60 research outputs found

    The effect of mindfulness group therapy on a broad range of psychiatric symptoms : A randomised controlled trial in primary health care

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    Background The need for psychotherapy in primary health care is on the increase but individual-based treatment is costly. The main aim of this randomised controlled trial (RCT) was to compare the effect of mindfulness-based group therapy (MGT) with treatment as usual (TAU), mainly individual-based cognitive behavioural therapy (CBT), on a broad range of psychiatric symptoms in primary care patients diagnosed with depressive, anxiety and/or stress and adjustment disorders. An additional aim was to compare the effect of MGT with TAU on mindful attention awareness. Methods This 8-week RCT took place in 2012 at 16 primary care centres in southern Sweden. The study population included both men and women, aged 20–64 years (n = 215). A broad range of psychiatric symptoms were evaluated at baseline and at the 8-week follow-up using the Symptom Checklist-90 (SCL-90). Mindful attention awareness was also evaluated using the Mindful Attention Awareness Scale (MAAS). Results In both groups, the scores decreased significantly for all subscales and indexes in SCL-90, while the MAAS scores increased significantly. There were no significant differences in the change in psychiatric symptoms between the two groups. The mindfulness group had a somewhat larger change in scores than the control group on the MAAS (P = 0.06, non-significant). Conclusions No significant differences between MGT and TAU, mainly individual-based CBT, were found in treatment effect. Both types of therapies could be used in primary care patients with depressive, anxiety and/or stress and adjustment disorders, where MGT has a potential to save limited resources. Trial registration ClinicalTrials.gov identifier: NCT01476371

    Characterization of long-term motor deficits in the 6-OHDA model of Parkinson's disease in the common marmoset.

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    Research aimed at developing new therapies for Parkinson's disease (PD) critically depend on valid animal models of the disease that allows for repeated testing of motor disabilities over extended time periods. We here present an extensive characterization of a wide range of motor symptoms in the 6-OHDA marmoset model of PD when tested over several months. The severity of motor deficits was quantified in two ways: (i) through manual scoring protocols appropriately adapted to include species specific motor behavior and (ii) using automated quantitative motion tracking based on image processing of the digital video recordings. We show that the automated methods allow for rapid and reliable characterization of motor dysfunctions, thus complementing the manual scoring procedures, and that robust motor symptoms lasting for several months could be induced when using a two-stage neurotoxic lesioning procedure involving one hemisphere at a time. This non-human primate model of PD should therefore be well suited for long-term evaluation of novel therapies for treatment of PD

    Severe breastfeeding difficulties: Existential lostness as a mother—Women's lived experiences of initiating breastfeeding under severe difficulties

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    A majority of women in Sweden initiate breastfeeding but almost a quarter stop or wean the infant in the first few weeks after birth because of difficulties. In order to develop care that facilitates initiation of breastfeeding and enables mothers to realize their expectations concerning breastfeeding, it is necessary to understand what having severe breastfeeding difficulties means for women who experience them. The aim of this study is to describe the lived experiences of initiating breastfeeding under severe difficulties. A reflective lifeworld research design was used. Eight women, seven primiparous and one multipara, were interviewed within 2 months of giving birth. The essential meaning of the phenomenon is described as “Existential lostness as a mother forcing oneself into a constant fight”. This pattern is further explicated through its constituents; shattered expectations, a lost time for closeness, being of no use to the infant, being forced to expose oneself, and gaining strength through sharing. The results show that mothers with severe breastfeeding difficulties feel alone and exposed because of their suffering and are lost in motherhood. Thus, adequate care for mothers should enhance the forming of a caring relationship through sharing rather than exposing

    A framework for mapping, visualisation and automatic model creation of signal-transduction networks

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    An intuitive formalism for reconstructing cellular networks from empirical data is presented, and used to build a comprehensive yeast MAP kinase network. The accompanying rxncon software tool can convert networks to a range of standard graphical formats and mathematical models

    Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy

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    Heart failure (HF) is a major cause of morbidity and mortality worldwide, highlighting an urgent need for novel treatment options, despite recent improvements. Aberrant Ca(2+) handling is a key feature of HF pathophysiology. Restoring the Ca(2+) regulating machinery is an attractive therapeutic strategy supported by genetic and pharmacological proof of concept studies. Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models. Mice harboring the PLN R14del pathogenic variant recapitulate the human dilated cardiomyopathy (DCM) phenotype; subcutaneous administration of PLN-ASO prevents PLN protein aggregation, cardiac dysfunction, and leads to a 3-fold increase in survival rate. In another genetic DCM mouse model, unrelated to PLN (Cspr3/Mlp(−/−)), PLN-ASO also reverses the HF phenotype. Finally, in rats with myocardial infarction, PLN-ASO treatment prevents progression of left ventricular dilatation and improves left ventricular contractility. Thus, our data establish that antisense inhibition of PLN is an effective strategy in preclinical models of genetic cardiomyopathy as well as ischemia driven HF

    GAD65 vaccination: 5 years of follow-up in a randomised dose-escalating study in adult-onset autoimmune diabetes.

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    AIMS/HYPOTHESIS: The aim of this study was to ascertain whether treatment of GAD65 autoantibody (GADA)-positive diabetic patients with alum-formulated recombinant GAD65 (GAD-alum) is safe and does not compromise beta cell function. METHODS: This Phase 2, placebo-controlled, dose-escalation clinical trial, which was randomized through a central office, was performed in 47 GADA-positive type 2 diabetic patients, who received subcutaneous injections of GAD-alum (4 [n = 9], 20 [n = 8], 100 [n = 9] or 500 [n = 8] mug) or placebo (n = 13) at weeks 1 and 4 of the trial. Participants and caregivers were blinded to group assignments. The primary outcome was safety as assessed by neurological tests, medications and beta cell function evaluated over 5 years, representing the end of the trial. RESULTS: No severe study-related adverse events occurred during the 5 year follow-up. None of the dose groups was associated with an increased risk of starting insulin treatment compared with the placebo group. The use of oral hypoglycaemic agents did not differ between the dose groups. After 5 years, fasting C-peptide levels declined in the placebo group (-0.24; 95% CI -0.41 to -0.07 log(10) nmol/l; p = 0.01) and the 500 microg dose group (-0.37; 95% CI -0.57 to -0.17 log(10) nmol/l; p = 0.003), but not in the 4 microg (-0.10; 95% CI -0.28 to 0.07 log(10) nmol/l; p = 0.20), 20 microg (0.04; 95% CI -0.12 to 0.19 log(10) nmol/l; p = 0.58) and 100 microg (0.00; 95% CI -0.20 to -0.20 log(10) nmol/l; p = 0.98) dose groups. CONCLUSIONS/INTERPRETATION: The primary outcome of safety was achieved, since no severe study-related adverse events occurred. TRIAL REGISTRATION: Because the study was initiated before 1 July 2005, the protocol was not registered in a registry. FUNDING: This trial was funded by the National Institutes of Health (grant numbers DK26190 and DK53004), the Swedish Research Council (grant number 72X-14064) and Diamyd Therapeutics (Stockholm, Sweden)
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