Therapeutic intervention for internalized stigma of severe mental illness: A systematic review and meta-analysis.

OBJECTIVE: Internalized stigma can lead to pervasive negative effects among people with severe mental illness (SMI). Although prevalence of internalized stigma is high, there is a dearth of interventions and meanwhile a lack of evidence as to their effectiveness. This study aims at unraveling the existence of different therapeutic interventions and the effectiveness internalized stigma reduction in people with SMI via a systematic review and meta-analysis. METHODS: Five electronic databases were searched. Studies were included if they (1) involved community or hospital based interventions on internalized stigma, (2) included participants who were given a diagnosis of SMI>50%, and (3) were empirical and quantitative in nature. RESULTS: Fourteen articles were selected for extensive review and five for meta-analysis. Nine studies showed significant decrease in internalized stigma and two showed sustainable effects. Meta-analysis showed that there was a small to moderate significant effect in therapeutic interventions (SMD=-0.43; p=0.003). Among the intervention elements, four studies suggested a favorable effect of psychoeducation. Meta-analysis showed that there was small to moderate significant effect (SMD=-0.40; p=0.001). CONCLUSION: Most internalized stigma reduction programs appear to be effective. This systematic review cannot make any recommendation on which intervention is more effective although psychoeducation seems most promising. More Randomized Controlled Trials (RCT) on particular intervention components using standard outcome measures are recommended in future studies.

Synthesis and antiarrhythmic activity of novel 3-alkyl-1-[omega-[4-[(alkylsulfonyl)amino]phenyl]-omega- hydroxyalkyl]-1H-imidazolium salts and related compounds. 2.

Novel analogues of the class III antiarrhythmic agent 1-[2-hydroxy-2-[4-[(methylsulfonyl)amino]phenyl]ethyl]-3-methyl-1H- imidazolium chloride, 1 (CK-1649), were prepared and investigated for their class III electrophysiological activity on isolated canine cardiac Purkinje fibers and ventricular muscle tissue. Structure-activity relationships are discussed for a series of 11 compounds. One compound, N-[4-[1-hydroxy-2-(4,5-dihydro-2-methyl-1H-imidazol-1- yl)ethyl]phenyl]methanesulfonamide hydrochloride, 9, was comparable in activity to 1 in vitro and prolonged the functional refractory period in anesthetized dogs when given intraduodenally. Unlike 1, compound 9 was ineffective at preventing ventricular tachycardia induced by programmed electrical stimulation in anesthetized dogs 24 h after an acute myocardial infarction.

Synthesis and class III antiarrhythmic activity of (phenylbut-2-enyl)ammonium salts. Effect of conformation on activity.

The syntheses of seven 4-(substituted phenyl)but-2-en(or yn)yl quaternary ammonium salts and four related tertiary amines are described. The Meerwein arylation reaction was the preferred synthetic method for the required intermediate 1-aryl-4-halo-2-butenes (15a-c, 18). In the case of 18, the trans stereochemistry of the Meerwein adduct of 2,3-dimethylbutadiene was established unambiguously by 2D NMR and X-ray studies. The title compounds represent conformationally restricted analogues of the class III antiarrhythmic agent clofilium (1) and exhibit comparable potency and efficacy in the in vitro evaluation using isolated canine Purkinje fibers. These results suggest that the alkylene chain in 1 is extended in the active conformation. Computer-aided conformational analysis (MM2) supports this conclusion. Selective catalytic hydrogen conditions were developed for the conversion of the unsaturated analogue 2 to clofilium (1) with minimal hydrogenolysis of the allylic quaternary ammonium moiety, thus completing a novel and efficient synthesis of this substance.

Radiopharmaceuticals XXVII. 18F-labeled 2-deoxy-2-fluoro-d-glucose as a radiopharmaceutical for measuring regional myocardial glucose metabolism in vivo: tissue distribution and imaging studies in animals.

18F-2-Deoxy-2-fluoro-D-glucose (18FDG) is rapidly extracted by the mouse heart, and the radioactivity in heart (3-4% per organ) remains relatively constant for 2 hr post injection. The brain uptake (2-3% per organ) remained relatively constant throughout the time course of the study. Liver, lungs, kidneys, small intestine, and blood all showed a rapid clearance of radioactivity after injection of 18FDG. At 120 min the heart-to-lung ratio was 12 and heart-to-liver ratio was 32. Urinary excretion of activity was approximately 16% of the injected dose at 60 min. The uptake of radioactivity by dog heart following the intravenous administration of 18FDG was 2.8-4.1% at 60 min and 2.4% at 135 min; it was regionally distributed, the areas of highest activity being the left ventricle and the interventricular septum. The brain activity was 2.1-3.5% at 120 min, with a ratio of gray matter-to-white matter of 2-3:1. Urinary excretion in dogs was 16% and 50% of the injected dose at 60 and 135 min. The chemical form of the activity in the urine, although unidentified, was not 18F-. Cross-sectional images of the myocardium of the dog after intravenous injection of 18FDG were obtained using emission tomography.

A fluorinated glucose analog, 2-fluoro-2-deoxy-D-glucose (F-18): nontoxic tracer for rapid tumor detection.

Rapid uptake of F-18 FDG was observed in a variety of transplanted and spontaneous tumors in animals. The tumor uptake reached a peak by 30 min and remained relatively constant up to 60 min, with a very slow wash-out of F-18 activity from the tumor thereafter. Tumor-to-normal tissue and tumor-to-blood ratios ranged from 2.10-9.15 and 2.61-17.82, respectively, depending on the type of tumor. A scintiscan of a seminoma in a dog showed very high uptake in the viable part and lack of uptake in the necrotic mass. Toxicological studies in mice using 1000 times human tracer dose (HTD) per wk for 3 wk and in dogs using 50 times HTD per wk for 3 wk did not show any evidence of acute or chronic toxicity.