Monitoring change in community-oriented treatment programs.

F H Bliss; R H Moos; E J Bromet

doi:10.1002/1520-6629(197610)4:4<315::aid-jcop2290040402>3.0.co;2-w

Home/Archive/PubMed

PubMed · 10243948

Monitoring change in community-oriented treatment programs.

F H Bliss·R H Moos·E J Bromet

View original source ↗Export metadata ↓

Abstract

Changes in the social climate of two alcoholism treatment programs were evaluated by repeated assessments with the Community-Oriented Programs Environment Scale (COPES). The programs were similar in size and treatment orientation, but differed in physical and organizational setting, program length, and patient and staff characteristics. Specific and unique changes occurring within the treatment programs resulted in corresponding changes in relevant dimensions of the programs' social climates. The practical utility of COPES evaluations in instituting quality control and evaluating the results of change in community-oriented treatment programs is discussed.

Explore related subjects

Alcoholism Community Mental Health Services Halfway Houses Health Facilities Health Facility Environment Humans Outcome and Process Assessment, Health Care Rehabilitation Centers Social Change Social Environment Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

F H Bliss, R H Moos, E J Bromet. 1976. Monitoring change in community-oriented treatment programs.. https://doi.org/10.1002/1520-6629(197610)4%3A4%3C315%3A%3Aaid-jcop2290040402%3E3.0.co%3B2-w

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

How does alcohol impair neuronal migration?

Maternal alcohol consumption during pregnancy can cause serious birth defects, of which fetal alcohol syndrome (FAS) is the most devastating. Recognized by characteristic craniofacial abnormalities and growth deficiency, this condition produces severe alcohol-induced damage in the developing brain. FAS children experience ataxia; deficits in intellectual functioning; and difficulties in learning, memory, problem solving, and attention. Multiple aspects of central nervous system development can be affected by alcohol exposure, but the most striking abnormalities are neuronal and glial migration. Little is known about cellular mechanisms by which alcohol affects the migration of immature neurons. Recently, it has been found that Ca(2+) signaling and cyclic nucleotide signaling are the central targets of the action of alcohol in neuronal cell migration. Most importantly, the aberrant migration of immature neurons caused by alcohol exposure is significantly ameliorated by controlling the activity of these second-messenger pathways. In this Mini-Review, we first describe how alcohol exposure impairs the migration of cerebellar granule cells and then discuss the signaling mechanisms involved.

Alcoholism↗

PubMed2007

The serotonin transporter gene and alcoholism: the two pathways to suicidal behavior.

Explore the source record for details and available documents.

Alcoholism↗

PubMed2007

The alcoholic lung: epidemiology, pathophysiology, and potential therapies.

Epidemiological evidence gathered only in the past decade reveals that alcohol abuse independently increases the risk of developing the acute respiratory distress syndrome by as much as three- to fourfold. Experimental models and clinical studies are beginning to elucidate the mechanisms underlying this previously unrecognized association and are revealing for the first time that chronic alcohol abuse causes discrete changes, particularly within the alveolar epithelium, that render the lung susceptible to acute edematous injury in response to sepsis, trauma, and other inflammatory insults. Recent studies in relevant animal models as well as in human subjects are identifying common mechanisms by which alcohol abuse targets both the alveolar epithelium and the alveolar macrophage, such that the risks for acute lung injury and pulmonary infections are inextricably linked. Specifically, chronic alcohol ingestion decreases the levels of the antioxidant glutathione within the alveolar space by as much as 80-90%, and, as a consequence, impairs alveolar epithelial surfactant production and barrier integrity, decreases alveolar macrophage function, and renders the lung susceptible to oxidant-mediated injury. These changes are often subclinical and may not manifest as detectable lung impairment until challenged by an acute insult such as sepsis or trauma. However, even otherwise healthy alcoholics have evidence of severe oxidant stress in the alveolar space that correlates with alveolar epithelial and macrophage dysfunction. This review focuses on the epidemiology and the pathophysiology of alcohol-induced lung dysfunction and discusses potential new treatments suggested by recent experimental findings.

Alcoholism↗