Doris González-Fernández, Oviya Muralidharan, Paulo A Neves, Zulfiqar A Bhutta
Background/objectives: Despite advances in maternal nutritional knowledge, the effect of maternal diet, micronutrient status and undernutrition, and the effect of maternal supplementation on fetal, neonatal and infant outcomes still have gaps in the literature. This overview of reviews is intended to assess the available information on these issues and identify the main maternal nutritional factors associated with offspring outcomes in low- and middle-income countries as possible targets for public health interventions.
Methods: The literature search was performed in Medline (PubMed) and Cochrane Library datasets in June 2024. Pre-specified outcomes in offspring were pooled using standard meta-analytical methods.
Results: We found consistent evidence on the impact of maternal undernutrition indicated by low body mass index (BMI), mid-upper arm circumference (MUAC), and stature, but not of individual micronutrient status, on intrauterine-growth retardation, preterm birth, low birth weight, and small for gestational age, with research showing a possible effect of maternal undernutrition in later child nutritional status. Studies on micronutrient supplementation showed possible beneficial effects of iron, vitamin D, and multiple micronutrients on birthweight and/or decreasing small for gestational age, as well as a possible effect of calcium on preterm birth reduction. Interventions showing more consistent beneficial outcomes were balanced protein-energy and lipid base supplements, which demonstrated improved weight in newborns from supplemented mothers and a decreased risk of adverse neonatal outcomes.
Conclusions: Further research is needed to identify the benefits and risks of maternal individual micronutrient supplementation on neonatal and further child outcomes.
{"title":"Associations of Maternal Nutritional Status and Supplementation with Fetal, Newborn, and Infant Outcomes in Low-Income and Middle-Income Settings: An Overview of Reviews.","authors":"Doris González-Fernández, Oviya Muralidharan, Paulo A Neves, Zulfiqar A Bhutta","doi":"10.3390/nu16213725","DOIUrl":"10.3390/nu16213725","url":null,"abstract":"<p><strong>Background/objectives: </strong>Despite advances in maternal nutritional knowledge, the effect of maternal diet, micronutrient status and undernutrition, and the effect of maternal supplementation on fetal, neonatal and infant outcomes still have gaps in the literature. This overview of reviews is intended to assess the available information on these issues and identify the main maternal nutritional factors associated with offspring outcomes in low- and middle-income countries as possible targets for public health interventions.</p><p><strong>Methods: </strong>The literature search was performed in Medline (PubMed) and Cochrane Library datasets in June 2024. Pre-specified outcomes in offspring were pooled using standard meta-analytical methods.</p><p><strong>Results: </strong>We found consistent evidence on the impact of maternal undernutrition indicated by low body mass index (BMI), mid-upper arm circumference (MUAC), and stature, but not of individual micronutrient status, on intrauterine-growth retardation, preterm birth, low birth weight, and small for gestational age, with research showing a possible effect of maternal undernutrition in later child nutritional status. Studies on micronutrient supplementation showed possible beneficial effects of iron, vitamin D, and multiple micronutrients on birthweight and/or decreasing small for gestational age, as well as a possible effect of calcium on preterm birth reduction. Interventions showing more consistent beneficial outcomes were balanced protein-energy and lipid base supplements, which demonstrated improved weight in newborns from supplemented mothers and a decreased risk of adverse neonatal outcomes.</p><p><strong>Conclusions: </strong>Further research is needed to identify the benefits and risks of maternal individual micronutrient supplementation on neonatal and further child outcomes.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Catherine Saenz, David J Sanders, Samantha J Brooks, Lacey Bracken, Aydan Jordan, Justen Stoner, Emaly Vatne, Marley Wahler, Ann F Brown
Background: This study's purpose was to evaluate the relationship between dance training volume, body composition, and habitual diet in female collegiate dancers.
Methods: Thirty-three female collegiate dancers from three dance programs (20.4 ± 1.05 yrs.; 165.4 ± 11.3 cm, BMI 21.3 ± 3.4 kg/m2) participated in "The Intercollegiate Artistic Athlete Research Assessment (TIAARA)" study. We assessed dance training volume, body composition, and habitual diet. Data were analyzed using descriptive statistics (means ± SD). Two-sample t-tests were conducted to compare reported intake values versus sports nutrition recommendations. Two-tailed Pearson correlations (r) were computed for body composition and dietary intake (p < 0.05).
Results: Collegiate dancers were enrolled in 16 ± 2.09 semester credits, with 7.7 ± 3.8 credits as dance movement courses and an additional 3.0 ± 1.5 h/week of rehearsal time. Body composition assessments included fat mass (24.4 ± 6.8%), lean mass (LM) (42.4 ± 10.1 kg), and total body water (32.6 ± 4.6 L). Habitual diets reflected a low-calorie diet (1399 ± 648 kcal/d), with ~20% of dancers consuming a very low-calorie diet (≤1000 kcal/d). Dancers reported under-consuming dietary protein (54.3 ± 26.2 g) and carbohydrate (171.8 ± 77.8 g). LM was positively correlated with daily total energy (r = 0.333), fat (r = 0.37), protein (r = 0.349), and leucine intake (r = 0.352).
Conclusions: Our findings emphasize the positive effect of adequate nutritional quantity and quality on body composition in female collegiate dancers.
{"title":"The Relationship Between Dance Training Volume, Body Composition, and Habitual Diet in Female Collegiate Dancers: The Intercollegiate Artistic Athlete Research Assessment (TIAARA) Study.","authors":"Catherine Saenz, David J Sanders, Samantha J Brooks, Lacey Bracken, Aydan Jordan, Justen Stoner, Emaly Vatne, Marley Wahler, Ann F Brown","doi":"10.3390/nu16213733","DOIUrl":"10.3390/nu16213733","url":null,"abstract":"<p><strong>Background: </strong>This study's purpose was to evaluate the relationship between dance training volume, body composition, and habitual diet in female collegiate dancers.</p><p><strong>Methods: </strong>Thirty-three female collegiate dancers from three dance programs (20.4 ± 1.05 yrs.; 165.4 ± 11.3 cm, BMI 21.3 ± 3.4 kg/m<sup>2</sup>) participated in \"The Intercollegiate Artistic Athlete Research Assessment (TIAARA)\" study. We assessed dance training volume, body composition, and habitual diet. Data were analyzed using descriptive statistics (means ± SD). Two-sample <i>t</i>-tests were conducted to compare reported intake values versus sports nutrition recommendations. Two-tailed Pearson correlations (r) were computed for body composition and dietary intake (<i>p</i> < 0.05).</p><p><strong>Results: </strong>Collegiate dancers were enrolled in 16 ± 2.09 semester credits, with 7.7 ± 3.8 credits as dance movement courses and an additional 3.0 ± 1.5 h/week of rehearsal time. Body composition assessments included fat mass (24.4 ± 6.8%), lean mass (LM) (42.4 ± 10.1 kg), and total body water (32.6 ± 4.6 L). Habitual diets reflected a low-calorie diet (1399 ± 648 kcal/d), with ~20% of dancers consuming a very low-calorie diet (≤1000 kcal/d). Dancers reported under-consuming dietary protein (54.3 ± 26.2 g) and carbohydrate (171.8 ± 77.8 g). LM was positively correlated with daily total energy (r = 0.333), fat (r = 0.37), protein (r = 0.349), and leucine intake (r = 0.352).</p><p><strong>Conclusions: </strong>Our findings emphasize the positive effect of adequate nutritional quantity and quality on body composition in female collegiate dancers.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hye-Jeong Yang, Ting Zhang, Min-Jung Kim, Haeng-Jeon Hur, Xuangao Wu, Dai-Ja Jang, Sunmin Park
Background/objectives: Schisandra chinensis Fructus (SCF) is a traditional medicinal herb containing lignans that improves glucose metabolism by mitigating insulin resistance. We aimed to investigate the therapeutic potential and action mechanism of SCF for Alzheimer's disease (AD) using a network pharmacology analysis, followed by experimental validation in an AD rat model.
Methods: The biological activities of SCF's bioactive compounds were assessed through a network pharmacology analysis. An AD rat model was generated by infusing amyloid-β peptide (Aβ) (25-35) into the hippocampus to induce Aβ accumulation. The AD rats were fed either 0.5% dextrin (AD-Con) or 0.5% SCF (AD-SCF group) in a high-fat diet for seven weeks. The rats in the normal/control group received an Aβ (35-25) infusion (no Aβ deposition) and were fed a control diet (Normal-C). Aβ deposition, memory function, inflammation, and glucose/lipid metabolism were evaluated.
Results: The network analysis revealed significant intersections between AD-related targets and bioactive SCF compounds, like gomisin A, schisandrin, and longikaurin A. Key AD genes prostaglandin-endoperoxide synthase-2 (PTGS2, cyclooxygenase-2) and acetylcholinesterase (AChE) were linked to SCF compounds. In the rats with AD induced by bilaterally infusing amyloid-β (25-35) into the hippocampus, the 0.5% SCF intake mitigated hippocampal amyloid-β deposition, neuroinflammation, memory deficits, and dysregulated glucose and lipid metabolism versus the AD controls. SCF reduced hippocampal AChE activity, inflammatory cytokine expression related to PTGS2, and malondialdehyde contents and preserved neuronal cell survival-related factors such as brain-derived neurotrophic factor and ciliary neurotrophic factor similar to normal rats. The neuroprotective effects validated the network analysis findings.
Conclusions: SCF could be a potential AD therapeutic agent by activating the parasympathetic nervous system to reduce hippocampal oxidative stress and inflammation, warranting further clinical investigations of its efficacy.
{"title":"Efficacy and Mechanism of <i>Schisandra chinensis</i> Fructus Water Extract in Alzheimer's Disease: Insights from Network Pharmacology and Validation in an Amyloid-β Infused Animal Model.","authors":"Hye-Jeong Yang, Ting Zhang, Min-Jung Kim, Haeng-Jeon Hur, Xuangao Wu, Dai-Ja Jang, Sunmin Park","doi":"10.3390/nu16213751","DOIUrl":"10.3390/nu16213751","url":null,"abstract":"<p><strong>Background/objectives: </strong><i>Schisandra chinensis</i> Fructus (SCF) is a traditional medicinal herb containing lignans that improves glucose metabolism by mitigating insulin resistance. We aimed to investigate the therapeutic potential and action mechanism of SCF for Alzheimer's disease (AD) using a network pharmacology analysis, followed by experimental validation in an AD rat model.</p><p><strong>Methods: </strong>The biological activities of SCF's bioactive compounds were assessed through a network pharmacology analysis. An AD rat model was generated by infusing amyloid-β peptide (Aβ) (25-35) into the hippocampus to induce Aβ accumulation. The AD rats were fed either 0.5% dextrin (AD-Con) or 0.5% SCF (AD-SCF group) in a high-fat diet for seven weeks. The rats in the normal/control group received an Aβ (35-25) infusion (no Aβ deposition) and were fed a control diet (Normal-C). Aβ deposition, memory function, inflammation, and glucose/lipid metabolism were evaluated.</p><p><strong>Results: </strong>The network analysis revealed significant intersections between AD-related targets and bioactive SCF compounds, like gomisin A, schisandrin, and longikaurin A. Key AD genes prostaglandin-endoperoxide synthase-2 (<i>PTGS2</i>, cyclooxygenase-2) and acetylcholinesterase (<i>AChE</i>) were linked to SCF compounds. In the rats with AD induced by bilaterally infusing amyloid-β (25-35) into the hippocampus, the 0.5% SCF intake mitigated hippocampal amyloid-β deposition, neuroinflammation, memory deficits, and dysregulated glucose and lipid metabolism versus the AD controls. SCF reduced hippocampal AChE activity, inflammatory cytokine expression related to <i>PTGS2</i>, and malondialdehyde contents and preserved neuronal cell survival-related factors such as brain-derived neurotrophic factor and ciliary neurotrophic factor similar to normal rats. The neuroprotective effects validated the network analysis findings.</p><p><strong>Conclusions: </strong>SCF could be a potential AD therapeutic agent by activating the parasympathetic nervous system to reduce hippocampal oxidative stress and inflammation, warranting further clinical investigations of its efficacy.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Namhyun Kim, Rachel Kolko Conlon, Samaneh Farsijani, Marquis Samuel Hawkins
Background/objectives: Sleep health has been associated with diet quality, but the relationship between chrononutrition patterns and multidimensional sleep health is unclear. This study identifies chrononutrition patterns among U.S. adults and examines their associations with multidimensional sleep health.
Methods: This cross-sectional analysis used data from the 2017-2020 National Health and Nutrition Examination Survey. Chrononutrition behaviors were assessed using two 24 h dietary recalls. Latent profile analysis was used to identify chrononutrition profiles. Multivariable survey regression models determined the associations between chrononutrition patterns and sleep health dimensions.
Results: The sample included 5228 subjects with a median age of 49 years. Of the sample, 52% of the participants were female, and 65% were White. In adjusted models, each additional hour between wake time and first instance of eating was associated with a 19% increase in the odds of poor timing (sleep midpoint < 2:00 a.m. or >4:00 a.m.; 95% CI: 1.07-1.33) and a 21% increase in poor duration (<7 or >9 h/night; 95% CI: 1.09-1.33). Each additional hour between last eating and bedtime was associated with 9% higher odds of poor duration (95% CI: 1.03-1.16). A one-hour longer eating window was associated with 10% lower odds of poor timing (95% CI: 0.84-0.98). We identified five chrononutrition profiles: Typical Eating (reference), Early Finished Eating, Later Heavy Eating, Extended Window Eating, and Restricted Window Eating. The Later Heavy Eating profile exhibited 96% higher odds of poor timing (95% CI: 1.09-3.51) and the Restricted Window Eating profile had 94% higher odds of poor duration (95% CI: 1.10-3.43).
Conclusions: These findings highlight the importance of unique chrononutrition patterns in relation to multidimensional sleep health. We provide a framework for future studies to identify personalized chrononutrition interventions and their role in improving sleep health.
{"title":"Association Between Chrononutrition Patterns and Multidimensional Sleep Health.","authors":"Namhyun Kim, Rachel Kolko Conlon, Samaneh Farsijani, Marquis Samuel Hawkins","doi":"10.3390/nu16213724","DOIUrl":"10.3390/nu16213724","url":null,"abstract":"<p><strong>Background/objectives: </strong>Sleep health has been associated with diet quality, but the relationship between chrononutrition patterns and multidimensional sleep health is unclear. This study identifies chrononutrition patterns among U.S. adults and examines their associations with multidimensional sleep health.</p><p><strong>Methods: </strong>This cross-sectional analysis used data from the 2017-2020 National Health and Nutrition Examination Survey. Chrononutrition behaviors were assessed using two 24 h dietary recalls. Latent profile analysis was used to identify chrononutrition profiles. Multivariable survey regression models determined the associations between chrononutrition patterns and sleep health dimensions.</p><p><strong>Results: </strong>The sample included 5228 subjects with a median age of 49 years. Of the sample, 52% of the participants were female, and 65% were White. In adjusted models, each additional hour between wake time and first instance of eating was associated with a 19% increase in the odds of poor timing (sleep midpoint < 2:00 a.m. or >4:00 a.m.; 95% CI: 1.07-1.33) and a 21% increase in poor duration (<7 or >9 h/night; 95% CI: 1.09-1.33). Each additional hour between last eating and bedtime was associated with 9% higher odds of poor duration (95% CI: 1.03-1.16). A one-hour longer eating window was associated with 10% lower odds of poor timing (95% CI: 0.84-0.98). We identified five chrononutrition profiles: Typical Eating (reference), Early Finished Eating, Later Heavy Eating, Extended Window Eating, and Restricted Window Eating. The Later Heavy Eating profile exhibited 96% higher odds of poor timing (95% CI: 1.09-3.51) and the Restricted Window Eating profile had 94% higher odds of poor duration (95% CI: 1.10-3.43).</p><p><strong>Conclusions: </strong>These findings highlight the importance of unique chrononutrition patterns in relation to multidimensional sleep health. We provide a framework for future studies to identify personalized chrononutrition interventions and their role in improving sleep health.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jordi Rovira, María José Ramirez-Bajo, Elisenda Bañon-Maneus, Pedro Ventura-Aguiar, Marta Arias-Guillén, Barbara Romano-Andrioni, Raquel Ojeda, Ignacio Revuelta, Héctor García-Calderó, Joan Albert Barberà, Ana Paula Dantas, Maribel Diaz-Ricart, Fàtima Crispi, Juan Carlos García-Pagán, Josep M Campistol, Fritz Diekmann
Background: Cardiovascular disease (CVD) remains the most common cause of mortality in chronic kidney disease (CKD) patients. Several studies suggest that the Mediterranean diet reduces the risk of CVD due to its influence on endothelial function, inflammation, lipid profile, and blood pressure. Integrating metabolomic and proteomic analyses of CKD could provide insights into the pathways involved in uremia-induced CVD and those pathways modifiable by the Mediterranean diet.
Methods: We performed metabolomic and proteomic analyses on serum samples from 19 patients with advanced CKD (aCKD) and 27 healthy volunteers. The metabolites were quantified using four different approaches, based on their properties. Proteomic analysis was performed after depletion of seven abundant serum proteins (Albumin, IgG, antitrypsin, IgA, transferrin, haptoglobin, and fibrinogen). Integrative analysis was performed using MetaboAnalyst 4.0 and STRING 11.0 software to identify the dysregulated pathways and biomarkers.
Results: A total of 135 metabolites and 75 proteins were differentially expressed in aCKD patients, compared to the controls. Pathway enrichment analysis showed significant alterations in the innate immune system pathways, including complement, coagulation, and neutrophil degranulation, along with disrupted linoleic acid and cholesterol metabolism. Additionally, certain key metabolites and proteins were altered in aCKD patients, such as glutathione peroxidase 3, carnitine, homocitrulline, 3-methylhistidine, and several amino acids and derivatives.
Conclusions: Our findings reveal significant dysregulation of the serum metabolome and proteome in aCKD, particularly in those pathways associated with endothelial dysfunction and CVD. These results suggest that CVD prevention in CKD may benefit from a multifaceted approach, including dietary interventions such as the Mediterranean diet.
{"title":"Mediterranean Diet Pattern: Potential Impact on the Different Altered Pathways Related to Cardiovascular Risk in Advanced Chronic Kidney Disease.","authors":"Jordi Rovira, María José Ramirez-Bajo, Elisenda Bañon-Maneus, Pedro Ventura-Aguiar, Marta Arias-Guillén, Barbara Romano-Andrioni, Raquel Ojeda, Ignacio Revuelta, Héctor García-Calderó, Joan Albert Barberà, Ana Paula Dantas, Maribel Diaz-Ricart, Fàtima Crispi, Juan Carlos García-Pagán, Josep M Campistol, Fritz Diekmann","doi":"10.3390/nu16213739","DOIUrl":"10.3390/nu16213739","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease (CVD) remains the most common cause of mortality in chronic kidney disease (CKD) patients. Several studies suggest that the Mediterranean diet reduces the risk of CVD due to its influence on endothelial function, inflammation, lipid profile, and blood pressure. Integrating metabolomic and proteomic analyses of CKD could provide insights into the pathways involved in uremia-induced CVD and those pathways modifiable by the Mediterranean diet.</p><p><strong>Methods: </strong>We performed metabolomic and proteomic analyses on serum samples from 19 patients with advanced CKD (aCKD) and 27 healthy volunteers. The metabolites were quantified using four different approaches, based on their properties. Proteomic analysis was performed after depletion of seven abundant serum proteins (Albumin, IgG, antitrypsin, IgA, transferrin, haptoglobin, and fibrinogen). Integrative analysis was performed using MetaboAnalyst 4.0 and STRING 11.0 software to identify the dysregulated pathways and biomarkers.</p><p><strong>Results: </strong>A total of 135 metabolites and 75 proteins were differentially expressed in aCKD patients, compared to the controls. Pathway enrichment analysis showed significant alterations in the innate immune system pathways, including complement, coagulation, and neutrophil degranulation, along with disrupted linoleic acid and cholesterol metabolism. Additionally, certain key metabolites and proteins were altered in aCKD patients, such as glutathione peroxidase 3, carnitine, homocitrulline, 3-methylhistidine, and several amino acids and derivatives.</p><p><strong>Conclusions: </strong>Our findings reveal significant dysregulation of the serum metabolome and proteome in aCKD, particularly in those pathways associated with endothelial dysfunction and CVD. These results suggest that CVD prevention in CKD may benefit from a multifaceted approach, including dietary interventions such as the Mediterranean diet.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background/objectives: Western-type diets (WDs) damage the intestinal barrier by disrupting the gut microbiota composition and causing inflammation, leading to the development of obesity, type 2 diabetes, and non-alcoholic fatty liver disease. Short-chain fatty acids (SCFAs) are produced by the gut microbiota and found in fermented foods and can stimulate the anti-inflammatory action of type 3 innate lymphoid cells (ILCS3s) in the intestine. This study hypothesised that supplementing miso, a Japanese fermented food, to a WD could increase the levels of SCFAs and thus stimulate ILC3s, decreasing inflammation in the intestine and protecting intestinal barrier integrity.
Methods: Mice with RORγt total (KI/KI) or partial (KI/w) knockout were fed a high-fat high-sugar diet (HFHSD) for eight weeks as a model of WD. Half of the mice received miso supplementation in addition to the HFHSD. Weight gain, glucose tolerance and insulin resistance, intestinal barrier integrity, intestinal immunity, and liver condition were assessed.
Results: Miso supplementation increased SCFA levels in the small intestine, which stimulated ILC3 function in KI/w mice. Glucose tolerance was improved, intestinal barrier integrity was ameliorated, and mucus production was increased. The level of IL-22 was increased, while pro-inflammatory ILC1s, M1 macrophages, TNF-α, and IL-1β were decreased. Liver condition was not affected.
Conclusions: This study demonstrated that miso supplementation influenced several factors involved in inflammation and intestinal barrier integrity by stimulating ILC3s in RORγt heterozygous mice. Moreover, it showed that the number of ILC3s is not the key factor in immune regulation, but rather the ability of ILC3 to produce IL-22 and employ it to control the immune response in the small intestine.
{"title":"Supplementation of Miso to a Western-Type Diet Stimulates ILC3s and Decreases Inflammation in the Small Intestine.","authors":"River Budau, Takuro Okamura, Yuka Hasegawa, Naoko Nakanishi, Masahide Hamaguchi, Michiaki Fukui","doi":"10.3390/nu16213743","DOIUrl":"10.3390/nu16213743","url":null,"abstract":"<p><strong>Background/objectives: </strong>Western-type diets (WDs) damage the intestinal barrier by disrupting the gut microbiota composition and causing inflammation, leading to the development of obesity, type 2 diabetes, and non-alcoholic fatty liver disease. Short-chain fatty acids (SCFAs) are produced by the gut microbiota and found in fermented foods and can stimulate the anti-inflammatory action of type 3 innate lymphoid cells (ILCS3s) in the intestine. This study hypothesised that supplementing miso, a Japanese fermented food, to a WD could increase the levels of SCFAs and thus stimulate ILC3s, decreasing inflammation in the intestine and protecting intestinal barrier integrity.</p><p><strong>Methods: </strong>Mice with RORγt total (KI/KI) or partial (KI/w) knockout were fed a high-fat high-sugar diet (HFHSD) for eight weeks as a model of WD. Half of the mice received miso supplementation in addition to the HFHSD. Weight gain, glucose tolerance and insulin resistance, intestinal barrier integrity, intestinal immunity, and liver condition were assessed.</p><p><strong>Results: </strong>Miso supplementation increased SCFA levels in the small intestine, which stimulated ILC3 function in KI/w mice. Glucose tolerance was improved, intestinal barrier integrity was ameliorated, and mucus production was increased. The level of IL-22 was increased, while pro-inflammatory ILC1s, M1 macrophages, TNF-α, and IL-1β were decreased. Liver condition was not affected.</p><p><strong>Conclusions: </strong>This study demonstrated that miso supplementation influenced several factors involved in inflammation and intestinal barrier integrity by stimulating ILC3s in RORγt heterozygous mice. Moreover, it showed that the number of ILC3s is not the key factor in immune regulation, but rather the ability of ILC3 to produce IL-22 and employ it to control the immune response in the small intestine.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sichang Qu, Yewen Zhu, Norbert Pfeiffer, Franz H Grus
Background: Observational studies have noted that patients with certain retinal degenerative diseases exhibit iron disturbances in the retina or vitreous compared to healthy controls. However, the connection between serum iron status and these diseases remains unclear. This study aims to explore the potential causal relationship between serum iron status biomarkers and the development of age-related macular degeneration (AMD), retinitis pigmentosa (RP), and diabetic retinopathy (DR). Methods: A two-sample Mendelian randomization (MR) analysis was conducted to investigate the causal relationship between serum iron status and several retinal degenerative diseases. Genome-wide association study (GWAS) summary-level data were extracted from public GWAS databases. Inverse-variance weighting (IVW), MR-Egger regressions, Simple model, Weighted median, and Weight mode were used as MR methods. Sensitivity analysis was conducted to confirm the robustness of the results by examining horizontal pleiotropy and heterogeneity through MR-Egger intercept and leave-one-out analysis. Results: The MR analysis revealed causal relationships between genetically predicted serum iron status biomarkers and various retinal diseases. Transferrin was positively associated with the odds of AMD (whether dry or wet) (OR = 1.167, 95% CI = 1.045-1.304, p = 0.006) and wet AMD (OR = 1.194, 95% CI = 1.018-1.402, p = 0.030). Ferritin was negatively associated with the odds of wet AMD (OR = 0.555, 95% CI = 0.333-0.927, p = 0.024). Serum iron (OR = 0.508, 95% CI = 0.260-0.993, p = 0.048) and transferrin saturation (OR = 0.508, 95% CI = 0.260-0.993, p = 0.048) were negatively associated with the odds of RP. Conclusions: These findings provide evidence supporting a potential causal relationship between serum iron status and various retinal degenerative diseases, highlighting a direction for future research into the underlying mechanisms of these diseases.
背景:观察性研究发现,与健康对照组相比,某些视网膜变性疾病患者的视网膜或玻璃体内会出现铁紊乱。然而,血清铁状态与这些疾病之间的联系仍不清楚。本研究旨在探讨血清铁状态生物标志物与老年性黄斑变性(AMD)、色素性视网膜炎(RP)和糖尿病视网膜病变(DR)之间的潜在因果关系。研究方法通过双样本孟德尔随机化(MR)分析,研究血清铁状态与几种视网膜退行性疾病之间的因果关系。从公共 GWAS 数据库中提取了全基因组关联研究(GWAS)的摘要级数据。采用反方差加权(IVW)、MR-Egger 回归、简单模型、加权中位数和加权模式作为 MR 方法。通过MR-Egger截距和leave-one-out分析检查水平多向性和异质性,进行了敏感性分析以确认结果的稳健性。结果磁共振分析揭示了基因预测的血清铁状态生物标志物与各种视网膜疾病之间的因果关系。转铁蛋白与老年性视网膜病变(无论是干性还是湿性)(OR = 1.167,95% CI = 1.045-1.304,p = 0.006)和湿性老年性视网膜病变(OR = 1.194,95% CI = 1.018-1.402,p = 0.030)的几率呈正相关。铁蛋白与湿性黄斑变性的几率呈负相关(OR = 0.555,95% CI = 0.333-0.927,p = 0.024)。血清铁(OR = 0.508,95% CI = 0.260-0.993,p = 0.048)和转铁蛋白饱和度(OR = 0.508,95% CI = 0.260-0.993,p = 0.048)与RP的几率呈负相关。结论这些发现为血清铁状态与各种视网膜退行性疾病之间的潜在因果关系提供了证据,为今后研究这些疾病的内在机制指明了方向。
{"title":"Serum Iron Status and Retinal Degenerative Diseases: A Mendelian Randomization Study on AMD, RP, and DR.","authors":"Sichang Qu, Yewen Zhu, Norbert Pfeiffer, Franz H Grus","doi":"10.3390/nu16213747","DOIUrl":"10.3390/nu16213747","url":null,"abstract":"<p><p><b>Background</b>: Observational studies have noted that patients with certain retinal degenerative diseases exhibit iron disturbances in the retina or vitreous compared to healthy controls. However, the connection between serum iron status and these diseases remains unclear. This study aims to explore the potential causal relationship between serum iron status biomarkers and the development of age-related macular degeneration (AMD), retinitis pigmentosa (RP), and diabetic retinopathy (DR). <b>Methods</b>: A two-sample Mendelian randomization (MR) analysis was conducted to investigate the causal relationship between serum iron status and several retinal degenerative diseases. Genome-wide association study (GWAS) summary-level data were extracted from public GWAS databases. Inverse-variance weighting (IVW), MR-Egger regressions, Simple model, Weighted median, and Weight mode were used as MR methods. Sensitivity analysis was conducted to confirm the robustness of the results by examining horizontal pleiotropy and heterogeneity through MR-Egger intercept and leave-one-out analysis. <b>Results</b>: The MR analysis revealed causal relationships between genetically predicted serum iron status biomarkers and various retinal diseases. Transferrin was positively associated with the odds of AMD (whether dry or wet) (OR = 1.167, 95% CI = 1.045-1.304, <i>p</i> = 0.006) and wet AMD (OR = 1.194, 95% CI = 1.018-1.402, <i>p</i> = 0.030). Ferritin was negatively associated with the odds of wet AMD (OR = 0.555, 95% CI = 0.333-0.927, <i>p</i> = 0.024). Serum iron (OR = 0.508, 95% CI = 0.260-0.993, <i>p</i> = 0.048) and transferrin saturation (OR = 0.508, 95% CI = 0.260-0.993, <i>p</i> = 0.048) were negatively associated with the odds of RP. <b>Conclusions</b>: These findings provide evidence supporting a potential causal relationship between serum iron status and various retinal degenerative diseases, highlighting a direction for future research into the underlying mechanisms of these diseases.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Sodium benzoate (SB) is widely used in food products, cosmetics, and medical solutions due to its antimicrobial properties. While it is generally considered safe and has potential neuroprotective benefits, SB has also been linked to adverse effects, including hepatic oxidative stress and inflammation. However, the potential effects of SB on obesity and lifespan remain poorly understood.
Objectives: In this study, we investigated the effects of SB on fat accumulation and lifespan using the nematode Caenorhabditis elegans (C. elegans) as a model system.
Methods: Wild-type worms were exposed to various SB concentrations (0%, 0.0004%, 0.0008%, 0.004%, and 0.1%) and 0.016% glucose as a positive control for 72 h in liquid or on NGM agar plates.
Result: Fat accumulation was assessed through the Oil Red O staining, which revealed that SB induced more fat accumulation compared to vehicle control, even at low concentrations, including the dosage of 0.0004%. Lifespan analysis also demonstrated that SB significantly reduced lifespan in wild-type worms, even at low concentrations. Further investigations found that SKN-1 (an Nrf2 homolog) is necessary for SB-induced fat accumulation and lifespan reduction. Moreover, SB inhibited the nuclear localization of SKN-1 under oxidative stress conditions.
Conclusion: These findings suggest that SB may induce fat accumulation and reduce lifespan by inhibiting the oxidative stress-mediated SKN-1 signaling pathway.
{"title":"Sodium Benzoate Induces Fat Accumulation and Reduces Lifespan via the SKN-1/Nrf2 Signaling Pathway: Evidence from the <i>Caenorhabditis elegans</i> Model.","authors":"Jiah D Lee, Jiwoo Lee, Jerry Vang, Xiaoping Pan","doi":"10.3390/nu16213753","DOIUrl":"10.3390/nu16213753","url":null,"abstract":"<p><strong>Background: </strong>Sodium benzoate (SB) is widely used in food products, cosmetics, and medical solutions due to its antimicrobial properties. While it is generally considered safe and has potential neuroprotective benefits, SB has also been linked to adverse effects, including hepatic oxidative stress and inflammation. However, the potential effects of SB on obesity and lifespan remain poorly understood.</p><p><strong>Objectives: </strong>In this study, we investigated the effects of SB on fat accumulation and lifespan using the nematode <i>Caenorhabditis elegans</i> (<i>C. elegans</i>) as a model system.</p><p><strong>Methods: </strong>Wild-type worms were exposed to various SB concentrations (0%, 0.0004%, 0.0008%, 0.004%, and 0.1%) and 0.016% glucose as a positive control for 72 h in liquid or on NGM agar plates.</p><p><strong>Result: </strong>Fat accumulation was assessed through the Oil Red O staining, which revealed that SB induced more fat accumulation compared to vehicle control, even at low concentrations, including the dosage of 0.0004%. Lifespan analysis also demonstrated that SB significantly reduced lifespan in wild-type worms, even at low concentrations. Further investigations found that SKN-1 (an Nrf2 homolog) is necessary for SB-induced fat accumulation and lifespan reduction. Moreover, SB inhibited the nuclear localization of SKN-1 under oxidative stress conditions.</p><p><strong>Conclusion: </strong>These findings suggest that SB may induce fat accumulation and reduce lifespan by inhibiting the oxidative stress-mediated SKN-1 signaling pathway.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Conventional cancer treatments include surgical resection, chemotherapy, hyperthermia, immunotherapy, hormone therapy, and locally targeted therapies such as radiation therapy. Standard cancer therapies often require the use of multiple agents, which can activate nuclear factor kappa B (NF-κB) in tumor cells, leading to reduced cell death and increased drug resistance. Moreover, the use of multiple agents also contributes to added toxicity, resulting in poor treatment outcomes. Cancer cells gradually develop resistance to almost all chemotherapeutics through various mechanisms, such as drug efflux, alterations in drug metabolism and transport, changes in signal transduction pathways, enhanced DNA repair capacity, evasion of apoptosis, increased mutations, reactivation of drug targets, interaction with the cancer microenvironment, cancer cell-stroma interactions, epithelial-mesenchymal transition (EMT)-mediated chemoresistance, epigenetic modifications, metabolic alterations, and the effect of cancer stem cells (CSCs). Developing new strategies to improve chemotherapy sensitivity while minimizing side effects is essential for achieving better therapeutic outcomes and enhancing patients' quality of life. One promising approach involves combining conventional cancer treatments with propolis and its flavonoids. These natural compounds may enhance tumor response to treatment while reducing toxicity. Propolis and its components can sensitize cancer cells to chemotherapeutic agents, likely by inhibiting NF-κB activation, reprogramming tumor-associated macrophages (TAMs; an M2-like phenotype), and thereby reducing the release of matrix metalloproteinase (MMP)-9, cytokines, chemokines, and the vascular endothelial growth factor (VEGF). By reducing TAMs, propolis and its components may also overcome EMT-mediated chemoresistance, disrupt the crosstalk between macrophages and CSCs, inhibit the maintenance of stemness, and reverse acquired immunosuppression, thus promoting an antitumor response mediated by cytotoxic T-cells. This review highlights the potential of flavonoids to modulate the responsiveness of cancer to conventional treatment modalities. The evidence suggests that novel therapeutic strategies incorporating flavonoids could be developed to improve treatment outcomes. The positive effects of combining propolis with chemotherapeutics include reduced cytotoxicity to peripheral blood leukocytes, liver, and kidney cells. Therefore, polyphenolic/flavonoid components may hold potential for use in combination with chemotherapeutic agents in the clinical treatment of various types of cancers.
{"title":"Potential Strategies for Overcoming Drug Resistance Pathways Using Propolis and Its Polyphenolic/Flavonoid Compounds in Combination with Chemotherapy and Radiotherapy.","authors":"Nada Oršolić, Maja Jazvinšćak Jembrek","doi":"10.3390/nu16213741","DOIUrl":"10.3390/nu16213741","url":null,"abstract":"<p><p>Conventional cancer treatments include surgical resection, chemotherapy, hyperthermia, immunotherapy, hormone therapy, and locally targeted therapies such as radiation therapy. Standard cancer therapies often require the use of multiple agents, which can activate nuclear factor kappa B (NF-κB) in tumor cells, leading to reduced cell death and increased drug resistance. Moreover, the use of multiple agents also contributes to added toxicity, resulting in poor treatment outcomes. Cancer cells gradually develop resistance to almost all chemotherapeutics through various mechanisms, such as drug efflux, alterations in drug metabolism and transport, changes in signal transduction pathways, enhanced DNA repair capacity, evasion of apoptosis, increased mutations, reactivation of drug targets, interaction with the cancer microenvironment, cancer cell-stroma interactions, epithelial-mesenchymal transition (EMT)-mediated chemoresistance, epigenetic modifications, metabolic alterations, and the effect of cancer stem cells (CSCs). Developing new strategies to improve chemotherapy sensitivity while minimizing side effects is essential for achieving better therapeutic outcomes and enhancing patients' quality of life. One promising approach involves combining conventional cancer treatments with propolis and its flavonoids. These natural compounds may enhance tumor response to treatment while reducing toxicity. Propolis and its components can sensitize cancer cells to chemotherapeutic agents, likely by inhibiting NF-κB activation, reprogramming tumor-associated macrophages (TAMs; an M2-like phenotype), and thereby reducing the release of matrix metalloproteinase (MMP)-9, cytokines, chemokines, and the vascular endothelial growth factor (VEGF). By reducing TAMs, propolis and its components may also overcome EMT-mediated chemoresistance, disrupt the crosstalk between macrophages and CSCs, inhibit the maintenance of stemness, and reverse acquired immunosuppression, thus promoting an antitumor response mediated by cytotoxic T-cells. This review highlights the potential of flavonoids to modulate the responsiveness of cancer to conventional treatment modalities. The evidence suggests that novel therapeutic strategies incorporating flavonoids could be developed to improve treatment outcomes. The positive effects of combining propolis with chemotherapeutics include reduced cytotoxicity to peripheral blood leukocytes, liver, and kidney cells. Therefore, polyphenolic/flavonoid components may hold potential for use in combination with chemotherapeutic agents in the clinical treatment of various types of cancers.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Daniel Emiliano de Farias Xavier, Rúbia Cartaxo Squizato de Moraes, Thallyta Alanna Ferreira Viana, Joicy Karla Grangeiro Pereira, Paulo César Trindade da Costa, Davyson Barbosa Duarte, Melyssa Kellyane Cavalcanti Galdino, Adélia da Costa Pereira de Arruda Neta, José Luiz de Brito Alves, Vinícius José Baccin Martins
Background/objectives: Depression, anxiety, and stress are highly prevalent mental disorders worldwide, and food consumption can change in individuals with these conditions. We aimed to assess the food consumption of women with depressive symptoms and compare it to a control without symptoms.
Methods: A cross-sectional study was conducted with 96 women, aged 18-59, allocated into two groups: control (n = 62) or depressive symptoms (n = 34). The participants underwent an anthropometric assessment, and food consumption was evaluated using a 24 h food recall and the NOVA classification. Depressive symptoms, anxiety, and stress were measured using the DASS-21 questionnaire.
Results: Anthropometric parameters did not differ between the groups. Women with depressive symptoms consumed fewer calories (p = 0.006), carbohydrates (p = 0.014), proteins (p = 0.036), and lipids (0.011) from unprocessed and minimally processed foods (UMPF) compared to the control women. A negative correlation was found between the dietary consumption energy of UMPF and symptoms of depression (r = -0.337; p = 0.001), anxiety (r = -0.262; p = 0.014), and stress (r = -0.260; p = 0.014), as well as a positive correlation between energy intake from ultra-processed foods (UPF) and symptoms of depression (r = 0.218; p = 0.042) and stress (r = 0.227; p = 0.034). Regression analysis showed that depressive symptoms accounted for 7.6% of the lower energy consumption from UMPF.
Conclusions: Women with depressive symptoms displayed lower UMPF consumption, and this was negatively correlated with symptoms of depression, anxiety, and stress. Professional dietary advice can improve health status in these patients.
{"title":"Food Consumption According to the NOVA Food Classification and Its Relationship with Symptoms of Depression, Anxiety, and Stress in Women.","authors":"Daniel Emiliano de Farias Xavier, Rúbia Cartaxo Squizato de Moraes, Thallyta Alanna Ferreira Viana, Joicy Karla Grangeiro Pereira, Paulo César Trindade da Costa, Davyson Barbosa Duarte, Melyssa Kellyane Cavalcanti Galdino, Adélia da Costa Pereira de Arruda Neta, José Luiz de Brito Alves, Vinícius José Baccin Martins","doi":"10.3390/nu16213734","DOIUrl":"10.3390/nu16213734","url":null,"abstract":"<p><strong>Background/objectives: </strong>Depression, anxiety, and stress are highly prevalent mental disorders worldwide, and food consumption can change in individuals with these conditions. We aimed to assess the food consumption of women with depressive symptoms and compare it to a control without symptoms.</p><p><strong>Methods: </strong>A cross-sectional study was conducted with 96 women, aged 18-59, allocated into two groups: control <i>(n</i> = 62) or depressive symptoms (<i>n</i> = 34). The participants underwent an anthropometric assessment, and food consumption was evaluated using a 24 h food recall and the NOVA classification. Depressive symptoms, anxiety, and stress were measured using the DASS-21 questionnaire.</p><p><strong>Results: </strong>Anthropometric parameters did not differ between the groups. Women with depressive symptoms consumed fewer calories (<i>p</i> = 0.006), carbohydrates (<i>p</i> = 0.014), proteins (<i>p</i> = 0.036), and lipids (0.011) from unprocessed and minimally processed foods (UMPF) compared to the control women. A negative correlation was found between the dietary consumption energy of UMPF and symptoms of depression (r = -0.337; <i>p</i> = 0.001), anxiety (r = -0.262; <i>p</i> = 0.014), and stress (r = -0.260; <i>p</i> = 0.014), as well as a positive correlation between energy intake from ultra-processed foods (UPF) and symptoms of depression (r = 0.218; <i>p</i> = 0.042) and stress (r = 0.227; <i>p</i> = 0.034). Regression analysis showed that depressive symptoms accounted for 7.6% of the lower energy consumption from UMPF.</p><p><strong>Conclusions: </strong>Women with depressive symptoms displayed lower UMPF consumption, and this was negatively correlated with symptoms of depression, anxiety, and stress. Professional dietary advice can improve health status in these patients.</p>","PeriodicalId":19486,"journal":{"name":"Nutrients","volume":"16 21","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11547796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142625068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}