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Biomedical subjects

P J Abbott

Publications and source records attributed to P J Abbott.

At least 19 recordsLinked to original sources
PubMed1998

AIDS risk behavior in opioid dependent patients treated with community reinforcement approach and relationships with psychiatric disorders.

This study examined the Community Reinforcement Approach's (CRA) effect on AIDS risk behaviors and the relationship between comorbid psychiatric disorders and the risk for AIDS behavior in opioid dependent patients entering methadone maintenance treatment. Additionally, we looked at AIDS risk behaviors as they related to the Addition Severity Index (ASI), Beck Depression Inventory, Symptom Checklist-90-Revised (SCL-90-R), and the Social Adjustment Scale-Self Report (SAS-SR). Subjects (N = 227) were drawn from a large clinical trial that examined the effectiveness of a Community Reinforcement Approach for treatment of opioid dependence. Both CRA and standard treatment demonstrated a significant effect on reduction of AIDS risk behaviors. There was no relationship found regarding comorbid psychiatric disorders with the risk for AIDS behavior. However, there were correlations with other psychiatric, social, and substance abuse variables. Multivariate analyses indicated that increased drug and legal ASI composite scores were the primary predictors of increased AIDS risk behavior.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Community reinforcement approach in the treatment of opiate addicts.

The authors studied the efficacy of the community reinforcement approach (CRA) as compared to standard counseling in opiate-dependent patients on methadone maintenance. One hundred eighty subjects were randomized to three treatment conditions: standard, CRA, and CRA with relapse prevention (CRA/RP). Of these, 151 subjects were followed up 6 months after intake. Since few of the RP sessions had been concluded at the 6-month follow-up, the two CRA groups were combined for analyses. Weekly urinalysis drug screens and Addiction Severity Index (ASI) scores at intake and 6 months were compared. The combined CRA groups did significantly better than the standard group in the following areas: consecutive opiate-negative urinalysis (3 weeks), and the 6-month ASI drug composite score. These results support the benefit of adding CRA strategies to the treatment of patients who are opiate dependent and on methadone maintenance. Because of insufficient treatment exposure to RP at the 6-month follow-up, the additive effect of RP could not be adequately evaluated; further follow-up will be required.

Behavior Therapy↗
PubMed1998

Traditional and western healing practices for alcoholism in American Indians and Alaska Natives.

The American Indian and Alaska Native population is a culturally diverse population with a current census of 1,959,000. Prior to White contact, there was historically little use of alcoholic beverages except for American Indians in the Southwest. After White contact, use and misuse of alcohol escalated rapidly; however, the prevalence, patterns, and problems of drinking alcoholic beverages vary enormously even in tribes closely linked geographically. American Indians and Alaska Natives have preserved and revitalized a number of traditional healing practices and applied these to the treatment of alcohol-related problems. These healing practices include the following: nativistic movements, sacred dances, sweat lodges, talking circle, four circles, and cultural enhancement programs. Additionally, Western treatment approaches have been applied in the treatment of problems related to alcohol, such as medication for detoxification, disulfiram (Antabuse), Alcoholics Anonymous, and behavioral interventions. Several investigators have completed a small number of naturalistic follow-up studies, but no one has undertaken a randomized controlled trial looking at specific methods of alcohol treatment in American Indians or Alaska Natives. American Indian and Alaska Native communities have adapted and integrated both Traditional and Western approaches to fit their own unique sociocultural needs.

Adult↗
PubMed1996

American Indian and Alaska native aboriginal use of alcohol in the United States.

Alcohol beverages prior to White contact originated with the Mayan and the Aztec Nations and spread to the American Indians of the Southwest. Surprisingly, there are a number of accounts of alcohol use among other American Indians and Alaska Natives. Beverages were limited to wine and beer, and included: balche, pulque, and "haren a pitahaya" wines, tulpi beer and other beverages. White contact brought dramatic shifts in the use and function of alcoholic beverages in American Indian and Alaska Native societies.

Alaska↗
PubMed1995

Ambulatory medical detoxification for alcohol.

In the past decade, ambulatory medical detoxification for alcohol withdrawal has become increasingly utilized due to pressures to contain cost of treatment and research demonstrating its effectiveness. The research that describes this area spans the last 15 years. This article reviews the available literature on ambulatory detoxification and attempts to summarize and synthesize what is known about this area in order to make ambulatory medical detoxification readily reproducible in clinical practice. Finally, this article concludes with an analysis of the advantages and disadvantages of outpatient alcohol detoxification as compared to inpatient treatment.

Ambulatory Care↗
PubMed1994

Psychiatric disorders of opioid addicts entering treatment: preliminary data.

Psychiatric disorders have become an increasing concern in the treatment of substance abusers. The introduction of the Human Immunodeficiency Virus (HIV) into this population has further complicated treatment. This study examines the prevalence of psychiatric disorders in an opioid dependent population maintained on methadone. Results from this preliminary analysis show high rates of psychiatric disorders in this population. Additionally, needle sharing behavior appears to be increased in patients with a diagnosis of dysthymia. These findings have direct implications for aggressive screening and treatment of psychiatric disorders in methadone maintenance clinics.

Adult↗
PubMed1992

Carcinogenic chemicals in food: evaluating the health risk.

The presence of a low level of potentially harmful chemicals in food continues to be a concern to many individuals. A major concern is that these chemicals, which can be synthetic or naturally occurring, may be a causative factor in human cancer. Synthetic chemicals in food may be present either as specific additives or as contaminants derived from environmental or agricultural chemicals. Food also contains a variety of naturally occurring chemicals derived from vegetables or other plants. These may in some cases be considered as contaminants, and are occasionally used as specific additives. New chemicals can also be formed during the cooking or preserving processes. The capacity of any of these chemicals to induce cellular damage and mutation is minimized by natural defence systems such as an efficient cellular detoxification system and DNA repair. The factors influencing tumour formation in humans are numerous and interrelated and exposure to minor dietary chemicals needs to be considered in this context. Thus, the results of animal carcinogenicity assays on individual chemicals need to be interpreted with care, taking into account the mechanisms by which mutagenic and other chemicals initiate cancer, as well as the level of human exposure to these chemicals. Further research is necessary to determine the role, if any, of minor dietary components in tumour formation. Meanwhile, there needs to be a more holistic approach to the multitude of factors, including total diet, that may influence human cancer incidence. In this way, the relative risk of dietary chemicals may be given a more meaningful perspective for health professionals and consumers alike.

Animals↗
PubMed1987

Methylcyclopentadienyl manganese tricarbonyl (MMT) in petrol: the toxicological issues.

Methylcyclopentadienyl manganese tricarbonyl (MMT), when used as an octane improver in petrol, leads to increased airborne levels of manganese in the form of Mn3O4. The potential health effects of increased airborne manganese are considered in this paper. Manganese, unlike lead which it can replace in petrol, is a normal and essential component of the human diet and the intake from airborne manganese is slight by comparison to the normal dietary intake. The major toxicological effects of manganese, observed after long occupational exposure, are on the lung (manganese pneumonia) and the central nervous system (manganism). The small increase in airborne manganese from the use of MMT in petrol is 3-4 orders of magnitude lower than the level required to produce toxic symptoms of manganese exposure, even in areas of high traffic density, and no health risk from the use of MMT is likely.

Air Pollutants↗
PubMed1986

Caffeine: a toxicological overview.

The health effects of caffeine have been examined in a review of its toxicological and pharmacological properties together with its effect on children. Caffeine commonly causes symptoms of an acute overdose and withdrawal symptoms. These may be identified as anxiety in moderate consumers and can lead to severe central nervous system effects in heavy consumers. Pharmacological effects occur even at low doses but their severity is influenced by wide individual variation and the development of tolerance. Nevertheless, chronic consumption of caffeine is implicated in various minor symptoms of ill health and is associated with elevated serum cholesterol levels. At the doses that are consumed by humans, there is little evidence at present to suggest effects on reproduction, teratogenesis, tumour formation or the incidence of myocardial infarction. A reduced consumption of caffeine is advocated for all age groups.

Abnormalities, Drug-Induced↗
PubMed1985

Stimulation of recombination between homologous sequences on carcinogen-treated plasmid DNA and chromosomal DNA by induction of the SOS response in Escherichia coli K12.

Previous studies have shown that transformation of Escherichia coli by plasmid DNA modified in vitro by carcinogens leads to RecA-dependant recombination between homologous plasmid and chromosomal DNA sequences. The mechanism of this recombination has now been studied using recombination-deficient mutants, and the influence of induction of the SOS response on the level of recombination investigated. Plasmid pNO1523, containing the str+ operon (Sms), has been modified in vitro by either irradiation with UV light, or by reaction with (+/-) trans-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) and used to transform streptomycin-resistant hosts. The formation of Ampr transformants which also carry streptomycin resistance was used as a measure of the level of recombination between plasmid and chromosomal DNA. Transformation of recB and recC mutants produced no change in the level of recombination while in the recF mutant a significant decrease was observed compared to the wild type host. Thermal induction of the SOS response in tif-1 and tif-1 umuC mutants followed by transformation led to a four-fold increase in recombination in both cases. The results suggest that the streptomycin-resistant transformants arise exclusively via a recombinational pathway which is largely dependant on the recF gene product, and that this pathway is influenced by induction of the SOS response. These results are discussed in terms of the mechanism of this recombination.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1985

Hostility, somatic symptoms, and hypochondriacal fears and beliefs.

The authors administered self-rating scales of anger-hostility, somatic symptoms, and hypochondriacal fears and beliefs to seven groups of patients and nonpatients. Somatic symptoms were positively correlated with anger-hostility and were negatively correlated with feelings of friendliness; the correlation coefficients ranged from low to moderately high and were significant in most groups. Somatic symptoms tended to be associated more strongly with symptoms of anxiety and depression than with those of hostility. The associations of hypochondriacal fears and beliefs with hostility were inconsistent, varied between groups and with the concern measured. The findings do not support the view that anger or hostility are main or specific etiological factors either in somatization or in hypochondriacal fears or beliefs.

Adult↗
PubMed1984

The effect of methyl substituents on the in vitro metabolism of cyclopenta[a]phenanthren-17-ones: implications for biological activity.

The in vitro metabolism of 15,16-dihydrocyclopenta[a]phenanthren-17-one and its 11- and 12-methyl derivatives has been compared. All three compounds form trans-3,4-dihydrodiols having quasi-diequatorial conformations and 3R,4R configurations. The trans-3,4-dihydrodiol of the mutagenic, but non-tumorigenic 15,16-dihydrocyclopenta[a]phenanthren-17-one appears to undergo stereospecific epoxidation to a syn-diol epoxide. By contrast the 3,4-dihydrodiol of the nontumorigenic 15,16-dihydro-12-methylcyclopenta[a]phenanthren-17-one appears to undergo stereospecific epoxidation to an anti diol-epoxide equivalent to that generated from 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one which is a strong carcinogen. These results are discussed with reference to the biological activities of the parent compounds.

Animals↗
PubMed1983

Strain-specific tumorigenesis in mouse skin induced by the carcinogen, 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one, and its relation to DNA adduct formation and persistence.

The incidence of skin tumors has been studied in three strains of mice, namely, TO, C57BL, and DBA/2, after treatment with the carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one. After either a single dose followed by croton oil promotion or a continual dose of the carcinogen, tumors were observed in the TO and C57BL strains, with the TO mice having the shorter mean latent period. The DBA/2 mice, however, appeared to be resistant to tumor formation by either treatment. To understand the mechanism of resistance, several criteria have been investigated. Metabolism of the carcinogen was assessed in terms of the total DNA adduct formation and the pattern of individual adducts after separation by high-pressure liquid chromatography, and no major differences between the three strains was found. Similarly, the rates of disappearance of the individual adducts when measured over 14 days posttreatment were not strain specific. Persistent binding of the carcinogen after 2 months was found in all three strains and could be reduced markedly if croton oil was administered throughout this period. The ability of the phorbol esters to cause biochemical changes in both sensitive and resistant strains was indicated by the induction of ornithine decarboxylase in each of the three strains after treatment with either croton oil or its active component, 12-O-tetradecanoylphorbol-13-acetate.

Animals↗
PubMed1981

DNA adducts of the carcinogen, 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one, in vivo and in vitro: high pressure liquid chromatographic separation and partial characterization.

The 11-methyl derivative (11-methyl ketone) is the most carcinogenic of the series of methylated derivatives based on 15,16-dihydro-cyclopenta[a]phenanthren-17-one. The nucleoside adducts derived from [3H]-11-methyl ketone-modified mouse skin DNA have been separated by both Sephadex LH-20 chromatography and reverse-phase h.p.l.c. and compared to those derived from DNA modified in vitro with the [14C]-11-methyl ketone using rat liver microsomes. The in vivo modified DNA separated to give 6 adducts (designated I--VI) on h.p.l.c. The major in vivo adduct (80% total adducts) co-chromatographed with the major in vitro adduct. The metabolites of the 11-methyl ketone (designated a--g) have been separated by h.p.l.c., and the adducts derived from each of these individual metabolites determined by further metabolism in the presence of DNA. H.p.l.c. separation of these adducts has allowed characterization of the in vivo adducts. The major adduct (V) and possibly one of the minor adducts (IV) were derived from the 3,4-dihydro-3,4-diol of the 11-methyl ketone (metabolite e). Adducts II and III were derived from the 16- and 15-monohydroxylated derivatives of the 11-methyl ketone and also from their corresponding 3,4-diols and therefore are likely to be the 16- and 15-hydroxy derivatives, respectively, of adduct V. Adduct VI, however, although derived from the 15-hydroxy-3,4-diol had a late retention time on h.p.l.c., suggesting either a non-diol-epoxide adduct or a deoxyadenosine adduct. The use of [3H-G]DNA has established that the major adduct (V) and the 16-hydroxy-derived adduct (II) contain deoxyguanosine. Reaction of the carcinogen with [3H-A]poly[dA-dT) gave adduct VI which was the only adduct peak shown to contain [3H]deoxyadenosine.

Animals↗
PubMed1981

Mass spectral characterisation of the major DNA--carcinogen adduct formed from the metabolically activated carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one.

E. coli DNA, labelled with [14C]adenine and [14C]-guanine, was allowed to react with the [3H]-labelled carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenanthren-17-one in the presence of a microsomal metabolising system. Enzymatic hydrolysis of the DNA followed by Sephadex LH20 chromatography of its constituent nucleosides established that the major DNA - carcinogen adduct involved guanine, and not adenine. This was confirmed by submitting calf thymus DNA, which had been allowed to react with the unlabelled carcinogen, to pyrolysis electron impact mass spectrometry without further derivatisation. Analysis of a selected ion product (m/z 368) by means of mass-analysed kinetic energy spectrometry, a technique which allows study of the further fragmentation of the single, selected ion, revealed that the guanine moiety was attached via the nitrogen atom of its exocyclic amino group to C-1 of a 1,2,3,4-tetrahydro-2,3,4-trihydroxy derivative of the original carcinogen.

Biotransformation↗