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M Davidson

Publications and source records attributed to M Davidson.

At least 253 records · Page 14Linked to original sources
PubMed1991

Continuous performance tests in schizophrenic patients: stimulus and medication effects on performance.

Medicated (n = 17) and unmedicated (n = 17) schizophrenic patients were compared to a normal control group (n = 19) on their performance on auditory and visual versions of the Continuous Performance Test (CPT). Within each stimulus modality, performance was examined on lexical and nonlexical target stimuli. Neuromotor competence was assessed on the basis of motor speed and proficiency. Normal subjects made fewer errors of all types than schizophrenic patients. Unmedicated patients made significantly more errors on nonlexical stimuli than medicated patients, with medication status found not to be associated with stimulus modality effects. Motor proficiency was associated with CPT performance in the medicated patients, but not the unmedicated ones, although this difference in correlations did not account for the group differences between these patients. The authors discuss the implications of these data for the type of cognitive and attentional functions that are affected by medication in schizophrenia.

Adult↗
PubMed1991

Effect of concurrent distraction on communication failures in schizophrenic patients. II. Medication status correlations.

In order to examine the effects of irrelevant distracting information on speech disorder, medicated (n = 13) and unmedicated (n = 18) schizophrenics were compared to a mixed affective sample (n = 15) on the frequencies of linguistic measures of verbal communication disorder. Patients conversed with an interviewer during the presence and absence of irrelevant information inserted into their conversation. Affective patients manifested no distraction-related increase in communication disorder. Schizophrenics on medication manifested a small, but nonsignificant, increase in communication disorders during the concurrent distraction condition. Unmedicated schizophrenics manifested a substantial increase in their communication disorders during distraction. These data suggest that medication reduces the extent to which speech processes in schizophrenia are vulnerable to overload-related deterioration and provide confirmation of the hypothesis that some component of positive thought disorder in schizophrenia is due to medication-responsive attention deficits.

Adult↗
PubMed1991

Time course and clinical predictors of treatment response in schizophrenia.

The severity of schizophrenic symptoms was examined in 50 male chronic patients while neuroleptic free for at least 3 weeks and during 6 weeks of treatment with haloperidol. The results suggested that 50% of the improvement associated with haloperidol administration occurred by the end of the first treatment week and that early improvement, at both 1 and 4 weeks of treatment, was predictable from drug-free symptom severity. There was a negative correlation between week 1 improvement and improvement during the next 3 weeks of treatment, suggesting that medication response is not linear. Finally, dose increases after 4 weeks of treatment with 20 mg of haloperidol did not lead to any clinical improvement. These results are discussed in terms of their implications for selecting chronic schizophrenic patients who will and will not benefit from medication treatment.

Adult↗
PubMed1991

The liver/erythrocyte pyruvate kinase gene complex [Pk-1] in the mouse: regulatory gene mutations.

Nine enzyme activity variants and one charge variant of liver/erythrocyte pyruvate kinase have been found amongst laboratory and wild mice. Four of the enzyme activity variants were previously reported to be caused by allelic differences in the structural gene, Pk-1s. Analysis of two putative regulatory gene mutations is now reported, both of which map at, or close to, the structural gene on chromosome 3. One of these mutations, in the inbred strain SWR, is tissue specific, affecting enzyme concentration in the liver but not the erythrocyte the other, which arose in a mutation experiment, doubles the enzyme concentration in both tissues. The organization and the nomenclature in the [Pk-1] gene complex are discussed and are compared with the organization of other comprehensively analysed gene complexes in the mouse.

Animals↗
PubMed1991

Cholinergic strategies in the treatment of Alzheimer's disease.

Since the identification of the cholinergic deficit, strategies aimed at enhancing cholinergic neurotransmission have dominated the field of pharmacology in Alzheimer's disease (AD). These strategies include increasing acetylcholine precursor availability, delaying synaptic degradation and stimulating muscarinic receptors. Although most clinical trials report mild symptomatic improvements in some patients, support for large-scale clinical use of cholinomimetics in AD is not yet available. This article presents the most representative clinical trials, discusses the limitations of the cholinergic strategies and suggests future directions in the treatment of AD.

Acetylcholine↗
PubMed1991

Affective and impulsive personality disorder traits in the relatives of patients with borderline personality disorder.

OBJECTIVE: This study tested the hypothesis that the risk for affective and impulsive personality disorder traits commonly found in patients with borderline personality disorder would be greater in the first-degree relatives of probands with borderline personality disorder than in two comparison groups. METHOD: Blind family history interviews were conducted with family informants to assess the extent to which first-degree relatives of 29 probands with borderline personality disorder, 22 probands with other personality disorders who met three or fewer of the criteria for borderline personality disorder, and 43 probands with schizophrenia fulfilled operationalized criteria for the two kinds of personality disorder traits and for other diagnostic categories. The crude proportions of adult relatives with each diagnosis, as well as the age-adjusted morbid risks, were assessed in the three groups of relatives. RESULTS: The risks for affective and impulsive personality disorder traits were independently greater in the 129 relatives of the borderline probands than in the 105 relatives of the probands with other personality disorders and the 218 relatives of the schizophrenic probands. There was no similarly greater risk for any other psychiatric disorder assessed, including major affective disorder. In addition, the relatives of borderline probands with current or past major depressive disorder showed a greater risk for major affective disorders than the relatives of never-depressed probands with other personality disorders but not the relatives of never-depressed borderline probands. CONCLUSIONS: These results suggest familial transmission of the hallmark borderline-related personality characteristics and raise the possibility that these familial traits may be partially independent.

Adult↗
PubMed1991

Dopamine in schizophrenia: a review and reconceptualization.

OBJECTIVE: The initial hypothesis that schizophrenia is a manifestation of hyperdopaminergia has recently been faulted. However, several new findings suggest that abnormal, although not necessarily excessive, dopamine activity is an important factor in schizophrenia. The authors discuss these findings and their implications. METHOD: All published studies regarding dopamine and schizophrenia and all studies on the role of dopamine in cognition were reviewed. Attention has focused on post-mortem studies, positron emission tomography, neuroleptic drug actions, plasma levels of the dopamine metabolite homovanillic acid (HVA), and cerebral blood flow. RESULTS: Evidence, particularly from intracellular recording studies in animals and plasma HVA measurements, suggests that neuroleptics act by reducing dopamine activity in mesolimbic dopamine neurons. Post-mortem studies have shown high dopamine and HVA concentrations in various subcortical brain regions and greater than normal dopamine receptor densities in the brains of schizophrenic patients. On the other hand, the negative/deficit symptom complex of schizophrenia may be associated with low dopamine activity in the prefrontal cortex. Recent animal and human studies suggest that prefrontal dopamine neurons inhibit subcortical dopamine activity. The authors hypothesize that schizophrenia is characterized by abnormally low prefrontal dopamine activity (causing deficit symptoms) leading to excessive dopamine activity in mesolimbic dopamine neurons (causing positive symptoms). CONCLUSIONS: The possible co-occurrence of high and low dopamine activity in schizophrenia has implications for the conceptualization of dopamine's role in schizophrenia. It would explain the concurrent presence of negative and positive symptoms. This hypothesis is testable and has important implications for treatment of schizophrenia and schizophrenia spectrum disorders.

Animals↗
PubMed1991

Plasma homovanillic acid in schizotypal personality disorder.

Schizotypal patients were found to have a significantly higher mean plasma HVA concentration than normal comparison subjects. Furthermore, plasma HVA concentration positively correlated with "psychotic-like" schizotypal symptoms. These results implicate dopaminergic mechanisms modulating the psychotic-like symptoms of schizotypal personality disorder.

Dopamine↗
PubMed1991

Diagnostic and pharmacological approaches in Alzheimer's disease.

Alzheimer's disease is a chronic progressive disease affecting higher intellectual functioning. The clinical diagnosis is made when the onset of illness is insidious, the course slowly progressive and all the treatable causes of dementia have been ruled out. The use of more stringent criteria has improved clinical diagnosis, but at best only 80% of patients are accurately diagnosed. Ultimately the diagnosis depends upon pathological confirmation. The neuritic plaques and neurofibrillary tangles described by Alzheimer, although not pathognomonic for the disease, continue to be the basis for pathological diagnosis. The aetiology and pathophysiology of Alzheimer's disease are presently unknown. Epidemiological studies have suggested a genetic basis for the disorder, and many biochemical studies have linked it to degeneration of central cholinergic neurons, and possibly to abnormalities of other neurotransmitter systems. A marker which would permit accurate diagnosis early in the course of disease would be of major importance to researchers and clinicians alike. No marker has been found to date, although recent research results are promising. Various pharmacological strategies have been employed in the treatment of Alzheimer's disease. More recently attempts have focused on enhancing central cholinergic transmission. Despite the well-founded rationale for these studies, results have been modest.

Alzheimer Disease↗
PubMed1991

Electronic data interchange: a strategic approach.

The potential of EDI is virtually unlimited, but the success of any EDI initiative hinges on its ability to directly support strategies that achieve your institution's business objectives. At its most fundamental level, EDI technology automates current business practices, speeding up the exchange of business information. This application of EDI most often is found in a hospital's material management department. But EDI integrated internally within a hospital and externally with suppliers and vendors has the potential to go beyond simple automation and to transform processes. This is where the full value of EDI can be realized. No matter which level of EDI participation hospital management decides is appropriate to fulfill its business objectives and strategies, EDI will affect the entire institution's exchange of information with its internal and external audiences. The question management must answer is: Will the hospital's EDI strategy be offensive and managed, or defensive and reactive? Today's environment leaves no room for a "no-strategy" EDI option. The options are either to proactively shape EDI, or reactively play catch-up. EDI can work for you. Adequately developing an EDI game plan in support of your business objectives and calling on your suppliers and other trading partners to work with you will ensure EDI is an asset to your facility.

Computer Communication Networks↗
PubMed1991

The use of benzodiazepines in the management of behavioral symptoms in demented patients.

Hard data on the efficacy of benzodiazepines in the treatment of behavioral disturbances in Alzheimer's disease are not available. Short-acting benzodiazepines, such as oxazepam, appear safer than long-acting benzodiazepines and more efficient than placebo in the short-term (4-8 weeks) treatment of behavioral disturbances in geriatric, psychogeriatric, and demented patients. It is unknown whether oxazepam is superior to neuroleptic drugs or other commonly prescribed sedatives in this context. To some extent these findings may apply to patients with Alzheimer's disease as well, but there are several arguments against an uncritical extrapolation of conclusions drawn from other geriatric populations to patients with Alzheimer's disease. When, despite the lack of well-founded knowledge in this field, such a treatment modality is chosen, short-acting benzodiazepines should be preferred over long-acting agents. Drug interactions and pharmacokinetic aspects of the specific agent in the individual patient should always be considered carefully. Future studies on the treatment of behavioral disturbances in Alzheimer's disease need to clarify which specific behavioral symptoms should be treated pharmacologically, which therapeutic agents have the most advantageous risk-benefit ratio in this context, and what is the optimal treatment duration.

Aged↗
PubMed1991

Murine respiratory mycoplasmosis: a model to study effects of oxidants.

Previous studies have shown that exposure to nitrogen dioxide at concentrations of 5 and 10 parts per million (ppm) decreases intrapulmonary killing of Mycoplasma pulmonis, and that this decrease is related to increased lung lesions and mortality. The specific objectives of the present study were to titrate the effects of nitrogen dioxide on pulmonary clearance of M. pulmonis, determine the mechanisms by which this organism is killed within the lungs, and determine the target that the nitrogen dioxide affects. Pathogen-free C57BL/6N mice were exposed to 0, 0.5, 1, 2, or 5 ppm of nitrogen dioxide (contamination with other oxides of nitrogen compounds was 5% or less) for four hours and then immediately were exposed to aerosols of viable, radiolabeled M. pulmonis strain UAB CT. One-half of the animals in each group were killed immediately after exposure to the infectious aerosols, and the rest were killed 24 hours later. The amount of radioactivity and the number of viable M. pulmonis were determined for each group. Exposure to less than 5 ppm of nitrogen dioxide had no effect on intrapulmonary killing of M. pulmonis, although exposure to 1 ppm of nitrogen dioxide did increase mechanical removal. We were unable to develop a completely in vitro mycoplasma killing method. However, we were able to demonstrate the in vitro killing of M. pulmonis that had been allowed to associate with alveolar macrophages in vivo. Thus, mouse lungs contain unidentified factors that allow cells to kill M. pulmonis. Furthermore, we obtained evidence that suggests that prior exposure to nitrogen dioxide abrogates killing in these experiments. We also have shown that exposure to nitrogen dioxide does not increase the protein content of bronchoalveolar lavage fluid. Using immunofluorescence, more than 95% of the cells recovered by lavage were macrophages; with double-label immunofluorescence, more than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. In assessing the cytological parameters of lung lavage cells from mice exposed to nitrogen dioxide, M. pulmonis, or both, we found that both insults affected the viability of recovered macrophages. Viability immediately after exposure as measured by trypan blue exclusion or by fluorescein diacetate uptake, was 89% +/- 4% and 88% +/- 4% in the control group, respectively; 56% +/- 19% and 64% +/- 11% in the group receiving M. pulmonis alone; 23% +/- 7% and 48% +/- 9% in the group receiving nitrogen dioxide alone; and 16% +/- 6% and 25% +/- 6% in the group receiving both M. pulmonis and 10 ppm nitrogen dioxide exposures.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollutants↗
PubMed1991

DTP immunization and susceptibility to infectious diseases. Is there a relationship?

A two-part study was carried out in Alaskan Native children to evaluate the potential risk of invasive bacterial disease and the occurrence of minor illnesses after immunization with diphtheria and tetanus toxoids and whole-cell pertussis vaccine (DTP). First, a case-control comparison was performed with 186 children who had invasive Haemophilus influenzae type b or Streptococcus pneumoniae disease (cases) and 186 healthy controls matched for sex, region of residence, birth date, and number of DTP immunizations. The proportion of cases and controls immunized in the 30-day period before onset of disease for cases or reference date for controls was identical, suggesting no association with DTP immunization. In a second analysis, the occurrence of any illness, particularly infectious diseases, in 104 study subjects was compared for the period 30 days before and after 377 DTP immunizations. The rate of illness before immunization was 53%, and after immunization, 43%, again suggesting no causative effects from DTP immunization. Despite the high rates of invasive bacterial disease and nearly compete DTP immunization status in this population, no consistent relationship could be demonstrated between DTP immunization and susceptibility to infectious diseases.

Alaska↗
PubMed1991

The treatment of cognitive impairment in Alzheimer's disease: beyond the cholinergic approach.

Despite the well-founded rationale for the use of cholinomimetic and monoaminergic agents in the treatment of Alzheimer's disease, thus far, these strategies have only led to modest results. None of the drugs assessed to date have been shown to improve cognitive function to a clinically significant degree in patients with Alzheimer's disease. Some agents have produced mild improvements on specific tests, whereas others seem to slow down the progression of the disease. This article provides a brief overview of the current trends in the treatment of cognitive dysfunction in Alzheimer's disease.

Alzheimer Disease↗
PubMed1990

Ethanol and synaptosomal calcium homeostasis.

The effect of ethanol on synaptosomal calcium homeostasis was studied in the rat using the fluorescent dye, fura-2, and 45Ca uptake. The mitochondrial poison, cyanide, caused a substantial rise in intracellular free Ca2+ concentration, [Ca2+]i, over that of control synaptosomes. This rise was enhanced by ethanol. Ethanol also augmented the rise in [Ca2+]i induced by ouabain, indicating that modulation of Na(+)-Ca2+ exchange is probably not the underlying mechanism. The Ca2+ channel blockers, verapamil and La3+, also failed to inhibit the rise in [Ca2+]i caused by ethanol. Preincubation of synaptosomes with caffeine, however, caused a significant decrease in the rise of [Ca2+]i due to ethanol, suggesting that ethanol exerts effects on Ca2+ homeostasis at the level of the endoplasmic reticulum.

Animals↗