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We extend classical ideal point estimation to allow voters to have different preferences when voting in different domains—for example, when voting on agricultural policy than when voting on defense policy. Our scaling procedure results in estimated ideal points on a common scale. As a result, we are able to directly compare a member’s revealed preferences across different domains of voting (different sets of motions) to assess if, for example, a member votes more conservatively on agriculture motions than on defense. In doing so, we are able to assess the extent to which voting behavior of an individual voter is consistent with a uni-dimensional spatial model—if a member has the same preferences in all domains. The key novelty is to estimate rather than assume the identity of “stayers”—voters whose revealed preference is constant across votes. Our approach offers methodology for investigating the relationship between the basic space and issue space in legislative voting (Poole 2007). There are several methodological advantages to our approach. First, our model allows for testing sharp hypotheses. Second, the methodology developed can be understood as a kind of partial-pooling model for item response theory scaling, resulting in less uncertainty of estimates. Related, our estimation method provides a principled and unified approach to the issue of “granularity” (i.e., the level of aggregation) in the analysis of roll-call data (Crespin and Rohde 2010; Roberts et al. 2016). We illustrate the model by estimating U.S. House of Representatives members’ revealed preferences in different policy domains, and identify several other potential applications of the model including: studying the relationship between committee and floor voting behavior; and investigating constituency influence and representation.
Serotonergic neurotransmission plays a key role in seasonal changes of mood and behaviour. Higher serotonin transporter availability in healthy human subjects in times of lesser light has been reported in recent studies. Furthermore, seasonal alterations of postsynaptic serotonin-1A receptors have been suggested by a recent animal study. Following that, this study aimed at identifying seasonal alterations of serotonin-1A receptor binding in the living human brain.
Thirty-six healthy, drug-naïve subjects were investigated using PET and the specific tracer [carbonyl-11C]WAY-100635. Regional serotonin-1A receptor binding (5-HT1A BPND) was related to the individual exposure to global radiation. Furthermore, the subjects were divided into two groups depending on individual exposure to global radiation, and the group differences in regional 5-HT1A BPND were determined.
Correlation analysis controlled for age and gender revealed highly significant positive correlations between regional postsynaptic 5-HT1A BPND and global radiation accumulated for 5 days (r=.32 to .48, p=.030 to .002). Highly significant differences in 5-HT1A BPND binding between subjects with low compared to high exposure to global radiation were revealed (T=-2.63 to -3.77, p .013 to .001). 20% to 30% lower 5-HT1A BPND was found in the subject group exposed to lower amount of global radiation.
Seasonal factors such as exposure to global radiation influence postsynaptic serotonin-1A receptor binding in various brain regions in healthy human subjects. In combination with seasonal alterations in serotonin turnover and 5-HTT availability revealed in recent studies, our results provide an essential contribution of molecular mechanisms in seasonal changes of human serotonergic neurotransmission.
Regional alterations of serotonergic neurotransmission and functional activation in the amygdalar region of patients with major depression are underpinning its important role in affective disorders. In this study we used fMRI and PET to describe functional and molecular alterations associtated with an astrocytoma in the left amygdalar region in a patient with organic depressive disorder compared to control subjects.
The serotonin-1A (5-HT1A) receptor binding (BPND) was quantified with PET (30 frames, 90 min, 4.4 mm FWHM) in 36 subjects using the radioligand [carbonyl-11C]WAY-100635, and a reference tissue model (MRTM2). In fMRI (3T, EPI inplane resolution 1.6*2.7 mm, 10 AC-PC orientated slices, ST = 3 mm, TE/TR = 31/1000 ms), 32 participants performed emotion discrimination and sensorimotor control tasks. Statistical analysis with SPM5 and unpaired t-tests were performed on molecular and functional data separately.
The astrocytoma was delineated in the serotonin-1A receptor distribution showing (p < 0.01, uncorrected) regional BPND decrease. The ipsilateral thalamus and bilateral habenula regions displayed (p < 0.001; uncorrected) BPND increase. The fMRI data showed significantly (p < 0.05; uncorrected) reduced activation in the affected amygdalar region, ipsilateral fusiform gyrus, bilateral orbitofrontal cortex and temporal regions and increased activation in the contralateral temporal pole.
Lower serotonin-1A receptor binding in the left amydala region reflects the glial provenance of the tumor. The increased receptor binding in the habenulae might be associated with altered monoaminergic neurotransmission and depressive symptoms according to the influence of the habenulae on monoaminergic nuclei. The functional data demonstrate neuroplastic changes beyond affected areas and might indicate compensatory mechanisms.
Dysfunction in the basal ganglia has been related to impaired reward processing and anhedonia, a core symptom of Major Depressive Disorder (MDD). In particular, the ventral striatum including the nucleus accumbens is increasingly implicated in the pathophysiology of MDD, but evidence for a specific role during episodes of full remission is lacking so far.
To investigate functional connectivity patterns of resting-state activity in patients in the remitted phase of MDD (rMDD).
To determine whether rMDD is related to disruptions of functional coupling between the ventral striatum and cortical regions.
Forty-three remitted depressed patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. Seed time series were extracted from the preprocessed data using individual masks for ventral striatum and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fishertransformed, group results were determined by comparing group mean smoothed z-scores with a two-sample ttest.
Increased resting-state functional connectivity was revealed between ventral striatum (seed region) and anterior cingulate cortex as well as orbitofrontal cortex in the rMDD group compared to healthy controls.
Our preliminary data is in accordance with the idea that increased functional coupling between the ventral striatum and two major emotion processing regions, the anterior cingulate cortex and the orbitofrontal cortex, may represent a neural mechanism contributing to the maintenance of full remission of MDD.
Maximal serotonin transporter (5-HTT) densities have been found in the cingulate cortex, a cortical region that has been critically implicated in emotion processing and the pathophysiology of Major Depressive Disorder. Furthermore, serotonin (5-HT) re-uptake inhibition is the first line strategy in the treatment of depression.
Since 5-HTTs are not restricted to neuronal cells, 5-HT uptake velocity (Vmax) can be easily measured on blood platelets subserving as peripheral model of neuronal 5-HTT function and related measures of neural activation.
To determine whether peripheral 5-HTT uptake velocity is related to neural activation in the cingulate cortex during emotion processing.
48 healthy subjects underwent an fMRI paradigm comprising emotional (angry/fearful faces and scenes) and neutral stimuli (simple shapes). 5-HT Vmax was determined in platelets. Subjects were genotyped for a common triallelic polymorphism in the promoter region of the 5-HTT gene (5-HTTLPR).
Significant negative correlations between Vmax and BOLD-signal in the anterior and posterior portion of the cingulate cortex have been found. Cluster maxima within both regions were detected in the subgenual anterior cortex (−1.5, 28.5, −3.5, t = −3.77) and the ventral posterior cingulate cortex (−4.5, −49.5,14.5, t = −3.06). Genotype did not impact on this relationship.
Our results indicate a clear dependency between a peripheral marker, platelet 5-HT uptake velocity, and neural activity in portions of the cingulate cortex for the first time.
Converging evidence suggests alterations of neural activation in the basal ganglia to represent neural correlates of Major Depressive Disorder (MDD). While a previous study reported increases of functional connectivity in resting state activity between the caudate nuclei and the posterior cingulate cortex in acutely depressed patients, it remains unclear whether this finding persists during full remission once antidepressant treatment has been discontinued.
To investigate patterns of functional coupling between the basal ganglia and cortical regions during resting-state conditions.
To determine whether increases of functional connectivity between caudate nuclei, putamen, and pallidum with cortical regions, in particular the cingulate cortex, pertain during remission of MDD.
Forty-three remitted depressed (rMDD) patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. Seed time series were extracted from the preprocessed data using individual masks for the basal ganglia and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fisher-transformed, group results were determined by comparing group mean smoothed z-scores with a two-sample t-test.
Increased resting-state functional connectivity was revealed between basal ganglia and cingulate as well as prefrontal cortex in the rMDD group compared to healthy controls.
Our preliminary results revealed increased functional coupling between the basal ganglia and wide parts of the cingulate and prefrontal cortex to possibly represent a specific neural pattern during remission of MDD.
While most neuroimaging studies have investigated acutely depressed patients, neural mechanisms underlying stable remission are rarely examined. Furthermore, the majority of previous functional MRI (fMRI) studies have focused on task-induced neural activity, while resting-state activity may be more reproducible across study centers.
To clarify patterns of functional coupling between subcortical structures and cortical resting state activity.
To determine whether alterations of functional coupling between the amygdala and cortical emotion processing regions characterize patients in the remitted phase of Major Depressive Disorder (rMDD).
Forty-three remitted depressed patients and thirty-five healthy controls were recruited at Medical University of Vienna, Vienna, Austria, and performed a six minute resting-state fMRI scan. The scans were corrected for slice timing and motion, as well as for mean white matter, mean CSF, and median gray matter signals. Seed time series were extracted using individual amygdala masks and correlated with all nodes in a surface based analysis using FreeSurfer, AFNI and SUMA. The resulting correlation coefficients were then Fisher-transformed, group results were determined by comparing group mean smoothed (to 8 mm FWHM) z-scores with a two-sample t-test.
Increased resting-state functional connectivity was revealed between amygdala (seed region) and posterior cingulate cortex as well as orbitofrontal cortex in the rMDD group compared to healthy controls.
Our preliminary results suggest altered functional coupling between amygdala and cortical emotion processing areas during resting state conditions, possibly representing a neural mechanism contributing to the maintenance of stable remission of MDD.
The natural course of Major Depressive Disorder (MDD) encompasses the occurrence of alternating intervals of major depressive episodes and remission. While several abnormalities in neural circuits related to acute MDD have been identified, the neural mechanisms underlying stable remission remain obscure.
Acute MDD is characterized by increased amygdala and subgenual anterior cingulate cortex (sACC) activation and decreased connectivity between the amygdala and the sACC. Consequently, we expect those regions to be affected during remission.
To determine whether active counter-regulatory mechanisms are implicated in the maintenance of full remission once antidepressant treatment has been discontinued.
Functional and structural magnetic resonance imaging was used to measure brain activation and volume of the amygdala and the sACC. Images were obtained from 38 healthy subjects without any psychiatric life-time diagnosis and 38 gender-matched drug-free remitted MDD patients. Furthermore, correlation analyses were performed with clinical variables.
Patients with rMDD exhibited lower activation in the amygdala and the sACC and increased functional coupling between the amygdala and sACC compared to controls. This connectivity was particularly pronounced in patients characterized by a long cumulated time of depressive episodes. Similarly, structural connectivity results showed increased association between the amygdala and sACC volume in rMDD patients compared to controls.
Remitted MDD is related to neural alterations within a neural circuit encompassing the amygdala and the sACC compared to controls. These findings suggest active counter-regulatory mechanisms likely contributing to the maintenance of remission once treatment has been discontinued.
Our aim was to identify areas of improvement for current Opioid Maintenance Treatment (OMT) approaches, by analysing European Quality Audit of Opioid Treatment (EQUATOR) data from 8 European countries (Austria, Denmark, France, Germany, Norway, Portugal, Sweden, UK).
A standardised face-to-face survey was administered to OMT patients (OMT-P) and active opioid user (AOU). Reasons for entering and staying out of OMT, rules pertaining to OMT, and factors facilitating OMT retention were compared between countries, and between OMT-P and AOU groups. Both groups were divided into those who never had OMT before [un-experienced OMT-P (n=573) and AOU (n=360)] and those who had been maintained at least once [experienced OMT-P (n=746) and AOU (n=377)].
Motives for starting OMT vary distinctly between countries (p≤0.001). Transnationally, experienced AOU reported concerns about their ability to follow treatment rules and negative treatment experiences as decisive reasons for staying out of OMT. Greater flexibility, less pressure to reduce their treatment dose and greater treatment structure were ranked significantly higher by experienced compared to un-experienced OMT-P as factors that might facilitate treatment retention (p≤0.05).
The major strength of this investigation was the homogenous methodology applied in all countries, which enabled new insights in variations between treatment systems and their impact on patient outcome. Treatment systems need to aim an optimal balance between flexibility and structure. Standardised approaches that still permit tailoring treatment to individual patient needs are crucial to yield maximum benefit for patients, and reduce the considerable societal economic burden of addiction.
Due to concerns over increasing fluoroquinolone (FQ) resistance among gram-negative organisms, our stewardship program implemented a preauthorization use policy. The goal of this study was to assess the relationship between hospital FQ use and antibiotic resistance.
Large academic medical center.
We performed a retrospective analysis of FQ susceptibility of hospital isolates for 5 common gram-negative bacteria: Acinetobacter spp., Enterobacter cloacae, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Primary endpoint was the change of FQ susceptibility. A Poisson regression model was used to calculate the rate of change between the preintervention period (1998–2005) and the postimplementation period (2006–2016).
Large rates of decline of FQ susceptibility began in 1998, particularly among P. aeruginosa, Acinetobacter spp., and E. cloacae. Our FQ restriction policy improved FQ use from 173 days of therapy (DOT) per 1,000 patient days to <60 DOT per 1,000 patient days. Fluoroquinolone susceptibility increased for Acinetobacter spp. (rate ratio [RR], 1.038; 95% confidence interval [CI], 1.005–1.072), E. cloacae (RR, 1.028; 95% CI, 1.013–1.044), and P. aeruginosa (RR, 1.013; 95% CI, 1.006–1.020). No significant change in susceptibility was detected for K. pneumoniae (RR, 1.002; 95% CI, 0.996–1.008), and the susceptibility for E. coli continued to decline, although the decline was not as steep (RR, 0.981; 95% CI, 0.975–0.987).
A stewardship-driven FQ restriction program stopped overall declining FQ susceptibility rates for all species except E. coli. For 3 species (ie, Acinetobacter spp, E. cloacae, and P. aeruginosa), susceptibility rates improved after implementation, and this improvement has been sustained over a 10-year period.
A Lagrangian study was conducted in a eutrophic estuary (Guanabara Bay, Brazil) to investigate in situ plankton trophodynamics under the influence of the cold, nutrient-rich South Atlantic Coastal Water in a short-term temporal variability (scale of hours). We tested the hypothesis that the base of the plankton food web is composed of small cells and that microzooplankton is the main consumer of this assemblage. Samples of pico-, nano- and microplankton, as well as copepods, were collected during spring, when the entry of upwelling water in the Bay is commonly observed, and near the surface every 3 h during the 1-day sampling period. Potential predation of dinoflagellates, ciliates, copepod nauplii, copepodites and adult copepods was estimated based on predator-prey size relationships. The main trophic links in the Guanabara Bay food web for the period analysed were nanophytoplankton-copepods, nanophytoplankton-ciliates, and autotrophic dinoflagellates-heterotrophic dinoflagellates. According to microphytoplankton availability, adult copepods could not satisfy their food requirement, and nanophytoplankton represented an important supplementary food source. In fact, diel variations of nano- and microplankton biomass were opposite to that of copepods suggesting predation control by the latter on the former. The trophodynamics of Guanabara Bay, under the influence of upwelling water, resulted in marked differences from other eutrophic estuaries around the world.
Obsessive–compulsive disorder (OCD) patients typically overmonitor their own behavior, as shown by symptoms of excessive doubt and checking. Although this is well established for the patients’ relationship with external stimuli in the environment, no study has explored their monitoring of internal body signals, a process known to be affected in anxiety-related syndromes. Here, we explored this issue through a cardiac interoception task that measures sensing of heartbeats. Our aim was to explore key behavioral and electrophysiological aspects of internal-cue monitoring in OCD, while examining their potential distinctiveness in this condition.
We administered a heartbeat detection (HBD) task (with related interoceptive confidence and awareness measures) to three matched groups (OCD patients, panic disorder patients, healthy controls) and recorded ongoing modulations of two task-relevant electrophysiological markers: the heart evoked potential (HEP) and the motor potential (MP).
Behaviorally, OCD patients outperformed controls and panic patients in the HBD task. Moreover, they exhibited greater amplitude modulation of both the HEP and the MP during cardiac interoception. However, they evinced poorer confidence and awareness of their interoceptive skills.
Convergent behavioral and electrophysiological data showed that overactive monitoring in OCD extends to the sensing of internal bodily signals. Moreover, this pattern discriminated OCD from panic patients, suggesting a condition-distinctive alteration. Our results highlight the potential of exploring interoceptive processes in the OCD spectrum to better characterize the population's cognitive profile. Finally, these findings may lay new bridges between somatic theories of emotion and cognitive models of OCD.
We report an epidemiological investigation of a cluster of Brevundimonas diminuta isolates cultured from sterile sites. Inoculation of supplement medium yielded growth of B. diminuta. Molecular typing indicated likely contamination of the lot. No B. diminuta was further isolated after replacement of the supplement with a new lot number.
Long-term records of wildfires and their controlling factors are important sources of information for informing land management practices. Here, dendrochronology and lake sediment analyses are used to develop a 3500-yr fire and vegetation history for a montane forest in Jasper National Park, Alberta, Canada. The tree-ring record (AD 1771-2012) indicates that this region historically experienced a mixed-severity fire regime, and that effective fire suppression excluded widespread fire events from the study area during the 20th century. A sediment core collected from Little Trefoil Lake, located near the Jasper townsite, is analyzed for subfossil pollen and macroscopic charcoal (>150 μm). When comparing the tree-ring record to the 3500-yr record of sediment-derived fire events, only high-severity fires are represented in the charcoal record. Comparisons between the charcoal record and historical climate and pollen data indicate that climate and vegetation composition have been important controls on the fire regime for most of the last 3500 yr. Although fire frequency is presently within the historical range of variability, the fire return interval of the last 150 yr is longer than expected given modern climate and vegetation conditions, indicating that humans have become the main control on fire activity around Little Trefoil Lake.
HD151018 is a normal O-type giant with periodic variability of the wind seen in both spectroscopy and linear polarimetry. The characteristics of the wind emission strongly indicate a magnetically confined wind. This work presents the observational results and an initial modelling of the polarimetric modulation of this star.
Impairments in facial emotion recognition (FER) have been detected in patients with Parkinson disease (PD). Presently, we aim at assessing differences in emotion recognition performance in PD patient groups with and without mild forms of cognitive impairment (MCI) compared to healthy controls.
Performance on a concise emotion recognition test battery (VERT-K) of three groups of 97 PD patients was compared with an age-equivalent sample of 168 healthy controls. Patients were categorized into groups according to two well-established classifications of MCI according to Petersen's (cognitively intact vs. amnestic MCI, aMCI, vs. non-amnestic MCI, non-aMCI) and Litvan's (cognitively intact vs. single-domain MCI, sMCI, vs. multi-domain MCI, mMCI) criteria. Patients and controls underwent individual assessments using a comprehensive neuropsychological test battery examining attention, executive functioning, language, and memory (Neuropsychological Test Battery Vienna, NTBV), the Beck Depression Inventory, and a measure of premorbid IQ (WST).
Cognitively intact PD patients and patients with MCI in PD (PD-MCI) showed significantly worse emotion recognition performance when compared to healthy controls. Between-groups effect sizes were substantial, showing non-trivial effects in all comparisons (Cohen's ds from 0.31 to 1.22). Moreover, emotion recognition performance was higher in women, positively associated with premorbid IQ and negatively associated with age. Depressive symptoms were not related to FER.
The present investigation yields further evidence for impaired FER in PD. Interestingly, our data suggest FER deficits even in cognitively intact PD patients indicating FER dysfunction prior to the development of overt cognitive dysfunction. Age showed a negative association whereas IQ showed a positive association with FER.
Vancomycin-resistant enterococci (VRE) infections are a public health threat associated with increased patient mortality and healthcare costs. Antibiotic usage, particularly cephalosporins, has been associated with VRE colonization and VRE bloodstream infections (VRE BSI). We examined the relationship between antimicrobial usage and incident VRE colonization at the individual patient level. Prospective, weekly surveillance was undertaken for incident VRE colonization defined by negative admission but positive surveillance swab in a medical intensive care unit over a 17-month period. Antimicrobial exposure was quantified as days of therapy (DOT)/1000 patient-days. Multiple logistic regression was used to analyse incident VRE colonization and antibiotic DOT, controlling for demographic and clinical covariates. Ninety-six percent (1398/1454) of admissions were swabbed within 24 h of intensive care unit (ICU) arrival and of the 380 patients in the ICU long enough for weekly surveillance, 83 (22%) developed incident VRE colonization. Incident colonization was associated in bivariate analysis with male gender, more previous hospital admissions, longer previous hospital stay, and use of cefepime/ceftazidime, fluconazole, azithromycin, and metronidazole (P < 0·05). After controlling for demographic and clinical covariates, metronidazole was the only antibiotic independently associated with incident VRE colonization (odds ratio 2·0, 95% confidence interval 1·2–3·3, P < 0·009). Our findings suggest that risk of incident VRE colonization differs between individual antibiotic agents and support the possibility that antimicrobial stewardship may impact VRE colonization and infection.
Preventable diseases not only cause suffering and physical harm, they also impose financial costs on private individuals and public authorities. By disregarding evidence of the safety and effectiveness of vaccines and choosing not to vaccinate their children, some parents are increasing the risk of outbreaks and their attendant costs. In a very real sense, since those families are not currently required to cover the full costs of outbreaks, they are externalizing those costs onto others – individuals affected and society at large. Since non-vaccinating can directly lead to costly outbreaks, this paper argues that it is both fair and desirable to impose those costs upon those making the choice not to vaccinate. There are, in fact, strong policy reasons to support doing so regardless of whether we use an approach based on fault or a no-fault framework. Not only can the decision not to vaccinate be seen as culpable, aside from the culpability consideration, it is appropriate to compel those deciding not to vaccinate to internalize the costs in order to prevent free riding and to mitigate harms to others.