Coping skills training and contingency management treatments for marijuana dependence: exploring mechanisms of behavior change

AIMS: Achieving abstinence in the treatment of marijuana dependence has been difficult. To date the most successful treatments have included combinations of motivation enhancement treatment (MET) plus cognitive-behavioral coping skills training (CBT) and/or contingency management (ContM) approaches. Although these treatment approaches are theoretically based, their mechanisms of action have not been explored fully. The purpose of the present study was to explore mechanisms of behavior change from a marijuana treatment trial in which CBT and ContM were evaluated separately and in combination. DESIGN: A dismantling design was used in the context of a randomized clinical trial. SETTING: The setting was an out-patient treatment research facility located in a university medical center. PARTICIPANTS: Participants were 240 adult marijuana smokers, meeting criteria for cannabis dependence. INTERVENTIONS: Participants were assigned to one of four 9-week treatment conditions: a case management control condition, MET/CBT coping skills training, ContM and MET/CBT + ContM. MEASUREMENTS: Outcome measures were total 90-day abstinence, recorded every 90 days for 12 months post-treatment. FINDINGS: Regardless of treatment condition, abstinence in near-term follow-ups was predicted most clearly by abstinence during treatment, but long-term abstinence was predicted by use of coping skills and especially by post-treatment self-efficacy for abstinence. CONCLUSIONS: It was concluded that the most efficacious treatments for marijuana dependence are likely to be those that increase self-efficacy.     

Plasma P-selectin is increased in thrombotic consumptive platelet disorders

P-selectin is a 140-kD protein found in the alpha-granules of platelets and the Weibel-Palade bodies of endothelial cells that on cell activation is expressed on the cell surface and also secreted into the plasma. The secreted form of P-selectin, like plasma P-selectin, differed from platelet membrane P-selectin in that its molecular mass was approximately 3 kD lower under reducing conditions. Both the secreted and plasma forms of P-selectin contained cytoplasmic sequence as determined by Western blot analysis with an affinity-purified rabbit anti-P-selectin cytoplasmic peptide antibody. We have measured plasma P- selectin and beta-thromboglobulin (beta TG) concurrently in (1) patients with consumptive thrombotic disorders, including disseminated intravascular coagulation (DIC), heparin-induced thrombocytopenia (HIT), and thrombotic thrombocytopenic purpura (TTP)/haemolytic uremic syndrome (HUS); (2) patients with idiopathic thrombocytopenic purpura (ITP); and (3) healthy controls. Patients with DIC, HIT, and TTP/HUS, but not ITP, had significantly elevated plasma P-selectin and beta TG levels when compared with their age-matched healthy controls. The increased plasma P-selectin and beta TG in patients with thrombotic disorders were likely to be the result of in vivo platelet and endothelial cell damage or activation. We also found that avoidance of veno-occlusion and other tedious measures customarily taken during blood collection and sample preparation to prevent in vitro platelet activation did not affect plasma P-selectin assay results. In addition, plasma P-selectin levels were not influenced by the presence of renal failure or heparin administration. These results indicate that plasma P- selectin may be a useful new marker for thrombotic diseases.     

A placebo controlled, dose-ranging, safety study of allogenic mesenchymal stem cells injected by endomyocardial delivery after an acute myocardial infarction.

AIMS: Although mesenchymal stem cells (MSCs) show promising signs in reducing myocardial infarct (MI) size, the safety of endomyocardial delivery and the most efficacious dose is unknown. METHODS AND RESULTS: Three days after MI, female Yorkshire swine (25-32 kg, age 2 months, n = 32) were randomized to endomyocardial delivery of one of three MSC doses (2.4 x 10(7), 2.4 x 10(8), 4.4 x 10(8) cells) or vehicle control. Animals were sacrificed at 12 weeks. There were no safety issues related to cell delivery and all animals tolerated the procedure. By magnetic resonance imaging infarct size (g) was decreased in the experimental groups and increased in the control group; 2.4 x 10(7): Delta -2.5 +/- 2.5 g, 2.4 x 10(8): -0.9 +/- 2.71 g, 4.4 x 10(8): -1.6 +/- 5.8 g, and control +3.6 +/- 3.4 g (P = 0.002, P = 0.016, and P = 0.055 compared with control, respectively). There was no effect on ejection fraction or left ventricular volumes. By histology there were no toxic effects of MSC delivery, however, few engrafted MSCs were observed. CONCLUSION: Direct MSC delivery into infarcted myocardium was safe and produced a local but not a functional effect. There was no dose-dependent effect. The effect of MSCs on infarct reduction may result from transient residence and subsequent paracrine effects.     

Cardiac CT in the Emergency Department: Contrasting Evidence from Registries and Randomized Controlled Trials

Purpose of Review

To compare outcomes between registries and randomized controlled trials of coronary computed tomographic angiography (CCTA)-based versus standard of care approaches to the initial evaluation of patients with acute chest pain.

Recent Findings

Randomized trials have demonstrated CCTA to be a safe and efficient tool for triage of low- to intermediate-risk patients presenting to the emergency department with chest pain. Recent studies demonstrate heterogeneous result using different standard of care approaches for evaluation of hard endpoints in comparison with standard evaluation. Also, there has been continued concern for increase in subsequent testing after coronary CTA.

Summary

Although CCTA improves detection of coronary artery disease, it is uncertain if it will bring improvement of long-term health outcomes at this point of time. Careful analysis of the previous results and further investigation will be required to validate evaluation of hard endpoints.

     

Three unrelated Rh D gene polymorphisms identified among blood donors with Rhesus CCee (r'r') phenotypes

Human red blood cells are traditionally typed as Rhesus (Rh)-positive or -negative depending on the presence or absence of the Rh D antigen. A recent report demonstrated that the Rh D gene is completely absent in Rh D-negative individuals. In this study, Rh D-negative blood donors with ccee (n = 25) and CCee (n = 3) phenotypes were examined for the presence of absence of the D gene. Polymerase chain reaction (PCR) probes that hybridize to the 5' and 3' regions of the Rh CcEe gene and the closely related D gene were used in a Southern analysis. The D gene was absent in all ccee phenotypes examined. The CCee phenotypes showed three Rh D polymorphisms: one donor lacked the D gene, one donor had a partial deletion on one D gene at the 3' region, and the remaining donor appeared to have one normal D gene within the intron/exon regions examined. We conclude that, while the D gene may be absent in the majority of Rh D-negative phenotypes, rarer polymorphisms also occur that prevent expression of the D antigen resulting in the Rh D-negative phenotype.     

B lymphoblastoid cell lines with normal and defective O-glycosylation established from an individual with blood group Tn

Individuals with the Tn blood group contain terminal serine/threonine- linked N-acetylgalactosamine residues in their blood cells. This is due to lack of UDP-D-galactose: D-N-acetyl galactosamine beta-D-galactosyl transferase from part of their red cells and probably from their leukocytes. We have established B lymphoblastoid cell lines from such an individual by in vitro infection of his lymphocytes with Epstein- Barr virus. The original line contained a mixture of cells reactive and nonreactive with Helix pomatia lectin (Hp). These cells were subcloned after staining with fluorescent Hp by a fluorescence-activated cell sorter (FACS) into homogeneous, phenotypically stable lines of Hp- positive (Hp+) and Hp-negative (Hp-) cells. The molecular differences between the membrane glycoproteins were characterized by carbohydrate- specific surface labeling techniques, Hp affinity chromatography, polyacrylamide slab gel electrophoresis and glycopeptide/oligosaccharide analysis. The major O-glycosidic membrane glycoprotein (GP105) was retained on Hp-Sepharose columns only from Hp+ cells, whereas the common leukocyte antigen (GP160-200) was partially retained on Hp columns from both lines. These proteins were isolated by immune precipitation with monoclonal antibodies and characterized. The results show that the GP105 glycoprotein from Hp+ cells contains terminal N-acetylgalactosamine residues but also more complex oligosaccharides. The common leukocyte antigen showed different electrophoretic mobilities in Hp+ and Hp- cells. UDP-galactose D-N- acetyl galactosamine beta-galactosyl transferase was almost absent in the Hp+ cells. These cell lines are useful for studies on the functional role and regulation of the biosynthesis of O-glycosidic carbohydrates.     

Determinants of Pain Treatment Response and Nonresponse: Identification of TMD Patient Subgroups

The purpose of the present study was to determine if we could identify a specific subtype of temporomandibular disorder (TMD) pain patients that does not respond to treatment. Patients were 101 men and women with chronic TMD pain recruited from the community and randomly assigned to 1 of 2 treatment conditions: a standard conservative care (STD) condition or a standard care plus cognitive-behavioral therapy condition (STD + CBT) in which patients received all elements of STD but also received cognitive-behavioral coping skills training. Growth mixture modeling, incorporating a series of treatment-related predictors, was used to distinguish several distinct classes of responders or nonresponders to treatment based on reported pain over a 1-year follow-up period. Results indicated that treatment nonresponders accounted for 16% of the sample and did not differ from treatment responders on demographics or temporomandibular joint pathology, but that they reported more psychiatric symptoms, poorer coping, and higher levels of catastrophizing. Treatment-related predictors of membership in treatment responder groups versus the nonresponder group included the addition of CBT to STD, treatment attendance, and decreasing catastrophization. It was concluded that CBT may be made more efficacious for TMD patients by placing further emphasis on decreasing catastrophization and on individualizing care.     

Myocardial infarct size quantification by MR imaging early after coronary artery occlusion in dogs

The feasibility of using magnetic resonance (MR) imaging to estimate myocardial infarct size was explored in an in vitro model using only the inherent differences in contrast between infarcted and noninfarcted myocardium. Eight dogs underwent coronary occlusion; their hearts were removed 6 hours later. Estimates of T2 for normal and infarcted myocardium were derived from MR images. Infarct size was quantified anatomically using triphenyltetrazolium-chloride (TTC) staining and compared with MR estimates. The T2 values derived from the images clearly discriminated between infarcted (126 +/- 22 msec) and normal myocardium (88 +/- 10 msec, P less than .05), providing images with good contrast between normal and infarcted myocardium. Comparable differences in T2 values were also noted from spectrometric determinations. Estimates of infarct size by MR imaging compared well with TTC estimates (r = 0.98) over a wide range of infarct sizes from 3% to 29% of the left ventricular mass. These results suggest the potential for in vivo quantification of infarct size based on the inherent contrast difference between infarcted and normal myocardium.