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(1) Introduction: Previous studies have found that diet can change gut microbiota, thereby affecting metabolic health. However, research on gestational diabetes mellitus (GDM) is still limited. Our study aimed to explore the mediating role of gut microbiota in the relationship between dietary patterns and GDM. (2) Methods: In this case-control study, 107 women with GDM at 24-28 weeks of gestation and 78 healthy pregnant women were enrolled. A semi-quantitative food frequency questionnaire (FFQ) was used to assess dietary intake over the previous month. Mediation analysis was performed to explore the link between dietary patterns, gut microbiota, and GDM. (3) Results: Among the five dietary patterns extracted, the high group (factor scores ≥ -0.07) of the vegetables-fruits dietary pattern had a 67% lower risk of developing GDM compared to the low group (factor scores < -0.07) (OR: 0.33; 95% CI: 0.15-0.74). In addition, a significant alteration was observed in gut microbiota composition among GDM pregnant women. Mediation analysis showed that the Lachnospiraceae family, Blautia, and Ruminococcus genus partially mediated the effect of vegetables-fruits dietary pattern on GDM, explaining 45.81%, 44.33%, and 31.53% of the association, respectively. (4) Conclusions: Adherence to vegetables-fruits dietary patterns during pregnancy may reduce the risk of GDM by altering gut microbiota composition.
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Diabetes Gestacional , Dieta , Frutas , Microbioma Gastrointestinal , Verduras , Humanos , Femenino , Diabetes Gestacional/microbiología , Embarazo , Adulto , Estudios de Casos y Controles , Dieta/estadística & datos numéricos , Conducta Alimentaria , Factores de Riesgo , Patrones DietéticosRESUMEN
Systemic lupus erythematosus (SLE) is a common autoimmune disease, and its pathogenesis mainly involves the aberrant activation of B cells through follicular helper T (Tfh) cells to produce pathogenic antibodies, which requires more effective and safe treatment methods. Dihydroartemisinin (DHA) is the main active ingredient of artemisinin and has immunosuppressive effects. In this study, in vitro experiments confirmed that DHA inhibited Tfh cell induction and weakened its auxiliary function in B cell differentiation; furthermore, DHA directly inhibited B cell activation, differentiation, and antibody production. Furthermore, a mouse model of SLE was established, and we confirmed that DHA significantly reduced the symptoms of SLE and lupus nephritis, and decreased serum immunoglobulin (Ig)G, IgM, IgA, and anti-dsDNA levels. Moreover, DHA reduced the frequencies of total Tfh cells, activated Tfh cells, and B cell lymphoma 6, and interleukin (IL)-21 levels in Tfh cells from the spleen and lymph nodes, as well as the levels of B cells, germinal center B cells, and plasma cells in the spleen, lymph nodes, and kidneys. Additionally, DHA inhibited Tfh cells by blocking IL-2-inducible T cell kinase (ITK) signaling and its downstream nuclear factor (NF)-κB, nuclear factor of activated T cell, and activating protein-1 pathways, and directly inhibited B cells by blocking Bruton's tyrosine kinase (BTK) signaling and the downstream NF-κB and Myc pathways. Overall, our results demonstrated that DHA inhibited Tfh cells by blocking ITK signaling and also directly inhibited B cells by blocking BTK signaling. Therefore, reducing the production of pathogenic antibodies might effectively treat SLE.
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Artemisininas , Linfocitos B , Lupus Eritematoso Sistémico , Artemisininas/farmacología , Animales , Lupus Eritematoso Sistémico/tratamiento farmacológico , Lupus Eritematoso Sistémico/inmunología , Lupus Eritematoso Sistémico/metabolismo , Ratones , Linfocitos B/efectos de los fármacos , Linfocitos B/inmunología , Linfocitos B/metabolismo , Linfocitos T Colaboradores-Inductores/efectos de los fármacos , Linfocitos T Colaboradores-Inductores/inmunología , Linfocitos T Colaboradores-Inductores/metabolismo , Femenino , Células T Auxiliares Foliculares/inmunología , Células T Auxiliares Foliculares/efectos de los fármacos , Células T Auxiliares Foliculares/metabolismo , Modelos Animales de Enfermedad , Diferenciación Celular/efectos de los fármacosRESUMEN
Despite the important breakthroughs of immune checkpoint inhibitors in recent years, the objective response rates remain limited. Here, we synthesize programmed cell death protein-1 (PD-1) antibody-iRGD cyclic peptide conjugate (αPD-1-(iRGD)2) through glycoengineering methods. In addition to enhancing tissue penetration, αPD-1-(iRGD)2 simultaneously engages tumor cells and PD-1+ T cells via dual targeting, thus mediating tumor-specific T cell activation and proliferation with mild effects on non-specific T cells. In multiple syngeneic mouse models, αPD-1-(iRGD)2 effectively reduces tumor growth with satisfactory biosafety. Moreover, results of flow cytometry and single-cell RNA-seq reveal that αPD-1-(iRGD)2 remodels the tumor microenvironment and expands a population of "better effector" CD8+ tumor infiltrating T cells expressing stem- and memory-associated genes, including Tcf7, Il7r, Lef1, and Bach2. Conclusively, αPD-1-(iRGD)2 is a promising antibody conjugate therapeutic beyond antibody-drug conjugate for cancer immunotherapy.
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Receptor de Muerte Celular Programada 1 , Microambiente Tumoral , Animales , Receptor de Muerte Celular Programada 1/inmunología , Receptor de Muerte Celular Programada 1/antagonistas & inhibidores , Ratones , Microambiente Tumoral/inmunología , Microambiente Tumoral/efectos de los fármacos , Humanos , Línea Celular Tumoral , Linfocitos T/inmunología , Linfocitos T/efectos de los fármacos , Ratones Endogámicos C57BL , Oligopéptidos/química , Oligopéptidos/farmacología , Linfocitos T CD8-positivos/inmunología , Linfocitos T CD8-positivos/efectos de los fármacos , Inmunoconjugados/farmacología , Inmunoconjugados/química , Femenino , Activación de Linfocitos/efectos de los fármacos , Activación de Linfocitos/inmunología , Linfocitos Infiltrantes de Tumor/inmunología , Linfocitos Infiltrantes de Tumor/efectos de los fármacos , Inhibidores de Puntos de Control Inmunológico/farmacologíaRESUMEN
Functional gastrointestinal disorders (FGIDs) are common digestive system diseases in children, which can severely affect the growth and development of infants and toddlers. Probiotics therapy, as a relatively safe treatment method, have attracted the attention of researchers. However, their effectiveness in treating FGIDs in infants and toddlers is still unclear. This article reviews the mechanisms of probiotics in treating FGIDs in infants and toddlers, explores the reasons for the inconsistency in various research results, and aims to provide assistance for the clinical treatment of FGIDs in infants and toddlers and future research.
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Enfermedades Gastrointestinales , Probióticos , Humanos , Probióticos/uso terapéutico , Enfermedades Gastrointestinales/terapia , Lactante , PreescolarRESUMEN
(1) Background: With autistic children's high pervasiveness of eating problems and inappropriate feeding behaviors by their caregivers, this study wanted to inspect the connection between caregivers' pressure to eat and food neophobia in these children. (2) Methods: Cross-sectional overview of 160 guardians of kids aged 2 to 7 years. After one-on-one questioning by the researcher, the collected information on the socio-demographic characteristics of the children with autism, caregiver feeding behavior, and new food neophobia (FN) scores was entered into the Questionnaire Star system. (3) Results: The mean FN score was 25.56 ± 6.46. The caregiver's pressure to eat positively related to children's FN (ß = 0.164 95% CI, 0.078, 2.163). In these children, we found a negative correlation between FN score and the frequency of vegetable intake (p ≤ 0.001), fruit intake (p ≤ 0.05), aquatic product intake (p ≤ 0.05), and dietary diversity score (p ≤ 0.01), and positively correlated with the frequency of snack intake (p ≤ 0.05). (4) Conclusions: Caregiver pressure to eat was positively associated with high levels of FN in Chinese kids with ASD, which in turn negatively impacted dietary quality. To improve eating habits, caregivers should reconsider their feeding strategies and avoid using forceful methods to ease food neophobia in these children.
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Mesenchymal stem cells (MSCs) have demonstrated potent immunomodulatory properties that have shown promise in the treatment of autoimmune diseases, including rheumatoid arthritis (RA). However, the inherent heterogeneity of MSCs triggered conflicting therapeutic outcomes, raising safety concerns and limiting their clinical application. This study aimed to investigate the potential of extracellular vesicles derived from human gingival mesenchymal stem cells (GMSC-EVs) as a therapeutic strategy for RA. Through in vivo experiments using an experimental RA model, our results demonstrate that GMSC-EVs selectively homed to inflamed joints and recovered Treg and Th17 cell balance, resulting in the reduction of arthritis progression. Our investigations also uncovered miR-148a-3p as a critical contributor to the Treg/Th17 balance modulation via IKKB/NF-κB signaling orchestrated by GMSC-EVs, which was subsequently validated in a model of human xenograft versus host disease (xGvHD). Furthermore, we successfully developed a humanized animal model by utilizing synovial fibroblasts obtained from patients with RA (RASFs). We found that GMSC-EVs impeded the invasiveness of RASFs and minimized cartilage destruction, indicating their potential therapeutic efficacy in the context of patients with RA. Overall, the unique characteristics - including reduced immunogenicity, simplified administration, and inherent ability to target inflamed tissues - position GMSC-EVs as a viable alternative for RA and other autoimmune diseases.
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Artritis Reumatoide , Vesículas Extracelulares , Células Madre Mesenquimatosas , MicroARNs , FN-kappa B , Linfocitos T Reguladores , Células Th17 , Artritis Reumatoide/terapia , Artritis Reumatoide/inmunología , Artritis Reumatoide/metabolismo , Humanos , Animales , Células Th17/inmunología , Células Th17/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , FN-kappa B/metabolismo , Linfocitos T Reguladores/inmunología , Linfocitos T Reguladores/metabolismo , Ratones , Células Madre Mesenquimatosas/metabolismo , Células Madre Mesenquimatosas/inmunología , Vesículas Extracelulares/metabolismo , Vesículas Extracelulares/trasplante , Quinasa I-kappa B/metabolismo , Transducción de Señal , Modelos Animales de Enfermedad , Encía/citología , Encía/metabolismo , Encía/patología , Encía/inmunología , Masculino , Fibroblastos/metabolismoRESUMEN
The substantial utilization of antibiotics causes their "pseudo-persistence" in offshore environments. Published studies on antibiotic surveillance in food webs have primarily emphasized on parent forms; however, the compositions and concentrations of conjugated antibiotics in aquatic organisms remain largely unexplored. This study systematically examined the distribution characteristics and trophodynamics of free antibiotics and their conjugated forms in an estuarine food web. Total antibiotic levels differed insignificantly between the surface and bottom waters. The total mean values of free antibiotics in crabs, fish, shrimps, sea cucumbers, and snails varied from 0.77 to 1.4 ng/g (wet weight). The numbers and values of antibiotics rose in these biological samples after enzymatic hydrolysis. Conjugated antibiotics accounted for 23.8-76.9% of the total antibiotics in the biological samples, revealing that conjugated forms play a non-negligible role in aquatic organisms. More number of antibiotics exhibited bioaccumulation capabilities after enzymatic hydrolysis. In the food web, the free forms of anhydroerythromycin and conjugated forms of trimethoprim and ciprofloxacin underwent trophic dilution, whereas the free forms of trimethoprim and conjugated forms of ofloxacin underwent trophic amplification. The present work provides new insights into the bioaccumulation and trophic transfer of free and conjugated antibiotics in food webs.
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Cadena Alimentaria , Contaminantes Químicos del Agua , Animales , Antibacterianos/análisis , Bioacumulación , Multimedia , Contaminantes Químicos del Agua/análisis , Organismos Acuáticos , Peces , Trimetoprim , Monitoreo del Ambiente , ChinaRESUMEN
Rheumatoid arthritis is an autoimmune disease characterized by synovium hyperplasia and bone destruction. Macrophage extracellular traps are released from macrophages under various stimuli and may generate stable autoantigen-DNA complexes, as well as aggravate autoantibody generation and autoimmune responses. We aimed to investigate the role of macrophage extracellular traps on the biologic behaviors of rheumatoid arthritis fibroblast-like synoviocytes. Synovial tissues and fibroblast-like synoviocytes were obtained from patients with rheumatoid arthritis. Extracellular traps in synovium and synovial fluids were detected by immunofluorescence, immunohistochemistry, and SYTOX Green staining. Cell viability, migration, invasion, and cytokine expression of rheumatoid arthritis fibroblast-like synoviocytes were assessed by CCK-8, wound-healing assay, Transwell assays, and quantitative real-time polymerase chain reaction, respectively. RNA sequencing analysis was performed to explore the underlying mechanism, and Western blot was used to validate the active signaling pathways. We found that extracellular trap formation was abundant in rheumatoid arthritis and positively correlated to anti-CCP. Rheumatoid arthritis fibroblast-like synoviocytes stimulated with purified macrophage extracellular traps demonstrated the obvious promotion in tumor-like biologic behaviors. The DNA sensor cGAS in rheumatoid arthritis fibroblast-like synoviocytes was activated after macrophage extracellular trap stimuli. RNA sequencing revealed that differential genes were significantly enriched in the PI3K/Akt signaling pathway, and cGAS inhibitor RU.521 effectively reversed the promotion of tumor-like biologic behaviors in macrophage extracellular trap-treated rheumatoid arthritis fibroblast-like synoviocytes and downregulated the PI3K/Akt activation. In summary, our study demonstrates that macrophage extracellular traps promote the pathogenically biological behaviors of rheumatoid arthritis fibroblast-like synoviocytes through cGAS-mediated activation of the PI3K/Akt signaling pathway. These findings provide a novel insight into the pathogenesis of rheumatoid arthritis and the mechanisms of macrophages in modulating rheumatoid arthritis fibroblast-like synoviocyte tumor-like behaviors.
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Artritis Reumatoide , Productos Biológicos , Trampas Extracelulares , Neoplasias , Sinoviocitos , Humanos , Sinoviocitos/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Trampas Extracelulares/metabolismo , Proliferación Celular , Transducción de Señal , Artritis Reumatoide/patología , Nucleotidiltransferasas , Neoplasias/patología , Fibroblastos , ADN/metabolismo , Productos Biológicos/farmacología , Células CultivadasRESUMEN
Focal iron overload is frequently observed in patients with rheumatoid arthritis (RA), yet its functional significance remains elusive. Herein, we report that iron deposition in lesion aggravates arthritis by inducing macrophage ferroptosis. We show that excessive iron in synovial fluid positively correlates with RA disease severity as does lipid hyperoxidation of focal monocyte/macrophages. Further study reveals high susceptibility to iron induced ferroptosis of the anti-inflammatory macrophages M2, while pro-inflammatory M1 are less affected. Distinct glutathione peroxidase 4 (GPX4) degradation depending on p62/SQSTM1 in the two cell types make great contribution mechanically. Of note, ferroptosis inhibitor liproxstatin-1 (LPX-1) can alleviate the progression of K/BxN serum-transfer induced arthritis (STIA) mice accompanied with increasing M2 macrophages proportion. We thus propose that the heterogeneous ferroptosis susceptibility of macrophage subtypes as well as consequent inflammation and immune disorders are potential biomarkers and therapeutic targets in RA.
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Artritis Reumatoide , Ferroptosis , Sobrecarga de Hierro , Humanos , Ratones , Animales , Artritis Reumatoide/metabolismo , Macrófagos/metabolismo , Sobrecarga de Hierro/patología , Hierro/metabolismoRESUMEN
AIM OF THE STUDY: Naoxinqing (NXQ) tablets are derived from persimmon leaves and are widely used in China for promoting blood circulation and removing blood stasis in China. We aimed to explore whether NXQ has the therapeutic effect on ischemic stroke and explored its possible mechanism. MATERIALS AND METHODS: The cerebral artery occlusion/reperfusion (MCAO/R) surgery was used to establish the cerebral ischemic/reperfusion rat model. NXQ (60 mg/kg and 120 mg/kg) were administered orally. The TTC staining, whole brain water content, histopathology staining, immunofluorescent staining, enzyme-linked immunosorbent assay (ELISA) and Western blot analyses were performed to determine the therapeutical effect of NXQ on MCAO/R rats. RESULTS: The study demonstrated that NXQ reduced the cerebral infarction volumes and neurologic deficits in MCAO/R rats. The neuroprotective effects of NXQ were accompanied by inhibited oxidative stress and inflammation. The nerve regeneration effects of NXQ were related to regulating the AMPKα/NAMPT/SIRT1/PGC-1α pathway. CONCLUSION: In summary, our results revealed that NXQ had a significant protective effect on cerebral ischemia-reperfusion injury in rats. This study broadens the therapeutic scope of NXQ tablets and provides new neuroprotective mechanisms of NXQ as an anti-stroke therapeutic agent.
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Isquemia Encefálica , Enfermedades Metabólicas , Fármacos Neuroprotectores , Daño por Reperfusión , Accidente Cerebrovascular , Ratas , Animales , Sirtuina 1/metabolismo , Accidente Cerebrovascular/tratamiento farmacológico , Encéfalo , Isquemia Encefálica/metabolismo , Enfermedades Metabólicas/tratamiento farmacológico , Daño por Reperfusión/tratamiento farmacológico , Daño por Reperfusión/prevención & control , Daño por Reperfusión/metabolismo , Infarto de la Arteria Cerebral Media/patología , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Fármacos Neuroprotectores/metabolismoRESUMEN
IL-2 inducible T cell kinase (ITK) is critical in T helper subset differentiation and its inhibition has been suggested for the treatment of T cell-mediated inflammatory diseases. T follicular helper (Tfh), Th17 and regulatory T cells (Treg) also play important roles in the development of rheumatoid arthritis (RA), while the role of ITK in the development of RA and the intricate balance between effector T and regulatory T cells remains unclear. Here, we found that CD4+ T cells from RA patients presented with an elevated ITK activation. ITK inhibitor alleviated existing collagen-induced arthritis (CIA) and reduced antigen specific antibody production. Blocking ITK kinase activity interferes Tfh cell generation. Moreover, ITK inhibitor effectively rebalances Th17 and Treg cells by regulating Foxo1 translocation. Furthermore, we identified dihydroartemisinin (DHA) as a potential ITK inhibitor, which could inhibit PLC-γ1 phosphorylation and the progression of CIA by rebalancing Th17 and Treg cells. Out data imply that ITK activation is upregulated in RA patients, and therefore blocking ITK signal may provide an effective strategy to treat RA patients and highlight the role of ITK on the Tfh induction and RA progression.
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Artritis Experimental , Artritis Reumatoide , Enfermedades Autoinmunes , Animales , Humanos , Artritis Experimental/tratamiento farmacológico , Artritis Reumatoide/tratamiento farmacológico , Diferenciación Celular , Linfocitos T Reguladores , Células Th17RESUMEN
OBJECTIVE: This research was devoted to estimating the outcomes of ginsenoside Rg1 on learning and memory ability and neuronal apoptosis in epileptic rats through ERK/CREB/BDNF pathway. METHODS: The epileptic rats induced by lithium chloride were stochastically separated into model subgroup, ginsenoside Rg1 different dose subgroups. The ginsenoside Rg1 subgroups were given 20, 30 and 40 mg/kg ginsenoside Rg1 by gavage individually. Another 6 normal rats were selected as the control subgroup. The seizures of each subgroup were estimated. Morris water maze was utilized for estimating the changes of cognitive function changes of rats. The injury and apoptosis of hippocampal neurons in each subgroup were detected by Nissl and TUNEL assays. HE staining was applied for the structural and pathomorphological changes of hippocampal neurons detection. The oxidative stress level in hippocampus of rats was estimated by ELISA. DCFH-DA probe was applied for the changes of reactive oxygen species (ROS) in brain tissue detection. The Bcl-2, Bax, ERK, p-ERK, CREB, p-CREB and BDNF levels in cerebral cortex were estimated by western blot, and PD98059, a blocker of ERK pathway, was used to intervene. RESULTS: In the control subgroup, Nissl bodies were abundant and evenly distributed, and cortical neurons were arranged neatly. In the model subgroup, the cytoplasmic staining of cortical neurons was insufficient and the arrangement of neurons was disordered. After treatment with ginsenoside Rg1, the morphology of neurons in the cerebral cortex was restored. The frequency of seizures, duration of seizures, Racine grade, escape latency, target quadrant residence time, MDA, TNF-α and ROS levels of cerebral cortex in the model subgroup boosted notablely versus the control subgroup. The frequency of crossing the original platform, the activity of SOD, the IL-10, p-ERK/ERK, p-CREB/CREB and BDNF levels in cerebral cortex were notablely lessened. The above-mentioned indexes in the ginsenoside Rg1 subgroup were notablely improved versus the model subgroup, and the three proteins levels in the PD98059 intervention subgroup were notablely lower. CONCLUSION: Ginsenoside Rg1 can improve cognitive dysfunction in epileptic rats, which may be concerned with ERK/CREB/BDNF pathway activation in cerebral cortex and lessening oxidative stress and inflammation.
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Factor Neurotrófico Derivado del Encéfalo , Ginsenósidos , Ratas , Animales , Sistema de Señalización de MAP Quinasas , Especies Reactivas de Oxígeno , Transducción de Señal , Ginsenósidos/farmacología , Hipocampo , Apoptosis , ConvulsionesRESUMEN
Background: Chinese college students used to eat in student canteens, making dietary consumption outside the cafeterias the main reason for the difference in sodium intake. This study aims to develop and validate a food frequency questionnaire (Sodium-FFQ) targeting dietary sodium intake outside the canteens among undergraduates in China. Methods: This cross-sectional study included 124 and 81 college students from comprehensive universities in the development and validation stage. A 24 h dietary recall and a food frequency questionnaire were used to develop the Sodium-FFQ. Food items were selected according to the foods that contributed more to the total sodium intake. Test-retest correlation coefficients with an interval of 14 days were employed to evaluate reproducibility. Validity was assessed against a single 24 h urine collection and a 3-day dietary record using correlation coefficients, Bland-Altman analyses, and cross-classification analysis of Kappa coefficients. Results: The Sodium-FFQ consists of 12 groups of foods with 48 items. The Spearman correlation coefficient of test-retest on sodium intake was 0.654 (p < 0.05), and that between the Sodium-FFQ, 3 × 24 h dietary record, and 24-h urinary sodium were 0.393 (p < 0.05) and 0.342 (p < 0.05), respectively. The Sodium-FFQ was correlated to 24 h urinary sodium-to-potassium ratio, with a Spearman coefficient of 0.370 (p < 0.05). The classification agreement of the Sodium-FFQ and 24 h urinary sodium was 68.4%, and the Kappa coefficient was 0.371 (p < 0.001). Conclusion: The Sodium-FFQ developed in this study presented an acceptable reproducibility, validity, and classification agreement. It indicates that the Sodium-FFQ could be a potential tool for promoting sodium restriction in college students.
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Macrophages play a critical role in ankylosing spondylitis by promoting autoimmune tissue inflammation through various effector functions. The inflammatory potential of macrophages is highly influenced by their metabolic environment. Here, we demonstrate that glycolysis is linked to the proinflammatory activation of human blood monocyte-derived macrophages in ankylosing spondylitis. Specifically, ankylosing spondylitis macrophages produced excessive inflammation, including TNFα, IL1ß, and IL23, and displayed an overactive status by exhibiting stronger costimulatory signals, such as CD80, CD86, and HLA-DR. Moreover, we found that patient-derived monocyte-derived M1-type macrophages (M1 macrophages) exhibited intensified glycolysis, as evidenced by a higher extracellular acidification rate. Upregulation of PKM2 and GLUT1 was observed in ankylosing spondylitis-derived monocytes and monocyte-derived macrophages, especially in M1 macrophages, indicating glucose metabolic alteration in ankylosing spondylitis macrophages. To investigate the impact of glycolysis on macrophage inflammatory ability, we treated ankylosing spondylitis M1 macrophages with 2 inhibitors: 2-deoxy-D-glucose, a glycolysis inhibitor, and shikonin, a PKM2 inhibitor. Both inhibitors reduced proinflammatory function and reversed the overactive status of ankylosing spondylitis macrophages, suggesting their potential utility in treating the disease. These data place PKM2 at the crosstalk between glucose metabolic changes and the activation of inflammatory macrophages in patients with ankylosing spondylitis.
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Espondilitis Anquilosante , Humanos , Espondilitis Anquilosante/metabolismo , Activación de Macrófagos , Macrófagos/metabolismo , Inflamación/metabolismo , Glucosa/metabolismoRESUMEN
(1) Background: Insufficient evidence exists regarding the dietary habits that may contribute to high sodium intake among college students in China. This cross-sectional study aimed to investigate the dietary sodium intake of college students in Hunan and its association with their dietary habits. (2) Methods: In total, 585 university students from Hunan were recruited for this study. The sodium Food Frequency Questionnaire (sodium-FFQ) and dietary habits were assessed. (3) Results: Excluding cooking salt and high-sodium seasonings, the daily dietary sodium intake among college students in Changsha, Hunan Province, was 1183.74 (563.38, 2054.86) mg/day. A vast majority (89%) of college students reported eating outside of school at least once a week, and approximately one-third (34%) ordered takeaways at least once a week. After adjusting for confounding factors, the associations between the frequency of eating out and ordering takeaways with college students' sodium intake remained significant. (4) Conclusions: The findings indicate that excessive dietary sodium intake among college students in Hunan is a growing concern. College students who frequently eat out and order takeaways tend to have a higher sodium intake. Future research should focus on identifying the main sources of dietary sodium and developing interventions that promote healthy dietary habits among college students.
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Conducta Alimentaria , Sodio en la Dieta , Humanos , Universidades , Estudios Transversales , Sodio , Estudiantes , Ingestión de AlimentosRESUMEN
Steroids have attracted particular attention as environmental contaminants because of their severe endocrine-disrupting effects. Previous studies have predominantly focused on parent steroids; however, the levels and proportions of the free and conjugated forms of their metabolites remain largely unclear, especially in food webs. Here, we first characterized the free and conjugated forms of parent steroids and their metabolites in 26 species in an estuarine food web. The steroids were dominated by their metabolites in water samples, whereas parent compounds were predominant in sediment samples. The total mean steroid concentrations in the biota samples that underwent non-enzymatic hydrolysis decreased in the following order: crabs (27 ng/g) > fish (5.9 ng/g) > snails (3.4 ng/g) > shrimps and sea cucumbers (1.2 ng/g); and those in the biota samples that underwent enzymatic hydrolysis decreased in the following order: crabs (57 ng/g) > snails (9.2 ng/g) > fish (7.9 ng/g) > shrimps and sea cucumbers (3.5 ng/g). The proportion of metabolites in the enzymatic hydrolysis biota samples was higher (38-79%) than that (2.9-65%) in non-enzymatic ones, indicating that the free and conjugated forms of metabolites in aquatic organisms were not negligible. Most synthetic steroids were either bioaccumulative or highly bioaccumulative. Importantly, in the invertebrate food web, 17α-methyltestosterone was biomagnified, while 17ß-boldenone underwent trophic dilution. Although the estuarine water had a median ecological risk level, the health risks via aquatic product consumption were very low. This study provides novel insights into the composition and trophic transfer of steroids in an estuarine food web for the first time and highlights that free and conjugated metabolites should receive more attention, particularly in biota samples.
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Cadena Alimentaria , Contaminantes Químicos del Agua , Animales , Monitoreo del Ambiente , Contaminantes Químicos del Agua/análisis , Peces , Esteroides/metabolismo , Agua , ChinaRESUMEN
In recent years, microplastics (MPs) as emerging carriers for environmental pollutants have attracted increasing worldwide attention. However, the adsorption of heavy metals on MPs, especially for biodegradable MPs, has been still poorly understood in estuarine environments. In this study, we investigated the aging of biodegradable and conventional MPs in the Pearl River Estuary after long-term exposure and their impacts on the adsorption of heavy metals from seawater. The results showed that the changes in surface characteristics were more prominent on biodegradable MPs than on conventional MPs after aging. Both biodegradable and conventional MPs could adsorb heavy metals, and their adsorption capacities fluctuated greatly on different MPs and different exposure times. The adsorption capacities of Cu, Pb, and As on biodegradable MPs were higher than those on conventional MPs, whereas Mn, Cr, and Co had lower adsorption on biodegradable MPs after 9-12 months by inductively coupled plasma-mass spectrometry (ICP-MS). The aging characteristics (CI, O/C, and Xc) of MPs accounted for a contribution of 51.0% on heavy metal adsorption, while the environmental factors (temperature, salinity, pH, and heavy metal concentration) only contributed to 13.2%. Therefore, the present study can provide important evidence on the environmental behaviors and ecological risks of biodegradable and conventional MPs in estuarine systems.
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Metales Pesados , Contaminantes Químicos del Agua , Microplásticos/química , Plásticos , Adsorción , Ríos , Estuarios , Contaminantes Químicos del Agua/análisis , Metales Pesados/análisis , ChinaRESUMEN
The production and use of hexabromocyclododecanes (HBCDs) have been strictly limited due to their persistence, toxicity and bioaccumulation. However, the release of HBCDs from related products and wastes would continue for a long time, which may cause many environmental problems. In this study, we investigated the occurrence and distribution of HBCDs and microplastics (MPs) in aquatic organisms inhabiting different substrates. HBCDs were measurable in the seawater, sediment, expanded polystyrene (EPS) substrates and organism samples. Mostly, the concentrations of HBCDs in organisms inhabiting EPS buoys were significantly higher than those of the same species inhabiting other substrates. Meanwhile, the diastereomeric ratio (α/γ) of HBCDs in organisms inhabiting EPS buoys was closer to that in EPS buoys. The fugacity values of HBCDs in EPS buoys were much higher than those in other media, implying that HBCDs can be transferred from EPS buoys to other media. Additionally, MPs derived from EPS buoys would be mistaken as food and ingested by aquatic organisms. The transfer of HBCDs from EPS buoys to aquatic organisms can be achieved by aqueous and dietary exposures. In combination, the contribution of MP ingestion to HBCDs for aquatic organisms should be very limited. These results supported EPS buoys as an important source of HBCDs for the aquatic ecosystem. To effectively control HBCDs pollution, it is necessary to discontinue or reduce the use of EPS buoys.
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Hidrocarburos Bromados , Contaminantes Químicos del Agua , Poliestirenos/análisis , Ecosistema , Plásticos , Monitoreo del Ambiente , Hidrocarburos Bromados/análisis , Organismos Acuáticos , Contaminantes Químicos del Agua/análisisRESUMEN
This study aimed to investigate the relationship between anxiety, depression, and gut microbiota in elderly patients with FC. METHODS: in this cross-sectional study, a total of 198 elderly participants (85 male and 113 female) aged over 60 years were recruited. The study was conducted in Changsha city, China. The participants completed an online questionnaire, including The Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), The Patient Assessment of Symptoms (PAC-SYM), and The Patient Assessment of Quality of Life (PAC-QoL). We selected the 16S rDNA V3 + V4 region as the amplification region and sequenced the gut microbiota using the Illumina Novaseq PE250 high-throughput sequencing platform. RESULTS: in total, 30.3% of patients with constipation had depression, while 21.3% had anxiety. The relative abundance of intestinal microbiota in the normal group was higher than that in the anxiety and depression group. According to LEfSe analysis, the relative abundance of g_Peptoniphilus and g_Geobacter in the people without depression and anxiety was higher. The relative abundance of g_Pseudoramibacter-Eubacterium and g_Candidatus-Solibacter in the depression group was lower, and the relative abundance of g_Bacteroides and g_Paraprevotella, g_Cc_115 in the anxiety group was higher. In addition, according to the correlation analysis, g_Aquicella and g_Limnohabitans were negatively correlated with constipation symptoms, anxiety, and depression. CONCLUSIONS: this study found that gut microbiota composition may be associated with a higher incidence of anxiety and depression in patients with FC, thus providing insight into the mechanisms that ameliorate mood disorders in patients with FC.
Asunto(s)
Microbioma Gastrointestinal , Anciano , Humanos , Masculino , Femenino , Persona de Mediana Edad , Calidad de Vida , Estudios Transversales , Pueblos del Este de Asia , Ansiedad/epidemiología , Estreñimiento/epidemiología , Clostridiales , Depresión/epidemiologíaRESUMEN
BACKGROUND: Previous studies have shown that berberine can inhibit glioma progression, although the underlying molecular mechanisms needed to be explored further. The aim of this study was to evaluate the suppressive effects of berberine on human glioma cells, and identify the underlying signaling pathways. MATERIAL AND METHODS: The cytotoxic effect of different concentrations of berberine against normal human glial cells (HEB) and 4 glioma cell lines was evaluated by the CCK-8 assay. Apoptosis was assayed by flow cytometry. In vitro migration and invasion were analyzed by the wound healing and transwell assays. The expression levels of specific proteins were measured by western blotting and ELISA. RESULTS: Berberine significantly inhibited the proliferation of human glioma U-87 cells, and induced apoptosis in the U-87 and LN229 cells by downregulating Bcl-2, and upregulating Bax and caspase-3. In addition, berberine also inhibited migration and invasion of the glioma cells. Furthermore, berberine exerted its effects on the proliferation, migration, invasion, and apoptosis of glioma cells by inhibiting the TGF-ß1/SMAD2/3 signaling pathway, and exogenous TGF-ß abrogated the pro-apoptotic and anti-oncogenic effects of berberine. CONCLUSIONS: Berberine inhibits glioma progression by targeting the TGF-ß1/SMAD2/3 signaling pathway.