16 research outputs found
Mixed evidence on the relationship between socioeconomic position and atopic dermatitis: A systematic review.
BACKGROUND: Lower socioeconomic position usually portends worse health outcomes, but multiple studies have found that atopic dermatitis is associated with higher socioeconomic position. The nature of this relationship remains unclear. OBJECTIVE: To systematically review the literature on socioeconomic position and atopic dermatitis and determine whether the association varies by patient or study characteristics. METHODS: A literature search was conducted in the PubMed and Embase databases. Individual-level studies addressing the association between all measures of socioeconomic position and the prevalence or incidence of atopic dermatitis were eligible for inclusion. Two independent reviewers screened all texts and extracted all data for qualitative synthesis. RESULTS: Eighty-eight studies met the inclusion criteria. Of the 88 studies, 42% (37) found a positive association between atopic dermatitis and socioeconomic position, 15% (13) found a negative association, and 43% (38) found a null or inconsistent association. Studies conducted in Europe, among children, and based on self-report of eczema were more likely to find a positive association with socioeconomic position. LIMITATIONS: Studies varied both in terms of the measurement of socioeconomic position and the definition of atopic dermatitis, limiting quantitative synthesis. CONCLUSION: The evidence of a positive association between atopic dermatitis and socioeconomic position is not consistent
Male and Female Mice Exhibit Divergent Responses of the Cortical Vasculature to Traumatic Brain Injury
Traumatic brain injuries (TBI) occur in 1.7 million people each year in the USA. Little is known about how the cerebrovasculature is altered after TBI. We previously reported that TBI elicits acute decrements in cerebral vessels near the injury site in rats followed by revascularization over the subsequent 2 weeks. Sexual dimorphism of the brain is well documented and different hormonal levels in males and females differentially modify the recovery process after injury. However, the effects of biological sex on the temporal evolution of revascularization following TBI are understudied. Using a model of controlled cortical impact in male and female mice, we set out to determine if the injury and the repair process are affected by sex
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Mixed evidence on the relationship between socioeconomic position and atopic dermatitis: A systematic review.
BackgroundLower socioeconomic position usually portends worse health outcomes, but multiple studies have found that atopic dermatitis is associated with higher socioeconomic position. The nature of this relationship remains unclear.ObjectiveTo systematically review the literature on socioeconomic position and atopic dermatitis and determine whether the association varies by patient or study characteristics.MethodsA literature search was conducted in the PubMed and Embase databases. Individual-level studies addressing the association between all measures of socioeconomic position and the prevalence or incidence of atopic dermatitis were eligible for inclusion. Two independent reviewers screened all texts and extracted all data for qualitative synthesis.ResultsEighty-eight studies met the inclusion criteria. Of the 88 studies, 42% (37) found a positive association between atopic dermatitis and socioeconomic position, 15% (13) found a negative association, and 43% (38) found a null or inconsistent association. Studies conducted in Europe, among children, and based on self-report of eczema were more likely to find a positive association with socioeconomic position.LimitationsStudies varied both in terms of the measurement of socioeconomic position and the definition of atopic dermatitis, limiting quantitative synthesis.ConclusionThe evidence of a positive association between atopic dermatitis and socioeconomic position is not consistent
Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes
Psychological trauma and obesity co-occur frequently and have been identified as major risk factors for psychiatric disorders. Surprisingly, preclinical studies examining how obesity disrupts the ability of the brain to cope with psychological trauma are lacking. The objective of this study was to determine whether an obesogenic Western-like high-fat diet (WD) predisposes rats to post-traumatic stress responsivity. Adolescent Lewis rats (postnatal day 28) were fed ad libitum for 8 weeks with either the experimental WD diet (41.4% kcal from fat) or the control diet (16.5% kcal from fat). We modeled psychological trauma by exposing young adult rats to a cat odor threat. The elevated plus maze and the open field test revealed increased psychological trauma-induced anxiety-like behaviors in the rats that consumed the WD when compared with control animals 1 week after undergoing traumatic stress (p < 0.05). Magnetic resonance imaging showed significant hippocampal atrophy (20% reduction) and lateral ventricular enlargement (50% increase) in the animals fed the WD when compared with controls. These volumetric abnormalities were associated with behavioral indices of anxiety, increased leptin and FK506-binding protein 51 (FKBP51) levels, and reduced hippocampal blood vessel density. We found asymmetric structural vulnerabilities to the WD, particularly the ventral and left hippocampus and lateral ventricle. This study highlights how WD consumption during adolescence impacts key substrates implicated in post-traumatic stress disorder. Understanding how consumption of a WD affects the developmental trajectories of the stress neurocircuitry is critical, as stress susceptibility imposes a marked vulnerability to neuropsychiatric disorders
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Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes.
Psychological trauma and obesity co-occur frequently and have been identified as major risk factors for psychiatric disorders. Surprisingly, preclinical studies examining how obesity disrupts the ability of the brain to cope with psychological trauma are lacking. The objective of this study was to determine whether an obesogenic Western-like high-fat diet (WD) predisposes rats to post-traumatic stress responsivity. Adolescent Lewis rats (postnatal day 28) were fed ad libitum for 8 weeks with either the experimental WD diet (41.4% kcal from fat) or the control diet (16.5% kcal from fat). We modeled psychological trauma by exposing young adult rats to a cat odor threat. The elevated plus maze and the open field test revealed increased psychological trauma-induced anxiety-like behaviors in the rats that consumed the WD when compared with control animals 1 week after undergoing traumatic stress (p < 0.05). Magnetic resonance imaging showed significant hippocampal atrophy (20% reduction) and lateral ventricular enlargement (50% increase) in the animals fed the WD when compared with controls. These volumetric abnormalities were associated with behavioral indices of anxiety, increased leptin and FK506-binding protein 51 (FKBP51) levels, and reduced hippocampal blood vessel density. We found asymmetric structural vulnerabilities to the WD, particularly the ventral and left hippocampus and lateral ventricle. This study highlights how WD consumption during adolescence impacts key substrates implicated in post-traumatic stress disorder. Understanding how consumption of a WD affects the developmental trajectories of the stress neurocircuitry is critical, as stress susceptibility imposes a marked vulnerability to neuropsychiatric disorders
Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes.
Psychological trauma and obesity co-occur frequently and have been identified as major risk factors for psychiatric disorders. Surprisingly, preclinical studies examining how obesity disrupts the ability of the brain to cope with psychological trauma are lacking. The objective of this study was to determine whether an obesogenic Western-like high-fat diet (WD) predisposes rats to post-traumatic stress responsivity. Adolescent Lewis rats (postnatal day 28) were fed ad libitum for 8 weeks with either the experimental WD diet (41.4% kcal from fat) or the control diet (16.5% kcal from fat). We modeled psychological trauma by exposing young adult rats to a cat odor threat. The elevated plus maze and the open field test revealed increased psychological trauma-induced anxiety-like behaviors in the rats that consumed the WD when compared with control animals 1 week after undergoing traumatic stress (p < 0.05). Magnetic resonance imaging showed significant hippocampal atrophy (20% reduction) and lateral ventricular enlargement (50% increase) in the animals fed the WD when compared with controls. These volumetric abnormalities were associated with behavioral indices of anxiety, increased leptin and FK506-binding protein 51 (FKBP51) levels, and reduced hippocampal blood vessel density. We found asymmetric structural vulnerabilities to the WD, particularly the ventral and left hippocampus and lateral ventricle. This study highlights how WD consumption during adolescence impacts key substrates implicated in post-traumatic stress disorder. Understanding how consumption of a WD affects the developmental trajectories of the stress neurocircuitry is critical, as stress susceptibility imposes a marked vulnerability to neuropsychiatric disorders
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Up-regulation of Wnt/β-catenin expression is accompanied with vascular repair after traumatic brain injury
Recent data suggest that repairing the cerebral vasculature after traumatic brain injury (TBI) may help to improve functional recovery. The Wnt/β-catenin signaling pathway promotes blood vessel formation during vascular development, but its role in vascular repair after TBI remains elusive. In this study, we examined how the cerebral vasculature responds to TBI and the role of Wnt/β-catenin signaling in vascular repair. We induced a moderate controlled cortical impact in adult mice and performed vessel painting to visualize the vascular alterations in the brain. Brain tissue around the injury site was assessed for β-catenin and vascular markers. A Wnt transgenic mouse line was utilized to evaluate Wnt gene expression. We report that TBI results in vascular loss followed by increases in vascular structure at seven days post injury (dpi). Immature, non-perfusing vessels were evident in the tissue around the injury site. β-catenin protein expression was significantly reduced in the injury site at 7 dpi. However, there was an increase in β-catenin expression in perilesional vessels at 1 and 7 dpi. Similarly, we found increased number of Wnt-GFP-positive vessels after TBI. Our findings suggest that Wnt/β-catenin expression contributes to the vascular repair process after TBI
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Mild Concussion, but Not Moderate Traumatic Brain Injury, Is Associated with Long-Term Depression-Like Phenotype in Mice.
Mild traumatic brain injuries can lead to long-lasting cognitive and motor deficits, increasing the risk of future behavioral, neurological, and affective disorders. Our study focused on long-term behavioral deficits after repeated injury in which mice received either a single mild CHI (mCHI), a repeated mild CHI (rmCHI) consisting of one impact to each hemisphere separated by 3 days, or a moderate controlled cortical impact injury (CCI). Shams received only anesthesia. Behavioral tests were administered at 1, 3, 5, 7, and 90 days post-injury (dpi). CCI animals showed significant motor and sensory deficits in the early (1-7 dpi) and long-term (90 dpi) stages of testing. Interestingly, sensory and subtle motor deficits in rmCHI animals were found at 90 dpi. Most importantly, depression-like behaviors and social passiveness were observed in rmCHI animals at 90 dpi. These data suggest that mild concussive injuries lead to motor and sensory deficits and affective disorders that are not observed after moderate TBI