The screening and treatment of undiagnosed depression in patients with chronic obstructive pulmonary disease (COPD) in a general practice.

AIMS AND OBJECTIVES: To screen for, and to treat, depression in COPD patients in a general practice surgery, and to test the feasibility of the screening method. METHODS: We sent The Beck Depression Inventory (BDI) Short-Form Questionnaire to all patients on the COPD register (n=69) by post, excluding those already diagnosed with depression (n=3). We sent appointments to all responders with moderate to severe depression and offered them treatment including antidepressants and pulmonary rehabilitation if the diagnosis was confirmed. RESULTS: Of the 66 patients to whom we sent questionnaires, 43 were returned completed and 13 of these had significant depression (30%). 10 of these patients were contactable and attended for review. The diagnosis of depression was confirmed in all 10 cases. Treatment options were discussed; five chose antidepressant medication, three chose pulmonary rehabilitation and two declined treatment. CONCLUSION: We identified and treated a significant number of depressed COPD patients in a general practice setting using this screening method. This method could have wider applications for screening, although further trials are needed.     

Benefits of enriched intervention compared with standard care for patients with recent-onset psychosis: a metaanalytic approach.

OBJECTIVE: To assess the effectiveness of enriched intervention (EI) on symptomatic and functional outcomes, compared with standard care (SC). METHOD: Studies were retrieved from search engines and, using a metaanalytic approach, we compared El trials with SC trials. Eleven EI sample trials (1053 patients) and 6 SC sample trials (500 patients), totalling data from 1553 patients (69% male), were examined. We calculated the effect sizes (ESs) of both symptomatic and functional improvement over a follow-up period of about 1 year. RESULTS: Significant differences between El and SC were observed at follow-up for the improvement of both positive and negative symptoms, respectively: positive, EI = -1.54 (95%CI, -1.63 to -1.45 ) and SC = -1.07 (95%CI, -1.19 to -0.94) (Qbetween = 40.3, df 1, P < 0.001); negative, EI= -0.44 (95%CI, -0.53 to -0.35) and SC = -0.18 (95%Cl, -0.31 to -0.05) (Qbetween = 10.6, df 1, P < 0.01). We also observed a significant difference between the El and the SC groups for functional improvement over the follow-up period with mean EI = 1.11 (95%CI, 0.99 to 1.23) and SC = 0.63 (95%CI, 0.49 to 0.77) (Qbetween = 24.5, df 1, P < 0.001). CONCLUSIONS: There is now quantitative evidence across multiple studies and sites to indicate that Els for patients with recent-onset psychosis are significantly more effective than SC for symptomatic and functional improvement over a period of about 1 year.     

Time after excision and temperature alter ex vivo tissue relaxation time measurements

Previously unreported effects of tissue storage were recently observed in the authors' experimental magnetic resonance (MR) studies. To evaluate the effect of elapsed time after excision and storage temperature on tissue relaxation time measurements, tissue samples from the liver, pancreas, kidney, testis, spleen, and brain were obtained in rats. T1 and T2 were first measured within 5 minutes of excision, and between subsequent measurements, tubes were kept in a water bath at 40°C, at room temperature (28°C), or in an ice bath (4°C). Cellular and organellar integrity was assessed with electron microscopy and correlated with the MR findings. At 40°C (20-MHz spectrometer), the T1 of liver decreased from 280 msec ± 8 to 212 msec ± 10 during the first 60 minutes; the T1 of pancreas decreased from 276 msec ± 3 to 208 msec ± 2. Other tissues showed less than a 5% decrease in T1. T2 changes were smaller than T1 changes in all tissues. Electron microscopy of pancreatic acinar cells showed postmortem changes in mitochondria evolving over the first 60 minutes after death. Manganese loading experiments implicated mitochondrial manganese stores in the observed enhanced postmortem decrease in T1. This study calls into question reported relaxation time data for liver and pancreas. MR studies of excised tissues must account for time and temperature to prevent systematic experimental errors.     

Morphogenetic adaptation of the looping embryonic heart to altered mechanical loads.

The biophysical mechanisms that drive and regulate cardiac looping are not well understood, but mechanical forces likely play a central role. Previous studies have shown that cardiac torsion, which defines left-right directionality, is caused largely by forces exerted on the heart tube by a membrane called the splanchnopleure (SPL). Here we show that, when the SPL is removed from the embryonic chick heart, torsion is initially suppressed. Several hours later, however, normal torsion is restored. This delayed torsion coincides with increased myocardial stiffness, especially on the right side of the heart. Exposure to the myosin inhibitor Y-27632 suppressed both responses, suggesting that the delayed torsion is caused by an abnormal cytoskeletal contraction. This hypothesis is supported further by computational modeling. These results suggest that the looping embryonic heart has the ability to adapt to changes in the mechanical environment, which may play a regulatory role during morphogenesis.     

Alterations in cholinergic and non-cholinergic neurotransmitter receptor densities in transgenic Tg2576 mouse brain with beta-amyloid plaque pathology.

Cholinergic deficits in Alzheimer's disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. To address the question whether beta-amyloid may contribute to these deficits, brain tissue from transgenic Tg2576 mice with Alzheimer plaque pathology at ages of 5 (still no significant plaque load) and 17 months (moderate to high cortical beta-amyloid plaque load) were examined for a number of cholinergic and non-cholinergic markers. Transgenic mice with no significant plaque load demonstrated reduced hemicholinium-3 (HCh-3) binding to choline uptake sites in anterior brain regions as compared to non-transgenic littermates, while in aged transgenic mice with high number of plaque deposits decreased HCh-3 binding levels were accompanied by increased vesicular acetylcholine transporter binding in selected cortical brain regions. In aged transgenic mice GABA(A), NMDA, AMPA, kainate, and beta-adrenergic as well 5-HT(1A)- and 5-HT(2A)-receptor binding levels were hardly affected, whereas alpha(1)- and alpha(2)-adrenoceptor binding was increased in selected cerebral cortical regions as compared to non-transgenic littermates. The development of changes in both cholinergic and non-cholinergic markers in transgenic Tg2576 mouse brain already before the onset of progressive plaque deposition provides in vivo evidence of a modulatory role of soluble beta-amyloid on cortical neurotransmission and may be referred to the deficits in learning and memory observed in these mice also before significant plaque load.