Predicting postoperative rehemorrhage in hypertensive intracerebral hemorrhage using noncontrast CT radiomics and clinical data with an interpretable machine learning approach.

In hypertensive intracerebral hemorrhage (HICH) patients, while emergency surgeries effectively reduce intracranial pressure and hematoma volume, their significant risk of causing postoperative rehemorrhage necessitates early detection and management to improve patient prognosis. This study sought to develop and validate machine learning (ML) models leveraging clinical data and noncontrast CT radiomics to pinpoint patients at risk of postoperative rehemorrhage, equipping clinicians with an early detection tool for prompt intervention. The study conducted a retrospective analysis on 609 HICH patients, dividing them into training and external verification cohorts. These patients were categorized into groups with and without postoperative rehemorrhage. Radiomics features from noncontrast CT images were extracted, standardized, and employed to create several ML models. These models underwent internal validation using both radiomics and clinical data, with the best model's feature significance assessed via the Shapley additive explanations (SHAP) method, then externally validated. In the study of 609 patients, postoperative rehemorrhage rates were similar in the training (18.8%, 80/426) and external verification (17.5%, 32/183) cohorts. Six significant noncontrast CT radiomics features were identified, with the support vector machine (SVM) model outperforming others in both internal and external validations. SHAP analysis highlighted five critical predictors of postoperative rehemorrhage risk, encompassing three radiomics features from noncontrast CT and two clinical data indicators. This study highlights the effectiveness of an SVM model combining radiomics features from noncontrast CT and clinical parameters in predicting postoperative rehemorrhage among HICH patients. This approach enables timely and effective interventions, thereby improving patient outcomes.

Gut Microbiota Mediates Lactobacillus rhamnosus GG Alleviation of Deoxynivalenol-Induced Anorexia.

Deoxynivalenol (DON) is a widespread mycotoxin and causes anorexia and emesis in humans and animals; Lactobacillus rhamnosus GG (LGG), a well-characterized probiotic, can improve intestinal barrier function and modulate immune response. Currently, it is unclear whether LGG has a beneficial effect on DON-induced anorexia. In the present study, mice were treated with DON, LGG, or both by gavage for 28 days to evaluate the effects of LGG on DON-induced anorexia. Antibiotic treatment and fecal microbiota transplant (FMT) experiment were also conducted to investigate the link between DON, LGG, and gut microbiota. LGG significantly increased the villus height and reduced the crypt depth in jejunum and ileum, enhanced the tight junction proteins expression in the intestine, and regulated the TLR4/NF-κB signaling pathway, consequently attenuating the intestinal inflammation caused by DON. In addition, LGG increased the relative abundance of Lactobacillus and butyric acid production of cecal contents; remodeled phenylalanine metabolism and tryptophan metabolism; reduced plasma peptide tyrosine tyrosine (PYY), 5-hydroxytryptamine (5-HT), and glucagon-like peptide-1 (GLP-1) concentrations; and promoted hypothalamic NPY and AgPR gene expression, which will further promote food intake and reduce weight loss, ultimately alleviating DON-induced anorexia in mice. Interestingly, antibiotic treatment diminished the intestinal toxicity of DON. The FMT experiment showed that DON-originated microbiota promotes intestinal inflammation and anorexia, while LGG + DON-originated microbiota has no adverse effects on mice. Both antibiotic treatment and FMT experiment have proved that gut microbiota was the primary vector for DON to exert its toxic effects and an essential mediator of LGG protection. In summary, our findings demonstrate that gut microbiota plays essential roles in DON-induced anorexia, and LGG can reduce the adverse effects caused by DON through its structure and regulate the gut microbiota, which may lay the important scientific foundation for future applications of LGG in food and feed products.

The impact of stereotype threat on endogenous poverty-elimination dynamics in generationally poor individuals.

Introduction: The study examines the impact of stereotype threat on generationally poor individuals and its effect on achievement motivation. It also explores the extent to which self-affirmation has an intervention effect on the negative impact of stereotype threat. Methods and results: In Study 1, statements that contained negative stereotypes were used to elicit stereotype threat in generationally poor individuals; the results show that stereotype threat reduced the performance of generationally poor individuals in a mental-rotation task. Study 2 used a questionnaire to measure the endogenous dynamics of generationally poor individuals attempting to escape poverty after experiencing stereotype threat; participants in the stereotype-threat group showed lower-level endogenous poverty-elimination dynamics than those in the control group. In Study 3, a self-affirmation intervention was administered to the stereotype-threat group after the stereotype threat was induced. Participants in the self-affirmation group were shown to have higher-level endogenous poverty-elimination dynamics than those in the control group. Discussion: These findings confirm the negative effect of stereotype threat on endogenous poverty-elimination dynamics and verify the effectiveness of self-affirmation in mitigating the negative effects of stereotype threat.

Lactobacillus rhamnosus GG ameliorates DON-induced intestinal damage depending on the enrichment of beneficial bacteria in weaned piglets.

BACKGROUND: Deoxynivalenol (DON) is one of the most common environmental pollutants that induces intestinal inflammation and microbiota dysbiosis. Lactobacillus rhamnosus GG (LGG) is a probiotic that not only has anti-inflammatory effects, but also shows protective effect on the intestinal barrier. However, it is still unknown whether LGG exerts beneficial effects against DON-induced intestinal damage in piglets. In this work, a total of 36 weaned piglets were randomized to one of four treatment groups for 21 d. The treatment groups were CON (basal diet); LGG (basal diet supplemented with 1.77 × 1011 CFU/kg LGG); DON (DON-contaminated diet) and LGG + DON (DON-contaminated diet supplemented with 1.77 × 1011 CFU/kg LGG). RESULT: Supplementation of LGG can enhance growth performance of piglets exposed to DON by improving intestinal barrier function. LGG has a mitigating effect on intestinal inflammation induced by DON exposure, largely through repression of the TLR4/NF-κB signaling pathway. Furthermore, supplementation of LGG increased the relative abundances of beneficial bacteria (e.g., Collinsella, Lactobacillus, Ruminococcus_torques_group and Anaerofustis), and decreased the relative abundances of harmful bacteria (e.g., Parabacteroides and Ruminiclostridium_6), and also promoted the production of SCFAs. CONCLUSIONS: LGG ameliorates DON-induced intestinal damage, which may provide theoretical support for the application of LGG to alleviate the adverse effects induced by DON exposure.

Dihydroartemisinin alleviates deoxynivalenol induced liver apoptosis and inflammation in piglets.

Deoxynivalenol (DON) is one of the mycotoxins that contaminate cereals and feed, thereby endangering human and animal health. Dihydroartemisinin (DHA), a derivative of artemisinin, has anti-inflammatory and antioxidant functions in addition to anti-malaria and anti-cancer. The purpose of this study was to investigate the effects of DHA on alleviating liver apoptosis and inflammation induced by DON in piglets. The experimental design followed a 2 (normal diet and DON-contaminated diet) × 2 (with and without supplementation of DHA) factorial arrangement. 36 weaned piglets were subjected to a 21-day experiment. Results showed that DON increased ALT activity, the levels of TNF-α, IL-1ß and IL-2, and reduced the levels of total protein (TP) and albumin (ALB) in the serum. However, DHA decreased the levels of TNF-α, IL-1ß and IL-2, and increased the levels of TP and ALB. Also, DON decreased glutathione (GSH) content and catalase (CAT) activity, and increased methane dicarboxylic aldehyde (MDA) content. But GSH content was increased by DHA. In addition, DHA decreased DON-induced increase in apoptosis rate of hepatocytes. Furthermore, DON activated death receptor pathway to promote apoptosis by up-regulating the protein expression of FasL and caspase-3, and the mRNA expression of FasL, TNFR1, caspase-8, Bid, Bax, CYC and caspase-3. However, DHA reduced caspase-3 protein expression, as well as the mRNA expression of FADD, Bid, Bax, CYC and caspase-3. Besides, DON also activated TNF/NF-κB pathway to induce an inflammatory response by up-regulating TNF-α protein expression, and the mRNA expression of TNFR1, RIP1, IKKß, IκBα, IL-1ß and IL-8. Nevertheless, DHA reduced the mRNA expression of RIP1, IκBα, NF-κB, IL-1ß and IL-6, and the protein expression of TNF-α and NF-κB. In conclusion, DHA improved DON-induced negative effects on serum biochemical parameters and inflammatory cytokine levels, hepatic antioxidant capacity, hepatic apoptosis and inflammation.

Lactobacillus rhamnosus GG ameliorates deoxynivalenol-induced kidney oxidative damage and mitochondrial injury in weaned piglets.

Deoxynivalenol (DON) is a common mycotoxin that pollutes food crops and adversely affects the health of animals, even humans. Lactobacillus rhamnosus GG (LGG) can alleviate intestinal injury, and anti-inflammatory and antioxidant effects. However, the potential of LGG in alleviating kidney injury induced by DON in piglets remains to be studied. The objective of this study was to investigate the adverse effect of DON on kidney injury and the protective ability of LGG. A total of twenty-seven weaned piglets were divided into three groups: CON group, DON group (3.11 mg kg-1 feed) and LGG + DON group (LGG powder 1 g kg-1 + DON 3.15 mg kg-1 feed). DON increased the MDA content, and decreased antioxidant enzyme activity (GSH-Px) and total antioxidant capacity (P < 0.05). Meanwhile, DON activated the Nrf2 antioxidant pathway. However, LGG supplementation alleviated the damage of DON to the kidney antioxidant system of piglets. Notably, DON significantly reduced the Sirt3 expression (P < 0.05), which was alleviated by LGG addition. The expression of mitochondrial biogenesis related factors such as VDAC1 and Cyt C was up-regulated by DON (P < 0.05), and LGG could improve mitochondrial ultrastructural abnormalities and mitochondrial dysfunction. In addition, LGG mitigated DON-induced mitochondrial fusion inhibition, and prevented DON-mediated mitochondrial autophagy. In conclusion, LGG play a protective role in DON-induced kidney toxicity, and dietary intervention may be a strategy to reduce mycotoxins.

Dispositional mindfulness and self-referential neural activity during the resting state.

Mindfulness-based interventions have been shown to impact a broad range of outcomes including enhanced attention, memory, and self-regulation. Previously, mindfulness training has been negatively correlated with brain activity across the default mode network nodes following mindfulness-based practice. Currently, little research has been done to understand the neural basis of differences in mindfulness levels in untrained individuals. In this study, we explored the relationship between the amplitude of low-frequency fluctuation (ALFF) and fractional ALFF (fALFF) during the resting state and the level of dispositional mindfulness, which was measured by using the Five Facet Mindfulness Questionnaire (FFMQ). The results showed that the total scores on the FFMQ were negatively correlated with the spontaneous activation of left premotor cortex. This indicates that individuals with higher levels of dispositional mindfulness might require less effort to control their irrelevant motor responses.

Lycopene Affects Intestinal Barrier Function and the Gut Microbiota in Weaned Piglets via Antioxidant Signaling Regulation.

BACKGROUND: In pig production, early and abrupt weaning frequently causes weaning stress, which manifests as oxidative damage, barrier disruption, and digestion and absorption capacity declines. Lycopene exhibits beneficial antioxidant capacity in both humans and other animal models. OBJECTIVES: The present study aimed to investigate the effects of lycopene supplementation on early weaning stress in piglets and the underlying mechanisms by examining the oxidative stress state, gut intestinal barrier function, and the gut microbiota. METHODS: Twenty-four 21-day-old weaned piglets [Duroc × (Landrace × Yorkshire); castrated males; 5.48 ± 0.10 kg initial body weight] were randomly assigned to 2 treatments. The piglets were fed a basal diet (control treatment) or a basal diet supplemented with 50 mg/kg lycopene (lycopene treatment) for 28 days. The serum lipid levels, serum and jejunum enzyme activities, jejunum morphology, mRNA and protein expression, and gut microbiota were determined. RESULTS: Compared with the control treatment, lycopene supplementation increased the serum catalase activity (P = 0.042; 62.0%); serum total cholesterol concentration (P = 0.020; 14.1%); and jejunum superoxide dismutase activity (P = 0.032; 21.4%), whereas it decreased serum (P = 0.039, 23.0%) and jejunum (P = 0.047; 20.9%) hydrogen peroxide concentrations. Additionally, lycopene increased the mRNA and protein expression of NFE2-like bZIP transcription factor 2 (214.0% and 102.4%, respectively) and CD36 (100.8% and 145.2%, respectively) in the jejunum, whereas it decreased the mRNA and protein expression of Kelch-like ECH-associated protein 1 (55.6% and 39.8%, respectively ). Lycopene also improved jejunal morphology, increasing the villus height (P = 0.018; 27.5%) and villus:crypt ratio (P < 0.001; 57.9%). Furthermore, it increased the abundances of potentially beneficial bacterial groups, including Phascolarctobacterium and Parasutterella, and decreased those of potentially pathogenic bacterial groups, including Treponema_2 and Prevotellaceae_unclassified. CONCLUSIONS: Lycopene supplementation strengthens the intestinal barrier function and improves the gut microbiota in weaned piglets by regulating intestinal antioxidant signaling.

Lycopene improves maternal reproductive performance by modulating milk composition and placental antioxidative and immune status.

Placental health and milk quality are important for maternal reproductive performance during pregnancy and lactation. Lycopene plays an important role in antioxidation, anti-inflammation and regulating lipid metabolism. The goal of the present study was to investigate the effects of dietary lycopene supplementation in the pig model on reproductive performance, placental health and milk composition during maternal gestation and lactation. In the present study, the litter size of live piglets was increased and the litter size of dead piglets was decreased by lycopene supplementation of the diet of sows. The litter weight at birth and weaning were increased in the lycopene group. Through placental proteomics, we enriched differentially expressed proteins (DEPs), gene ontology (GO) terms, and Kyoto encyclopedia of proteins and genomes (KEGG) pathways involved in immunity, anti-inflammation, antioxidants, and lipid metabolism and transport. Furthermore, in terms of placental health, we analyzed the levels of related enzymes, metabolites and mRNA expression in the placenta. Lycopene was shown to reduce mRNA expression and the levels of placental inflammatory factors, increase the content of immunoglobulin, improve the antioxidant capacity, and improve lipid metabolism and lipid transport in the placenta. In terms of sow milk composition, lycopene increased the levels of immunoglobulins in colostrum and lactose in colostrum and milk. Overall, the results of the present study demonstrate that dietary lycopene supplementation of sows during gestation and lactation improves the reproductive performance to a certain extent; this may be due to lycopene improving the placental health and milk composition of sows.

Deoxynivalenol exposure induces liver damage in mice: Inflammation and immune responses, oxidative stress, and protective effects of Lactobacillus rhamnosus GG.

Deoxynivalenol (DON), one of the most common environmental pollutants, substantially affects human and animal health. Much attention has been paid to the ability of probiotics to modulate inflammation and immune responses. In this work, the toxic effects of DON on the liver and the protective effects of Lactobacillus rhamnosus GG (LGG) were investigated. We treated mice with oral gavage of DON (2.4 mg/kg bw/day), LGG (1 × 109 CFU/mouse/day) or both for 28 days. The results showed that DON triggered liver inflammation, reflected by pathological changes and liver function damage but LGG oral administration significantly attenuated these changes. Notably, DON treatment activated the TLR4/NF-κB signaling pathway which contribute to produce inflammatory cytokines, but oral administration of LGG inhibited all the effects of DON. DON treatment can also induce oxidative stress and activate Keap1-Nrf2 signaling pathway, leading to the activation of Nrf2 and the downstream genes, while LGG treatment can improve the antioxidant capacity of liver and protected mice from DON injury. In conclusion, LGG was able to negate the detrimental effects of DON on the liver and may contribute as a potential dietary intervention strategy to reduce mycotoxicity.

Lycopene modulates lipid metabolism in rats and their offspring under a high-fat diet.

The purpose of this study was to investigate the effects of lycopene supplementation on lipid metabolism in rats and their offspring. The experiment was conducted on 60 female rats divided into four groups: normal diet, normal diet with 200 mg kg-1 lycopene, high-fat diet, and high-fat diet with 200 mg kg-1 lycopene. The plasma levels of TG, LDL-C, AST and ALT in female rats fed a high-fat diet were significantly increased (P < 0.05). Lycopene supplementation reduced the plasma TG, LEP and AST levels (P < 0.05). In addition, the activity of ACC and mRNA expression of SREBP1c, FAS, PPARγ, CPT1, HMGCR, ACC, PLIN1 and FATP1 in the liver were also increased after feeding a high-fat diet (P < 0.05), whereas the expression of HSL was decreased (P < 0.05). Lycopene increased the activity of HSL and the expression of ATGL in the liver (P < 0.05), and the activity of ACC and mRNA expression of HMGCR and ACC were decreased (P < 0.05). For the offspring, maternal feeding of a high-fat diet reduced the plasma HDL-C levels (P < 0.05), but lycopene supplementation reduced the plasma TC levels (P < 0.05). Maternal high-fat diet also decreased the activity of HSL and the expression of CD36, PLIN1 and FATP1 in the liver while increasing the expression of PPARγ (P < 0.05). Maternal lycopene supplementation decreased the activities of ACC and FAS in the liver and decreased the expression of PPARγ, ACC and PLIN1 (P < 0.05). Maternal feeding of a high-fat diet increased the level of oxidative stress in the liver, the level of blood lipids in plasma and the rate of lipid production in the liver of rats and their offspring. Maternal lycopene supplementation can reduce the level of oxidative stress in rats and their offspring, reduce the level of blood lipids in plasma, and also reduce the rate of lipid production in the liver of rats and offspring.

Lycopene Modulates Placental Health and Fetal Development Under High-Fat Diet During Pregnancy of Rats.

Lycopene plays an important role in improving immunity, promoting antioxidant capacity, and regulating fat metabolism. The placenta, an important organ for nutrients exchange between mother and child during pregnancy, directly affects fetal development. This study aims to characterize effects of lycopene on placental health and fetal development under a high-fat diet, and utilize RNA sequencing (RNA-seq) to investigate and integrate the differences of molecular pathways and biological processes in placenta. For placental health, high-fat diet during pregnancy increases placental oxidative stress, inflammation, and fat deposition. However, lycopene reduces the negative effects of high-fat diet on placenta to some extent, and further promotes fetal development. Under high-fat diet, lycopene reduces the levels of Interleukin 17 (IL-17), Interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) in placenta (p < 0.05) through the IL-17 pathway. Furthermore, lycopene supplementation in high-fat diet increases Glutaredoxin (Glrx) gene and protein expression in the placenta (p < 0.05), increases Glutathione peroxidase (GSH-Px) and Total antioxidant capacity (T-AOC) levels (p < 0.05), decreases reactive oxygen species (ROS) (p < 0.01) and Hydrogen peroxide (H2 O2 ) levels (p < 0.05) in placenta. In addition, lycopene supplementation in high fat diet increases the expression of Lep gene and protein in placenta and increases the level of leptin (p < 0.05). In terms of fetal development, the average fetal weight and fetal litter weight are increased by lycopene compared to high-diet treatment.

3D particle-in-cell simulations of electron magnetic confinement in electron cyclotron resonance ion sources.

The electron confinement in an electron cyclotron resonance ion source is considered a critical factor that has a great influence on the working efficiency. In this paper, a three-dimensional electromagnetic particle-in-cell code is presented for simulations of the electron confinement in minimum-B structures. Electron dynamics under the effect of electromagnetic fields is modeled through a leapfrog scheme by solving Maxwell's equations and the particle equations of motion iteratively. Some characteristics of electron magnetic confinement are obtained through a benchmarking example. Preliminary results of the simulation show good agreement with the well-known effects.

Materialism Moderates the Effect of Accounting for Time on Prosocial Behaviors.

Accounting for time is defined as putting a price on time. Researchers have demonstrated that accounting for time reduces the time individuals spend on others; however, its association with monetary donations has not been examined. We hypothesized that accounting for time will activate a utility mindset that would affect one's allocation of time and money. In Study 1, the mediating effect of utility mindsets on the relationship between accounting for time and prosocial behavior was examined. In Study 2, we examined the effect of accounting for time on time spent helping and donating money, and the moderating role of material values on the relationship between accounting for time and prosocial behavior. Results showed that accounting for time activated a mindset of utility maximization that, in turn, reduced participants' prosocial behavior; moreover, materialism moderated the effect of accounting for time on prosocial behavior.