show impaired learning and memory and hippocampal dysfunction. Thus, acetylcholinergic systems may be primarily or secondarily disrupted in the hippocampal formation of schizophrenic patients. The present study tested the hypothesis that [(3)H]pirenzepine-labeled muscarinic cholinergic receptor levels are altered in the hippocampal formation of patients with schizophrenia. METHODS: We have used quantitative autoradiography to measure [(3)H]pirenzepine binding to M(1) and M(4) receptors in the hippocampal formation from 15 schizophrenic and 18 nonschizophrenic subjects. RESULTS: The mean density of [(3)H]pirenzepine binding was reduced in all regions studied, including the dentate gyrus, subdivisions of Ammon's Horn (CA1-CA4), subiculum, and the parahippocampal gyrus, of the schizophrenic cohort. Moreover, unlike controls, there was no significant variation between the mean levels of [(3)H]pirenzepine binding across the subregions of the hippocampal formation from schizophrenic subjects. CONCLUSIONS: These findings provide support for a possible involvement of the muscarinic cholinergic system in the pathology and/or treatment of schizophrenia.

Adult↗
PubMed2000

Serotonin(2A) receptors are reduced in the planum temporale from subjects with schizophrenia.

[(3)H]ketanserin binding to 5HT(2A) receptors was measured in the left planum temporale (sensory speech cortex) from schizophrenic and non-schizophrenic (control) subjects using both particulate membranes and tissue sections. There was a significant decrease in the affinity of [(3)H]ketanserin binding to particulate membranes from schizophrenic subjects who were treated with phenothiazines up to death. Adding 2nM chlorpromazine to brain tissue from control subjects caused a similar decrease in the affinity of [(3)H]ketanserin binding to particulate membranes. This suggests that the decrease in affinity observed in the phenothiazine-treated subjects was due to residual drugs. In addition, there was a significant decrease in the density of [(3)H]ketanserin binding in both particulate membranes and tissue sections from schizophrenic subjects which did not appear to be due to residual antipsychotic drugs. Analysis of the laminar distribution of 5HT(2A) receptors showed that this decrease was greatest in cortical layer III. The decrease in the density of 5HT(2A) receptors was significant whether schizophrenic subjects were receiving phenothiazines or haloperidol at the time of death, and there was no correlation between the last recorded dose of antipsychotic drug and 5HT(2A) receptor density. These data suggest that a decrease in the density of 5HT(2A) receptors in the planum temporale may be associated with the pathology of schizophrenia.

Adolescent↗
PubMed2000

Comparative proteome analysis of the hippocampus implicates chromosome 6q in schizophrenia.

Comparative brain proteome analysis is a new strategy to discover proteins and therefore genes whose altered expression may underlie schizophrenia. This strategy does not require an a priori theory of the pathogenesis or the mode of inheritance of schizophrenia. Using proteome analysis we previously compared the hippocampal proteome, that is, those proteins expressed by the hippocampal genome, of seven schizophrenic individuals with the hippocampal proteome of seven control individuals, matched for age and post mortem delay.1 We found 18 proteins that were significantly altered in concentration in the schizophrenic hippocampus (P < 0.05), when compared to control tissue. One of these proteins was characterised, by N-terminal sequencing, as diazepam binding inhibitor whose gene maps to 6q12-q21. Here we characterise a further three of the 18 proteins as: manganese superoxide dismutase, 6q25.3, T-complex protein 1, 6q25.3-q26 and collapsin response mediator protein 2, 8p21. That three of these four characterised proteins should map to the long arm of the same chromosome is significant (P < 0.002) and suggests the importance of chromosome 6q in schizophrenia. These results indicate that antioxidant defence is altered in the schizophrenic hippocampus and suggest that segregation distortion, of schizophrenia susceptibility genes, may be a possible causative factor in the high incidence of schizophrenia. Molecular Psychiatry (2000) 5, 85-90.

Carrier Proteins↗
PubMed2000

Muscarinic1 and 2 receptor mRNA in the human caudate-putamen: no change in m1 mRNA in schizophrenia.

Studies using tissue obtained at autopsy suggest that changes in cholinergic neurons could be important in the pathology of schizophrenia.1-4 We have previously reported a decrease in [3H]pirenzepine binding5 and [3H]AF-DX 384 binding6 to caudate-putamen (CP) from subjects who had schizophrenia. Under the conditions chosen, [3H]pirenzepine would predominately bind to muscarinic1 (M1) and muscarinic4 (M4) receptors,7whereas [3H]AF-DX 384 would mainly bind to muscarinic2 (M2) and M4 receptors.8 Given the relative concentrations of M1, M2 and M4 receptors in the human CP and the magnitude of the decreases in radioligand binding in schizophrenia, our results most likely reflected a change in the density of M1 and M2 receptors in the CP from the schizophrenic subjects. In situ hybridisation has now been used to determine levels of m1 and m2 mRNA in CP from 14 schizophrenic and 16 control subjects previously used for radioligand binding. m2 mRNA in the CP from the schizophrenic and control subjects was below the sensitivity of in situhybridisation. There was no difference in the levels of m1 mRNA in CP from schizophrenic and control subjects (mean +/- SEM: 103 +/- 16 vs106 +/- 17 fmol [35S]oligonucleotide probe g-1estimated tissue equivalents, P = 0.91). In conclusion, data from our radioligand binding studies show decreases in [3H]pirenzepine binding that are likely to reflect a decrease in the density of M1 receptors in CP from schizophrenic subjects. Our data in this study show the absence of a concomitant change in mRNA coding for that receptor.

Adult↗
PubMed2000

Signal transmission, rather than reception, is the underlying neurochemical abnormality in schizophrenia.

OBJECTIVE: This review aims to summarise the outcome of studies on changes in the molecular architecture of the brain of subjects with schizophrenia and formulate a hypothesis on mechanisms involved in the pathology of the illness. METHOD: The outcomes from key studies using neuroimaging techniques and tissue obtained post-mortem that have been directed toward identifying abnormalities in the molecular architecture of the brain in subjects with schizophrenia were summarised. Using the results from these studies hypotheses were formulated on the underlying pathological process that precipitate schizophrenia. RESULTS: Studies using neuroimaging techniques or tissue obtained post-mortem have revealed changes in the dopaminergic, serotoninergic, glutamatergic, GABAergic and cholinergic systems of the brain in schizophrenia. Some of these studies have identified abnormalities in presynaptic proteins or functioning that may be central to the pathology of schizophrenia. CONCLUSIONS: There appears to be diverse changes in the molecular cytoarchitecture of the brains from subjects with schizophrenia. It could be that it is by affecting these multiple systems that the atypical antipsychotic drugs produce their improved clinical outcomes. Abnormal functioning of presynaptic processes could be central to the pathology of schizophrenia. If the 'presynaptic' hypothesis is proven, future antipsychotic drug design should be directed away from post-synaptic receptor antagonism toward the modulating the functions of presynaptic neurones.

Brain↗
PubMed2000

What is a prescribing error?

OBJECTIVE: To develop a practitioner led definition of a prescribing error for use in quantitative studies of their incidence. DESIGN: Two stage Delphi technique. SUBJECTS: A panel of 34 UK judges, which included physicians, surgeons, pharmacists, nurses and risk managers. MAIN OUTCOME MEASURES: The extent to which judges agreed with a general definition of a prescribing error, and the extent to which they agreed that each of 42 scenarios represented a prescribing error. RESULTS: Responses were obtained from 30 (88%) of 34 judges in the first Delphi round, and from 26 (87%) of 30 in the second round. The general definition of a prescribing error was accepted. The panel reached consensus that 24 of the 42 scenarios should be included as prescribing errors and that five should be excluded. In general, transcription errors, failure to communicate essential information, and the use of drugs or doses inappropriate for the individual patient were considered prescribing errors; deviations from policies or guidelines were not. CONCLUSIONS: Health care professionals are in broad agreement about the types of events that should be included and excluded as prescribing errors. A general definition of a prescribing error has been developed, together with more detailed guidance regarding the types of events that should be included. This definition allows the comparison of prescribing error rates among different prescribing systems and different hospitals, and is suitable for use in both research and clinical governance initiatives.

Attitude of Health Personnel↗
PubMed2000

Ionotropic glutamate receptors and expression of N-methyl-D-aspartate receptor subunits in subregions of human hippocampus: effects of schizophrenia.

OBJECTIVE: Multiple quantifiable biologic abnormalities have been localized to the hippocampus in schizophrenia. Alterations in glutamate-mediated transmission at N-methyl-D-aspartic acid (NMDA)-sensitive receptors in hippocampus have been implicated in the pathophysiology of the illness. The authors tested the hypothesis that glutamatergic transmission within and efferent from hippocampus is altered in schizophrenia. METHOD: The authors analyzed postmortem hippocampal tissue from individuals with schizophrenia and from healthy individuals. The tissue samples had been collected by two brain tissue banks, one in Maryland and the other in Melbourne, Australia. lonotropic receptor binding for the NMDA, kainate, and (3)H-amino-3-hydroxy-5-methylisoxazol-4-propionate (AMPA) receptors was quantified by using usual radioligand techniques. In situ hybridization autoradiography was used to quantify mRNA for the NMDA receptor subunits NR1, NR2A, and NR2B. RESULTS: Ligand binding to the ionotropic glutamate receptors (NMDA, kainate, and AMPA) did not differ significantly overall or in any subregion between the schizophrenia tissue and the healthy comparison tissue. The only exception was AMPA receptor binding in hippocampal subregion CA2, which was slightly but significantly less in schizophrenia. However, the level of mRNA for the NMDA receptor subunits NR1 and NR2B was significantly different between groups; in several hippocampal subregions, the level of NR1 mRNA was lower and the level of NR2B mRNA higher in schizophrenia. CONCLUSIONS: Because the NR1 subunit of the NMDA receptor is critical to full receptor activity, a reduction of NR1 in hippocampus in schizophrenia suggests a functional impairment in glutamatergic transmission at the NMDA receptor, resulting in reduced glutamatergic transmission within and possibly efferent from the hippocampus in schizophrenia. This defect could underlie a hypoglutamatergic state in regions of limbic cortex, consistent with published results from other lines of research in schizophrenia.

Adult↗
PubMed2000

Schizophrenia: an illness of distorted reality.

Schizophrenia is a seriously disturbing disorder, both for the victim and for their families. Although treatments are available which can effectively control symptoms, their side effects are severe enough to cause many sufferers to discontinue taking them and their actions are not properly understood.

Antipsychotic Agents↗
PubMed1999

The binding of [3H]AF-DX 384 is reduced in the caudate-putamen of subjects with schizophrenia.

Clinical studies of cholinergic pharmacotherapy, together with the putative role of the muscarinic receptor system in the neurophysiology of human behavior, support a possible muscarinic cholinergic involvement in schizophrenia. The present study has measured the density of [3H]AF-DX 384 labelled receptors (muscarinic M2 and M4) in the caudate-putamen, obtained at autopsy, from 19 subjects who had schizophrenia, and 20 subjects who did not have schizophrenia. [3H]AF-DX 384 binding was reduced in caudate-putamen from schizophrenic subjects (104 +/- 10.3 vs 145 +/- 901 fmol mg(-1) TE; mean +/- s.e.; p = 0.007). Preliminary analysis of patient drug data as well as rat studies suggest that the reduced [3H]AF-DX 384 binding in caudate-putamen of schizophrenic subjects is not wholly due to antipsychotic drug treatment, or anticholinergic medication for the treatment of extrapyramidal effects. These data suggest that the muscarinic cholinergic system may be involved in the pathology of schizophrenia.

Adult↗
PubMed1999

No change in the density of the serotonin1A receptor, the serotonin4 receptor or the serotonin transporter in the dorsolateral prefrontal cortex from subjects with schizophrenia.

Changes in serotonin receptors and the serotonin transporter have been reported in the dorsolateral prefrontal cortex from subjects with schizophrenia, an area of the brain thought to be important in the pathology of the illness. To further our understanding on how such changes could play a role in the pathology of the illness, in situ radioligand binding with autoradiography was used to measure the density of the serotonin1A receptor, the serotonin4 receptor and the serotonin transporter in the dorsolateral prefrontal cortex, obtained at autopsy, from 10 schizophrenic and 10 control subjects. The binding of [3H]8-OH-DPAT to serotonin1A receptor, [3H]GR113808 to the 5HT4 receptor and [3H]citalopram to serotonin transporter was not altered in subjects with schizophrenia. significantly, only in tissue from the control subjects was there a relationship between age and the density of the serotonin4 receptor in Brodmann's areas 8 (r = 0.71, P = 0.02) and 10 (r = -0.67, P = 0.03). Importantly, this confounding factor did not influence the comparison of the density of serotonin4 receptor in the tissue from the schizophrenic and control subjects. This study has failed to show a difference in the density of serotonin1A receptor, the serotonin4 receptor or the serotonin transporter in the dorsolateral prefrontal cortex (Brodmann's areas 8, 9 and 10) from subjects with schizophrenia. These data suggest that not all serotonergic markers are altered in the dorsolateral prefrontal cortex from schizophrenic subjects.

Carrier Proteins↗
PubMed1999

Hospital drug distribution systems in the UK and Germany--a study of medication errors.

The aim of this study was to compare the incidence of medication errors and the stages of the drug distribution system at which they occur in a United Kingdom (UK) hospital using the ward pharmacy system, a German hospital using the unit dose system and a German hospital using their traditional system. Medication errors were identified by observing the preparation and administration of regularly scheduled solid oral medication. In the UK hospital using the ward pharmacy system, the medication error rate was 8.0% (95% confidence interval 6.2-9.8%). The majority of these errors occurred at the stage of medication administration. In the hospital using the traditional German system, the error rate was 5.1% (4.4-5.8%). With the German unit dose system, the error rate was 2.4% (2.0-2.8%). In both German systems the errors were mainly attributable to the stage of transcription. It was noted that patient turnover was much higher in the wards using the ward pharmacy system and therefore the study sites may not be comparable. However, recommendations can be made in order to reduce the error rate associated with each system. Errors associated with the ward pharmacy system may be reduced if medication is stored in individual patient medicine cabinets and patients' own drugs used. Errors occurring with the traditional system and the unit dose system may be reduced if the original prescription is used for medication administration.

Data Collection↗
PubMed1999

When should pharmacists visit their wards? An application of simulation to planning hospital pharmacy services.

This paper reports a pilot study of the use of simulation in planning hospital pharmacy services. The objectives were to create a simulation model of the hospital drug distribution system, to use the model to investigate a simple problem and to assess the potential for simulation to aid decision making in hospital pharmacy management. The problem chosen for investigation focused on the UK ward pharmacy system, where a pharmacist visits each ward daily to initiate the supply of newly prescribed non-stock medication. A simulation model was used to investigate how changing the time of the ward pharmacist's visit could affect the mean time delay between the prescription of a non-stock drug and the arrival of that drug on the ward. The simulation results suggest that the time of day at which pharmacists visit their wards can have a major impact on delay times, and that the relative benefit of different visit times is likely to vary between wards. Simulation was found to be a useful approach to investigating different service alternatives without the expense and disruption of assessing each in practice.

Computer Simulation↗
PubMed1999

A comparative proteome analysis of hippocampal tissue from schizophrenic and Alzheimer's disease individuals.

The proteins expressed by a genome have been termed the proteome. Comparative proteome analysis of brain tissue offers a novel means to identify biologically significant gene products that underlie psychopathology. In this study we collected post mortem hippocampal tissue from the brains of seven schizophrenic, seven Alzheimer's disease (AD) and seven control individuals. Hippocampal proteomes were visualised by two-dimensional gel electrophoresis of homogenised tissue. A mean of 549 (s.d. 35) proteins were successfully matched between each disease group and the control group. In comparison with the control hippocampal proteome, eight proteins in the schizophrenic hippocampal proteome were found to be decreased and eight increased in concentration, whereas, in the AD hippocampal proteome, 35 proteins were decreased and 73 were increased in concentration (P<0.05). One protein, which was decreased in concentration in both diseases, was characterised as diazepam binding inhibitor (DBI) by N-terminal sequence analysis. DBI can regulate the action of the GABA(A) receptor. Protein changes involved 6% of the assessed AD hippocampal proteome, whereas, in schizophrenia protein changes involved less than 1% of the assessed hippocampal proteome. We conclude that schizophrenia has a subtle neuropathological presentation and comparative proteome analysis is a viable means by which to investigate diseases of the brain at the molecular level.

Adult↗