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51.	Gupta, Sunjai, et al. (författare) The role of inflammation in the relationship of self-rated health with mortality and implications for public health : Data from the English Longitudinal Study of Aging (ELSA) 2020 Ingår i: Brain, Behavior, & Immunity. - Amsterdam, the Netherlands : Elsevier. - 0889-1591 .- 1090-2139 .- 2666-3546. ; 8, s. 100139-100139 Tidskriftsartikel (refereegranskat)abstract Self-rated health (SRH) predicts mortality after adjustment for potential confounders, including measures of health status. Prodromal disease might lead to worsened SRH and higher mortality. But no study of SRH and mortality has focussed on inflammation. The objective of this study is to investigate the influence of inflammation upon the association between SRH and mortality in a British cohort. The English Longitudinal Study of Ageing (ELSA) involves interviewing participants aged over 50 every two years. We analysed data for 3405 men and 4139 women. Mortality for consenting members was detected by linkage with UK National Health Care registry up to March 2012. Demographic, clinical, and health behaviours at wave 2 were treated as confounders, as well as inflammation-related disease and C-reactive protein (CRP). A five-step hierarchical multivariable logistic regression was estimated. An association was observed between SRH and mortality after adjusting for all variables. In men, compared to those with excellent health, CRP only, and CRP and inflammation-related disease combined, could explain 7.03% and 24.35% of increased risk of dying associated with poor health, respectively. For women, the corresponding figures were 8.95% and 24.28%, respectively. Inflammation is associated with increased risk of death, and may help to explain approximately a quarter of the association between SRH and mortality. Individuals with relatively poor SRH may be aware of underlying inflammation that increases the risk of illness and death, and this may lead to increased use of services, for example. Identifying the cause and treating inflammation in those without a diagnosis may help to increase survival and life quality among those who perceive their health to be relatively poor.
52.	Hamzik, Namik, et al. (författare) Interleukin-6 primarily produced by non-hematopoietic cells mediates the lipopolysaccharide-induced febrile response 2013 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 33, s. 123-130 Tidskriftsartikel (refereegranskat)abstract Interleukin-6 (IL-6) is critical for the lipopolysaccharide (LPS)-induced febrile response. However, the exact source(s) of IL-6 involved in regulating the LPS-elicited fever is still to be identified. One known source of IL-6 is hematopoietic cells, such as monocytes. To clarify the contribution of hematopoietically derived IL-6 to fever, we created chimeric mice expressing IL-6 selectively either in cells of hematopoietic or, conversely, in cells of non-hematopoietic origin. This was performed by extinguishing hematopoietic cells in wild-type (WT) or IL-6 knockout (IL-6 KO) mice by whole-body irradiation and transplanting them with new stem cells. Mice on a WT background but lacking IL-6 in hematopoietic cells displayed normal fever to LPS and were found to have similar levels of IL-6 protein in the cerebrospinal fluid (CSF) and in plasma and of IL-6 mRNA in the brain as WT mice. In contrast, mice on an IL-6 KO background, but with intact IL-6 production in cells of hematopoietic origin, only showed a minor elevation of the body temperature after peripheral LPS injection. While they displayed significantly elevated levels of IL-6 both in plasma and CSF compared with control mice, the increase was modest compared with that seen in LPS injected mice on a WT background, the latter being approximately 20 times larger in magnitude. These results suggest that IL-6 of non-hematopoietic origin is the main source of IL-6 in LPS-induced fever, and that IL-6 produced by hematopoietic cells only plays a minor role.
53.	Hansson, Lina S., 1992-, et al. (författare) Perception of unfamiliar caregivers during sickness – Using the new Caregiver Perception Task (CgPT) during experimental endotoxemia 2024 Ingår i: Brain, behavior, and immunity. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0889-1591 .- 1090-2139. ; 119, s. 741-749 Tidskriftsartikel (refereegranskat)abstract Social withdrawal is a well-established part of sickness behavior, but in some contexts sick animals might gain from keeping close instead of keeping away. For instance, sick individuals are more willing to be near known individuals who can provide care and safety (close others) compared to when healthy. Yet, interactions with some strangers might also be beneficial (i.e., healthcare professionals), but it is not known how sickness interplay with social behavior towards such individuals. Here, we assessed if sickness affects perception of caregivers, and developed a new task, the Caregiver Perception Task (CgPT). Twenty-six participants performed the CgPT, once after an injection of lipopolysaccharide (LPS, 0.8 ng/kg body weight, n = 24), and once after an injection of saline (n = 25), one hour and forty-five minutes post-injection. During the task, participants watched short video clips of three types of caregivers: a healthcare professional taking care of a sick individual, a healthcare professional not taking care of a sick individual, and a non-healthcare professional taking care of their sick adult child or partner. After each video clip, the likability, trustworthiness, professionalism, and willingness to interact with and receive care from the caregiver were rated on visual analogue scales. Results showed that participants injected with saline rated healthcare professionals who did not take care of a sick individual less positively on all aspects compared to healthcare professionals who took care of a sick individual. Moreover, compared to saline, LPS increased the participants’ willingness to receive care from healthcare professionals and non-healthcare professionals providing care, but not from healthcare professionals not providing care. Thus, our results indicate that sick individuals may approach unknown individuals with potential to provide care and support.
54.	Hansson, Lina S., 1986-, et al. (författare) Pointing out sickness : Detection of sickness from gait patterns 2021 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 98, s. 21-21 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Background: The ability to detect sick individuals is crucial for survival, by allowing avoidance of contagion. We have shown that humans can detect sick individuals from facial cues and body odors, but perception of these cues requires close proximity to the infectious person. Given that gait patterns can be detected from a distance and are altered during sickness, it would be beneficial to detect sickness from biological motion. Methods: We collected videos and point-light displays of walking individuals who were either made sick experimentally with an injection of lipopolysaccharide, or who were healthy (placebo). In study 1, 106 naive subjects watched these displays and rated them as coming from someone sick or healthy. In study 2, 106 other subjects rated health, sadness and tiredness of the displays on a VAS scale. Results: In Study 1, the sensitivity was 59% for videos and 57% for point-light displays, while the specificity was 74% for videos and 61% for point-light displays. Additional results will be presented at the conference. Conclusion: This study will indicate if sickness can be detected from gait patterns, possibly adding to immune defensive behaviors by facilitating avoidance of contagious peers.
55.	Hansson, Lina S., et al. (författare) Regulation of emotions during experimental endotoxemia : A pilot study 2021 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 93, s. 420-424 Tidskriftsartikel (refereegranskat)abstract Even though dysfunctional emotion regulation is prominent in depression and a link between depression and inflammation is well established, there is little knowledge about how inflammation affects the regulation of emotions. The aim of this pilot study was to explore the effect of experimentally induced inflammation on the cognitive reappraisal of emotions, and to assess domain specificity by comparing success in regulation of emotions towards two unpleasant stimuli classes (general negative stimuli and disgust stimuli). In a between-subject design, ten healthy participants were injected with an intravenous injection of lipopolysaccharide (2 ng/kg body weight) and eleven were injected with saline. Participants performed a cognitive reappraisal task, in which they had to down-regulate or up-regulate their emotions towards general negative stimuli and disgust stimuli, 5–6 h post-injection. Contrary to our hypotheses, participants injected with lipopolysaccharide reported greater success in down-regulating emotional responses towards unpleasant stimuli as compared to the saline group. In addition, both groups were poorer at down-regulating emotions towards disgust stimuli as compared to general negative stimuli. The current pilot study indicates that cognitive reappraisal of emotions is affected during experimental endotoxemia, and suggests that disgust stimuli might be difficult to reappraise.
56.	Hansson, Lina S., et al. (författare) The walking sick : Perception of experimental sickness from biological motion 2023 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 113, s. 319-327 Tidskriftsartikel (refereegranskat)abstract Identification of sick conspecifics allows for avoidance of infectious threats, and is therefore an important behavioral defense against diseases. Here, we investigated if humans can identify sick individuals solely from biological motion and posture (using point-light displays). Additionally, we sought to determine which movements and sickness parameters would predict such detection. We collected video clips and derived point-light displays (one stride presented in a loop) of sick walkers (injected with lipopolysaccharide at 2.0 ng/kg body weight) and the same walkers when healthy (injected with saline). We then presented these displays to two groups, one group classified each walker as sick or healthy (study 1, n = 106), and the other group scored the walkers’ health on a visual analogue scale (study 2, n = 106). The raters were able to identify sick individuals above chance, and rated sick walkers as having worse health, both from observing video clips and point-light displays. Furthermore, both sickness detection and worse apparent health were predicted by inflammation-induced increase in rigidity and slower walking, but not other cues. Altogether, these findings indicate that biological motion can serve as a sickness cue, possibly allowing humans to identify sick conspecifics from a distance, and thereby allowing for disease avoidance.
57.	Hansson, Lina S., 1986-, et al. (författare) The walking sick : what predicts the detection of walking sick individuals? 2022 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 106, s. 36-36 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Methods: In two studies, raters watched video recordings and point-light displays (i.e. dots depicting the body joints) of walking individuals who were either experimentally sick (after injection with lipopolysaccharide at 2.0 ng/kg bw) or healthy (after a placebo injection). In study 1, 106 raters classified each walking individual as either sick or healthy. In study 2, 106 other raters graded health of the stimuli on a visual analogue scale. We assessed the predicting effect on sickness detection (study 1) and apparent health (study 2) of walking parameters (objective measures of stride length, width, time, as well as knee angle, arm angle, and head angle) and well-known sickness responses (Sickness Questionnaire score, pain intensity, body temperature, and interleukin-6 concentration).Results: In study 1, shorter steps was the only predictor of the detection of sick individuals from video recordings (β=0.712(0.257), p=0.02). In the point-light displays, slower, wider, stiffer and shorter steps, all predicted a better sickness detection (β=0.0003(0.0001)-0.415(0.126), p<0.05).In study 2, lipopolysaccharide-induced slower, shorter and stiffer steps (B=5.214(1.888)-6.385(2.083), p<0.01), as well as higher interleukin-6 concentrations (B=0.051(0.020), p=0.01), predicted worse health ratings of sick individuals in the video recordings. In the point-light displays, lipopolysaccharide-induced slower, shorter and stiffer steps, and more head tilting, predicted worse health ratings of sick individuals (B=4.185(1.892)-6.701(2.092), p<0.05).Conclusions: The results imply that specific changes in walking parameters may aid in sickness detection, possibly regulating approach-avoidance behaviors towards sick peers.
58.	Henderson, Audrey J., et al. (författare) Skin colour changes during experimentally-induced sickness 2017 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 60, s. 312-318 Tidskriftsartikel (refereegranskat)abstract Skin colour may be an important cue to detect sickness in humans but how skin colour changes with acute sickness is currently unknown. To determine possible colour changes, 22 healthy Caucasian participants were injected twice, once with lipopolysaccharide (LPS, at a dose of 2ng/kg body weight) and once with placebo (saline), in a randomised cross-over design study. Skin colour across 3 arm and 3 face locations was recorded spectrophotometrically over a period of 8h in terms of lightness (L(∗)), redness (a(∗)) and yellowness (b(∗)) in a manner that is consistent with human colour perception. In addition, carotenoid status was assessed as we predicted that a decrease it skin yellowness would reflect a drop in skin carotenoids. We found an early change in skin colouration 1-3h post LPS injection with facial skin becoming lighter and less red whilst arm skin become darker but also less red and less yellow. The LPS injection also caused a drop in plasma carotenoids from 3h onwards. However, the timing of the carotenoid changes was not consistent with the skin colour changes suggesting that other mechanisms, such as a reduction of blood perfusion, oxygenation or composition. This is the first experimental study characterising skin colour associated with acute illness, and shows that changes occur early in the development of the sickness response. Colour changes may serve as a cue to health, prompting actions from others in terms of care-giving or disease avoidance. Specific mechanisms underlying these colour changes require further investigation.
59.	Hetze, S, et al. (författare) Taste-immune associative learning amplifies immunopharmacological effects and attenuates disease progression in a rat glioblastoma model 2022 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 106, s. 270-279 Tidskriftsartikel (refereegranskat)
60.	Holleman, Jasper, et al. (författare) Diurnal cortisol, neuroinflammation, and neuroimaging visual rating scales in memory clinic patients 2024 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 118, s. 499-509 Tidskriftsartikel (refereegranskat)abstract BACKGROUND: Neuroinflammation is a hallmark of the Alzheimer's disease (AD) pathogenic process. Cortisol dysregulation may increase AD risk and is related to brain atrophy. This cross-sectional study aims to examine interactions of cortisol patterns and neuroinflammation markers in their association with neuroimaging correlates.METHOD: 134 participants were recruited from the Karolinska University Hospital memory clinic (Stockholm, Sweden). Four visual rating scales were applied to magnetic resonance imaging or computed tomography scans: medial temporal lobe atrophy (MTA), global cortical atrophy (GCA), white matter lesions (WML), and posterior atrophy. Participants provided saliva samples for assessment of diurnal cortisol patterns, and underwent lumbar punctures for cerebrospinal fluid (CSF) sampling. Three cortisol measures were used: the cortisol awakening response, total daily output, and the ratio of awakening to bedtime levels. Nineteen CSF neuroinflammation markers were categorized into five composite scores: proinflammatory cytokines, other cytokines, angiogenesis markers, vascular injury markers, and glial activation markers. Ordinal logistic regressions were conducted to assess associations between cortisol patterns, neuroinflammation scores, and visual rating scales, and interactions between cortisol patterns and neuroinflammation scores in relation to visual rating scales.RESULT: Higher levels of angiogenesis markers were associated with more severe WML. Some evidence was found for interactions between dysregulated diurnal cortisol patterns and greater neuroinflammation-related biomarkers in relation to more severe GCA and WML. No associations were found between cortisol patterns and visual rating scales.CONCLUSION: This study suggests an interplay between diurnal cortisol patterns and neuroinflammation in relation to brain structure. While this cross-sectional study does not provide information on causality or temporality, these findings suggest that neuroinflammation may be involved in the relationship between HPA-axis functioning and AD.
61.	Hou, Ruihua, et al. (författare) The role of inflammation in anxiety and depression in the European U-BIOPRED asthma cohorts 2023 Ingår i: Brain, behavior, and immunity. - : Academic Press. - 0889-1591 .- 1090-2139. ; 111, s. 249-258 Tidskriftsartikel (refereegranskat)abstract Background: Growing evidence indicates high comorbid anxiety and depression in patients with asthma. However, the mechanisms underlying this comorbid condition remain unclear. The aim of this study was to investigate the role of inflammation in comorbid anxiety and depression in three asthma patient cohorts of the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) project. Methods: U-BIOPRED was conducted by a European Union consortium of 16 academic institutions in 11 European countries. A subset dataset from subjects with valid anxiety and depression measures and a large blood biomarker dataset were analysed, including 198 non-smoking patients with severe asthma (SAn), 65 smoking patients with severe asthma (SAs), 61 non-smoking patients with mild-to-moderate asthma (MMA), and 20 healthy non-smokers (HC). The Hospital Anxiety and Depression Scale was used to measure anxiety and depression and a series of inflammatory markers were analysed by the SomaScan v3 platform (SomaLogic, Boulder, Colo). ANOVA and the Kruskal-Wallis test were used for multiple-group comparisons as appropriate. Results: There were significant group effects on anxiety and depression among the four cohort groups (p < 0.05). Anxiety and depression of SAn and SAs groups were significantly higher than that of MMA and HC groups (p < 0.05. There were significant differences in serum IL6, MCP1, CCL18, CCL17, IL8, and Eotaxin among the four groups (p < 0.05). Depression was significantly associated with IL6, MCP1, CCL18 level, and CCL17; whereas anxiety was associated with CCL17 only (p < 0.05). Conclusions: The current study suggests that severe asthma patients are associated with higher levels of anxiety and depression, and inflammatory responses may underlie this comorbid condition.
62.	Humble, Mats B., 1952-, et al. (författare) Inflammasome activation in psychosis : Consequence of peripheral dyslipidaemia or reflection of an inflammatory pathogenesis? 2022 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 101, s. 284-285 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
63.	Isgren, Anniella, et al. (författare) Increased cerebrospinal fluid interleukin-8 in bipolar disorder patients associated with lithium and antipsychotic treatment. 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 43, s. 198-204 Tidskriftsartikel (refereegranskat)abstract Inflammation has been linked to the pathophysiology of bipolar disorder based on studies of inflammation markers, such as cytokine concentrations, in plasma and serum samples from cases and controls. However, peripheral measurements of cytokines do not readily translate to immunological activity in the brain. The aim of the present study was to study brain immune and inflammatory activity. To this end, we analyzed cytokines in cerebrospinal fluid from 121 euthymic bipolar disorder patients and 71 age and sex matched control subjects. Concentrations of 11 different cytokines were determined using immunoassays. Cerebrospinal fluid IL-8 concentrations were significantly higher in patients as compared to controls. The other cytokines measured were only detectable in part of the sample. IL-8 concentrations were positively associated to lithium- and antipsychotic treatment. The findings might reflect immune aberrations in bipolar disorder, or be due to the effects of medication.
64.	Isgren, Anniella, et al. (författare) Markers of neuroinflammation and neuronal injury in bipolar disorder: Relation to prospective clinical outcomes. 2017 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 65, s. 195-201 Tidskriftsartikel (refereegranskat)abstract Neuroimmune mechanisms have been linked to the pathophysiology of bipolar disorder based on studies of biomarkers in plasma, cerebrospinal fluid (CSF), and postmortem brain tissue. There are, however, no longitudinal studies investigating if CSF markers of neuroinflammation and neuronal injury predict clinical outcomes in patients with bipolar disorder. We have in previous studies found higher CSF concentrations of interleukin-8 (IL-8), monocyte chemoattractant protein 1 (MCP-1/CCL-2), chitinase-3-like protein 1 (CHI3L1/YKL-40), and neurofilament light chain (NF-L) in euthymic patients with bipolar disorder compared with controls. Here, we investigated the relationship of these CSF markers of neuroinflammation and neuronal injury with clinical outcomes in a prospective study. 77 patients with CSF analyzed at baseline were followed for 6-7years. Associations of baseline biomarkers with clinical outcomes (manic/hypomanic and depressive episodes, suicide attempts, psychotic symptoms, inpatient care, GAF score change) were investigated. Baseline MCP-1 concentrations were positively associated with manic/hypomanic episodes and inpatient care during follow-up. YKL-40 concentrations were negatively associated with manic/hypomanic episodes and with occurrence of psychotic symptoms. The prospective negative association between YKL-40 and manic/hypomanic episodes survived multiple testing correction. Concentrations of IL-8 and NF-L were not associated with clinical outcomes. High concentrations of these selected CSF markers of neuroinflammation and neuronal injury at baseline were not consistently associated with poor clinical outcomes in this prospective study. The assessed proteins may be involved in adaptive immune processes or reflect a state of vulnerability for bipolar disorder rather than being of predictive value for disease progression.
65.	Janelidze, Shorena, et al. (författare) Cytokine levels in the blood may distinguish suicide attempters from depressed patients. 2011 Ingår i: Brain, Behavior, and Immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 25, s. 335-339 Tidskriftsartikel (refereegranskat)abstract Elevated plasma cytokines is a common finding in Major Depressive Disorder (MDD), although not consistent. It is currently not known whether the inflammatory changes are confined to any specific subgroup of depressive patients. We here analyzed three inflammatory markers in suicidal and non-suicidal depressive patients, as well as healthy controls. Plasma interleukin (IL)-2, IL-6 and tumor necrosis factor (TNF)-α were measured in 47 suicide attempters, 17 non-suicidal depressed patients and 16 healthy controls. Study participants were evaluated using the Comprehensive Psychopathological Rating Scale (CPRS) with subscales for anxiety and degree of depression, as well as the Suicide Assessment Scale (SUAS). We found increased levels of IL-6 and TNF-α as well as decreased IL-2 concentrations in suicide attempters compared to non-suicidal depressed patients and healthy controls. The results were adjusted for potential confounders of cytokine expression, such as age, sex, body mass index (BMI), degree of depression, anxiety, personality disturbance, abuse and type of medication. These results demonstrate for the first time that suicidal patients display a distinct peripheral blood cytokine profile compared to non-suicidal depressed patients. Thus, our study provides further support for a role of inflammation in the pathophysiology of suicidality.
66.	Kanegawa, Naoki, et al. (författare) In vivo evidence of a functional association between immune cells in blood and brain in healthy human subjects 2016 Ingår i: Brain, behavior, and immunity. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0889-1591 .- 1090-2139. ; 54, s. 149-157 Tidskriftsartikel (refereegranskat)abstract Microglia, the resident macrophages in the central nervous system, are thought to be maintained by a local self-renewal mechanism. Although preclinical and in vitro studies have suggested that the brain may contain immune cells also from peripheral origin, the functional association between immune cells in the periphery and brain at physiological conditions is poorly understood. We examined 32 healthy individuals using positron emission tomography (PET) and [C-11]PBR28, a radioligand for the 18-kDa translocator protein (TSPO) which is expressed both in brain microglia and blood immune cells. In 26 individuals, two measurements were performed with varying time intervals. In a subgroup of 19 individuals, of which 12 had repeat examinations, leukocyte numbers in blood was measured on each day of PET measurements. All individuals were genotyped for TSPO polymorphism and categorized as high, mixed, and low affinity binders. We assessed TSPO binding expressed as total distribution volume of [C-11]PBR28 in brain and in blood cells. TSPO binding in brain was strongly and positively correlated to binding in blood cells both at baseline and when analyzing change between two PET examinations. Furthermore, there was a significant correlation between change of leukocyte numbers and change in TSPO binding in brain, and a trend level correlation to change in TSPO binding in blood cells. These in vivo findings indicate an association between immunological cells in blood and brain via intact BBB, suggesting a functional interaction between these two compartments, such as interchange of peripherally derived cells or a common regulatory mechanism. Measurement of radioligand binding in blood cells may be a way to control for peripheral immune function in PET studies using TSPO as a marker of brain immune activation. (C) 2016 Elsevier Inc. All rights reserved.
67.	Karlsson, H, et al. (författare) Association between erythrocyte sedimentation rate and IQ in Swedish males aged 18-20 2010 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 24:6, s. 868-873 Tidskriftsartikel (refereegranskat)
68.	Karshikoff, Bianka, et al. (författare) Editorial : Vulnerability and protective factors for inflammation-associated somatoform and mental disorders 2022 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 106, s. 227-230 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Over the past 30 years, research in psychoneuroimmunology and immunopsychiatry points to immune processes playing a part in the development and maintenance of various non-communicable disorders, including chronic pain (Grace et al., 2014), chronic fatigue (Lacourt et al., 2018), depression (Zunszain et al., 2013), anxiety (Michopoulos et al., 2016), psychosis (Ullah et al., 2021) and neurodegeneration (Park et al., 2020). Many of these disorders are characterized by a complex symptomatology, various comorbidities, and a difficulty to treat the disorder satisfactorily. Although recent research shows that immune alterations and inflammatory components may contribute to the pathophysiology of these diseases, inflammation is probably not sufficient to independently induce these disorders or maintain them. Not all individuals with a heightened inflammatory activity will develop one of these disorders, and some individuals with these disorders show no changes in immune parameters. This suggests the involvement of additional factors that interact with the immune system to cause vulnerability to, or a protection against, inflammation-associated disorders.In this special issue of Brain, Behavior and Immunity, we welcomed articles investigating predictors and moderators of inflammation-associated disorders, comorbidities, and behavioral changes. The studies included in this issue range from experimental human and animal studies to clinical investigations applying proteomic approaches. The disorders discussed include those related to aging and neurodegenerative diseases, psychiatric disorders, fatigue, and pain. The authors contributing to this special issue tackle some fundamental questions, including: Why do not all individuals with a heightened inflammatory activity develop one of these disorders? How can we protect against the neuropsychiatric effects of inflammation? Does inflammation interact with other pathological processes of clinical conditions such as Parkinson’s disease and Alzheimer’s disease?
69.	Karshikoff, B., et al. (författare) LPS increases pain sensitivity by decreased pain inhibition and increased insular activation 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 49, s. e1-e1 Tidskriftsartikel (refereegranskat)abstract We have shown that women are more prone to developing LPS-induced pain sensitivity than men, and that the descending endogenous pain inhibition is disrupted in women during experimental systemic inflammation. The aim of the present study was to investigate some of the central neural mechanisms underlying our previous findings. 51 participants (29 women) were injected with 0.6 ng/kg LPS or saline and went through a thumb-pressure pain fMRI paradigm 2 h after injection. As hypothesized, the subjects injected with LPS had decreased activity in the ventromedial prefrontal cortex and rostral anterior cingulate cortex (rACC), areas involved in descending pain inhibition. In addition, the LPS group had higher activity in the anterior insula, an area involved in medial/affective pain processing and interoception. These effects were not sex dependent. However, the male participants had overall stronger descending pain inhibition, reflected as a stronger rACC activity compared to women. It is possible that the more robust activation of descending pain inhibition rendered the men more resistant to the immune provocation, which may explain previously seen sex differences in LPS-induced pain sensitivity. Our findings give an indication to how the pain matrix is affected during a sickness response. The results strengthen the proposed link between systemic inflammation and weakened pain regulation in chronic pain disorders, and offers a possible mechanism underlying the female predominance in chronic pain disorders.
70.	Karshikoff, B., et al. (författare) Modality and sex differences in pain sensitivity during human endotoxemia 2014 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 46, s. 35-43 Tidskriftsartikel (refereegranskat)abstract Systemic inflammation can induce pain hypersensitivity in animal and human experimental models, and has been proposed to be central in clinical pain conditions. Women are overrepresented in many chronic pain conditions, but experimental studies on sex differences in pain regulation during systemic inflammation are still scarce. In two randomized and double blind placebo controlled experiments, we used low doses of lipopolysaccharide (LPS) as an experimental model of systemic inflammation. The first study employed 0.8ng/kg LPS in a within-subject design of 8 individuals (1 woman), and the second study 0.6ng/kg LPS in a between-subject design of 52 participants (29 women). We investigated the effect on (a) pressure, heat, and cold pain thresholds, (b) suprathreshold noxious heat and cold sensitivity, and (c) conditioned pain modulation (CPM), and differences between men and women. LPS induced significantly lower pressure pain thresholds as compared to placebo (mean change with the 0.8ng/kg dose being -64±30kPa P=.04; with the 0.6ng/kg dose -58±55kPa, P<.01, compared to before injection), whereas heat and cold pain thresholds remained unaffected (P's>.70). Suprathreshold noxious pain was not affected by LPS in men (P's⩾.15). However, LPS made women rated suprathreshold noxious heat stimuli as more painful (P=.01), and showed a tendency to rate noxious cold pain as more painful (P=.06) as compared to placebo. Furthermore, LPS impaired conditioned pain modulation, a measure of endogenous pain inhibition, but this effect was also restricted to women (P<.01, for men P=.27). Pain sensitivity correlated positively with plasma IL-6 and IL-8 levels. The results show that inflammation more strongly affects deep pain, rather than cutaneous pain, and suggest that women's pain perception and modulation is more sensitive to immune activation than men's.
71.	Karshikoff, Bianka, et al. (författare) Why sickness hurts : A central mechanism for pain induced by peripheral inflammation 2016 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 57, s. 38-46 Tidskriftsartikel (refereegranskat)abstract Low-grade systemic inflammation has been implicated in chronic pain, as well as in comorbid diseases like depression and fatigue. We have previously shown that women's pain perception and regulation is more affected by systemic inflammation than that of men. Here we investigated the neural substrates underlying these effects using an fMRI paradigm previously employed in a clinical population. Fifty-one participants (29 women) were injected with 0.6ng/kg lipopolysaccharide (LPS) or saline to induce a peripheral inflammatory response. The subjects were then tested with a pressure pain fMRI paradigm designed to capture descending pain inhibitory activity 2h after injection, and blood was sampled for cytokine analysis. The subjects injected with LPS became more pain sensitive compared to the placebo group, and the heightened pain sensitivity was paralleled by decreased activity in the ventrolateral prefrontal cortex and the rostral anterior cingulate cortex (rACC) compared to placebo; areas involved in descending pain regulation. The LPS group also had higher activity in the anterior insular cortex, an area underpinning affective and interoceptive pain processing. Women displayed overall less pain-evoked rACC activity compared to men, which may have rendered women less resilient to immune provocation, possibly explaining sex differences in LPS-induced pain sensitivity. Our findings elucidate the pain-related brain circuits affected by experimental peripheral inflammation, strengthening the theoretical link between systemic inflammation and weakened pain regulation in chronic pain disorders. The results further suggest a possible mechanism underlying the female predominance in many chronic pain disorders.
72.	Kern, Silke, et al. (författare) Higher CSF interleukin-6 and CSF interleukin-8 in current depression in older women. Results from a population-based sample. 2014 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 41, s. 55-58 Tidskriftsartikel (refereegranskat)abstract The literature regarding cerebrospinal fluid (CSF) cytokines in geriatric depression is sparse. The aim of this study was to examine associations between CSF interleukin-6 (IL-6), interleukin-8 (IL-8) and depression in a population-based sample of older women who were followed for 17years.
73.	Kosek, Eva, et al. (författare) The translocator protein gene is associated with symptom severity and cerebral pain processing in fibromyalgia 2016 Ingår i: Brain Behavior and Immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 58, s. 218-227 Tidskriftsartikel (refereegranskat)abstract The translocator protein (TSPO) is upregulated during glia activation in chronic pain patients. TSPO constitutes the rate-limiting step in neurosteroid synthesis, thus modulating synaptic transmission. Related serotonergic mechanisms influence if pro- or anti-nociceptive neurosteroids are produced. This study investigated the effects of a functional genetic polymorphism regulating the binding affinity to the TSPO, thus affecting symptom severity and cerebral pain processing in fibromyalgia patients. Gene-to-gene interactions with a functional polymorphism of the serotonin transporter gene were assessed. Fibromyalgia patients (n = 126) were genotyped regarding the polymorphisms of the TSPO (rs6971) and the serotonin transporter (5-HTTLPR/rs25531). Functional magnetic resonance imaging (n = 24) was used to study brain activation during individually calibrated pressure pain. Compared to mixed/low TSPO affinity binders, the high TSPO affinity binders rated more severe pain (p = 0.016) and fibromyalgia symptoms (p = 0.02). A significant interaction was found between the TSPO and the serotonin transporter polymorphisms regarding pain severity (p < 0.0001). Functional connectivity analyses revealed that the TSPO high affinity binding group had more pronounced pain-evoked functional connectivity in the right frontoparietal network, between the dorsolateral prefrontal area and the parietal cortex. In conclusion, fibromyalgia patients with the TSPO high affinity binding genotype reported a higher pain intensity and more severe fibromyalgia symptoms compared to mixed/low affinity binders, and this was modulated by interaction with the serotonin transporter gene. To our knowledge this is the first evidence of functional genetic polymorphisms affecting pain severity in FM and our findings are in line with proposed glia-related mechanisms. Furthermore, the functional magnetic resonance findings indicated an effect of translocator protein on the affective-motivational components of pain perception.
74.	Koskuvi, Marja, et al. (författare) Lower complement C1q levels in first-episode psychosis and in schizophrenia 2024 Ingår i: Brain, Behavior, and Immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 117, s. 313-319 Tidskriftsartikel (refereegranskat)abstract Recent evidence has implicated complement component (C) 4A in excessive elimination of synapses in schizophrenia. C4A is believed to contribute to physiological synapse removal through signaling within the C1q initiated classical activation axis of the complement system. So far, a potential involvement of C1q in the pathophysiology of schizophrenia remains unclear. In this study, we first utilized large-scale gene expression datasets (n = 586 patients with schizophrenia and n = 986 controls) to observe lower C1QA mRNA expression in prefrontal cortex tissue of individuals with schizophrenia (P = 4.8x10-05), while C1QA seeded co-expression networks displayed no enrichment for schizophrenia risk variants beyond C4A. We then used targeted liquid chromatography-mass spectrometry (LS-MS) to measure cerebrospinal fluid (CSF) levels of C1qA in 113 individuals with first-episode psychosis (FEP), among which 66 individuals was later diagnosed with schizophrenia, and 87 healthy controls. CSF concentrations of C1qA were lower in individuals diagnosed with FEP (P = 0.0001), also after removing subjects with a short-term prescription of an antipsychotic agent (P = 0.0005). We conclude that C1q mRNA and protein levels are lower in schizophrenia and that further experimental studies are needed to understand the functional implications.
75.	Lai, Jacqueline, 1980, et al. (författare) Immune responses in perinatal brain injury. 2017 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 63, s. 210-223 Forskningsöversikt (refereegranskat)abstract The perinatal period has often been described as immune deficient. However, it has become clear that immune responses in the neonate following exposure to microbes or as a result of tissue injury may be substantial and play a role in perinatal brain injury. In this article we will review the immune cell composition under normal physiological conditions in the perinatal period, both in the human and rodent. We will summarize evidence of the inflammatory responses to stimuli and discuss how neonatal immune activation, both in the central nervous system and in the periphery, may contribute to perinatal hypoxic-ischemic brain injury.
76.	Lasselin, Julie, 1986-, et al. (författare) Advantages and methodological considerations of experimental endotoxemia in humans : Towards a standardized procedure for its application in PNI 2021 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 98, s. 28-29 Tidskriftsartikel (refereegranskat)abstract Experimental endotoxemia is now recognized as a highly useful tool to better understand inflammation-induced behavioral changes and their underlying mechanisms. Advantages of this model include the ability to assess the causal effects of inflammatory mediators in a safe and highly controlled context, to assess the homeostatic (regulatory) response to inflammatory mediators within a relatively short time frame, as well as to translate findings between animals and humans. Various groups have used this model in humans, leading to variations in experimental procedures that likely affect the studied outcomes. As the use of experimental endotoxemia develops, there is a need of a standardization of the procedure to make the best use of this model in PNI. The participants in this discussion group are all leaders in the use of the model of experimental endotoxemia in humans in PNI, and will discuss the advantages, limitations, clinical relevance, and methodological considerations of this model. This discussion is intended as a first step towards developing common and optimized procedures for the use of this model across PNI groups.
77.	Lasselin, Julie, et al. (författare) Biological motion during inflammation in humans 2020 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 84, s. 147-153 Tidskriftsartikel (refereegranskat)abstract Biological motion is a powerful perceptual cue that can reveal important information about the inner state of an individual. Activation of inflammatory processes likely leads to changes in gait, posture, and mobility patterns, but the specific characteristics of inflammation-related biological motion have not been characterized. The aim of this study was to determine the effect of inflammation on gait and motion in humans. Systemic inflammation was induced in 19 healthy volunteers with an intravenous injection of lipopolysaccharide (2 ng/kg body weight). Biological motion parameters (walking speed, stride length and time, arm, leg, head, and shoulder angles) were assessed during a walking paradigm and the timed-up-and-go test. Cytokine concentrations, body temperature, and sickness symptoms were measured. During inflammation, compared to placebo, participants exhibited shorter, slower, and wider strides, less arm extension, less knee flexion, and a more downward-tilting head while walking. They were also slower and took a shorter First step in the timed-up-and-go test. Higher interleukin-6 concentrations, stronger sickness symptoms, and lower body temperature predicted the inflammation-related alterations in biological motion. These findings show that biological motion contains clear information about the inflammatory status of an individual, and may be used by peers or artificial intelligence to recognize that someone is sick or contagious.
78.	Lasselin, Julie, et al. (författare) Effect of long-term sleep restriction and subsequent recovery sleep on the diurnal rhythms of white blood cell subpopulations. 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 47:SI, s. 93-99 Tidskriftsartikel (refereegranskat)abstract While acute modifications of sleep duration induces a wide array of immune function alterations, less is known of how longer periods with insufficient sleep affect immune functions and how they return to normal once recovery sleep is obtained. The purpose of the present study was to investigate the effects of five days of restricted sleep and a subsequent 7-day period of sleep recovery on white blood cell (WBC) subpopulation count and diurnal rhythms. Nine healthy males participated in a sleep protocol consisting of two baseline days (8h of sleep/night), five nights with restricted sleep (4h of sleep/night) and seven days of recovery sleep (8h of sleep/night). During nine of these days, blood was drawn hourly during night-time end every third hour during daytime, and differential WBC count was analyzed. Gradual increase across the days of sleep restriction was observed for total WBC (p<.001), monocytes (p<.001), neutrophils (p<.001) and lymphocytes (p<.05). Subsequent recovery sleep resulted in a gradual decrease in monocytes (p<.001) and lymphocytes (p=.001), but not in neutrophils that remained elevated over baseline level at the end of the 7-day recovery period. These effects were associated with altered diurnal rhythms of total WBC and neutrophils, restricted sleep being associated with higher levels during the night and at awakening, resulting in a flattening of the rhythm. The diurnal alterations were reversed when recovery sleep was allowed, although the amplitude of total WBC, neutrophils and monocytes was increased at the end of the recovery period in comparison to baseline. Altogether, these data show that long-term sleep restriction leads to a gradual increase of circulating WBC subpopulations and alterations of the respective diurnal rhythms. Although some of the effects caused by five days of restricted sleep were restored within the first days of recovery, some parameters were not back to baseline even after a period of seven recovery days.
79.	Lasselin, Julie, et al. (författare) Fatigue and sleepiness responses to experimental inflammation and exploratory analysis of the effect of baseline inflammation in healthy humans 2020 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 83, s. 309-314 Tidskriftsartikel (refereegranskat)abstract Inflammation is believed to be a central mechanism in the pathophysiology of fatigue. While it is likely that dynamic of the fatigue response after an immune challenge relates to the corresponding cytokine release, this lacks evidence. Although both fatigue and sleepiness are strong signals to rest, they constitute distinct symptoms which are not necessarily associated, and sleepiness in relation to inflammation has been rarely investigated. Here, we have assessed the effect of an experimental immune challenge (administration of lipopolysaccharide, LPS) on the development of both fatigue and sleepiness, and the associations between increases in cytokine concentrations, fatigue and sleepiness, in healthy volunteers. In addition, because chronic-low grade inflammation may represent a risk factor for fatigue, we tested whether higher baseline levels of inflammation result in a more pronounced development of cytokine-induced fatigue and sleepiness. Data from four experimental studies was combined, giving a total of 120 subjects (LPS N = 79, 18 (23%) women; Placebo N = 69, 12 (17%) women). Administration of LPS resulted in a stronger increase in fatigue and sleepiness compared to the placebo condition, and the development of both fatigue and sleepiness closely paralleled the cytokine responses. Individuals with stronger increases in cytokine concentrations after LPS administration also suffered more from fatigue and sleepiness (N = 75), independent of gender. However, there was no support for the hypothesis that higher baseline inflammatory markers moderated the responses in fatigue or sleepiness after an inflammatory challenge. The results demonstrate a tight connection between the acute inflammatory response and development of both fatigue and sleepiness, and motivates further investigation of the involvement of inflammation in the pathophysiology of central fatigue.
80.	Lasselin, Julie, et al. (författare) Immunological and behavioral responses to in vivo lipopolysaccharide administration in young and healthy obese and normal-weight humans 2020 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 88, s. 283-293 Tidskriftsartikel (refereegranskat)abstract Obesity is associated with an increase prevalence of neuropsychiatric symptoms and diseases, such as depression. Based on the facts that pro-inflammatory cytokines are able to modulate behavior, and that obesity is characterized by a chronic low-grade inflammatory state, inflammation has been hypothesized to contribute to the neuropsychiatric comorbidity in obese individuals. However, a causal link between inflammation and the development of neuropsychiatric symptoms is hard to establish in humans. Here, we used an inflammatory stimulus, i.e. the intravenous injection of lipopolysaccharide (LPS), in a double-blind placebo-controlled design, to determine the vulnerability of obese individuals to inflammation-induced behavioral changes. The hypothesis was that obese individuals would show heightened behavioral response compared to normal-weight subjects for the same inflammatory stimulus, reflecting an increased sensitivity to the behavioral effects of pro-inflammatory cytokines. LPS (dose 0.8 ng/kg body weight, adjusted for estimated blood volume in obese subjects) and placebo (saline) were intravenously injected in 14 obese healthy subjects and 23 normal-weight healthy subjects in a within-subject, randomized, crossover design. LPS administration induced, in both groups, an acute increase in blood concentrations of cytokines (interleukin-6, tumor necrosis factor-alpha, and IL-10), as well as in body temperature, cortisol, norepinephrine, sickness symptoms, fatigue, negative mood, and state anxiety. There were little differences in the immune and behavioral responses to LPS between obese and normal-weight subjects, but the cortisol response to LPS was strongly attenuated in obese individuals. Higher percentage of body fat was related to a lower cortisol response to LPS. Taken together, the population of young and healthy obese individuals in this study did not exhibit an increased behavioral sensitivity to cytokines, but an attenuated cortisol response to the immune challenge. Future studies will need to determine whether additional physiological and psychological factors interact with the state of obesity to increase the risk for inflammation-induced neuropsychiatric symptoms.
81.	Lasselin, Julie, et al. (författare) Inflammation in the visceral adipose tissue of obese subjects: relationship with circulating inflammation and association with bariatric surgery outcomes 2014 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 40, s. e29-e29 Tidskriftsartikel (refereegranskat)abstract The inflammatory state of the adipose tissue, in particular visceral adipose tissue, is believed to contribute to systemic chronic low-grade inflammation associated with obesity. Nevertheless, the precise characterization of the inflammatory profile of obese subjects, associating adipose and systemic inflammatory markers, is still needed. In addition, the question whether inflammatory specificities in obesity influence the outcomes of bariatric surgery, such as weight reduction, remains to be elucidated. To address these questions, thirty-seven obese patients were included in the present study and about 70% of them were followed up to fourteen months after bariatric surgery. Systemic concentrations of inflammatory markers were assessed using ELISA before bariatric surgery. Samples of visceral adipose tissue were extracted during bariatric surgery and gene expression of cytokines and immune cells markers were evaluated using qRT-PCR. Our results indicate that cytokines were strongly inter-correlated in the adipose tissue. In addition, we have found significant associations of adipose expression of macrophage and T cells markers with adipose expression and with systemic levels of cytokines, including TNF-α and IL-6. Importantly, a higher inflammatory state of the visceral adipose tissue before bariatric surgery predicted a lower weight reduction after surgery, notably at early stages post-surgery. Taking together, these findings highlight the importance of the inflammatory state of the visceral adipose tissue in obesity-related inflammation, and its relevance regarding its impact on outcomes of obesity treatments.
82.	Lasselin, Julie, 1986-, et al. (författare) Inflammation-related gait- Analysis of biological motion using the Microsoft® Kinect® during experimentally-induced sickness 2017 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 66 Tidskriftsartikel (refereegranskat)abstract Biological motion is a powerful communication cue and we have recently shown that sickness can be detected from gait pattern. However, it is unclear which gait characteristics are modulated by health status and whether change in gait pattern relates to inflammation and to the degree of sickness. The current study aimed at answering these questions by assessing biological motion characteristics in 19 individuals during experimentally-induced sickness, obtained by intravenous injection of lipopolysaccharide (2 ng/kg bw), and after placebo administration. Joint 3-D coordinates were recorded using the Microsoft® Kinect® during a walking paradigm and a mobility test (time-up-and-go test). Results indicate that gait during experimentally-induced sickness is characterized by slower and shorter strides, resulting in slower walking speed, as well as a slower time to stand up from a chair. In addition, sick subjects appear to swing their arms and to lift their legs less than when healthy, as reflected by smaller elbow angle during arm extension and larger knee angle during leg flexion compared to the placebo condition. Alterations in the overall gait pattern during experimentally-induced sickness was associated with interleukin-6 peak concentrations and a trend was observed with sickness symptoms. Altogether, these findings suggest that gait pattern might signal sickness/inflammatory status and could be used as an objective assessment of sickness, as well as to determine evolution of health status in individuals over time.
83.	Lasselin, Julie (författare) Is inflammation-associated depression atypical depression? 2020 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 87, s. 193-194 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Major depressive disorder (MDD) remains today a challenge to treat and to prevent, mostly because of the highly heterogeneous features and multifactorial processes underlying the disease. During the last two decades, some hope have emerged from clinical and experimental evidence revealing the role of inflammation in the pathophysiology of depression (Miller and Raison, 2016). This research provides support for the use of anti-inflammatory treatments in depressed patients. However, it is estimated that only about 30% of depressed patients exhibit signs of inflammation and would benefit from anti-inflammatory treatments (Chamberlain et al., 2018). Therefore, it has become clear that the solution to better treatments against major depression is to develop therapies tailored to match subpopulations of patients. To this aim, it is crucial to define and characterize these subpopulations, such as proposed by Cosgrove et al. (2020) in their recent article published in Brain, Behavior, and Immunity.
84.	Lasselin, Julie, et al. (författare) Low-grade inflammation is a major contributor of impaired attentional set shifting in obese subjects 2016 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 58, s. 63-68 Tidskriftsartikel (refereegranskat)abstract Impairment in cognitive flexibility and set shifting abilities has been described in obesity. This alteration is critical as it can interfere with obesity management strategies. Recent evidences suggest that chronic low-grade inflammation may be involved in cognitive deficits associated with obesity, but the potential involvement in reduced flexibility remains unknown. The objective of this study was to assess the contribution of low-grade inflammation, determined by circulating levels of high-sensitivity C-reactive protein (hsCRP), in reduced cognitive flexibility and shifting abilities of obese subjects relatively to a group of non-obese participants. Performance in the intra/extra-dimensional set shift (IED) test, extracted from the CANTAB, was assessed in 66 obese subjects and 20 non-obese participants. Obese subjects with concentrations of hsCRP above 5 mg/L exhibited reduced performance on the IED test in comparison to obese subjects with lower levels of hsCRP and non-obese participants. This difference was particularly manifest in the number of errors made during the extra-dimensional shift (EDS errors). In contrast, performance before the extra-dimensional shift was spared. Linear regression analyses revealed that the association between obesity and IED alterations was significant only when the condition hsCRP >5 mg/L was entered in the model. These findings are important as they indicate that, rather than obesity itself, low-grade inflammation represents a major contributor of IED performance in obese subjects.
85.	Lasselin, Julie, et al. (författare) Mood disturbance during experimental endotoxemia : Predictors of state anxiety as a psychological component of sickness behavior 2016 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 57, s. 30-37 Tidskriftsartikel (refereegranskat)abstract Lipopolysaccharide (LPS) administration is a well-established model to assess afferent immune-to-brain communication and behavioral aspects of inflammation. Nevertheless, only few studies in comparatively small samples have assessed state anxiety as a psychological component of sickness behavior despite possible clinical implications for the pathophysiology of neuropsychiatric conditions. Thus, the goal of the present analyses carried out in a large, pooled dataset from two independent study sites was to analyze the state anxiety response to LPS administration and to investigate predictors (i.e., cytokine changes; pre-existing anxiety and depression symptoms assessed with the Hospital Anxiety and Depression Scale) of the LPS-induced state anxiety changes at different time points after LPS administration. Data from 186 healthy volunteers who participated in one of six randomized, placebo-controlled human studies involving intravenous administration of LPS at doses of 0.4-0.8ng/kg body weight were combined. State anxiety as well as circulating interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10 concentrations were significantly increased 2h and 3h after LPS administration, with a peak at 2h, and returned to baseline 6h after administration. Greater changes in IL-6 from baseline to 3h after LPS administration significantly and independently predicted a more pronounced LPS-induced state anxiety response. In addition, higher pre-existing subclinical anxiety symptoms significantly predicted a lower increase in state anxiety 3h and 6h after LPS-administration, which was mediated by TNF-α changes. In conclusion, our findings give additional support for a putative role of inflammatory mechanisms in the pathophysiology of stress-related and anxiety disorders and give new insight on the potential role of pre-existing subclinical affective symptoms.
86.	Lasselin, Julie, et al. (författare) Pre-existent anxiety symptoms is associated with modified behavioral response during endotoxemia 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 49, s. e29-e30 Tidskriftsartikel (refereegranskat)abstract Experimental endotoxin administration is a well-established model to analyze the effect of inflammation on the development of mood impairments. However, it remains unknown from previous studies in comparatively small samples whether pre-existing inter-individual differences modulate the behavioral response during endotoxemia. We addressed this question in the present study using a merged database combining data from multiple studies performed at two study sites. In 286 healthy volunteers who either received low-dose intravenous injection of lipopolysaccharide (LPS, 0.4–0.8 ng/kg, n = 168) or saline (n = 118), plasma concentrations of TNF-alpha and IL-6 were analyzed before and 2, 3.5 and 6 hours post injection together with state anxiety symptoms (STAI). Pre-existent symptoms of anxiety and depression (HADS) were assessed before injection. LPS administration induced an increase in state anxiety 2 hours post injection that was positively correlated with increases in TNF-alpha and IL-6, but not with pre-existent HADS scores (when adjusted for age, sex, BMI, LPS dose, and study design). However, higher levels of pre-existent HADS anxiety symptoms predicted a stronger subsequent reduction in state anxiety at 3.5 and 6 hours post LPS injection. Taken together, these data suggest that although inter-individual differences in anxiety or depression symptoms do not appear to explain the extent of mood impairments during endotoxemia, at least in non-patient samples, they still lead to a modified mood response with a faster and stronger decline.
87.	Lasselin, Julie, et al. (författare) Sickness behavior is not all about the immune response : Possible roles of expectations and prediction errors in the worry of being sick 2018 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 74, s. 213-221 Tidskriftsartikel (refereegranskat)abstract BackgroundPeople react very differently when sick, and there are only poor correlations between the intensity of the immune response and sickness behavior. Yet, alternative predictors of the individual differences in sickness are under-investigated. Based on the predictive coding model of placebo responses, where health outcomes are function of bottom-up sensory information and top-down expectancies, we hypothesized that individual differences in behavioral changes during sickness could be explained by individual top-down expectancies and prediction errors.MethodsTwenty-two healthy participants were made sick by intravenously administering lipopolysaccharide (2 ng/kg body weight). Their expectations of becoming sick were assessed before the injection.ResultsParticipants having lower expectations of becoming sick before the injection reacted with more emotional distress (i.e., more negative affect and lower emotional arousal) than those with high expectations of becoming sick, despite having similar overall sickness behavior (i.e., a combined factor including fatigue, pain, nausea and social withdrawal). In keeping with a predictive coding model, the “prediction error signal”, i.e., the discrepancy between the immune signal and sickness expectancy, predicted emotional distress (reduction in emotional arousal in particular).ConclusionThe current findings suggest that the emotional component of sickness behavior is, at least partly, shaped by top-down expectations. Helping patients having a realistic expectation of symptoms during treatment of an illness may thus reduce aggravated emotional responses, and ultimately improve patients’ quality of life and treatment compliance.Registration“Endotoxin-induced Inflammatory and Behavioral Responses and Predictors of Individual Differences”, https://clinicaltrials.gov/ct2/show/NCT02529592, registration number: NCT02529592.
88.	Lasselin, Julie, et al. (författare) Sleep during naturally occurring respiratory infections : A pilot study 2019 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 79, s. 236-243 Tidskriftsartikel (refereegranskat)abstract There is strong experimental support that infections increase the drive for sleep in animals, and it is widely believed that more sleep is part of an adaptive immune response. While respiratory infections (RI) are very prevalent in humans, there is a striking lack of systematic knowledge on how it affects sleep. We recruited 100 people, among whom 28 became sick with an RI during the study period (fulfilling criteria for influenza-like illness, ILI, or acute respiratory infection, ARI). We measured sick participants' sleep at home, both objectively (actigraphy) and subjectively (diary ratings), for one week as well as four weeks later when healthy. During the week with RI, people spent objectively longer time in bed and had a longer total sleep time compared to the healthy week. During the infection, participants also had more awakenings, but no significant differences in sleep latency or sleep efficiency. While sick, people also reported increased difficulties falling asleep, worse sleep quality, more restless sleep and more shallow sleep, while they did not report sleep to be less sufficient. Most problems occurred at the beginning of the sickness week, when symptoms were strong, and showed signs of recovery thereafter (as indicated by interactions between condition and day/night of data collection for all the 10 sleep outcomes). The degree of symptoms of RI was related to a worse sleep quality and more restless sleep, but not to any of the objective sleep outcomes or the other subjective sleep variables. Having a higher body temperature was not significantly related to any of the sleep variables. This study suggests that having a respiratory infection is associated with spending more time in bed and sleeping longer, but also with more disturbed sleep, both objectively and subjectively. This novel study should be seen as being of pilot character. There is a need for larger studies which classify pathogen type and include baseline predictors, or that manipulate sleep, in order to understand whether the sleep alterations seen during infections are adaptive and whether sleep interventions could be used to improve recovery from respiratory infections.
89.	Lee, BK, et al. (författare) Maternal hospitalization with infection during pregnancy and risk of autism spectrum disorders 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 44, s. 100-105 Tidskriftsartikel (refereegranskat)
90.	Lekander, Mats, et al. (författare) Intrinsic functional connectivity of insular cortex and symptoms of sickness during acute experimental inflammation 2016 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 56, s. 34-41 Tidskriftsartikel (refereegranskat)abstract Task-based fMRI has been used to study the effects of experimental inflammation on the human brain, but it remains unknown whether intrinsic connectivity in the brain at rest changes during a sickness response. Here, we investigated the effect of experimental inflammation on connectivity between areas relevant for monitoring of bodily states, motivation, and subjective symptoms of sickness. In a double blind randomized controlled trial, 52 healthy volunteers were injected with 0.6 ng/kg LPS (lipopolysaccharide) or placebo, and participated in a resting state fMRI experiment after approximately 2h 45 minutes. Resting state fMRI data were available from 48 participants, of which 28 received LPS and 20 received placebo. Bilateral anterior and bilateral posterior insula sections were used as seed regions and connectivity with bilateral orbitofrontal and cingulate (anterior and middle) cortices was investigated. Back pain, headache and global sickness increased significantly after as compared to before LPS, while a non-significant trend was shown for increased nausea. Compared to placebo, LPS was followed by increased connectivity between left anterior insula and left midcingulate cortex. This connectivity was significantly correlated to increase in back pain after LPS and tended to be related to increased global sickness, but was not related to increased headache or nausea. LPS did not affect the connectivity from other insular seeds. In conclusion, the finding of increased functional connectivity between left anterior insula and middle cingulate cortex suggests a potential neurophysiological mechanism that can be further tested to understand the subjective feeling of malaise and discomfort during a sickness response.
91.	Lekander, Mats, et al. (författare) Longitudinal relationship between inflammation and poor self-rated health in elderly 2015 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 49, s. e37-e37 Tidskriftsartikel (refereegranskat)abstract Self-rated health (SRH) predicts future objective health and summarizes information in a way that goes beyond the biomedical health model. Low-grade inflammation contributes to poor SRH, but previous findings rely on cross-sectional analyses. We therefore studied the relationship between SRH and IL-6 in a longitudinal study of elderly. Participants (m = 74 years; range 60–93; 41% male) were studied in 6-month waves over a period up to 5 years. SRH was measured with a one-item question (excellent to poor). Serum was collected following the interview visit (median interval 40 days), frozen at −80 °C and later analyzed with high-sensitivity ELISA for IL-6. Overall, 999 observations were available for analysis. When analyzed as a between-subject effect, a stable relationship was observed between SRH and logIL-6 (β = −.088; p < .001). However, the within-subject effect of SRH on IL-6 was not significant. The effects were not explained by gender, age, BMI, neuroticism, or statin use. There was no main effect of interview-to-blood sample interval, neither between nor within subjects. Putative variations over time in the relation between SRH and IL-6 could thus not be captured with the present design. With the advantage of a longitudinal design and multiple sampling occasions, the present data strongly support the stability of the previously reported cross-sectional relationship between higher levels of inflammatory cytokines and less favorable health appraisals across individuals.
92.	Lekander, Mats, et al. (författare) Subjective health perception in healthy young men changes in response to experimentally restricted sleep and subsequent recovery sleep 2013 Ingår i: Brain Behavior and Immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 34, s. 43-46 Tidskriftsartikel (refereegranskat)abstract Sleep and subjective health are both prospectively related to objective indices of health and health care use. Here, we tested whether five days with restricted sleep and subsequent recovery days affect subjective health and is related to increased levels of circulating IL-6 and TNF-alpha and fatigue. Nine healthy men (23-28 years) went through a 6-week sleep protocol with subjects as their own controls in a repeated measures design with a total of 11 nights in a sleep laboratory. The experimental part of the protocol included three baseline days (sleep 23-07 h), five days with sleep restriction (03-07 h) and three recovery days (23-07 h) in the sleep laboratory. Subjective health and fatigue was recorded daily. Eight blood samples were drawn each day (every third hour) on 8 days of the protocol and analyzed with respect to IL-6 and TNF-alpha. Subjective health deteriorated gradually during restricted sleep (p = .002) and returned to baseline levels after three days of recovery. IL-6 and TNF-alpha did not change significantly. Fatigue increased gradually during sleep restriction (p = .001), which significantly contributed to the association between restricted sleep and subjective health. The study is the first to show that subjective health is directly responsive to changes in sleep length and related to increased fatigue. Thus, subjective health is differently appraised after manipulation of one of its presumed determinants. Larger experimental studies would be beneficial to further distinguish causation from association regarding the underpinnings of subjective health. (C) 2013 Published by Elsevier Inc.
93.	Leone, Marica, et al. (författare) Association of severe childhood infections with depression and intentional self-harm in adolescents and young adults 2022 Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 99, s. 247-255 Tidskriftsartikel (refereegranskat)abstract Early-life infections have been linked with subsequent depression and self-harm. Examination of specific groups of infections and the role of familial factors may elucidate this observed relationship. We addressed these considerations in our investigations of the association of severe childhood infections with the risks of depression and self-harm in adolescence and early-adulthood. This population-based cohort study included all individuals born in Sweden between 1982 and 1996, with follow-up through 2013 (N = 1,506,070). Severe childhood infections were identified using inpatient and outpatient diagnoses from birth through age 12. Any infection as well as specific groups of infections were investigated. We examined diagnoses of depression and self-harm within inpatient and outpatient care and death by self-harm between ages 13 and 31. Cox proportional hazards regression models were used to estimate absolute risks, hazard ratios (HRs), and 95% CIs. When adjusting for sex and birth year, individuals exposed to any childhood infection demonstrated increased absolute risk differences for both outcomes (2.42% [95% CI, 0.41%-4.43%] of being diagnosed with depression up until age 31, and 0.73% [-2.05%-3.51%] of self-harm up until age 31) and increased relative risks (HR, 1.22 [1.20-1.24] for depression and HR, 1.29 [1.25-1.32] for self-harm). When controlling for unmeasured factors shared between family members by comparing discordant siblings, no strong association persisted. Our findings show that childhood infections may not be involved in the etiology of later depression and self-harm, and highlight the importance of identifying these genetic and environmental familial risk factors, which may serve as targets for interventions.
94.	Lindqvist, Daniel, et al. (författare) Cerebrospinal fluid inflammatory markers in Parkinson's disease - Associations with depression, fatigue, and cognitive impairment. 2013 Ingår i: Brain Behavior and Immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 33:Jul.,31, s. 183-189 Tidskriftsartikel (refereegranskat)abstract Neuroinflammation may be involved in the pathophysiology of Parkinson's disease (PD) and specifically in non-motor symptoms such as depression, fatigue and cognitive impairment. The aim of this study was to measure inflammatory markers in cerebrospinal fluid (CSF) samples from PD patients and a reference group, and to investigate correlations between non-motor symptoms and inflammation. We quantified C-reactive protein (CRP), interleukin-6, tumor necrosis factor-alpha, eotaxin, interferon gamma-induced protein-10, monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein 1-β in CSF samples from PD patients (N=87) and the reference group (N=33). Sixteen of the PD patients had a dementia diagnosis (PDD). We assessed symptoms of fatigue, depression, anxiety and cognitive function using the Functional Assessment of Chronic Illness Therapy-Fatigue, the Hospital Anxiety and Depression Scale, and the Mini Mental State Examination, respectively. There were no significant differences in mean levels of inflammatory markers between PD patients and the reference group. After controlling for age, gender and somatic illness, patients with PDD had significantly higher levels of CRP compared to non-demented PD patients (p=0.032) and the reference group (p=0.026). Increased levels of inflammatory markers in CSF were significantly associated with more severe symptoms of depression, anxiety, fatigue, and cognition in the entire PD group. After controlling for PD duration, age, gender, somatic illness and dementia diagnosis, high CRP levels were significantly associated with more severe symptoms of depression (p=0.010) and fatigue (p=0.008), and high MCP-1 levels were significantly associated with more severe symptoms of depression (p=0.032). Our results indicate that non-motor features of PD such as depression, fatigue, and cognitive impairment are associated with higher CSF levels of inflammatory markers.
95.	Lindqvist, Daniel, et al. (författare) Increased pro-inflammatory milieu in combat related PTSD - A new cohort replication study 2017 Ingår i: Brain Behavior and Immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 59, s. 260-264 Tidskriftsartikel (refereegranskat)abstract INTRODUCTION: Several lines of evidence indicate that increased inflammation is associated with Post-Traumatic Stress Disorder (PTSD). We have previously reported that peripheral inflammatory markers are significantly higher in combat-exposed veterans with than without PTSD. This study was designed to replicate these findings in a new study cohort using the same population and recruitment strategies.METHODS: Sixty-one male war veterans (31 PTSD and 30 control subjects) were included in this replication study. Levels of Interleukin-6, Tumor Necrosis Factor-alpha, Gamma interferon, and high-sensitivity C-reactive protein were quantified in blood samples. A standardized "total pro-inflammatory score" was calculated to limit the number of statistical comparisons. The Clinician Administered PTSD Scale (CAPS) rating scale was used to assess PTSD symptom severity.RESULTS: PTSD subjects had significantly higher total pro-inflammatory scores compared to non-PTSD subjects in unadjusted analysis (Cohen's d=0.75, p=0.005) as well as after adjusting for potentially confounding effects of age, BMI, smoking, and potentially interfering medications and somatic co-morbidities (p=0.023). There were no significant correlations between inflammatory markers and severity of symptoms within the PTSD group.CONCLUSIONS: We replicated, in a new sample, our previous finding of increased inflammatory markers in combat-exposed PTSD subjects compared to combat-exposed non-PTSD controls. These findings strongly add to the growing literature suggesting that immune activation may be an important aspect of PTSD pathophysiology, although not directly correlated with current PTSD symptom levels in the PTSD group.
96.	Lindqvist, Daniel, et al. (författare) Proinflammatory milieu in combat-related PTSD is independent of depression and early life stress. 2014 Ingår i: Brain Behavior and Immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 42:Jun 12, s. 81-88 Tidskriftsartikel (refereegranskat)abstract Chronic inflammation may be involved in combat-related post-traumatic stress disorder (PTSD) and may help explain comorbid physical diseases. However, the extent to which combat exposure per se, depression, or early life trauma, all of which are associated with combat PTSD, may confound the relationship between PTSD and inflammation is unclear.
97.	Liu, XC, et al. (författare) Behavioral disturbances in adult mice following neonatal virus infection or kynurenine treatment--role of brain kynurenic acid 2014 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 36, s. 80-89 Tidskriftsartikel (refereegranskat)
98.	Lizano, Paulo, et al. (författare) Peripheral inflammatory subgroup differences in anterior Default Mode network and multiplex functional network topology are associated with cognition in psychosis 2023 Ingår i: BRAIN BEHAVIOR AND IMMUNITY. - 0889-1591 .- 1090-2139. ; 114, s. 3-15 Tidskriftsartikel (refereegranskat)abstract Introduction: High-inflammation subgroups of patients with psychosis demonstrate cognitive deficits and neuroanatomical alterations. Systemic inflammation assessed using IL-6 and C-reactive protein may alter func-tional connectivity within and between resting-state networks, but the cognitive and clinical implications of these alterations remain unknown. We aim to determine the relationships of elevated peripheral inflammation subgroups with resting-state functional networks and cognition in psychosis spectrum disorders. Methods: Serum and resting-state fMRI were collected from psychosis probands (schizophrenia, schizoaffective, psychotic bipolar disorder) and healthy controls (HC) from the B-SNIP1 (Chicago site) study who were stratified into inflammatory subgroups based on factor and cluster analyses of 13 cytokines (HC Low n = 32, Proband Low n = 65, Proband High n = 29). Nine resting-state networks derived from independent component analysis were used to assess functional and multilayer connectivity. Inter-network connectivity was measured using Fisher z -transformation of correlation coefficients. Network organization was assessed by investigating networks of positive and negative connections separately, as well as investigating multilayer networks using both positive and negative connections. Cognition was assessed using the Brief Assessment of Cognition in Schizophrenia. Linear regressions, Spearman correlations, permutations tests and multiple comparison corrections were used for analyses in R. Results: Anterior default mode network (DMNa) connectivity was significantly reduced in the Proband High compared to Proband Low (Cohen's d =-0.74, p = 0.002) and HC Low (d =-0.85, p = 0.0008) groups. Internetwork connectivity between the DMNa and the right-frontoparietal networks was lower in Proband High compared to Proband Low (d =-0.66, p = 0.004) group. Compared to Proband Low, the Proband High group had lower negative (d = 0.54, p = 0.021) and positive network (d = 0.49, p = 0.042) clustering coefficient, and lower multiplex network participation coefficient (d =-0.57, p = 0.014). Network findings in high inflammation subgroups correlate with worse verbal fluency, verbal memory, symbol coding, and overall cognition. Conclusion: These results expand on our understanding of the potential effects of peripheral inflammatory signatures and/or subgroups on network dysfunction in psychosis and how they relate to worse cognitive performance. Additionally, the novel multiplex approach taken in this study demonstrated how inflammation may disrupt the brain's ability to maintain healthy co-activation patterns between the resting-state networks while inhibiting certain connections between them.
99.	Lodin, Karin, et al. (författare) Self-rated health is associated with fatigue, but not inflammatory cytokines or fraction of exhaled nitric oxide in men and women with allergic asthma 2013 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 32:Suppl., s. e31-e31 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract Allergic asthma is a chronic inflammatory disorder with both local and systemic inflammation and is associated with elevated levels of cytokines as well as exhaled fraction of nitric oxide (FeNO). Fatigue is a prominent symptom. Poor self-rated health has previously been associated to fatigue and inflammatory markers. However, it is not known if self-rated health is associated with fatigue and inflammation also in patients with asthma. Here, we investigated the associations between self-rated health, fatigue, inflammatory cytokines and FeNO in patients with asthma. Self-rated health, fatigue, levels of cytokines and FeNO were assessed in 184 (93 men, 91 women) non-smoking patients with allergic asthma aged 18–64 years in a one-year longitudinal study with five repeated measurements, two for cytokine levels. Analyses of associations between repeated measurements were performed using mixed regression models. More fatigue was associated with poor self-rated health in both men and women (p < 0.001). Fatigue was also associated to elevated levels of IL-1beta and TNF-alpha in women (p < 0.01). However, no association between self-rated health, inflammatory cytokines and FeNO were found. In conclusion, fatigue is an important determinant of self-rated health also in patients with asthma. In addition, fatigue was associated to elevated levels of inflammatory cytokines in women. Possibly, variance in inflammation may be of less importance in a chronic inflammatory condition such as asthma in relation to how subjective health is appraised.
100.	Luckemann, L, et al. (författare) Behavioral conditioning of anti-proliferative and immunosuppressive properties of the mTOR inhibitor rapamycin 2019 Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 79, s. 326-331 Tidskriftsartikel (refereegranskat)

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