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2.  Brief alcohol intervention in a psychiatric outpatient setting: a randomized controlled study 
Background
Although brief alcohol intervention (BI) is widely studied, studies from psychiatric outpatient settings are rare. The aim of this study was to investigate the effects of two variants of BI in psychiatric outpatients. By using clinical psychiatric staff to perform the interventions, we sought to collect information of the usefulness of BI in the clinical setting.
Methods
Psychiatric outpatients with Alcohol Use Disorders Identification Test (AUDIT) scores indicating hazardous or harmful drinking were invited to participate in the study. The outpatients were randomized to minimal (assessment, feedback, and an informational leaflet) or BI (personalized advice added). Measurements were performed at baseline and at six and 12 months after the intervention. The primary outcome was change in AUDIT score at the 12-month follow-up.
Results
In all, 150 patients were enrolled and received either a minimal intervention (n = 68) or BI (n = 82). At 12 months, there was a small reduction in AUDIT score in both groups, with no significant differences in outcome between groups. At 12-month follow-up, 21% of participants had improved from a hazardous AUDIT score level to a nonhazardous level, and 8% had improved from a harmful level to a hazardous level (8%).
Conclusions
Brief alcohol interventions may result in a reduction of AUDIT score to a small extent in psychiatric patients with hazardous or harmful alcohol use. Results suggest that BI may be of some value in the psychiatric outpatient setting. Still, more profound forms of alcohol interventions with risky-drinking psychiatric patients need elaboration.
doi:10.1186/1940-0640-7-23
PMCID: PMC3507638  PMID: 23186026
Brief intervention; Alcohol intervention; Hazardous use; Harmful use; Psychiatric outpatients
3.  Competing Definitions of Schizophrenia: What Can Be Learned From Polydiagnostic Studies? 
Schizophrenia Bulletin  2006;33(5):1178-1200.
The contemporary diagnoses of schizophrenia (sz)—Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition(DSM-IV) and International Classification of Diseases,10th Revision(ICD-10)—are widely considered as important scientific achievements. However, these algorithms were not a product of explicit conceptual analyses and empirical studies but defined through consensus with the purpose of improving reliability. The validity status of current definitions and of their predecessors remains unclear. The so-called “polydiagnostic approach” applies different definitions of a disorder to the same patient sample in order to compare these definitions on potential validity indicators.
We reviewed 92 polydiagnostic sz studies published since the early 1970s. Different sz definitions show a considerable variation concerning frequency, concordance, reliability, outcome, and other validity measures. The DSM-IV and the ICD-10 show moderate reliability but both definitions appear weak in terms of concurrent validity, eg, with respect to an aggregation of a priori important features. The first-rank symptoms of Schneider are not associated with family history of sz or with prediction of poor outcome. The introduction of long duration criteria and exclusion of affective syndromes tend to restrict the diagnosis to chronic stable patients. Patients fulfilling the majority of definitions (core sz patients) do not seem to constitute a strongly valid subgroup but rather a severely ill subgroup. Paradoxically, it seems that a century after the introduction of the sz concept, research is still badly needed, concerning conceptual and construct validity of sz, its essential psychopathological features, and phenotypic boundaries.
doi:10.1093/schbul/sbl065
PMCID: PMC3304082  PMID: 17158508
validation; diagnosis; polydiagnostic approach; concordance; schizophrenia concept; psychopathology; review
4.  Expression of Toll-like Receptor 9 in nose, peripheral blood and bone marrow during symptomatic allergic rhinitis 
Respiratory Research  2007;8(1):17.
Background
Allergic rhinitis is an inflammatory disease of the upper airway mucosa that also affects leukocytes in bone marrow and peripheral blood. Toll-like receptor 9 (TLR9) is a receptor for unmethylated CpG dinucleotides found in bacterial and viral DNA. The present study was designed to examine the expression of TLR9 in the nasal mucosa and in leukocytes derived from different cellular compartments during symptomatic allergic rhinitis.
Methods
The study was based on 32 patients with seasonal allergic rhinitis and 18 healthy subjects, serving as controls. Nasal biopsies were obtained before and after allergen challenge. Bone marrow, peripheral blood and nasal lavage fluid were sampled outside and during pollen season. The expression of TLR9 in tissues and cells was analyzed using immunohistochemistry and flow cytometry, respectively.
Results
TLR9 was found in several cell types in the nasal mucosa and in different leukocyte subpopulations derived from bone marrow, peripheral blood and nasal lavage fluid. The leukocyte expression was generally higher in bone marrow than in peripheral blood, and not affected by symptomatic allergic rhinitis.
Conclusion
The widespread expression of TLR9 in the nasal mucosa along with its rich representation in leukocytes in different compartments, demonstrate the possibility for cells involved in allergic airway inflammation to directly interact with bacterial and viral DNA.
doi:10.1186/1465-9921-8-17
PMCID: PMC1810251  PMID: 17328813
5.  Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis 
Respiratory Research  2005;6(1):100.
Background
Toll-like receptors enable the host to recognize a large number of pathogen-associated molecular patterns such as bacterial lipopolysaccharide, viral RNA, CpG-containing DNA and flagellin. Toll-like receptors have also been shown to play a pivotal role in both innate and adaptive immune responses. The role of Toll-like receptors as a primary part of our microbe defense system has been shown in several studies, but their possible function as mediators in allergy and asthma remains to be established. The present study was designed to examine the expression of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with intermittent allergic rhinitis, focusing on changes induced by exposure to pollen.
Methods
27 healthy controls and 42 patients with seasonal allergic rhinitis volunteered for the study. Nasal biopsies were obtained before and during pollen season as well as before and after allergen challenge. The seasonal material was used for mRNA quantification of Toll-like receptors 2, 3 and 4 with real-time polymerase chain reaction, whereas specimens achieved in conjunction with allergen challenge were used for immunohistochemical localization and quantification of corresponding proteins.
Results
mRNA and protein representing Toll-like receptors 2, 3 and 4 could be demonstrated in all specimens. An increase in protein expression for all three receptors could be seen following allergen challenge, whereas a significant increase of mRNA only could be obtained for Toll-like receptor 3 during pollen season.
Conclusion
The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation.
doi:10.1186/1465-9921-6-100
PMCID: PMC1243240  PMID: 16146574
6.  Concentration-dependent effects of native and polymerised α1-antitrypsin on primary human monocytes, in vitro 
BMC Cell Biology  2004;5:11.
Background
α1-antitrypsin (AAT) is one of the major serine proteinase inhibitors controlling proteinases in many biological pathways. There is increasing evidence that AAT is able to exert other than antiproteolytic effects. To further examine this question we compared how various doses of the native (inhibitory) and the polymerised (non-inhibitory) molecular form of AAT affect pro-inflammatory responses in human monocytes, in vitro. Human monocytes isolated from different donors were exposed to the native or polymerised form of AAT at concentrations of 0.01, 0.02, 0.05, 0.1, 0.5 and 1 mg/ml for 18 h, and analysed to determine the release of cytokines and to detect the activity of NF-κB.
Results
We found that native and polymerised AAT at lower concentrations, such as 0.1 mg/ml, enhance expression of TNFα (10.9- and 4.8-fold, p < 0.001), IL-6 (22.8- and 23.4-fold, p < 0.001), IL-8 (2.4- and 5.5-fold, p < 0.001) and MCP-1 (8.3- and 7.7-fold, p < 0.001), respectively, compared to buffer exposed cells or cells treated with higher doses of AAT (0.5 and 1 mg/ml). In parallel to increased cytokine levels, low concentrations of either conformation of AAT (0.02–0.1 mg/ml) induced NF-κB p50 activation, while 1 mg/ml of either conformation of AAT suppressed the activity of NF-κB, compared to controls.
Conclusions
The observations reported here provide further support for a central role of AAT in inflammation, both as a regulator of proteinase activity, and as a signalling molecule for the expression of pro-inflammatory molecules. This latter role is dependent on the concentration of AAT, rather than on its proteinase inhibitory activity.
doi:10.1186/1471-2121-5-11
PMCID: PMC400726  PMID: 15050036
7.  Circulating monocytes from healthy individuals and COPD patients 
Respiratory Research  2003;4(1):11.
Background
Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction associated with inflammation in which monocytes/macrophages are the predominant inflammatory cells. The only known genetic factor related to COPD is inherited PiZZ deficiency of α1-antitrypsin (AAT), an inhibitor of serine proteases.
Methods
We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency.
Results
After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD patient monocytes than from controls. LPS-stimulated release of IL-6 and MCP-1 was greater from COPD patient's monocytes relative to controls, while activation of control cells resulted in enhanced secretion of ICAM-1 and MMP-9 compared to COPD patients. Independent of disease status, monocytes from PiZZ AAT carriers released less TNFα (by 2.3-fold, p < 0.03).
Conclusions
The basal and LPS-stimulated secretion of specific pro-inflammatory molecules from circulating monocytes differs between healthy and COPD subjects. These findings may be valuable for further studies on the mechanisms involved in recruitment and activation of inflammatory cells in COPD.
doi:10.1186/1465-9921-4-11
PMCID: PMC239032  PMID: 14624669

Results 1-7 (7)