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Wildlife translocations, which involve the introduction of naive hosts into new environments with novel pathogens, invariably pose an increased risk of disease. The meningeal worm Parelaphostrongylus tenuis is a nematode parasite of the white-tailed deer (Odocoileus virginianus), which serves as its primary host and rarely suffers adverse effects from infection. Attempts to restore elk (Cervus canadensis) to the eastern US have been hampered by disease caused by this parasite. Using DNA sequence data from mitochondrial and nuclear genes, we examined the hypothesis that elk translocated within the eastern US could be exposed to novel genetic variants of P. tenuis by detailing the genetic structure among P. tenuis taken from white-tailed deer and elk at a source (Kentucky) and a release site (Missouri). We found high levels of diversity at both mitochondrial and nuclear DNA in Missouri and Kentucky and a high level of differentiation between states. Our results highlight the importance of considering the potential for increased disease risk from exposure to novel strains of parasites in the decision-making process of a reintroduction or restoration.
The paper suggests an innovative design research and intervention approach using a poststructuralist organizational education perspective. The potential of a high impact trans-epistemic design process is shown for the field of industry 4.0 and the specific context of cognitive assistive systems (CASs). The multi-layered approach addresses the design of technical, social and educational complexity to implement CASs sustainably on the shopfloor and exploit their potential in industry 4.0. Finally, we will shed light on how the approach can enhance deep organizational transformation in industry.
Poor sleep is a common complaint in postpartum depression (PPD). Depression as well as sleep disturbances may affect parenting functions and mother-infant relationship. The purpose of this study was to examine the relationship between objective sleep data, parenting stress and bonding in PPD.
Forty-five mothers (age: 34.5 ± 5.4 years SD) suffering from PPD were examined 212 ± 156 days (SD) after parturition. Depression was measured by Hamilton Depression Rating Scale (HDRS-ADS) and Beck Depression Inventory (BDI). Parenting stress and bonding were assessed by self report scales, i.e. Parenting Stress Index (PSI) and Postpartum Bonding Questionnaire (PBQ). In a subsample of 10 participants sleep parameters were assessed by actigraphy and sleep logs during seven consecutive days. Actigraphic sleep parameters were put in relation to severity of depression, PSI and PBQ scores.
Poor sleep, i.e. low total sleep time (TST) was negatively correlated to depression (HRDS-ADS) (r = -.63; p < .05). Low TST was associated with poor bonding (r = -.82; p = .02), especially attitudes of “rejection and anger”. Severity of depression (BDI) was correlated with parenting stress (r =.50; p =.005). Mothers with high parenting stress tended to have more difficulties in bonding (r =.65; p =.016). Neither sleep parameters nor parenting stress and bonding were correlated with the infant's age.
In PPD poor sleep should be recognized and treated early, because it is associated to parenting stress and disturbed bonding, which might have a detrimental impact on mother-infant relationship.
We report the results from the first 12 months of a 2-year maintenance phase of a study evaluating long-term efficacy and safety of venlafaxine extended-release (XR) in preventing recurrence of depression.
Patients with recurrent unipolar depression (N=1096) were randomly assigned in a 3:1 ratio to 10-week treatment with venlafaxine XR (75 mg/d to 300 mg/d) or fluoxetine (20 mg/d to 60 mg/d). Responders (HAM-D17 total score ≤12 and ≥50% decrease from baseline) entered a 6-month, double-blind, continuation phase on the same medication. Continuation phase responders enrolled into the maintenance treatment period consisting of 2 consecutive 12-month phases. At the start of each maintenance phase, venlafaxine XR responders were randomly assigned to double-blind treatment with venlafaxine XR or placebo; fluoxetine responders continued for each period. Time to recurrence (HAM-D17 total score >12 and <50% reduction from acute phase baseline at 2 consecutive visits or the last visit prior to discontinuation) was evaluated using Kaplan-Meier methods and compared between groups using log-rank tests.
At the end of the continuation phase, venlafaxine XR responders were randomly assigned to venlafaxine XR (n=164) or placebo (n=172); 129 patients in each group were evaluated for efficacy. The cumulative probability of recurrence through 12 months was 23.1% (95% CI: 15.3, 30.9) for venlafaxine XR and 42.0% (95% CI: 31.8, 52.2) for placebo (P=0.005).
Twelve months of venlafaxine XR maintenance treatment was effective in preventing recurrence in depressed patients who had been successfully treated with venlafaxine XR during acute and continuation therapy.
This study evaluated the efficacy and safety of venlafaxine extended-release (XR) in preventing recurrence of depression.
Outpatients with recurrent unipolar depression (N=1096) were randomly assigned in a 3:1 ratio to 10-week treatment with venlafaxine XR (75 mg/d to 300 mg/d) or fluoxetine (20 mg/d to 60 mg/d). Responders (HAM-D17 ≤12 and ≥50% decrease from baseline) entered a 6-month, double-blind, continuation phase on the same medication. Continuation phase responders enrolled into maintenance treatment consisting of 2 consecutive 12-month phases. At the start of each maintenance phase, venlafaxine XR responders were randomized to double-blind treatment with venlafaxine XR or placebo; fluoxetine responders continued on fluoxetine. Time to recurrence (HAM-D17 >12 and <50% reduction from acute phase baseline at 2 consecutive visits or the last valid visit prior to discontinuation) was evaluated using Kaplan-Meier methods and compared between groups using log-rank tests.
In the second maintenance phase, the cumulative probabilities of recurrence through 12 months in the venlafaxine XR (n=43) and placebo (n=40) groups were 8.0% (95% CI: 0.0, 16.8) and 44.8% (95% CI: 27.6, 62.0), respectively (P<0.001). The probabilities of recurrence over 24 months for patients assigned to venlafaxine XR (n=129) or placebo (n=129) for the first maintenance phase were 28.5% (95% CI 18.3, 37.8) and 47.3% (95% CI 36.4, 58.2), respectively (P=0.005).
An additional 12 months of venlafaxine XR maintenance therapy was effective in preventing recurrence in depressed patients who had responded to venlafaxine XR after acute, continuation, and 12 months' initial maintenance therapy.
In a recent randomised controlled trial (Exercise-I) the effect of aerobic indoor cycling on hippocampal volume as well as magnetic resonance imaging (MRS) metabolites, neuropsychological and clinical variables an physical fitness were determined comparing patients with multi-episode schizophrenia and healthy controls (Pajonk et al. 2010).
In a subsequent three-armed study (Exercise-II) male and female patients with schizophrenia attending a day hospital program or an outpatient clinic were randomised to either aerobic exercise training (cycling) or playing table football as control group for 3×30 minutes per week over a period of three months. After six weeks of intervention additional cognitive training was conducted (CogPack®, 2×30 minutes per week). All patients were undergoing treatment receiving either first or second generation antipsychotics with no differences in dosage or duration of illness between groups. Cycling at heart rate corresponding to a blood lactate concentration of 1,5–2 mmol/L was performed on standardized bikes in a local gym and the amount of exercise was monitored by measuring power (Watt/kg) heart rate, gas exchange (VO2, carbon dioxide output) and blood lactate levels. In the exercise groups, parameters of physical fitness increased. In schizophrenia patients, negative symptoms, short- and long-term memory, executive function as well as GAF score improved mainly during the intervention period of week 6 up to three months.
Data of the impact of this intervention on brain structure and function as well as clinical and neuropsychological variables in multi-episode schizophrenia will be presented.
The KIBRA rs17070145 “CC” and the CLSTN2 rs6439886 “TT” genotypes have been associated with poor episodic memory performance in healthy persons. Episodic memory is also impaired in depression. Therefore, we hypothesized that depressed persons with the “CC/TT” genotype combination would perform worse in comparison to other KIBRA and CLSTN2 combinations.
To examine the effects of KIBRA and CLSTN2 on episodic memory performance in nondepressed and depressed elderly persons (60+).
Genotyping from peripheral blood samples and episodic memory testing were performed in the population-based SNAC-K study. All non-demented participants (n = 2332) were categorized according to depression status (nondepressed/depressed) following ICD-10 criteria. Dichotomous variables were used for KIBRA (any T/CC) and CLSTN2 (any C/TT).
A three-factor MANCOVA revealed no main effects, but two significant interaction effects for episodic memory performance. Post hoc test for KIBRA × CLSTN2 revealed that persons with the “CC/TT” genotype exhibited poorer performance on free recall and recognition. Further, the three-way interaction (KIBRA × CLSTN2 × depression) showed that the negative effect of the “CC/TT” genotype was most pronounced among depressed persons Depressed “CC/TT” consistently performed at the lowest level.
The combination of the KIBRA “CC” and the CLSTN2 “TT” genotypes was associated with poorer episodic memory performance in both nondepressed and depressed persons. Depression in combination with the “CC/TT” genotype was especially disadvantageous for episodic memory performance. This supports the view that effects of specific SNPs on performance may be most easily disclosed at suboptimal levels of cognitive ability, e.g. in depression.
Iraq and Afghanistan Veterans with posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI) history have high rates of performance validity test (PVT) failure. The study aimed to determine whether those with scores in the invalid versus valid range on PVTs show similar benefit from psychotherapy and if psychotherapy improves PVT performance.
Veterans (N = 100) with PTSD, mild-to-moderate TBI history, and cognitive complaints underwent neuropsychological testing at baseline, post-treatment, and 3-month post-treatment. Veterans were randomly assigned to cognitive processing therapy (CPT) or a novel hybrid intervention integrating CPT with TBI psychoeducation and cognitive rehabilitation strategies from Cognitive Symptom Management and Rehabilitation Therapy (CogSMART). Performance below standard cutoffs on any PVT trial across three different PVT measures was considered invalid (PVT-Fail), whereas performance above cutoffs on all measures was considered valid (PVT-Pass).
Although both PVT groups exhibited clinically significant improvement in PTSD symptoms, the PVT-Pass group demonstrated greater symptom reduction than the PVT-Fail group. Measures of post-concussive and depressive symptoms improved to a similar degree across groups. Treatment condition did not moderate these results. Rate of valid test performance increased from baseline to follow-up across conditions, with a stronger effect in the SMART-CPT compared to CPT condition.
Both PVT groups experienced improved psychological symptoms following treatment. Veterans who failed PVTs at baseline demonstrated better test engagement following treatment, resulting in higher rates of valid PVTs at follow-up. Veterans with invalid PVTs should be enrolled in trauma-focused treatment and may benefit from neuropsychological assessment after, rather than before, treatment.
Attention impairment is an under-investigated feature and diagnostic criterion of Major Depressive Disorder (MDD) that is associated with poorer outcomes. Despite increasing knowledge regarding mechanisms of attention in healthy adults, we lack a detailed characterization of attention impairments and their neural signatures in MDD.
Here, we focus on selective attention and advance a deep multi-modal characterization of these impairments in MDD, using data acquired from n = 1008 patients and n = 336 age- and sex-matched healthy controls. Selective attention impairments were operationalized and anchored in a behavioral performance measure, assessed within a battery of cognitive tests. We sought to establish the accompanying neural signature using independent measures of functional magnetic resonance imaging (15% of the sample) and electroencephalographic recordings of oscillatory neural activity.
Greater impairment on the behavioral measure of selective attention was associated with intrinsic hypo-connectivity of the fronto-parietal attention network. Not only was this relationship specific to the fronto-parietal network unlike other large-scale networks; this hypo-connectivity was also specific to selective attention performance unlike other measures of cognition. Selective attention impairment was also associated with lower posterior alpha (8–13 Hz) power at rest and was related to more severe negative bias (frequent misidentifications of neutral faces as sad and lingering attention on sad faces), relevant to clinical features of negative attributions and brooding. Selective attention impairments were independent of overall depression severity and of worrying or sleep problems.
These results provide a foundation for the clinical translational development of objective markers and targeted therapeutics for attention impairment in MDD.
Environmental factors such as sunshine hours, temperature and UV radiation (UVR) are known to influence seasonal fluctuations in vitamin D concentrations. However, currently there is poor understanding regarding the environmental factors or individual characteristics that best predict neonatal 25-hydroxyvitamin D (25(OH)D) concentrations. The aims of this study were to (1) identify environmental and individual determinants of 25(OH)D concentrations in newborns and (2) investigate whether environmental factors and individual characteristics could be used as proxy measures for neonatal 25(OH)D concentrations. 25-Hydroxyvitamin D3 (25(OH)D3) was measured from neonatal dried blood spots (DBS) of 1182 individuals born between 1993 and 2002. Monthly aggregated data on daily number of sunshine hours, temperature and UVR, available from 1993, were retrieved from the Danish Meteorological Institute. The individual predictors were obtained from the Danish National Birth register, and Statistics Denmark. The optimal model to predict 25(OH)D3 concentrations from neonatal DBS was the one including the following variables: UVR, temperature, maternal education, maternal smoking during pregnancy, gestational age at birth and parity. This model explained 30 % of the variation of 25(OH)D3 in the neonatal DBS. Ambient UVR in the month before the birth month was the best single-item predictor of neonatal 25(OH)D3, accounting for 24 % of its variance. Although this prediction model cannot substitute for actual blood measurements, it might prove useful in cohort studies ranking individuals in groups according to 25(OH)D3 status.
Studies have suggested that vitamin D status at birth may be associated with a range of neonatal outcomes. The aim of this study was to assess the association between neonatal 25-hydroxyvitamin D3 (25(OH)D3) concentration and gestational age, birth weight, Ponderal Index and size for gestational age. Neonatal capillary blood stored as dried blood spots was used to assess 25(OH)D3 concentrations among 2686 subjects selected from a random population sub-sample of individuals, born in Denmark from 1 May 1981 to 31 December 2002. There was an inverse association between 25(OH)D3 concentration and gestational age at birth of −0·006 (95 % CI −0·009, −0·003, P<0·001) weeks of gestation per 1 nmol/l increase in 25(OH)D3 concentration. An inverted U-shaped association between 25(OH)D3 and birth weight and Ponderal Index (P=0·04) was found, but no association with size for gestational age was shown. This study suggests that neonatal 25(OH)D3 concentration is associated with anthropometric measures at birth known to be correlated with many subsequent health outcomes such as obesity and type 2 diabetes.
To assess hospital surgical-site infection (SSI) identification and reporting following colon surgery and abdominal hysterectomy via a statewide external validation
Infection preventionists (IPs) from the California Department of Public Health (CDPH) performed on-site SSI validation for surgical procedures performed in hospitals that voluntarily participated. Validation involved chart review of SSI cases previously reported by hospitals plus review of patient records flagged for review by claims codes suggestive of SSI. We assessed the sensitivity of traditional surveillance and the added benefit of claims-based surveillance. We also evaluated the positive predictive value of claims-based surveillance (ie, workload efficiency).
Upon validation review, CDPH IPs identified 239 SSIs following colon surgery at 42 hospitals and 76 SSIs following abdominal hysterectomy at 34 hospitals. For colon surgery, traditional surveillance had a sensitivity of 50% (47% for deep incisional or organ/space [DI/OS] SSI), compared to 84% (88% for DI/OS SSI) for claims-based surveillance. For abdominal hysterectomy, traditional surveillance had a sensitivity of 68% (67% for DI/OS SSI) compared to 74% (78% for DI/OS SSI) for claims-based surveillance. Claims-based surveillance was also efficient, with 1 SSI identified for every 2 patients flagged for review who had undergone abdominal hysterectomy and for every 2.6 patients flagged for review who had undergone colon surgery. Overall, CDPH identified previously unreported SSIs in 74% of validation hospitals performing colon surgery and 35% of validation hospitals performing abdominal hysterectomy.
Claims-based surveillance is a standardized approach that hospitals can use to augment traditional surveillance methods and health departments can use for external validation.
Endophenotypes are laboratory-based measures hypothesized to lie in the causal chain between genes and clinical disorder, and to serve as a more powerful way to identify genes associated with the disorder. One promise of endophenotypes is that they may assist in elucidating the neurobehavioral mechanisms by which an associated genetic polymorphism affects disorder risk in complex traits. We evaluated this promise by testing the extent to which variants discovered to be associated with schizophrenia through large-scale meta-analysis show associations with psychophysiological endophenotypes.
We genome-wide genotyped and imputed 4905 individuals. Of these, 1837 were whole-genome-sequenced at 11× depth. In a community-based sample, we conducted targeted tests of variants within schizophrenia-associated loci, as well as genome-wide polygenic tests of association, with 17 psychophysiological endophenotypes including acoustic startle response and affective startle modulation, antisaccade, multiple frequencies of resting electroencephalogram (EEG), electrodermal activity and P300 event-related potential.
Using single variant tests and gene-based tests we found suggestive evidence for an association between contactin 4 (CNTN4) and antisaccade and P300. We were unable to find any other variant or gene within the 108 schizophrenia loci significantly associated with any of our 17 endophenotypes. Polygenic risk scores indexing genetic vulnerability to schizophrenia were not related to any of the psychophysiological endophenotypes after correction for multiple testing.
The results indicate significant difficulty in using psychophysiological endophenotypes to characterize the genetically influenced neurobehavioral mechanisms by which risk loci identified in genome-wide association studies affect disorder risk.
Two generalist parasitoids, Dolichogenidea tasmanica (Cameron) (Hymenoptera: Braconidae) and Therophilus unimaculatus (Turner) (Hymenoptera: Braconidae) attack early instars of tortricid moths, including the light brown apple moth, Epiphyas postvittana (Walker) (Lepidoptera: Tortricidae). The two parasitoids co-exist in natural habitats, while D. tasmanica is dominant in vineyards, whereas T. unimaculatus occurs mainly in adjacent native vegetation. This difference suggests possible competition between the two species, mediated by habitat. Here, we report on the extent of interspecific differences in host discrimination and the outcome of interspecific competition between the two parasitoids. The parasitoids did not show different behavioural responses to un-parasitized hosts or those that were parasitized by the other species. Larvae of D. tasmanica out-competed those of T. unimaculatus, irrespective of the order or interval between attacks by the two species. The host larvae that were attacked by two parasitoids died more frequently before a parasitoid completed its larval development than those that were attacked by a single parasitoid. Dissection of host larvae parasitized by both species indicated that first instars of D. tasmanica attacked and killed larval T. unimaculatus.