Helminth infection is highly prevalent in indigenous chickens reared in semi-scavenging/ scavenging systems in Bangladesh. Here, we estimated the prevalence of gizzard worm infection in indigenous chickens, the detection of the worm-induced pathologies, the development of ex vivo cultural protocol, and anthelmintic efficacy. We randomly collected and examined 390 chickens and isolated worms from the gizzard and proventriculus. The isolated worms were identified as Cheilospirura hamulosa Diesing, 1861. The overall prevalence of C. hamulosa was 33.1% (129 out of 390). Prevalence of the worm was almost similar in both sexes but significantly (p <0.05) higher in adult chickens (44.3%) and in the summer season (47.1%). In heavy infections, C. hamulosa destroyed the muscular layer of the gizzard. The presence of brown necrotic tissues and curd-like caseous materials was detected in the affected gizzards. In severe cases, the horny lining of the gizzard was inflamed, necrotized and marked by multiple holes and brick-red colored spots. Liquefied, fetid materials oozed out from the muscular layer in extensive cases. Histopathological examination showed marked infiltrations of eosinophils. In serum-supplemented M199 and DMEM, adult C. hamulosa survived well and reproduced. Levamisole (LEV) and ivermectin (IVM) efficiently killed the worm. However, albendazole (ABZ), mebendazole (MBZ) and piperazine (PPZ) did not kill the worms. Our results suggest that C. hamulosa is highly prevalent in semi-scavenging chickens in Bangladesh. LEV and IVM can be used to treat and control the infection in chickens.

Growing evidence suggests that psychedelic-assisted therapies can alleviate depression, anxiety, posttraumatic stress, and substance use disorder, offering relatively safe profiles, enhanced efficacy, and lasting effects after a few applications. Athletes often experience high levels of stress and pressure, making them susceptible to these psychiatric conditions. However, the effects of psychedelic substances on athletic performance remain largely unknown. Before potential acceptance, evaluating their impact on physical and physiological measures beyond mental health outcomes is crucial. Here, we aim to explore this topic and highlight research directions to advance our understanding. Preclinical studies suggest that psilocybin/psilocin, lysergic acid diethylamide (LSD), N,N-dimethyltryptamine (DMT), and ayahuasca possess anti-inflammatory and anti-nociceptive properties. Studies investigating the effects of classical psychedelics or 3,4-methylenedioxymethamphetamine (MDMA) on factors such as muscle strength, motor coordination, locomotion, endurance, fluid and electrolyte balance, hormonal regulation, and metabolism are still scarce. While adhering to regulatory frameworks, further research in animal models, athletes, and non-athletes is needed to address these gaps, compare psychedelics with commonly used psychoactive drugs, and explore the potential prophylactic and regenerative benefits of specific interventions.

Green tea, a plant rich in bioactive compounds, has been highlighted for its beneficial effects. In the present systematic review and meta-analysis of randomised controlled trials (RCTs), the impact of green tea on inflammatory and oxidative markers is investigated. Using pre-defined keywords, online databases (PubMed, Scopus, Web of Science Core Collection, and Google Scholar) were searched for relevant articles, published from inception up to February 2024. The outcomes included C-reactive protein (CRP), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX). Analyses of subgroups, linear, and non-linear associations were also carried out. Out of 1264 records initially retrieved, 38 RCTs were included. Supplementation with green tea improved the following indicators: IL-1β (weighted mean difference (WMD): −0.10 pg/mL; 95% CI: −0.15, -0.06), MDA (WMD: −0.40 mcmol/L; 95 % CI: −0.63, −0.18), TAC (WMD: 0.09 mmol/L; 95% CI: 0.05, 0.13), SOD (WMD: 17.21 u/L; 95% CI: 3.24, 31.19), and GPX (WMD: 3.90 u/L; 95% CI: 1.85, 5.95); but failed to improve others, including CRP (WMD: 0.01 mg/L; 95% CI: −0.14, 0.15), IL-6 (WMD: −0.34 pg/mL; 95% CI:−0.94, 0.26), and TNF-α (WMD: −0.07 pg/mL; 95% CI: −0.42, 0.28). Supplementation with green tea can improve the body’s oxidative status. However, the results showed no significant effect of green tea on inflammatory markers, except for IL-1β. Further studies are needed to determine the effectiveness of green tea, particularly on inflammatory status.

A randomised parallel intervention study was conducted with male patients diagnosed with CHD. Participants were assigned to three groups: Group A abstained from alcohol (n 20), Group B consumed red wine (n 21) and Group C (n 16) consumed an alcoholic beverage without wine micro-constituents. Biological samples were collected at baseline, 4 and 8 weeks. Enzyme activities of acetyl-CoA:lyso-platelet-activating factor (PAF) acetyltransferase, cytidine 5’-diphospho (CDP)-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase (PAF-cholinephosphotransferase), PAF-acetylhydrolase in leukocyte homogenates, serum lipoprotein-associated phospholipase-A2 and plasma markers of thrombosis were measured. PAF-, ADP- and collagen-induced platelet aggregation was measured in human platelet-rich plasma. Red wine consumption led to a 15·3 % reduction in LysoPAF-acetyltransferase activity at 4 weeks (P= 0·008) compared with baseline and Group A (P= 0·01). PAF-cholinephosphotransferase activity was reduced by 11·1 % at 8 weeks (P= 0·04) compared with baseline and by 24·9 % compared with Group C (P= 0·02). PAF-acetylhydrolase activity was reduced by 36·2 % at 8 weeks compared with baseline (P= 0·001) and compared with Group A (P< 0·000) and Group C (P= 0·009). Fibrinogen levels in Group B reduced by 6–9 % at 4 (P= 0·04) and 8 weeks (P= 0·01) compared with baseline while D-dimer in Group C increased by 16·1 % at 8 weeks (P= 0·005) compared with baseline. Platelet aggregation against PAF and collagen was reduced in Group B (82·6 and 35·4 %, respectively), and in Group C (158·4 and 37·1 %, respectively) compared with baseline and Group A (P< 0·05). In conclusion, moderate wine consumption improved the activity of PAF-metabolism enzymes regardless of ethanol and reduced platelet aggregation, probably through mechanisms different from those of ethanol.

Insulin-like growth factor 1 (IGF-1) is an important growth factor in childhood. We aimed to investigate the impact of food supplements for the treatment of moderate acute malnutrition (MAM) on serum IGF-1 (sIGF-1). Secondary analysis of a randomised 2 × 2 × 3 factorial nutrition trial was performed. Children aged 6–23 months with MAM received 2093 kJ/d as lipid-based nutrient supplement (LNS) or corn soy blend (CSB), containing either dehulled soya or soya isolate and different quantities of dried skimmed milk (0 %, 20 % or 50 % of total protein) for 12 weeks. The trial was double-blind with regard to soya and milk but not to matrix (LNS v. CSB). sIGF-1 was measured at inclusion and after 12 weeks of supplementation. Of 1609 children enrolled, 1455 (90 %) had sIGF-1 measured at both time points. During supplementation, sIGF-1 increased 6·7 (95 % CI 6·1, 7·3) ng/ml compared with an expected age-dependent decrease of 0·3 (95 % CI 0·2, 0·4) ng/ml. Children who received LNS v. CSB had a lower increase in sIGF-1 (–8 %, 95 % CI − 12, −3). The effect of LNS was partly attenuated when sIGF-1 was corrected for inflammation. Children who received soya isolate compared with dehulled soya had a higher increase in sIGF-1 (6 %, 95 % CI 1, 12). Milk content did not affect sIGF-1. Overall, sIGF-1 increased during supplementation. The lower increase with LNS v. CSB was only partly explained by increased inflammation with LNS and needs further investigation. Isolate v. dehulled soya led to a higher increase which may be due to antinutrients in dehulled soya.

A co-relation between Schistosoma japonicum (Sj) and liver cancer (LC) in humans has been reported in the literature; however, this association is circumstantial. Due to the inconclusive nature of this association, the International Agency for Research on Cancer has placed Sj in Group 2B for LC, signifying it to be a ‘possible carcinogen’. Many epidemiological, pathological and clinical studies have identified multiple factors, linked with Sj infection, which can lead to liver carcinogenesis. These factors include chronic inflammation in response to deposited eggs (which leads to fibrosis, cirrhosis and chromosomal instability at cellular level), hepatotoxic effects of egg-antigens, co-infection with hepatitis viruses, and up-regulation of glycolysis linked genes among others which predisposes hepatic tissue towards malignant transformation. The objective of this work is to present the current understanding on the association of Sj infection with LC. Mechanisms and factors linked with Sj infection that can lead to LC are emphasized, along with measures to diagnose and treat it. A comparison of liver carcinogenesis is also provided for cases linked with and independent of Sj infection. It appears that Sj, alone or with another carcinogen, is an important factor in liver carcinogenesis, but further studies are warranted to conclusively label ‘infection with Sj alone’ as a liver carcinogen.

Current evidence points to a research-practice gap in mental health. There is a specific unmet need to identify novel strategies to improve diagnostic criteria, especially when clinical manifestations overlap as in the case of bipolar (BD) and major depressive disorder (MDD). Based on the rapidly evolving notion that affective disorders are characterized by disrupted brain-body communication, current efforts of neuropsychiatric research are converging towards the identification of specific clusters of peripheral interconnected biomarkers. We argue that these can capture the complexity of the disease as they are linked to the fundamental pathophysiological mechanisms underlying BD or MDD, and can thus deliver an unbiased biosignature. Here we provide a critical viewpoint on the promises and challenges of biomarkers to identify reliable biosignatures of affective disorders. Novel methodological insight and relevant biomarkers are discussed with a main focus on immunometabolic derangements and disrupted redox balance. Major advancements are reviewed taking into consideration that an unbiased diagnosis can only derive from a deep understanding of how biological, psychological, and social factors interact ultimately affecting the clinical manifestation of affective disorders.

Mastitis in dairy cows is an important factor restricting the healthy development of dairy industry. Natural extracts have become a research hotspot to alleviate and prevent diseases because of their unique properties. The purpose of this study was to investigate the effects of resveratrol (RES) on the mitochondrial biosynthesis, antioxidation, and anti-inflammatory in bovine mammary epithelial cells (BMECs) and its mechanism involved. Blood samples were collected from six healthy cows and six mastitis affected cows, respectively, and lipopolysaccharide (LPS) was used to treat BMECs to construct inflammation models, gene interference is achieved by transfection. The results showed that messenger RNA (mRNA) expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) was down-regulated and mitochondrial biogenesis-related gene expression was disrupted in the blood of mastitis cows and LPS-induced BMECs. RES is the best active substance to activate PGC-1α. The addition of RES can effectively alleviate the production of BMECs reactive oxygen species (ROS) and mitochondrial damage induced by LPS, and improve the antioxidation and anti-inflammatory ability, while the alleviation effect of RES is inhibited after interfering with protein kinase AMP-activated catalytic subunit α 1 (PRKAA1). In summary, our study emphasizes that PRKAA1 is a key gene mediating the activation of PGC-1α by RES, which regulates mitochondrial biosynthesis, inhibits ROS release, attenuates mitochondrial damage, and improves mitochondrial antioxidant capacity through the activation of PGC-1α by PRKAA1, thus attenuating the inflammatory response in BMECs.

Chia seeds have gained attention for their potential anti-inflammatory properties, which may be attributed to their high content of omega-3 fatty acids, dietary fibre, and antioxidants. This study aims to provide an overview of the current understanding regarding the effects of chia seeds on inflammatory markers, specifically C-reactive protein (CRP), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α). A comprehensive literature search was conducted on PubMed, Scopus, Web of Science, Cochrane, and Google Scholar up to June 2024. Randomized controlled trials (RCTs) assessing the effect of chia seed on CRP or/and IL-6 or/and TNF-α. Data were extracted and analysed using a random-effects model, and reported as weighted mean differences (WMD) with 95% confidence intervals (CI). Subgroup and sensitivity analyses were also performed. Four RCTs involving 210 participants were included in the meta-analysis. The results showed that chia consumption significantly decreased CRP (WMD: –0.64 mg/dl; 95% CI: –1.24, –0.04; P = 0.03). But it had no significant effect on IL-6 (WMD: 0.29 pg/dl; 95% CI: –0.40, 0.98; P = 0.41), and TNF-α (WMD: 0.05%; 95% CI: –0.21 to 0.30; P = 0.72). Chia consumption can significantly decrease CRP, but no significant effect was observed on IL-6 and TNF-α. To prove our findings, more studies with a larger sample size are needed.

Metabolic dietary patterns, including the Empirical Dietary Index for Hyperinsulinaemia (EDIH) and Empirical Dietary Inflammatory Pattern (EDIP), are known to impact multiple chronic diseases, but the role of the colonic microbiome in mediating such relationships is poorly understood. Among 1,610 adults with faecal 16S rRNA data in the TwinsUK cohort, we identified the microbiome profiles for EDIH and EDIP (from food frequency questionnaires) cross-sectionally using elastic net regression. We assessed the association of the dietary pattern-related microbiome profile scores with circulating biomarkers in multivariable-adjusted linear regression. In addition, we used PICRUSt2 to predict biological pathways associated with the enriched microbiome profiles, and further screened pathways for associations with the dietary scores in linear regression analyses. Microbiome profile scores developed with 32 (EDIH) and 15 (EDIP) genera were associated with higher insulin and homeostatic model assessment of insulin resistance. Six genera were associated with both dietary scores: Ruminococcaceae_UCG-008, Lachnospiraceae_UCG-008, Defluviitaleaceae_UCG-011 Anaeroplasma, inversely and Negativibacillus, Streptococcus, positively. Further, pathways in fatty acid biosynthesis, sugar acid degradation, and mevalonate metabolism were associated with insulinaemic and inflammatory diets. Dietary patterns that exert metabolic effects on insulin and inflammation may influence chronic disease risk by modulating gut microbial composition and function.

A positive association has been demonstrated between consumption of sucrose-sweetened beverages and the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD). Since the administration of 30 % sucrose in the drinking water (sucrose-rich diet (SRD)) to rats has proven to be a good model of systemic insulin resistance, the aim of our study was to analyse the effect of caloric restriction applied on SRD-treated rats by switching back to a standard diet, on liver morphology, function and metabolism. Consumption of an SRD causes a metabolic shift towards gluconeogenesis and fatty acid synthesis leading to an increase in TAG levels in plasma and in the liver that were associated with a decrease in insulin sensitivity. Moreover, our results show that animals fed an SRD develop steatohepatitis characterised by the generation of oxidative stress, endoplasmic reticulum (ER) stress, inflammation and apoptosis. Although no histological changes were observed after a 2-week caloric restriction, key pathways associated with the progression of MASLD as inflammation, ER stress and apoptosis were slowed down. Notably, this 2-week intervention also increased liver insulin sensitivity (evaluated by AKT activity in this tissue) and drove the lipid metabolic profile towards oxidation, thus lowering circulating TAG levels. In summary, the present study uncovers underlying mechanisms affected, and their metabolic consequences, during the first stages of the phenotypic reversal of steatohepatitis by switching back to a standard diet after receiving sucrose-sweetened water for several weeks.

Lipids play an important role in human nutrition. Although adequate lipid consumption is necessary for an optimal functioning of the human body, overconsumption of saturated fatty acids can lead to postprandial hypertriglyceridaemia, which triggers the development of atherosclerosis. Important parameters that impact postprandial lipaemia and inflammation are related to the matrix structure and the fat-soluble micronutrient profile of ingested foods/lipids, but the specific effect of these parameters should be further studied, as most of the available studies evaluate their effect at fasting state. This review specifically explores the effects of food structure and fat-soluble micronutrients, from either micronutrient-rich foods or supplements, on postprandial hypertriglyceridaemia and inflammation. The review also highlights the potential of emerging biomarkers such as miRNAs or circulating microvesicles, as an alternative to the widely use biomarkers (e.g. low-density lipoproteins or blood concentration of pro-inflammatory cytokines), to identify inflammation associated with postprandial hypertriglyceridaemia at early stages.