Personality Change following Internet-Based Cognitive Behavior Therapy for Severe Health Anxiety

Personality traits have traditionally been viewed as stable, but recent studies suggest that they could be affected through psychological treatment. Internet-based cognitive behavior therapy (ICBT) for severe health anxiety (DSM-IV hypochondriasis) has been shown to be effective in reducing health anxiety, but its effect on measures of personality traits has not been investigated. The main aim of this study was to investigate the impact of ICBT on personality traits in the three broad dimensions -neuroticism, extraversion and aggression. We hypothesized that participants in ICBT would reduce their level of neuroticism compared to controls that did not receive the active treatment. No specific predictions were made regarding extraversion and aggression. Data from a randomized controlled trial were used in which participants were allocated to 12 weeks of ICBT (n=40) or to a basic attention control condition (n=41). Personality traits were assessed with the Swedish Universities Scales of Personality and the primary outcome of health anxiety was the Health Anxiety Inventory. There was a significant interaction effect of group and time on neuroticism-related scales, indicating larger pre-to post-treatment reductions in the Internet-based CBT group compared to the control condition. Analyses at 6-month follow-up showed that changes were stable. Traits relating to extraversion and aggression were largely unchanged. This study is the first to demonstrate that a brief ICBT intervention for severe health anxiety causes long-term changes in measures of personality traits related to neuroticism. The treatment thus has a broader impact than just reducing health anxiety.Funding Agencies|Stockholm County council; Karolinska Institutet</p

Study on resting, roosting, foraging and nesting sites of few bird species at Mysore district, Karnataka, India

Three rhizosphere fungal isolates viz., PGPFYCM-2, PGPFYCM-8 and PGPFYCM-14 of Trichoderma harzianum, applied as seed treatment to a highly susceptible sunflower cultivar were evaluated for their ability to promote growth and induce resistance in sunflower against downy mildew disease caused by Plasmopara halstedii. Treatment of sunflower seeds with both conidial suspension (1þinspace×þinspace108 spores ml−1) and talc formulations (2.1þinspace×þinspace107 spores g−1) at 8 gþinspacekg−1 seeds and 10 gþinspacekg−1 seeds, significantly promoted growth and reduced disease incidence under both greenhouse and field conditions. Among the treatments, PGPFYCM-14 (1þinspace×þinspace108 spores ml−1) was highly significant (Pþinspace=þinspace0.05) in inducing resistance of 63 and 69 %, followed by PGPFYCM-2 which offered 41 and 42 % disease protection under greenhouse and field conditions respectively. Formulation treatments of PGPFYCM-14 also protected the plants significantly (Pþinspace=þinspace0.05) when compared to the untreated control. There was a significant increase in NPK macronutrients uptake in all the treated plants compared to the untreated control and maximum NPK uptake was observed with PGPFYCM-14 (1þinspace×þinspace108 spores ml−1). Under in vitro conditions, all the tested isolates expressed increase in seed germination and vigour index over the control. Tested plant growth promoting fungal (PGPF) isolates remain significant in enhancing vegetative and reproductive growth parameters, including plant height, early flowering, reduced crop duration, ear head size and crop yield under field conditions when compared to the untreated control

Therapist guided internet based cognitive behavioural therapy for body dysmorphic disorder: single blind randomised controlled trial

OBJECTIVES To evaluate the efficacy of therapist guided internet based cognitive behavioural therapy (CBT) programme for body dysmorphic disorder (BDD-NET) compared with online supportive therapy. DESIGN A 12 week single blind parallel group randomised controlled trial. SETTING Academic medical centre. PARTICIPANTS 94 self referred adult outpatients with a diagnosis of body dysmorphic disorder and a modified Yale-Brown obsessive compulsive scale (BDD-YBOCS) score of &amp;gt;= 20. Concurrent psychotropic drug treatment was permitted if the dose had been stable for at least two months before enrolment and remained unchanged during the trial. INTERVENTIONS Participants received either BDD-NET (n=47) or supportive therapy (n=47) delivered via the internet for 12 weeks. MAIN OUTCOME MEASURES The primary outcome was the BDD-YBOCS score after treatment and follow-up (three and six months from baseline) as evaluated by a masked assessor. Responder status was defined as a &amp;gt;= 30% reduction in symptoms on the scale. Secondary outcomes were measures of depression (MADRS-S), global functioning (GAF), clinical global improvement (CGI-I), and quality of life (EQ5D). The six month follow-up time and all outcomes other than BDD-YBOCS and MADRS-S at 3 months were not pre-specified in the registration at clinicaltrials.gov because of an administrative error but were included in the original trial protocol approved by the regional ethics committee before the start of the trial. RESULTS BDD-NET was superior to supportive therapy and was associated with significant improvements in severity of symptoms of body dysmorphic disorder (BDD-YBOCS group difference -7.1 points, 95% confidence interval -9.8 to -4.4), depression (MADRS-S group difference -4.5 points, -7.5 to -1.4), and other secondary measures. At follow-up, 56% of those receiving BDD-NET were classed as responders, compared with 13% receiving supportive therapy. The number needed to treat was 2.34 (1.71 to 4.35). Self reported satisfaction was high. CONCLUSIONS CBT can be delivered safely via the internet to patients with body dysmorphic disorder. BDD-NET has the potential to increase access to evidence based psychiatric care for this mental disorder, in line with NICE priority recommendations. It could be particularly useful in a stepped care approach, in which general practitioner or other mental health professionals can offer treatment to people with mild to moderate symptoms at low risk of suicide.Funding Agencies|Stockholm County Council; Karolinska Institutet; Swedish Research Council [K2013-61X-22168-01-3]; Swedish Society of Medicine (Soderstromska Konigska sjukhemmet) [SLS3B4451]</p

The Golgi-Localized gamma-Ear-Containing ARF-Binding (GGA) Proteins Alter Amyloid-beta Precursor Protein (APP) Processing through Interaction of Their GAE Domain with the Beta-Site APP Cleaving Enzyme 1 (BACE1)

Proteolytic processing of amyloid-β precursor protein (APP) by beta-site APP cleaving enzyme 1 (BACE1) is the initial step in the production of amyloid beta (Aβ), which accumulates in senile plaques in Alzheimer's disease (AD). Essential for this cleavage is the transport and sorting of both proteins through endosomal/Golgi compartments. Golgi-localized γ-ear-containing ARF-binding (GGA) proteins have striking cargo-sorting functions in these pathways. Recently, GGA1 and GGA3 were shown to interact with BACE1, to be expressed in neurons, and to be decreased in AD brain, whereas little is known about GGA2. Since GGA1 impacts Aβ generation by confining APP to the Golgi and perinuclear compartments, we tested whether all GGAs modulate BACE1 and APP transport and processing. We observed decreased levels of secreted APP alpha (sAPPα), sAPPβ, and Aβ upon GGA overexpression, which could be reverted by knockdown. GGA-BACE1 co-immunoprecipitation was impaired upon GGA-GAE but not VHS domain deletion. Autoinhibition of the GGA1-VHS domain was irrelevant for BACE1 interaction. Our data suggest that all three GGAs affect APP processing via the GGA-GAE domain.status: publishe

Data from: The Golgi-localized γ-ear-containing ARF-binding (GGA) proteins alter amyloid-β precursor protein (APP) processing through interaction of their GAE domain with the beta-site APP cleaving enzyme 1 (BACE1)

Proteolytic processing of amyloid-β precursor protein (APP) by beta-site APP cleaving enzyme 1 (BACE1) is the initial step in the production of amyloid beta (Aβ), which accumulates in senile plaques in Alzheimer’s disease (AD). Essential for this cleavage is the transport and sorting of both proteins through endosomal/Golgi compartments. Golgi-localized γ-ear-containing ARF-binding (GGA) proteins have striking cargo-sorting functions in these pathways. Recently, GGA1 and GGA3 were shown to interact with BACE1, to be expressed in neurons, and to be decreased in AD brain, whereas little is known about GGA2. Since GGA1 impacts Aβ generation by confining APP to the Golgi and perinuclear compartments, we tested whether all GGAs modulate BACE1 and APP transport and processing. We observed decreased levels of secreted APP alpha (sAPPα), sAPPβ, and Aβ upon GGA overexpression, which could be reverted by knockdown. GGA-BACE1 co-immunoprecipitation was impaired upon GGA-GAE but not VHS domain deletion. Autoinhibition of the GGA1-VHS domain was irrelevant for BACE1 interaction. Our data suggest that all three GGAs affect APP processing via the GGA-GAE domain

The Golgi-Localized γ-Ear-Containing ARF-Binding (GGA) Proteins Alter Amyloid-β Precursor Protein (APP) Processing through Interaction of Their GAE Domain with the Beta-Site APP Cleaving Enzyme 1 (BACE1) - Table 1

<p>The Golgi-Localized γ-Ear-Containing ARF-Binding (GGA) Proteins Alter Amyloid-β Precursor Protein (APP) Processing through Interaction of Their GAE Domain with the Beta-Site APP Cleaving Enzyme 1 (BACE1) - Table 1 </p

uncropped and unadjusted Westernblots

uncropped and unadjusted Westernblo

Deletion of GGA GAE domain but not VHS domain disrupts BACE1-GGA interaction in CoIPs.

<p>(A) HEK293 cells were co-expressed with BACE1-HA and either myc-tagged GGA_wt, -ΔVHS, -ΔGAT, or-ΔGAE constructs. Equal expression was controlled by Western blot (left panels). BACE1-HA was immunoprecipitated with anti-HA beads (Miltenyi Biotec), and precipitation and co-precipitation of the GGAs was controlled by Western blot (right panels). Deletion of the VHS domain of GGA 1, 2, or 3 did not disturb interaction with BACE1 compared with wt GGAs (Lanes 1+2). Likewise, deletion of the GAT domain had no effect on binding to BACE1 (Lane 3), whereas deletion of the GAE domain dramatically reduced binding of GGAs and BACE1 (Lane 4). (B) HEK293 cells were co-expressed with BACE1-cterm-HA and either myc-tagged GGA_wt, -ΔVHS, -ΔGAT, or-ΔGAE constructs. Equal expression was controlled by Western blot (left panels). BACE1-cterm-HA was immunoprecipitated with anti-HA beads (Miltenyi Biotec), and precipitation and co-precipitation of the GGAs was controlled by Western blot (right panels). Comparable to full-length BACE1, deletion of the VHS domain of GGA1, 2, or 3 did not disturb interaction with BACE1-cterm compared with wt GGAs (Lanes 1+2). Likewise, deletion of the GAT domain had no effect on binding to BACE1 (Lane 3), whereas deletion of the GAE domain dramatically reduced binding of GGAs and BACE1-cterm (Lane 4). (C) We tested whether BACE1 GGA1-GAE domain interaction is due to a direct binding of both proteins by using <i>in vitro</i> CoIP. Myc-tagged GGA1-wt, -ΔVHS, and-ΔGAE and HA-tagged BACE1 were expressed separately in HEK293 (left panel) and purified by immunoprecipitation using magnetic beads (Miltenyi Biotec) labeled with the corresponding antibodies (middle panel). Purified proteins were mixed and immunoprecipitated with anti-HA beads. Both GGA1-wt and GGA1-ΔVHS were co-precipitated by BACE1, but GGA1-ΔGAE was not, indicating direct binding of BACE1 and the GGA1-GAE domain.</p