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This chapter aims to elucidate the associations between ethnic and racial discrimination and biological and physiological processes among ethnically and racially minoritized adolescents, focusing on hypothalamic–pituitary–adrenal (or HPA) axis functioning, inflammation processes, and allostatic load. We first discuss the theoretical foundation for ethnic and racial discrimination and biological processes. Next, we synthesize empirical evidence on the links between ethnic and racial discrimination and HPA axis functioning (operationalized as cortisol activity including its diurnal rhythms, stress reactivity, and cumulative levels), inflammatory processes (operationalized as inflammatory biomarkers such as C-reactive protein and Interlukin-6), and allostatic load (a combination of indicators including neuroendocrine, inflammatory, cardiovascular, and metabolic biomarkers). Finally, we chart directions for future research and discuss implications for mitigating the detrimental effects of ethnic and racial discrimination on biological and physiological processes among ethnically and racially minoritized adolescents.
The maternal diet is believed to influence child neurodevelopment, at least in part, through inflammation, as dietary components can have pro- or anti-inflammatory effects. We examined the association between the energy-adjusted dietary inflammatory index (E-DII) during pregnancy and offspring symptoms of behavioral and emotional problems at 5.5 and 10 years, using data from the French nationwide ELFE birth cohort. Dietary intake during pregnancy was assessed using a validated food frequency questionnaire and an E-DII score was generated. Child behavioral and emotional symptoms, (including hyperactivity-inattention, conduct, peer-relationship, and emotional problems), were evaluated by parents using the Strengths and Difficulties Questionnaire at 5.5 (n=9627) and 10 years (n=8362) for: hyperactivity-inattention, conduct, peer-relationship, and emotional problems. Children were classified into three categories based on thresholds used to identify clinically relevant symptoms: “Normal”, “Borderline”, and “Atypical”. Multinomial logistic regression, adjusted for potential confounders was used to estimate odds ratios and 95% confidence intervals. An increasing maternal E-DII score during pregnancy was associated with higher odds of offspring classified with atypical hyperactivity-inattention and conduct problem scores at 5.5 and 10 years, atypical peer-relationship problem scores at 10-years, and atypical emotional problem scores at 10 years (differentially by sex). A more proinflammatory diet during pregnancy was consistently associated with higher odds of symptoms of externalizing problems throughout childhood and with internalizing problems at 10 years. Future research should explore the mechanisms by which prenatal exposure to maternal diet-induced inflammation may contribute to these outcomes.
Dairy polar lipids have demonstrated anti-inflammatory properties and protective effects on intestinal integrity, potentially mitigating the adverse impacts of weaning in piglets by modulating microbiota composition and intermediary metabolism. This study evaluated a dairy by-product rich in polar lipids on the microbiome and plasma lipid mediators of weaned piglets. A total of 240 male piglets (21 days old; 6.3 ± 0.5 kg) received either a soybean lipid-based diet (SD) or a polar lipid-based diet (PD) from weaning to day 21, followed by a common diet until day 42. Within each diet, animals were provided with one of the three milk replacers (MRs) for the first 7 days: (1) Commercial MR (CO); (2) Polar lipid-based MR (PO); and (3) Soybean lipid-based MR (SO). Fecal and plasma samples were analyzed to assess microbial composition and lipid mediator profiles. Taxonomical distance between diets increased over time, whereas MR type had no effect. The PD diet significantly altered microbiota composition, increasing, for instance, the relative abundance of Firmicutes-belonging genera of the Lachnospiraceae family (Coprococcus, Roseburia), and increasing levels of ethanolamides (e.g., AEA, PEA, SEA, and DPEA). In contrast, the SD diet increased pro-inflammatory lipid mediators (e.g., 13-HODE, 13-KODE) derived from linoleic acid. Polar lipid supplementation in diet, but not in MRs, influenced microbiota diversity and lipid mediator profiles, suggesting a potential long-term impact on immune regulation and metabolism, highlighting their potential to enhance resilience during early-life stress. Future studies should explore these effects under traditional weaning conditions or other stress models.
Current fibre recommendations are based on historical data and may underestimate the intake required for optimal cardiometabolic protection. We examined whether fibre intakes exceeding current guidelines are associated with additional improvements in inflammation and lipid metabolism. We analysed data from 7,008 adults (≥20 years) from the NHANES 2015-2018 with 24-h dietary recall and biomarker data (CRP, total cholesterol [TC], LDL, HDL, triglycerides [TG]). Fibre intake was expressed relative to recommendations from the Institute of Medicine (IOM) and the Academy of Nutrition and Dietetics (AND), and associations with biomarkers were assessed using multivariable regression models. Higher fibre intake was consistently associated with lower CRP concentrations, with the greatest reductions observed at intakes >150% of the IOM recommendation (>55.7 g/day; 95% CI: 48.6–56.7). Among men, both TC and LDL cholesterol decreased significantly at intakes >150% of IOM values (>69.8 g/day; 95% CI: 64.2–75.4). Triglycerides were significantly lower when fibre intake exceeded AND recommendations (>41.0 g/day; 95% CI: 32.6–49.5). No clear associations were observed for HDL cholesterol. The associations found in this study make us consider the possibility that the benefits of fibre on systemic inflammation and lipid profile may extend beyond current recommended levels. Public health guidelines may need to reconsider fibre targets to better reflect condition-specific benefits rather than minimum thresholds for adequacy should this hypothesis be duly proven by future longitudinal studies.
Background: In patients with cyanotic congenital heart disease (CHD), aortopulmonary collateral arteries (APCAs) commonly develop as a compensatory source of pulmonary blood flow. However, APCAs increase pulmonary vascular resistance and ventricular preload, potentially complicating the establishment of Fontan circulation. Coil embolisation of APCAs is routinely performed before Fontan completion, but post-procedural fever is frequently observed and may delay subsequent surgery. This study aimed to identify factors associated with post-embolisation fever, with a particular focus on the influence of coil type. Methods and Results: We retrospectively reviewed 97 paediatric patients who underwent APCA coil embolisation between 2007 and 2023. Patients were categorised according to coil type: platinum coils only (P group, n = 52), both platinum and hydrogel coils (P–H group, n = 29), or hydrogel coils only (H group, n = 16). The incidence of post-embolisation fever (≥38°C) and inflammatory markers were compared among groups. Histopathological characteristics of embolised vessels were also assessed. Overall, post-embolisation fever occurred in 64% of patients. The incidence of fever was significantly lower in the H group (25.0%) than in the P group (73.0%) and P–H group (68.9%) (p < 0.01). C-reactive protein levels increased significantly after fever onset, whereas white blood cell counts showed no meaningful change. Histopathological evaluation demonstrated prominent fibrin deposition and inflammatory cell infiltration in vessels embolised with platinum coils, while vessels treated with hydrogel coils exhibited only mild inflammatory changes. Conclusions: Hydrogel coils were associated with a lower incidence of post-embolisation fever and a milder inflammatory response than platinum coils. These findings suggest that coil selection may play an important role in minimising post-procedural inflammation and facilitating perioperative management in children preparing for the Fontan procedure.
Small-quantity lipid-based nutrient supplements (SQ-LNS) have been shown to improve growth, development and survival among young children in low-resource settings. One hypothesised pathway is through improvements in intestinal health, including modulation of the gut microbiome and reductions in environmental enteric dysfunction (EED). This study examined the effects of SQ-LNS on the gut microbiome and markers of EED and systemic inflammation among young children in Lusaka, Zambia. We conducted intention-to-treat analyses of 302 children aged 27–35 months in a 2 × 2 cluster-randomised trial. Serum biomarkers of EED (soluble CD14, intestinal fatty acid-binding protein) and inflammation (α-1-acid glycoprotein and C-reactive protein) were assessed in 240 children via the Micronutrient and Environmental Enteric Dysfunction Assessment Tool. Differences by SQ-LNS assignment were assessed using unadjusted and adjusted ordinary least squares regression models. Rectal swab samples from 299 children underwent 16S rRNA gene sequencing. Taxonomic profiles were visualised using stacked bar plots, alpha diversity was quantified using Shannon diversity indices and beta diversity was assessed using non-metric multidimensional scaling based on Bray–Curtis dissimilarity matrices. We found that SQ-LNS had no significant effect on EED or inflammation biomarkers and was not associated with differences in gut microbiome α diversity, beta diversity or overall microbial community composition. In exploratory analyses, Enterococcus abundance was lower among children receiving SQ-LNS. Overall, 18 months of SQ-LNS supplementation was not associated with broad changes in intestinal health among young Lusakan children. These findings suggest that the benefits of SQ-LNS operate through pathways other than intestinal health, such as improved nutrient availability.
The receptor for advanced glycation end-products (RAGE) is a unique multi-ligand member of the immunoglobulin superfamily that exists in both membrane-bound and soluble forms. Under physiological conditions, RAGE expression is low in most tissues; however, it is markedly upregulated in response to tissue injury, inflammation or metabolic stress. Ligand-induced activation of RAGE initiates complex intracellular signalling cascades that regulate inflammation, extracellular matrix remodelling, cell proliferation, survival and migration.
Methods
While the contribution of RAGE to diabetes and chronic inflammatory diseases is well established, its role in gynaecological disorders remains insufficiently characterized.
Results
This comprehensive review summarizes current evidence on the involvement of RAGE in the pathogenesis of benign gynaecological disorders, such as endometriosis and polycystic ovary syndrome (PCOS), pregnancy-related complications and malignant neoplasms of the female reproductive tract.
Conclusions
It also discusses emerging therapeutic strategies aimed at targeting the RAGE pathway, highlighting their potential translational relevance in gynaecological practice.
Acute malnutrition (wasting) remains a global public health problem. Ready-to-use therapeutic foods (RUTF) and supplemental foods (RUSF) for treatment of severe acute malnutrition (SAM) and moderate acute malnutrition (MAM), respectively, come in the form of macro- and micronutrient-dense pastes. These lipid-dense treatments provide the energy and nutrients needed to support growth but have significant rates of relapse. Their role in reversing pathophysiological contributors to malnutrition, such as intestinal barrier dysfunction, intestinal dysbiosis, and systemic inflammation have not been evaluated. Traditional lipid-dense RUTFs and RUSFs are rich in pro-inflammatory omega-6 polyunsaturated fatty acids (PUFAs) but low in anti-inflammatory omega-3 PUFAs, which could fuel malnutrition-related pathological inflammation. We reasoned that reduced dietary omega-6 (n-6) PUFAs and increased dietary long-chain omega-3 (n-3) PUFAs found in fish oil would reduce malnutrition-related pathological inflammation. In an established mouse model of MAM, we observed that altering the dietary n-3/n-6 PUFA ratio through replacing dietary corn oil with fish oil improved the diversity and composition of the caecal microbiota, improved intestinal mucosal barrier and immune defence, reduced translocation of bacteria and bacterial lipopolysaccharides (LPS), and dampened systemic inflammation. Furthermore, dietary fish oil protected against weight loss upon systemic challenge with bacterial LPS. The anti-inflammatory effects of dietary fish oil did not compromise host defence against challenge with the intestinal pathogen, Citrobacter rodentium. Collectively, these results suggest that dietary fish oil blunts inflammation that contributes to the pathogenesis of MAM. Inclusion of fish oil in dietary interventions may be beneficial in prevention or reduction of malnutrition-associated inflammation.
The β-galactoside-binding protein galectin-3 is currently a hotly pursued therapeutic target in cancer, inflammation and fibrosis-associated diseases due to its multi-mode actions and broad impact on the pathogenesis and progress of the diseases. Various natures of galectin-3 inhibitors have been developed and investigated, and several have shown promising results in early-phase clinical trials. All these galectin-3 antagonists were designed to target the canonical carbohydrate-binding site, the S-face, of the galectin-3 carbohydrate recognition domain (CRD). This review discussed the current galectin-3 antagonists and explored their modes of actions, focusing particularly on their targeting regions on galectin-3. It discussed the tri-modular structure of galectin-3 and the roles of different segments in galectin-3 actions. It proposed that, in addition to the canonical carbohydrate-binding sites on the S-face, the non-canonical carbohydrate-binding interface, the F-face of the galectin-3 CRD as well as its flexible N-terminal domain are also targetable in the design of galectin-3-targeted therapeutics. Given the high degree of structural similarities of CRDs among galectin family members but unique nature of galectin-3 N-terminus, antagonists developed against the N-terminal domain of galectin-3 can potentially offer greater target specificity by avoiding cross-reactivity with other galectin members. Antagonists that can interact with more than one segment of galectin-3, or a combination of antagonists against different galectin-3 segments, may potentially provide improved efficacy and therapeutic effectiveness for treatment of galectin-3-mediated pathologies and diseases.
Schizophrenia spectrum disorders (SSD) are complex illnesses influenced by genetic, biological and psycho-social factors, necessitating large clinical deep-phenotyped cohorts. Here, we describe the Region Midt Schizophrenia (RMS) Cohort, which aims to establish such a large, representative cohort with long-term follow-up, enabling large-scale studies on SSD aetiology and prognosis.
Methods:
The RMS cohort includes patients aged ≥15 years diagnosed with a first-episode SSD recruiting at 6 Danish psychiatric hospitals. Baseline and follow-up assessments at 1, 2, 3 and 12 months and 2, 3, 5 and 10 years cover sociodemographic measures, psychotic and negative symptoms, adverse childhood experiences (ACEs), level of functioning, sleep, actigraphy, cognition, side effects and medication adherence. Blood is collected at baseline and months 3 and 12 and at years 2, 3, 5 and 10 enabling comprehensive molecular analyses, for example, genetics and omics. Age-and sex-matched healthy controls will complete a baseline assessment including blood draw. Participants give informed consent for linkage with Danish nationwide register-based data.
Status and perspectives:
By February 23rd, 2026, a total of 131 participants with SSD have been recruited (109 with schizophrenia, median age 25 years (IQR 8), 54% females). Retention rates at 1, 2, 3 and 12 months are 86%, 80%, 78% and 75%, respectively. Our vision is continuous recruitment of 100 participants/year, establishing a large, deep-phenotyped and representative clinical cohort with long-term follow-up. The RMS cohort will serve as the basis for several studies on aetiological and prognostic factors and is designed to match with similar international cohorts enabling further collaborations.
This chapter presents a case of a 34-year-old male with chest pain due to a post-viral myopericarditis. The case highlights the approach to a young patient with chest pain, and details many of the pertinent historical details and exam findings that support this diagnosis. The approach to diagnostic testing, risk stratification based on echocardiography and laboratory values, and spectrum of disease and management are described.
Multidimensional metabolic dysregulation is implicated in hypertension development, but the utility of comprehensive metabolic vulnerability indices for assessing hypertension risk associations remains unclear. This prospective cohort study analysed 150 591 participants from the United Kingdom Biobank. The metabolic vulnerability index and its components – inflammation vulnerability index (IVX) and metabolic malnutrition index (MMX) – were calculated from six metabolites (GlycA, small HDL particles, leucine, valine, isoleucine and citrate) measured by NMR spectroscopy. Cox proportional hazards models assessed associations with incident hypertension, adjusting for demographic, lifestyle and clinical factors. Restricted cubic spline analyses examined dose–response relationships, and subgroup analyses explored effect modifications by polygenic risk score, BMI and C-reactive protein levels. During follow-up, 32 198 participants developed hypertension. After comprehensive adjustment, IVX and metabolic vulnerability index (MVX) showed significant positive associations with hypertension risk (highest v. lowest quartile: hazard ratio (HR) = 1·25 (95 % CI: 1·20, 1·31) and HR = 1·19 (95 % CI: 1·15, 1·24), respectively, P < 0·001). Each standard deviation increase in IVX and MVX was associated with 9 % and 7 % higher hypertension risk, respectively. Conversely, MMX demonstrated a slight protective effect (HR = 0·96 (95 % CI: 0·92, 0·99), P = 0·016) and exhibited a U-shaped relationship with hypertension risk. Notably, associations between IVX/MVX and hypertension were significantly stronger in non-obese individuals (BMI < 30) compared with obese participants (BMI ≥ 30) (P-interaction < 0·001 and P = 0·007, respectively). Results remained robust in sensitivity analyses excluding extreme values and early hypertension cases. Metabolic vulnerability, particularly its inflammatory component, is independently associated with hypertension risk beyond traditional risk factors. These findings highlight the potential utility of comprehensive metabolomic profiling for early identification of individuals at elevated hypertension risk.
Jaboticaba, Plinia cauliflora [Mart.] Kausel (Myrtaceae) is a native Brazilian fruit high in bioactive compounds with potent antioxidant and anti-inflammatory properties. We present the first protocol (randomised crossover with a washout period) for a clinical trial investigating the effects of consuming jaboticaba peel extract on inflammation, oxidative stress and gut dysbiosis in patients with chronic kidney disease (CKD) undergoing haemodialysis. Thirty eligible patients will be randomly assigned to the intervention group (3·3 g/d of jaboticaba peel extract, providing 650 mg/d of phenolic compounds) or to the placebo group (corn starch). The total daily dose will be administered as four capsules, divided into two doses per day, for 2 months. Following the washout period (2 months), patients will continue the supplementation in a crossover design for the same duration. Blood and fecal samples, food intake data and anthropometric measurements will be evaluated. Inflammatory markers and antioxidant enzymes will be assessed using real-time protein chain reaction, cytokine plasma levels will be measured by Luminex, and uremic toxin plasma levels will be analysed using high-performance LC. The fecal microbiome will be evaluated through high-throughput sequencing of the 16S rRNA gene amplicons. Conducting a rigorously designed trial using jaboticaba will provide essential information and generate new evidence to support nutritional strategies that utilise typical Brazilian fruits for patients with CKD.
Lactosylceramides (LacCers) are glycosphingolipids that play essential roles in physiological and pathological processes across immune, endocrine, and neurological systems, with mechanistic studies demonstrating that LacCers modulate inflammatory signalling, oxidative stress responses, membrane microdomain organisation, and control aspects of mitochondrial function. Historically, LacCers were quantified predominantly as a total lipid subclass, limiting the ability to discern how individual species contribute to biological processes in clinical contexts. Recent advances in mass spectrometry based lipidomics now enable LacCer species to be resolved by acyl-chain length and saturation, offering far greater biochemical and clinical insights.
Methods
In this narrative review, we examine evidence from population based lipidomic studies describing how LacCer composition varies across healthy and diseased states.
Results
In metabolic and vascular disorders, multiple studies report elevations in specific short- and medium-chain LacCer species, whereas patterns involving longer-chain species appear more heterogeneous. Altered LacCer profiles have also been described in neurodegenerative disease, chronic kidney disease, and cancers, with species-level differences varying by disease-context, tissue type, and analytical platform.
Conclusions
Our findings describe disease- and tissue-specific variations in LacCer acyl-chain composition, underscoring the value of species-level resolution for mechanistic understanding and informing the application of LacCer profiles in future biomarker and therapeutic studies.
Systemic inflammation is hypothesized to contribute to post-traumatic stress disorder (PTSD) vulnerability. Few studies have examined inflammation shortly after trauma as a predictor of later PTSD symptoms. We examined whether inflammation from the emergency department (ED) post-trauma is associated with PTSD symptom severity over the following 6 months.
Methods
Our sample included 742 AURORA participants, a longitudinal cohort of patients in 29 EDs across the United States after a traumatic stressor, followed up to 6 months. Plasma cytokines were assessed from a study blood draw in the ED: an inflammatory index (standardized sum of generally pro-inflammatory markers interleukin [IL]-6, IL-8, tumor necrosis factor alpha [TNF-α], interferon gamma [IFN-γ]), and generally anti-inflammatory IL-10. PTSD symptoms were self-reported at 2 weeks, 8 weeks, 3 months, and 6 months post-ED. Covariate-adjusted repeated-measures regressions estimated associations between inflammation and PTSD symptoms, overall and sex-stratified.
Results
Among 742 participants (age m = 40.0 [13.7]; 479 [64.6%] female), PTSD symptoms were elevated then modestly decreased over follow-up. Higher ED inflammation was associated with higher PTSD symptoms across follow-up (standardized symptoms β = 0.05, 95% CI: 0.01–0.09), adjusted for potential confounders. Higher pro-inflammatory index levels and IL-6, IL-8, and TNF-α were associated with higher PTSD symptoms in males only, while higher IL-10 was associated with higher PTSD symptoms in females only.
Conclusions
Pro-inflammatory levels shortly after traumatic stress are associated with heightened PTSD symptoms, particularly among males. Inflammatory markers may prove useful additions to prediction models for PTSD following trauma, with attention to sex differences.
The effects of maternal broccoli powder (BP) intake on inflammation and AMPK activation in weaning offspring programmed by maternal undernutrition remain poorly understood. This study aimed to investigate whether maternal BP intake during lactation ameliorates inflammation and affects AMPK phosphorylation in the hypothalamus and liver of weaning offspring subjected to maternal undernutrition. Pregnant rats received either a normal protein (NP, 20% casein) or a low protein (LP, 8% casein) diet. During lactation, dams were provided with either a normal protein diet without or with 0.74% BP (NP/NP or NP/NPBP) or a low protein diet without or with 0.74% BP (LP/LP or LP/LPBP). Blood, liver (left lateral lobular region), and hypothalamic samples (region estimated to include the arcuate nucleus and ventromedial hypothalamus) were collected on postnatal day 21. In the liver, macrophage count, NFκB p65 protein expression, and TNF-α mRNA expression were lower in LP/LPBP than in LP/LP. In the hypothalamus, Iba1 mRNA expression, NFκB p65 protein expression, and TNF-α mRNA expression were reduced in LP/LPBP compared to LP/LP. AMPK phosphorylation was upregulated in both the liver and hypothalamus of LP/LPBP offspring relative to LP/LP. In the liver, mTOR and Akt phosphorylation were downregulated in LP/LPBP compared to LP/LP. Additionally, Dnmt1 levels were lower in LP/LPBP than in LP/LP in the liver, whereas in the hypothalamus, Dnmt1 and Dnmt3a mRNA expression levels were higher in NP/NPBP than in NP/NP. In conclusion, maternal BP intake during lactation decreased inflammation and increased AMPK phosphorylation in the liver and hypothalamus of weaning rats programmed by maternal undernutrition.
Anxiety disorders are prevalent neuropsychiatric conditions associated with neuroinflammation and altered cytokine signalling in the hippocampus. This study aimed to evaluate the anxiolytic-like effects of alpha-pinene and its potential modulation of hippocampal neuroinflammatory pathways in a reserpine-induced anxiety model.
Methods:
Adult male Wistar rats were randomly assigned to four groups: control (vehicle), reserpine (0.5 mg/kg, i.p.), and reserpine co-treated with alpha-pinene at 50 or 100 mg/kg. Treatments were administered intraperitoneally for 10 consecutive days. Behavioural assays – including the Open Field Test, Elevated Plus Maze, and Light/Dark Box Test – assessed locomotor activity and anxiety-like behaviours. Following testing, hippocampal tissues were collected for molecular analyses, including real-time PCR for TLR4, MyD88, and NF-κB expression, and ELISA quantification of IL-1β and IL-6 levels.
Results:
Reserpine induced robust anxiety-like behaviours, accompanied by significant upregulation of TLR4, MyD88, and NF-κB expression and increased hippocampal IL-1β and IL-6. Alpha-pinene treatment at both doses significantly attenuated anxiety-like behaviours and reduced neuroinflammatory markers, suggesting involvement of the TLR4/MyD88/NF-κB pathway.
Conclusion:
Alpha-pinene exhibits anxiolytic-like effects in reserpine-treated rats, potentially via suppression of hippocampal neuroinflammation, supporting further investigation into its therapeutic potential for anxiety disorders.
Using National Health and Nutrition Examination Survey data (2011–2020), we assessed the association between the nutritional risk index (NRI) and stroke risk among 22 839 adults (mean age, 49·61 (sd 17·07) years), including 910 individuals (3·98 %) with stroke. Weighted multivariable logistic regression and restricted cubic spline (RCS) analysis were used to characterise the association, with subgroup analyses to examine consistency across populations and mediation analyses to investigate the roles of lipid and inflammatory biomarkers. Higher continuous NRI was inversely associated with stroke, with each 1-unit increase associated with 4 % lower odds (OR = 0·96, 95 % CI: 0·95, 0·97), and participants in the highest NRI quartile (Q4) had a significantly lower stroke risk than those in the lowest NRI quartile (Q1) (OR 0·60, 95 % CI 0·42, 0·85). RCS analysis indicated a linear relationship (P for nonlinearity > 0·05), and the protective effect of higher NRI remained robust across nearly all subgroups examined. Mediation analyses revealed that total cholesterol, systemic immune-inflammation index, product of platelet and neutrophil count, neutrophil:lymphocyte ratio and lymphocyte:monocyte ratio each partially mediated the NRI–stroke association, with mediation effects ranging from 1·71 % to 13·65 %. These findings suggest that favourable nutritional status, reflected by higher NRI, is linked to lower stroke risk, with lipid metabolism and inflammation playing mediating roles in this association. Further longitudinal and mechanistic studies are warranted.
Tail biting in pigs is a serious problem both from an animal welfare and an economic perspective. Once the behaviour starts, it is important to identify it and intervene immediately to restrict the spread and risk of secondary problems, such as infections. In this study, we tested whether thermal camera imaging could be used as an aid for early detection of tail biting. We also assessed links between skin temperature, tail health and saliva biomarkers for stress and inflammation. Bitten tails were slightly warmer based on thermal imaging than non-lesioned tails. However, the difference was not sufficiently large or specific to enable its use as a practical tool in the early detection of tail lesions. The methodology, however, warrants further investigation. Shortened, but healed tails had a lower skin temperature than tails of other health categories. In combination with a lower saliva cortisol level in pigs with shortened tails, potentially indicative of chronic stress, this supports previous studies indicating chronic pain in shortened pig tails, and/or chronic stress as a result of being a victim of tail biting. These findings provide a further insight into the link between stress, infections and tail biting, while also illustrating potential for skin temperature changes to be used as an early indicator of health and welfare challenges in pigs.
Increasing evidences show that inflammation might be involved in bipolar disorder (BD), but the association between abnormal brain function and inflammation in BD is still unclear. In this study, we tried to explore the disrupted brain functional network topology, peripheral inflammatory cytokine levels, and their correlations in unmedicated bipolar II depression (BDII-D).
Methods
In this study, 65 individuals with unmedicated BDII-D and 50 healthy controls (HCs) underwent resting-state magnetic resonance imaging scans. Graph theory analysis was performed to investigate the topological properties of the whole-brain functional connectome at both global and nodal levels. Besides, serum levels of 17 inflammatory cytokines were measured in both BDII-D and HCs. Correlations between topological properties, clinical variables, and peripheral inflammatory cytokine levels in BDII-D were calculated.
Results
Compared with HCs, at the global level, BDII-D showed significantly higher $ \lambda $, decreased $ \gamma $, $ \sigma $, Eglo, and Eloc; at the nodal level, BDII-D showed decreased Enodal in the right olfactory cortex, left pallidum, and vermis. Besides, BDII-D showed higher levels of interleukin-8 (IL-8), interleukin-10 (IL-10), and granulocyte colony-stimulating factor (G-CSF) compared with the HCs. In BDII-D, $ \gamma $ and $ \sigma $ were significantly negatively correlated with the Hamilton Depression Rating Scale (HDRS) scores and number of episodes. Also, IL-8 level showed significant negative correlation with $ \gamma $, $ \sigma $, and Enodal of the left pallidum in BDII-D.
Conclusions
Reduced information segregation and integration, and lower nodal efficiency in the left pallidum were associated with proinflammatory cytokine IL-8 level and might contribute to severe depressive symptoms in unmedicated BDII-D.