Brain, behavior, & immunity - health最新文献

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Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity 在早产儿脑病双击大鼠模型中,胎儿定时发炎和出生后缺氧会导致大脑皮层白质损伤、神经元间失衡和行为障碍
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-07-05 DOI: 10.1016/j.bbih.2024.100817
{"title":"Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity","authors":"","doi":"10.1016/j.bbih.2024.100817","DOIUrl":"10.1016/j.bbih.2024.100817","url":null,"abstract":"<div><p>Extreme preterm birth-associated adversities are a major risk factor for aberrant brain development, known as encephalopathy of prematurity (EoP), which can lead to long-term neurodevelopmental impairments. Although progress in clinical care for preterm infants has markedly improved perinatal outcomes, there are currently no curative treatment options available to combat EoP. EoP has a multifactorial etiology, including but not limited to pre- or postnatal immune activation and oxygen fluctuations. Elucidating the underlying mechanisms of EoP and determining the efficacy of potential therapies relies on valid, clinically translatable experimental models that reflect the neurodevelopmental and pathophysiological hallmarks of EoP. Here, we expand on our double-hit rat model that can be used to study EoP disease mechanisms and therapeutic options in a preclinical setting. Pregnant Wistar dams were intraperitoneally injected with 10 μg/kg LPS on embryonic day (E)20 and offspring was subjected to hypoxia (140 min, 8% O<sub>2</sub>) at postnatal day 4. Rats exposed to fetal inflammation and postnatal hypoxia (FIPH) showed neurodevelopmental impairments, such as reduced nest-seeking ability, ultrasonic vocalizations, social engagement, and working memory, and increased anxiety and sensitivity. Impairments in myelination, oligodendrocyte maturation and interneuron development were examined as hallmarks for EoP, in different layers and coordinates of the cortex using histological and molecular techniques. Myelin density and complexity was decreased in the cortex, which partially coincided with a decrease in mature oligodendrocytes. Furthermore, interneuron populations (GAD67+ and PVALB+) were affected. To determine if the timing of inducing fetal inflammation affected the severity of EoP hallmarks in the cortex, multiple timepoints of fetal inflammation were compared. Inflammation at E20 combined with postnatal hypoxia gave the most severe EoP phenotype in the cortex. In conclusion, we present a double-hit rat model which displays various behavioral, anatomical and molecular hallmarks of EoP, including diffuse white matter injury. This double-hit model can be used to investigate pathophysiological mechanisms and potential therapies for EoP.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000954/pdfft?md5=487b4ee5589e8c90ae36d8e9b68fd3ec&pid=1-s2.0-S2666354624000954-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141688971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Associations between IL-1β, IL-6, and TNFα polymorphisms and longitudinal trajectories of cognitive function in non-demented older adults IL-1β、IL-6 和 TNFα 多态性与非痴呆老年人认知功能纵向轨迹的关系
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-06-29 DOI: 10.1016/j.bbih.2024.100816
Karen A. Lawrence , Elana M. Gloger , Cristina N. Pinheiro , Frederick A. Schmitt , Suzanne C. Segerstrom
{"title":"Associations between IL-1β, IL-6, and TNFα polymorphisms and longitudinal trajectories of cognitive function in non-demented older adults","authors":"Karen A. Lawrence ,&nbsp;Elana M. Gloger ,&nbsp;Cristina N. Pinheiro ,&nbsp;Frederick A. Schmitt ,&nbsp;Suzanne C. Segerstrom","doi":"10.1016/j.bbih.2024.100816","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100816","url":null,"abstract":"<div><p>Inflammation is implicated in Alzheimer's disease (AD), and specific single nucleotide polymorphisms (SNPs) in inflammatory cytokine genes are associated with increased AD risk. Whether the same polymorphisms also predict domain-specific cognitive change in cognitively healthy older adults is unclear. Specific SNPs in three cytokine genes, IL-1β (rs16944), IL-6 (rs1800795), and TNFα (rs1800629) were assessed for association with longitudinal trajectories spanning up to 16 years of global cognitive function, episodic memory, attention and working memory, and executive function in a sample of 324 non-demented older adults. Only rs1800629 (TNFα) was associated with significant change in global cognitive function over time [γ = 5.22; 95% CI: 0.61, 9.83; p = 0.027]. Despite an association with AD risk, rs16944 and rs1800795 may not predict cognitive decline in cognitively healthy older adults. The presence of an A at rs1800629 (TNFα) may have broad, protective effects on cognitive function, over time. More validation studies are needed to determine whether specific cytokine SNPs are associated with respective serum levels to further understanding of AD biomarkers that may also serve as markers of cognitive decline.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000942/pdfft?md5=27d368287a563f3eb1b32e49154d7aa3&pid=1-s2.0-S2666354624000942-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141542482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Estimating survival in data-driven phenotypes of mental health symptoms and peripheral biomarkers: A prospective study 估算心理健康症状数据驱动表型和外周生物标志物的存活率:前瞻性研究
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-06-25 DOI: 10.1016/j.bbih.2024.100815
Santiago Allende , Peter J. Bayley
{"title":"Estimating survival in data-driven phenotypes of mental health symptoms and peripheral biomarkers: A prospective study","authors":"Santiago Allende ,&nbsp;Peter J. Bayley","doi":"10.1016/j.bbih.2024.100815","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100815","url":null,"abstract":"<div><h3>Background</h3><p>Chronic psychological stress has widespread implications, including heightened mortality risk, mental and physical health conditions, and socioeconomic consequences. Stratified precision psychiatry shows promise in mitigating these effects by leveraging clinical heterogeneity to personalize interventions. However, little attention has been given to patient self-report.</p></div><div><h3>Methods</h3><p>We addressed this by combining stress-related self-report measures with peripheral biomarkers in a latent profile analysis and survival model. The latent profile models were estimated in a representative U.S. cohort (<em>n</em> = 1255; mean age = 57 years; 57% female) and cross-validated in Tokyo, Japan (<em>n</em> = 377; mean age = 55 years; 56% female).</p></div><div><h3>Results</h3><p>We identified three distinct groups: “Good Mental Health”, “Poor Mental Health”, and “High Inflammation”. Compared to the “Good Mental Health” group, the “High Inflammation” and “Poor Mental Health” groups had an increased risk of mortality, but did not differ in mortality risk from each other.</p></div><div><h3>Conclusions</h3><p>This study emphasizes the role of patient self-report in stratified psychiatry.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000930/pdfft?md5=9df732907839560a6a4f7fda07b095b4&pid=1-s2.0-S2666354624000930-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141478983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Absence of association between maternal adverse events and long-term gut microbiome outcomes in the Australian autism biobank 澳大利亚自闭症生物库中孕产妇不良事件与长期肠道微生物组结果之间没有关联
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-06-21 DOI: 10.1016/j.bbih.2024.100814
Svetlina Vasileva , Chloe X. Yap , Andrew J.O. Whitehouse , Jacob Gratten , Darryl Eyles
{"title":"Absence of association between maternal adverse events and long-term gut microbiome outcomes in the Australian autism biobank","authors":"Svetlina Vasileva ,&nbsp;Chloe X. Yap ,&nbsp;Andrew J.O. Whitehouse ,&nbsp;Jacob Gratten ,&nbsp;Darryl Eyles","doi":"10.1016/j.bbih.2024.100814","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100814","url":null,"abstract":"<div><h3>Introduction</h3><p>Maternal immune activation (MIA) and prenatal maternal stress (MatS) are well-studied risk factors for psychiatric conditions such as autism and schizophrenia. Animal studies have proposed the gut microbiome as a mechanism underlying this association and have found that risk factor-related gut microbiome alterations persist in the adult offspring. In this cross-sectional study, we assessed whether maternal immune activation and prenatal maternal stress were associated with long-term gut microbiome alterations in children using shotgun metagenomics.</p></div><div><h3>Methods</h3><p>This cross-sectional study included children diagnosed with autism (N = 92), siblings without a diagnosis (N = 42), and unrelated children (N = 40) without a diagnosis who were recruited into the Australian Autism Biobank and provided a faecal sample. MIA exposure was inferred from self-reported data and included asthma/allergies, complications during pregnancy triggering an immune response, auto-immune conditions, and acute inflammation. Maternal stress included any of up to 9 stressful life events during pregnancy, such as divorce, job loss, and money problems. Data were analysed for a total of 174 children, of whom 63 (36%) were born to mothers with MIA and 84 (48%) were born to mothers who experienced maternal stress during pregnancy (where 33 [19%] experienced both). Gut microbiome data was assessed using shotgun metagenomic sequencing of the children's faecal samples.</p></div><div><h3>Results</h3><p>In our cohort, MIA, but not MatS, was associated with ASD. Variance component analysis revealed no associations between any of the gut microbiome datasets and neither MIA nor MatS. After adjusting for age, sex, diet and autism diagnosis, there was no significant difference between groups for bacterial richness, α-diversity or β-diversity. We found no significant differences in species abundance in the main analyses. However, when stratifying the cohort by age, we found that <em>Faecalibacterium prausnitzii E</em> was significantly decreased in MIA children aged 11–17.</p></div><div><h3>Discussion</h3><p>Consistent with previous findings, we found that children who were born to mothers with MIA were more likely to be diagnosed with autism. Unlike within animal studies, we found negligible microbiome differences associated with MIA and maternal stress. Given the current interest in the microbiome-gut-brain axis, researchers should exercise caution in translating microbiome findings from animal models to human contexts and the clinical setting.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000929/pdfft?md5=f43b5b24af886c8ab55397d3170a9df9&pid=1-s2.0-S2666354624000929-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141478982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
GRM7 deficiency, from excitotoxicity and neuroinflammation to neurodegeneration: Systematic review of GRM7 deficient patients GRM7缺乏症,从兴奋毒性和神经炎症到神经变性:对GRM7缺乏症患者的系统回顾
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-06-17 DOI: 10.1016/j.bbih.2024.100808
Majid Zaki-Dizaji , Mohammad Foad Abazari , Hossein Razzaghi , Irene Shkolnikov , Brian R. Christie
{"title":"GRM7 deficiency, from excitotoxicity and neuroinflammation to neurodegeneration: Systematic review of GRM7 deficient patients","authors":"Majid Zaki-Dizaji ,&nbsp;Mohammad Foad Abazari ,&nbsp;Hossein Razzaghi ,&nbsp;Irene Shkolnikov ,&nbsp;Brian R. Christie","doi":"10.1016/j.bbih.2024.100808","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100808","url":null,"abstract":"<div><p>The metabotropic glutamate receptor 7 (mGluR7) is a presynaptic G-protein-coupled glutamate receptor that modulates neurotransmitter release and synaptic plasticity at presynaptic terminals. It is encoded by GRM7, and recently variants have been identified in patients with autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), developmental delay (DD), intellectual disability (ID), and brain malformations. To gain updated insights into the function of GRM7 and the phenotypic spectrum of genetic variations within this gene, we conducted a systematic review of relevant literature utilizing PubMed, Web of Science, and Scopus databases. Among the 14 articles meeting the inclusion criteria, a total of 42 patients (from 28 families) harboring confirmed mutations in the <em>GRM7</em> gene have been documented. Specifically, there were 17 patients with heterozygous mutations, 20 patients with homozygous mutations, and 5 patients with compound heterozygous mutations. Common clinical features included intellectual behavioral disability, seizure/epilepsy, microcephaly, developmental delay, peripheral hypertonia and hypomyelination. Genotype-phenotype correlation was not clear and each variant had unique characteristics including gene dosage, mutant protein surface expression, and degradation pathway that result with a spectrum of phenotype manifestations through ASD or ADHD to severe DD/ID with brain malformations. Neuroinflammation may play a role in the development and/or progression of GRM7-related neurodegeneration along with excitotoxicity. The clinical and functional data presented here demonstrate that both autosomal dominant and recessive inheritance of GRM7 mutation can cause disease spectrum phenotypes through ASD or ADHD to severe DD/ID and seizure with brain malformations.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000863/pdfft?md5=be8035c61f8bfb4d16933d8fc5b3e29b&pid=1-s2.0-S2666354624000863-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141435201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications 神经炎症生物标志物的变化与 COVID-19 神经系统并发症患者的疾病严重程度和神经影像学改变相关。
IF 3.7
Brain, behavior, & immunity - health Pub Date : 2024-06-13 DOI: 10.1016/j.bbih.2024.100805
Fernanda G.Q. Barros-Aragão , Talita P. Pinto , Victor C. Carregari , Nathane B.S. Rezende , Thaís L. Pinheiro , Guilherme Reis-de-Oliveira , Mauro J. Cabral-Castro , Daniel C. Queiroz , Paula L.C. Fonseca , Alessandro L. Gonçalves , Gabriel R. de Freitas , Felipe K. Sudo , Paulo Mattos , Fernando A. Bozza , Erika C. Rodrigues , Renato S. Aguiar , Rosana S. Rodrigues , Carlos O. Brandão , Andrea S. Souza , Daniel Martins-de-Souza , Fernanda Tovar-Moll
{"title":"Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications","authors":"Fernanda G.Q. Barros-Aragão ,&nbsp;Talita P. Pinto ,&nbsp;Victor C. Carregari ,&nbsp;Nathane B.S. Rezende ,&nbsp;Thaís L. Pinheiro ,&nbsp;Guilherme Reis-de-Oliveira ,&nbsp;Mauro J. Cabral-Castro ,&nbsp;Daniel C. Queiroz ,&nbsp;Paula L.C. Fonseca ,&nbsp;Alessandro L. Gonçalves ,&nbsp;Gabriel R. de Freitas ,&nbsp;Felipe K. Sudo ,&nbsp;Paulo Mattos ,&nbsp;Fernando A. Bozza ,&nbsp;Erika C. Rodrigues ,&nbsp;Renato S. Aguiar ,&nbsp;Rosana S. Rodrigues ,&nbsp;Carlos O. Brandão ,&nbsp;Andrea S. Souza ,&nbsp;Daniel Martins-de-Souza ,&nbsp;Fernanda Tovar-Moll","doi":"10.1016/j.bbih.2024.100805","DOIUrl":"10.1016/j.bbih.2024.100805","url":null,"abstract":"<div><p>COVID-19 induces acute and persistent neurological symptoms in mild and severe cases. Proposed concomitant mechanisms include direct viral infection and strain, coagulopathy, hypoxia, and neuroinflammation. However, underlying molecular alterations associated with multiple neurological outcomes in both mild and severe cases are majorly unexplored. To illuminate possible mechanisms leading to COVID-19 neurological disease, we retrospectively investigated in detail a cohort of 35 COVID-19 mild and severe hospitalized patients presenting neurological alterations subject to clinically indicated cerebrospinal fluid (CSF) sampling. Clinical and neurological investigation, brain imaging, viral sequencing, and cerebrospinal CSF analyses were carried out. We found that COVID-19 patients presented heterogeneous neurological symptoms dissociated from lung burden. Nasal swab viral sequencing revealed a dominant strain at the time of the study, and we could not detect traces of SARS-CoV-2's spike protein in patients' CSF by multiple reaction monitoring analysis. Patients presented ubiquitous systemic hyper-inflammation and broad alterations in CSF proteomics related to inflammation, innate immunity, and hemostasis, irrespective of COVID-19 severity or neuroimaging alterations. Elevated CSF interleukin-6 (IL6) correlated with disease severity (sex-, age-, and comorbidity-adjusted mean Severe 24.5 pg/ml, 95% confidence interval (CI) 9.62–62.23 vs. Mild 3.91 pg/mL CI 1.5–10.3 patients, p = 0.019). CSF tumor necrosis factor-alpha (TNFα) and IL6 levels were higher in patients presenting pronounced neuroimaging alterations compared to those who did not (sex-, age-, and comorbidity-adjusted mean TNFα Pronounced 3.4, CI 2.4–4.4 vs. Non-Pronounced 2.0, CI 1.4–2.5, p = 0.022; IL6 Pronounced 33.11, CI 8.89–123.31 vs Non-Pronounced 6.22, CI 2.9–13.34, p = 0.046). Collectively, our findings put neuroinflammation as a possible driver of COVID-19 acute neurological disease in mild and severe cases.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000838/pdfft?md5=6f74e24526870f18a56f81152f67da55&pid=1-s2.0-S2666354624000838-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141399820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Maternal immune activation affects female offspring whisker movements during object exploration in a rat model of neurodevelopmental disorders 在神经发育障碍大鼠模型中,母体免疫激活会影响雌性后代在物体探索过程中的胡须运动
Brain, behavior, & immunity - health Pub Date : 2024-06-12 DOI: 10.1016/j.bbih.2024.100807
Ugne Simanaviciute , Harry G. Potter , Reinmar Hager , Jocelyn Glazier , Emma Hodson-Tole , John Gigg , Robyn Grant
{"title":"Maternal immune activation affects female offspring whisker movements during object exploration in a rat model of neurodevelopmental disorders","authors":"Ugne Simanaviciute ,&nbsp;Harry G. Potter ,&nbsp;Reinmar Hager ,&nbsp;Jocelyn Glazier ,&nbsp;Emma Hodson-Tole ,&nbsp;John Gigg ,&nbsp;Robyn Grant","doi":"10.1016/j.bbih.2024.100807","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100807","url":null,"abstract":"<div><p>Poly I:C rat offspring are used to investigate the effects of <em>in utero</em> exposure to maternal immune activation (MIA) and have been suggested as a model of neurodevelopmental disorders (NDD). The behavioural symptoms of this model are diverse and can vary with external factors, including the choice of background strain and husbandry practices. Measuring whisker movements provides quantitative, robust measurements of sensory, motor and cognitive behaviours in rodents. In this study, whisker movements were investigated in 50-day-old male and female offspring of MIA-exposed rat dams and compared to age-matched offspring of control (vehicle) dams. Rat offspring were filmed using high-speed videography in a sequential object exploration task with smooth and textured objects. Poly I:C treatment effects were found in female offspring that did not increase whisker mean angular position during object exploration, especially for the smooth object, indicating an attentional deficit. Whisker tracking during object exploration is demonstrated here, for the first time, as a useful, quick and non-invasive tool to identify both treatment effects and sex differences in a model of MIA-induced NDDs.</p></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000851/pdfft?md5=b46e9cf5a8ccfa41ba26c94d5a22e9cb&pid=1-s2.0-S2666354624000851-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Complement C4, C4A and C4a – What they do and how they differ 补体 C4、C4A 和 C4a - 它们的作用和区别
Brain, behavior, & immunity - health Pub Date : 2024-06-11 DOI: 10.1016/j.bbih.2024.100809
Meike Heurich , Melanie Föcking , David Cotter
{"title":"Complement C4, C4A and C4a – What they do and how they differ","authors":"Meike Heurich ,&nbsp;Melanie Föcking ,&nbsp;David Cotter","doi":"10.1016/j.bbih.2024.100809","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100809","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000875/pdfft?md5=44757fb17c4cd668160d6f5f87d46955&pid=1-s2.0-S2666354624000875-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
In order to reliably assess nurses’ optimism, resilience and experience during the pandemic, all influencing factors must be taken into account 为了可靠地评估护士在大流行病期间的乐观情绪、应变能力和经验,必须考虑到所有影响因素
Brain, behavior, & immunity - health Pub Date : 2024-06-11 DOI: 10.1016/j.bbih.2024.100810
Josef Finsterer
{"title":"In order to reliably assess nurses’ optimism, resilience and experience during the pandemic, all influencing factors must be taken into account","authors":"Josef Finsterer","doi":"10.1016/j.bbih.2024.100810","DOIUrl":"https://doi.org/10.1016/j.bbih.2024.100810","url":null,"abstract":"","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666354624000887/pdfft?md5=a9bcccc43fd4c0f96877b2fb6aa679a3&pid=1-s2.0-S2666354624000887-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141325958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correlating maternal and cord-blood inflammatory markers and BDNF with human fetal brain activity recorded by magnetoencephalography: An exploratory study 母体和脐带血炎症标志物及 BDNF 与脑磁图记录的胎儿大脑活动的相关性:探索性研究
Brain, behavior, & immunity - health Pub Date : 2024-06-11 DOI: 10.1016/j.bbih.2024.100804
Luis Mercado , Shannon Rose , Diana Escalona-Vargas , Nafisa Dajani , Eric R. Siegel , Hubert Preissl , Hari Eswaran
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