Fatty Acid Binding Protein Research Articles

Markers of Environmental Enteric Dysfunction Are Associated with Poor Growth and Developmental Outcomes among Young Children in Lusaka, Zambia

To examine cross-sectional relationships between biomarkers of environmental enteric dysfunction (EED), an acquired subclinical condition of the small intestine, and anthropometric and developmental outcomes among children in Lusaka, Zambia. Serum samples were collected from 240 children aged 27 to 35months enrolled in a cluster-randomized trial assessing the effects of growth charts and small-quantity lipid-based nutrient supplements on linear growth. Samples were analyzed using the 11-plex Micronutrient and EED Assessment Tool, which incorporates 2 biomarkers of EED, namely intestinal fatty acid-binding protein (I-FABP), a marker of epithelial damage, and soluble CD14 (sCD14), a marker of microbial translocation. Associations between log2-transformed biomarker concentrations and anthropometric (height-for-age z-score [HAZ], weight-for-height z-score, and weight-for-age z-score) and developmental (Global Scales of Early Development development for age z-score and saccadic reaction time [SRT]) outcomes were assessed using linear regression analyses adjusted for background characteristics. Mean±SD HAZ was -1.94±1.10. Higher sCD14 and I-FABP concentrations were significantly associated with lower HAZ (β: -0.21, 95% CI: -0.41, -0.01 and β: -0.20, 95% CI: -0.32, -0.08, respectively). Higher I-FABP concentrations were significantly associated with lower development-for-age z-score (β: -0.22, 95% CI: -0.40, -0.03) and slower SRT (β: 7.37ms, 95% CI: 2.02, 12.72) as were higher alpha-1-acid glycoprotein concentrations (HAZ β: -0.38, 95% CI: -0.72, -0.03; SRT β: 11.14ms, 95% CI: 0.94, 21.72). In children in Lusaka, biomarkers of EED were associated with poor anthropometric and developmental outcomes, underscoring the need for interventions to address EED to improve child health globally. ClinicalTrials.gov identifier for parent trial: NCT05120427. https://clinicaltrials.gov/ct2/show/NCT05120427.

APOEε4 alters ApoE and Fabp7 in frontal cortex white matter in prodromal Alzheimer's disease

The ApoE ε4 allele (APOEε4) is a major genetic risk factor for sporadic Alzheimer's disease (AD) and is linked to demyelination and cognitive decline. However, its effects on the lipid transporters apolipoprotein E (ApoE) and fatty acid-binding protein 7 (Fabp7), which are crucial for the maintenance of myelin in white matter (WM) during the progression of AD remain underexplored. To evaluate the effects of APOEε4 on ApoE, Fabp7 and myelin in the WM of the frontal cortex (FC), we examined individuals carrying one ε4 allele that came to autopsy with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI) and mild to moderate AD compared with non-carrier counterparts. ApoE, Fabp7 and Olig2 immunostaining was used to visualize cells, whereas myelin basic protein (MBP) immunocytochemistry and luxol fast blue (LFB) histochemistry of myelin in the WM of the FC were combined with quantitative morphometry. We observed increased numbers of ApoE-positive astrocytes in the WM of both NCI and MCI APOEε4 carriers compared with non-carriers, whereas Fabp7-positive cells were elevated only in AD. Conversely, Olig2 cell counts and MBP immunostaining decreased in MCI APOEε4 carriers compared to non-carriers, while LFB levels were higher in NCI APOEε4 carriers compared to non-carriers. Although no correlations were found between ApoE, Fabp7, and cognitive status, LFB measurements were positively correlated with perceptual speed, global cognition, and visuospatial scores in APOEε4 carriers across clinical groups. The present findings suggest that the ε4 allele compromises FC myelin homeostasis by disrupting the lipid transporters ApoE, Fabp7 and myelination early in the onset of AD. These data support targeting cellular components related to WM integrity as possible treatments for AD.

Network Pharmacology and Computational Approach to Explore the Potential Underlying Mechanism of Centella asiatica in the Treatment of Diabetes Mellitus

Background: Centella asiatica is a tropical medicinal herb traditionally used for the treatment of different diseases, such as arthritis, kidney disease, diabetes mellitus, etc. Diabetes mellitus is emerging as a global health concern, demanding research to provide insights into it. Objective: The current research study aimed at employing the Network Pharmacology and Molecular Docking approach to unearth and validate the possible molecular mechanism involved in the treatment of diabetic mellitus with herbal constituents from Centella asiatica. Methods: The phytocompounds and targets of Centella asiatica were screened from different databases. An herb-core-target-ingredient-diabetes mellitus network was established via Cystoscope 3.7.2. Next, Go and KEGG enrichment analysis was performed. Lastly, the interaction between ligands and targets was investigated via molecular docking. Results: According to the results obtained, we identified 49 core targets of diabetes mellitus and 37 active ingredients of Centella asiatica. Next, Go and KEGG resulted in a total of 455 biological processes for the treatment of diabetes mellitus. The KEGG enrichment analysis reported that the targets were related to metabolic pathways, insulin signaling pathways, glycolysis/gluconeogenesis, oxidative stress, insulin resistance, etc. On the basis of KEGG enrichment and protein-protein interaction, we selected Fructose-1-6 bisphosphate1 (FBP1), Glucokinase (GCK), Cytochromes P450 (CYP19A1), fatty acid binding protein 1 (FABP1), Interleukin 2 (IL2) and angiotensin-converting enzyme (ACE), and phytocompounds from Centella asiatica for docking. From the docking study, it was concluded that several targets had a stable binding affinity with Centella asiatica phytocompounds. result: Results: According to the results obtained, we identified 49 core-targets of diabetes mellitus and 37 active ingredients of Centella asiatica. Next, Go and KEGG resulted in total 455 biological process for treatments of diabetes mellitus. The KEGG enrichment analysis reported that the targets were related to metabolic pathways, insulin signaling pathways glycolysis/gluconeogenesis, oxidative stress, insulin-resistance etc. On the basis of KEGG enrichment and protein-protein interaction, we selected Fructose-1-6 bisphosphate1 (FBP1), Glucokinase (GCK), Cytochromes P450 (CYP19A1), fatty acid binding protein 1 (FABP1), Interleukin 2 (IL2) and angiotensin converting enzyme (ACE) and phytocompounds from Centella for Docking. From docking study, it is concluded that several targets have stable binding affinity with Centella phytocompounds Conclusion: We explored the biological mechanism of phytocompounds involved in the treatment of diabetes mellitus through different biological processes and signaling pathways, and lastly, docking provides us commending results that direct for experiments ahead.

MELK prevents radiofrequency ablation-induced immunogenic cell death and antitumor immune response by stabilizing FABP5 in hepatocellular malignancies

BackgroundRadiofrequency ablation (RFA) is an efficient treatment with unlimited potential for liver cancer that can effectively reduce patient mortality. Understanding the biological process related with RFA treatment is important for improving treatment strategy. This study aimed to identify the critical targets for regulating the efficacy of RFA.MethodsThe RFA treatment in hepatocellular carcinoma (HCC) tumor models in vivo, was analyzed by RNA sequencing technology. The heat treatment in vitro for HCC tumor cells was also constructed to explore the mechanism after RFA treatment in tumor cells. Nanoparticles with high affinity to tumor cells were applied as a new therapy to interfere with the expression of maternal embryonic leucine zipper kinase (MELK).ResultsIt was found that RFA treatment upregulated MELK expression, and MELK inhibition promoted RFA efficacy by immunogenic cell death and the antitumor response, including anti-tumoral macrophage polarization and increased CD8+ T cell cytotoxicity in HCC. Mechanically, MELK binds to fatty acid-binding protein 5 (FABP5), and affects its ubiquitination through the K48R pathway to increase its stability, thereby activating protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling axis to weaken the RFA-mediated antitumor effect. In addition, the synthesis of arginylglycylaspartic acid (RGD)-lipid nanoparticles (LNPs) targeting tumor cell-intrinsic MELK enhanced RFA efficacy in HCC.ConclusionMELK is a therapeutic target by regulating RFA efficacy in HCC, and targeting MELK via RGD-LNPs provides new insight into improving RFA efficacy in HCC clinical treatment and combating the malignant progression of liver cancer.

The Influence of Dietary Supplements on Exercise-Induced Gut Damage and Gastrointestinal Symptoms: A Systematic Review and Meta-Analysis

Endurance exercise, especially under heat stress, temporarily compromises the integrity of the intestinal barrier in healthy individuals. Consequently, there is growing interest in developing effective dietary strategies to alleviate exercise-induced gastrointestinal symptoms and gut damage. This meta-analysis investigated the effects of dietary supplements on mitigating these challenges. The search was performed in November 2024 following PRISMA guidelines, and 26 peer-reviewed studies were included across three meta-analyses: (1) gastrointestinal symptoms, (2) circulating intestinal fatty acid-binding protein (i-FABP), and (3) exercise performance. The moderating effect of variables was assessed via sub-group analysis and meta-regression. Overall, there was no pooled effect of supplement interventions on gastrointestinal symptoms (Hedges’ g = 0.42, 95% CI −0.17: 1.02, p = 0.15), and probiotics had a moderate significant effect for gastrointestinal symptoms (Hedges’ g = −0.62, 95% CI −1.01; 1.01, p = 0.05). There was a significant increase in i-FABP concentrations pre- to post exercise (∆ 106%; Hedges’ g = 1.01, 95% CI 0.63; 1.38, p = 0.01). There were no pooled or sub-group differences for exercise performance for any supplements (p = 0.53). Moderate-to-large heterogeneity was observed across studies (I2 ≥ 58.6%), and candidate moderators (exercise duration, modality, and environmental temperature) had no significant effect on any outcomes (p > 0.05). A significant increase in circulating i-FABP during exercise was observed. However, when examining the effects of different supplement categories, although significance was observed for a select few supplements, the changes in i-FABP, gastrointestinal symptoms, and exercise performance were outside of clinical relevance. Although probiotics showed a moderate significant effect for gastrointestinal symptoms, the conflicting findings across studies may have been due to inadequate control of confounding variables across studies. Further research is required to assess the alternative dietary supplements’ effects on gastrointestinal health and exercise performance, particularly under varied environmental conditions, where more rigorous control for cofounding factors is implemented.

High-Glucose-Induced Metabolic and Redox Alterations Are Distinctly Modulated by Various Antidiabetic Agents and Interventions Against FABP5/7, MITF and ANGPTL4 in Melanoma A375 Cells

Hyperglycemia-induced effects on cellular metabolic properties and reactive oxygen species (ROS) generation play pivotal roles in the pathogenesis of malignant melanoma (MM). This study assessed how metabolic states, ROS production, and related gene expression are modulated by antidiabetic agents. The anti-diabetic agents metformin (Met) and imeglimin (Ime), inhibitors of fatty acid-binding proteins 5/7 (MF6) and microphthalmia-associated transcription factor (MITF) (ML329), and siRNA-mediated knockdown of angiopoietin-like protein 4 (ANGPTL4), which affect mitochondrial respiration, ROS production, and related gene expression, were tested in A375 (MM cell line) cells cultured in low (5.5 mM) and high glucose (50 mM) conditions. Cellular metabolic functions were significantly and differently modulated by Met, Ime, MF6, or ML329 and knockdown of ANGPTL4. High glucose significantly enhanced ROS production, which was alleviated by Ime but not by Met. Both MF6 and ML329 reduced ROS levels under both low and high glucose conditions. Knockdown of ANGPTL4 enhanced the change in glucose-dependent ROS production. Gene expression related to mitochondrial respiration and the pathogenesis of MM was significantly modulated by different glucose conditions, antidiabetic agents, MF6, and ML329. These findings suggest that glucose-dependent changes in cellular metabolism and redox status are differently modulated by antidiabetic agents, inhibition of fatty acid-binding proteins or MITF, and ANGPTL4 knockdown in A375 cells.

FABP4 as a therapeutic host target controlling SARS-CoV-2 infection.

Host metabolic fitness is a critical determinant of infectious disease outcomes. Obesity, aging, and other related metabolic disorders are recognized as high-risk disease modifiers for respiratory infections, including coronavirus infections, though the underlying mechanisms remain unknown. Our study highlights fatty acid-binding protein 4 (FABP4), a key regulator of metabolic dysfunction and inflammation, as a modulator of SARS-CoV-2 pathogenesis, correlating strongly with disease severity in COVID-19 patients. We demonstrate that loss of FABP4 function, by genetic or pharmacological means, reduces SARS-CoV-2 replication and disrupts the formation of viral replication organelles in adipocytes and airway epithelial cells. Importantly, FABP4 inhibitor treatment of infected hamsters diminished lung viral titers, alleviated lung damage and reduced collagen deposition. These findings highlight the therapeutic potential of targeting host metabolism in limiting coronavirus replication and mitigating the pathogenesis of infection.

Metabolic Reprogramming of Neural Stem Cells by Chiral Nanofiber for Spinal Cord Injury.

Exogenous neural stem cells (NSCs) have great potential to reconstitute damage spinal neural circuitry. However, regulating the metabolic reprogramming of NSCs for reliable nerve regeneration has been challenging. This report discusses the biomimetic dextral hydrogel (DH) with right-handed nanofibers that specifically reprograms the lipid metabolism of NSCs, promoting their neural differentiation and rapid regeneration of damaged axons. The underlying mechanism is the intrinsic stereoselectivity between DH and fatty acid-binding protein 5 (FABP5), which facilitates the transportation of fatty acids bound to FABP5 into the mitochondria and endoplasmic reticulum, subsequently augmenting fatty acid oxidation (FAO) levels and enriching sphingosine biosynthesis. In the rat SCI model, DH significantly improved the Basso-Beattie-Bresnahan (BBB) locomotor scores (over 3-fold) and the hindlimbs' compound muscle action potential (over 4-fold) compared with the untreated group, conveying a significant return of functional recovery. This finding of nanoscale chirality-dependent NSCs metabolic reprogramming provides insights into understanding stem cell physiology and presents opportunities for regenerative medicine.

Expression of fatty acid binding proteins in mesenteric adipose tissue.

Adipose is a complex tissue comprised of adipocytes, immune cells, endothelial and progenitor stem cells. In humans, there are at least nine defined adipose depots, each containing variable numbers of genetically identified adipocyte clusters suggesting remarkable heterogeneity and potential functionality in each depot with respect to lipid metabolism. Although subcutaneous and visceral depots are commonly analyzed for biochemical and molecular functions, the mesenteric depot has been overlooked yet strongly implicated in lipid mediated immune surveillance. Since fatty acid binding proteins (FABPs) are primary cellular conduits to lipid trafficking, we evaluated the expression patterns for four major fatty acid binding proteins (FABP1, FABP3, FABP4 and FABP5) using a combination of gene expression, immunoblotting, and immunofluorescence in mesenteric fat from both young and old, male and female C57Bl/6J mice. All four FABPs were expressed at the mRNA and protein level in murine mesenteric adipose tissue. While there was no statistical change in expression of mesenteric FABP isoforms with sex or age, the expression of mesenteric FABP1 was increased, and FABP4 decreased, in both males and females as compared to perigonadal and inguinal depots. Surprisingly, immunofluorescence staining revealed that compared to subcutaneous or perigonadal depots, mesenteric fat expresses FABP3, but little FABP5, in adipocytes. These results highlight the diversity in adipose tissue and the importance of evaluating the mesenteric depot in the context of lipid transport and metabolism.

The obesogenic effects of Bisphenol A and its analogues are differentially regulated via PPARγ transactivation in mouse 3T3-L1 cells.

Exposure to environmental pollutants with obesogenic activity is being recognised as one of the contributing factors to the obesity epidemic. Bisphenol A (BPA) has been shown to stimulate adipogenesis in both human and mouse preadipocytes, to increase body weight and affect lipid metabolism in animal and epidemiological studies. Regulatory action and public concern has prompted industry to replace BPA with other structurally similar analogues that may have similar effects. In this study we investigated the effects of fifteen BPA analogues on adipogenesis in the mouse 3T3-L1 pre-adipocyte cell model in order to determine their adipogenic activity relative to BPA. 3T3-L1 cells were treated with increasing concentrations of BPA and replacements and mRNA expression of the mature adipocyte markers fatty acid binding protein 4 (Fabp4), perilipin (Plin) lipoprotein lipase (Lpl)and peroxisome proliferator-activated receptor (Ppar)γ and lipid accumulation were assessed. In addition, a luciferase reporter assay for PPARγ transactivation was employed to investigate mechanism of action. Our results show that BPC, BPS-MAE, BPS-MPE and TGSA, were the most adipogenic bisphenols, as shown by a robust increase in lipid accumulation and mRNA expression of adipogenic markers. BPS-MPE, BPC, BTUM, TGSA and D8 increased PPARγ transcriptional activity. Despite its ability to activate PPARγ in the transcriptional assay D8 did not affect adipogenesis in this cell model.

Effect of FABP4 Gene Polymorphisms on Fatty Acid Composition, Chemical Composition, and Carcass Traits in Sonid Sheep.

Fatty acids (FAs) are a group of organic compounds that are regulated by polygenic and environmental factors and affect the taste, nutritional value, and quality of meat. Lamb meat is rich in FAs required by the human body, which has directed more attention to sheep research and meat production. The fatty acid-binding protein 4 (FABP4) gene is considered a candidate gene that can affect FA composition in livestock. Therefore, the aim of this study was to screen for genetic polymorphisms of FABP4 and confirm the association between these polymorphisms and FAs, chemical composition, and carcass traits in Sonid lambs. The results of the association study showed that g.57764667T>C, g.57764436T>G, g.57764242G>A, and g.57757988A>G were associated with the composition of certain long-chain FAs, and g.57764242G>A, g.57764436T>G, and g.57758026G>A were associated with free amino acid levels. In addition, g.57764667T>C and g.57757988A>G were associated with carcass weight and live weight in Sonid lambs. Therefore, the polymorphisms of the FABP4 gene are expected to be a genetic selection marker for superior traits in Sonid sheep breeding, which also provides new insights into how the ovine FABP4 gene affects traits of lamb quality.

Lupeol Attenuates Palmitate-Induced Hypertrophy in 3T3-L1 Adipocytes.

Obesity is characterized by the enlargement of adipose tissue due to an increased calorie intake exceeding the body's energy expenditure. Changes in the size of adipose tissue can lead to harmful consequences, with excessive fat accumulation resulting in adipocyte hypertrophy and promoting metabolic dysfunction. These adiposity-associated pathologies can be influenced by dietary components and their potential health benefits. Lupeol, a pharmacologically active pentacyclic triterpenoid found in medicinal plants, vegetables, and fruits, has been shown to exhibit antioxidant and anti-inflammatory properties. This study investigated the role of lupeol on adipocyte hypertrophy by evaluating key adipogenic regulators in vitro. First, 3T3-L1 MBX mouse embryonic cells were differentiated into adipocytes and hypertrophy was induced using 500 µM palmitic acid. The treated adipocytes showed a significantly increased lipid droplet size, confirming adipocyte hypertrophy. Both adipocytes and hypertrophied adipocytes were then treated with or without 60 µM lupeol, following a dose-dependent study. Lipid droplet size was assessed and validated by Oil Red O staining. Western blot analysis was performed to measure the expression of adipogenic and inflammatory markers. Differentiated adipocytes showed increased fatty acid-binding protein 4 (FABP4) expression and Oil Red O staining, indicating an increased lipid content. Western blot analysis revealed that lupeol treatment reduced the expression of FABP4, peroxisome proliferator-activated receptor-γ (PPARγ), and adipokines. In conclusion, the results suggest that lupeol reverts the inflammatory and adipogenic markers that are enhanced in adipocyte hypertrophy. Through its anti-inflammatory effects, lupeol offers protective effects against adipocyte hypertrophy and contributes to reducing hypertrophic adiposity.

FABP5 regulates ROS-NLRP3 inflammasome in glutamate-induced retinal excitotoxic glaucomatous model.

Fatty acid binding proteins (FABPs) are a class of small molecular mass intracellular lipid chaperone proteins that bind to hydrophobic ligands, such as long-chain fatty acids. FABP5 expression was significantly upregulated in the N-methyl-d-aspartic acid (NMDA) model, the microbead-induced chronic glaucoma model, and the DBA/2J mice. Previous studies have demonstrated that FABP5 can mediate mitochondrial dysfunction and oxidative stress in ischemic neurons, but the role of FABP5 in oxidative stress and cell death in retina NMDA injury models is unclear. In this study, we found that FABP5 is significantly altered in a model of glutamate excitotoxicity and is regulated by Stat3. Inhibition of FABP5 alleviated oxidative stress imbalance and activation of NLRP3 inflammasome, reduced the release of inflammatory factors, and ultimately attenuated glutamate excitotoxicity-induced retinal ganglion cell loss. Meanwhile, caspase1 inhibitors could alleviate the retinal ganglion cell loss induced by glutamate excitotoxicity. In conclusion, FABP5 inhibition protects retina ganglion cells from excitotoxic damage by suppressing the ROS-NLRP3 inflammasome pathway. FABP5 maybe a promising new target for glaucoma diagnosis and treatment.

Limited Diagnostic Value of miRNAs in Early Trauma-Induced Liver Injury: Only miRNA-122 Emerges as a Late-Phase Marker.

Background/Objectives: Liver injury is common after abdominal trauma. However, the established biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), lack accuracy. This study investigates whether specific liver-related microRNAs (miRNAs) are released into the circulation in trauma patients with liver injury and whether they can indicate liver damage in the early phase after major trauma. Methods: A retrospective analysis of prospectively collected data and blood samples from 26 trauma patients was conducted. The levels of miRNA-21-5p, -122-5p, -191-5p, -192-3p, and -212-3p were measured in patients with computed tomography-confirmed liver trauma (LT group, n = 12) and polytrauma patients without liver trauma (PT group, n = 14) upon emergency room (ER) admission, and 24 and 48 h after trauma. Additionally, liver-type fatty acid binding protein (L-FABP) was measured, as it has recently been discussed in the context of abdominal trauma. Results: Only miRNA-122-5p showed a significant increase in the LT group compared to the PT group, but only at the 48 h time point (p = 0.032). Conversely, L-FABP (p = 0.018) and ALT (p = 0.05) were significantly elevated in the LT group compared to the PT group at the time of ER admission. There was a moderate correlation between miRNA-122-5p and AISAbdomen (p = 0.056) and transfused red blood cell concentrates (p = 0.055). L-FABP correlated strongly with the ALT levels (p = 0.0009) and the length of stay in the ICU (p = 0.0086). Conclusions: In this study, the liver-specific miRNA-122-5p did not effectively indicate liver injury in the early acute post-traumatic phase. Future research with a large sample size should investigate whether other miRNAs can more accurately predict liver injury and the extent of hepatocellular injury, particularly in the acute post-traumatic phase.

Cardiac fatty acid binding protein as a biomarker for long-term prognosis of clinically manifested heart failure and severe post-infarction left ventricular myocardial remodeling

The aim of the study is to evaluate cardiac fatty acid binding protein as a prognostic biomarker for the occurrence of severe post-infarction structural and functional remodeling of the left ventricular myocardium and heart failure with clinical manifestations in patients with acute myocardial infarction during long-term follow-up. Material and methods. The study included 95 patients with acute myocardial infarction and ST-segment elevation (mean age 56.8 ± 9.8 years). Upon admission to the emergency room, all patients underwent clinical and laboratory studies to determine cardiac fatty acid binding protein (cFABP) and high-sensitivity troponin T (hs-TnT). At the end of the long-term follow-up (Me = 36 months), the patients were examined for clinically evident heart failure (NYHA functional class II and higher), high-sensitivity C-reactive protein (hsCRP) was determined in the blood, and echocardiography was performed. According to the echocardiography data, the presence and severity of structural and functional remodeling of the left ventricle myocardium (SFR LV) were established. Results. It was determined that the presence of clinically evident heart failure is directly associated with age, the Charlton comorbidity index, cFABP ≥10 ng/ml upon admission to the hospital and has a direct tendency to be associated with hs-TnT upon admission to the hospital. The presence of severe structural and functional remodeling of the left ventricle myocardium is directly associated with age, obesity, creatinine, cFABP ≥ 10 ng/ml and hs-TnT upon admission to hospital, and there is also a direct tendency towards an association with age. It was revealed that hs-TnT upon admission to hospital is directly associated with hsCRP ≥ 2 mg/l at the end of long-term followup. Conclusions. the presence of cFABP ≥ 10 ng/ml in the blood of patients with acute myocardial infarction upon admission to hospital is associated with an increase in the probability of developing clinically evident heart failure during long-term follow-up by 4.27 times, and severe structural and functional remodeling of the left ventricle myocardium is 3.07 times more likely, which is due to the size of the infarction lesion and the subsequent development of myocardial fibrosis.

Feeding Preferences and Salivary Protein Profiles of Spodoptera frugiperda on Saccharum Species.

The invasion of the fall armyworm poses substantial threats to local agricultural safety, including the sugarcane industry. Exploring the insect-resistance mechanism is crucial for breeding resistant varieties. This study selected three representative materials from the Saccharum genus─Saccharum officinarum L. (Badila), S. spp. hybrid (GT58), and Saccharum spontaneum (SES208), to investigate feeding preferences and developmental fitness of Spodoptera frugiperda. Larvae exhibited a strong preference and highest fitness parameters in Badila leaves compared to SES208. Additionally, proteomic analyses of larval saliva from insects feeding on Badila and SES208 were carried out to test the types and abundance of proteins on different hosts. Furthermore, we identified fatty acid-binding protein 1-like activates plant defense responses, while aldehyde dehydrogenase negatively suppressed plant defense response. Our findings suggest that the plasticity of salivary proteins induced by different host plants, and also offer new insights into the molecular interactions between S. frugiperda and plants.

Evaluation of Intestinal Permeability Using Serum Biomarkers in Learning Early About Peanut Allergy Trial.

Intestinal barrier dysfunction may lead to a break in tolerance and development of food allergy (FA). There is contradictory evidence on whether intestinal permeability (IP) is altered in IgE-mediated FA. Thus, we sought to determine whether IP differed between children with eczema who did (FA group) or did not (atopic controls, ACs) develop FA and whether peanut sensitization, allergy, and early introduction impacted IP using serum biomarkers zonulin, soluble CD14, and Intestinal Fatty Acid Binding Protein among randomly selected participants enrolled in the Learning Early About Peanut allergy trial. FA group was defined as having at least one FA at either baseline (4-11 months) or 60 months of age (V60). ACs had eczema at baseline and no FA at either visit. Serum IP markers (sIPMs) were measured by ELISA at baseline and V60, and their relationship with the clinical characteristics of participants was analyzed using parametric tests and linear regression models. We evaluated 237 FA subjects and 76 ACs. sIPM levels were similar in FA subjects and ACs at baseline and V60. Age when the child first developed any FA (< 1 year vs. > 1 year), eczema severity, peanut sensitization, peanut allergy, and early peanut introduction were not statistically significantly associated with sIPM levels. Total IgE and eosinophil levels, peanut-specific IgE, IgG4, and IgG4/IgE ratio were not correlated with sIPM levels. No differences in sIPMs were detected to support altered IP in infants with FA compared to ACs or following early peanut introduction among peanut-sensitized children.

Effects of long-term volleyball training on multimodal responses in adolescent female athletes: a follow-up study.

The aim of this study was to examine the effects of long-term (10 months) volleyball training on biochemical responses in adolescent female athletes since the cumulative effects of chronic training on this population are not yet clear. Twenty-one adolescent female volleyball players competing at the national level served as the participants. All athletes carried out volleyball training, which consisted of ball handling, specialized drills, and practical game-style exercises, including physical training in the school gymnasium. The average training cycle consisted of 6 days per week, with a total of about 2 to 2.5 hours of volleyball training per day. In order to determine the cumulative effects on autonomic, immune, renal function and bone resorption, salivary and urinary samples were collected before volleyball training on 3 consecutive days (days 1, 3 and 5) at months 0 and 10, respectively. No significant changes in body mass, salivary secretion rate, urinary albumin, L-type fatty acid binding protein and type I collagen cross-linked N-telopeptide concentration were found. In contrast, significant decreases were noted in salivary α-amylase activity (% change: -22.9), total protein (%change: -21.4), and immunoglobulin A concentration (% change: -20.1). The results of this study imply that the autonomic function after chronic volleyball training in adolescent female athletes may be enhanced due to training adaptation, although the immune function may be attenuated as a result of cumulative overtraining. Moreover, long-term volleyball training in adolescent female athletes appears to suppress bone resorption and not to induce cumulative damage to renal function.

Advanced Dual-Mode Microfluidic Sensing Platform Based on Amphiphilic Polymer-Capped Perovskite Nanozymes Induced Photoelectrochemical Signal Amplification and Fluorescence Emission.

A novel dual-mode microfluidic sensing platform integrating photoelectrochemical (PEC) and fluorescence (FL) sensors was developed for the sensitive monitoring of heart fatty acid binding protein (h-FABP). First, BiVO4/AgInS2 (BVAIS) composites with excellent photoelectric activity were synthesized as sensing matrices. The BVAIS heterojunction with a well-matched internal energy level structure provided a stable photocurrent. Second, an innovative signal amplification strategy based on octylamine-modified poly(acrylic acid) (OPA)-capped CsPbBr3 (OPCB) nanocrystals (NCs) with excellent catalytic activity and fluorescence property was proposed. On the OPCB nanozyme possessing ascorbate oxidase-like catalytic activity could catalyze the oxidation of ascorbic acid, which achieved quenching of the photocurrent signals by competitively consuming the electron donor. On the other hand, the OPCB NCs that overcame the water stability defect processed good luminescence performance and were able to produce obvious FL signals. Mutually verified dual-response signals effectively enhance the precision of test outcomes and avoid false-positive or false-negative results. Finally, the constructed microfluidic sensing platform realized sensitive detection of h-FABP in the linear range of 0.0001-150 ng/mL (PEC mode) and 0.001-150 ng/mL (FL mode), with detection limits of 36 fg/mL and 0.32 pg/mL, respectively. The present work provided a new perspective for designing an efficient dual-mode sensing strategy to achieve sensitive detection of disease markers.

Effects of Aneurysmal Subarachnoid Hemorrhage in Patients Without In-Hospital Infection on FABP-I, LBP, and sCD-14.

Aneurysmal subarachnoid hemorrhage (aSAH) is a serious condition complicated by delayed cerebral ischemia (DCI), where inflammation plays a key role. Although altered gut permeability is noted in other conditions, its significance in aSAH remains unclear. Fatty acid-binding protein (FABP-I), lipopolysaccharide-binding protein (LBP), and soluble CD-14 (sCD-14) are established markers of barrier dysfunction. This study investigates gut permeability marker changes in early and late aSAH phases. The study included 177 aSAH patients and 100 controls. Serum samples were collected on days 1 (D1) and 9 (D9) after ictus. FABP-I, LBP, and sCD-14 levels were measured via ELISA, and clinical data were recorded. Outcomes were assessed using the 90-day modified Rankin scale (mRS 0-3 = favorable outcome). Serum FABP-I was significantly lower in aSAH patients (p < 0.05), while LBP and sCD-14 were higher (p < 0.001) compared to controls. FABP-I did not differ between outcome groups, but LBP and sCD-14 were significantly elevated in unfavorable outcomes (p < 0.001). These markers differed in patients without in-hospital infection, with higher levels noted in DCI patients during the later phase (p < 0.05). In aSAH patients without infection, differences in LBP and sCD-14 levels between outcome groups suggest potential endotoxin release from microbial systems, contributing to neuroinflammation and influencing outcomes.