Pub Date : 2023-06-01DOI: 10.1097/JN9.0000000000000010
Yi-Chao Ma, Wen-Qi Li, Chen Wei, Fei Wang, Yiqun Liao, Bin Zhao, Yuji Chen, Qi Zhao, Jie Qiu, Dong Tang
Abstract Background Observational studies have shown that inflammatory bowel disease (IBD), such as ulcerative colitis (UC) and Crohn disease (CD), is associated with gingivitis and periodontal disease (GP). This study aims to investigate whether there is a causal relationship between IBD and GP. Methods This study assessed the causal relationship between IBD and GP through a two-sample Mendelian randomization (MR) study. The required data were obtained through the IEU OpenGWAS project. Instrumental variable screening and the MR and sensitivity analyses were performed using the “TwoSampleMR” R package. Results IBD, UC, and CD may have a causal effect on GP (IBD, inverse variance weighting [IVW] OR = 1.05, 95% CI = 1.00–1.10, P = 0.03; UC, IVW OR = 1.05, 95% CI = 1.00–1.11, P = 0.03; CD, weighted median OR = 1.06, 95% CI = 1.00–1.13, P = 0.04; simple mode OR = 1.15, 95% CI = 1.02–1.31, P = 0.03). Scatterplots, forest plots, and funnel plots showed a significant relationship between IBD and GP and confirmed the robustness of the model. In sensitivity testing, no horizontal pleiotropy or heterogeneity was found in this study. Conclusions This study found a possible causal relationship between IBD (UC and CD) and GP, which deserves to be considered in clinical practice.
摘要 背景 观察性研究表明,溃疡性结肠炎(UC)和克罗恩病(CD)等炎症性肠病(IBD)与牙龈炎和牙周病(GP)有关。本研究旨在探讨 IBD 与 GP 之间是否存在因果关系。方法 本研究通过双样本孟德尔随机化(MR)研究评估 IBD 与 GP 之间的因果关系。所需数据通过 IEU OpenGWAS 项目获得。使用 "TwoSampleMR "R软件包进行了工具变量筛选、MR分析和敏感性分析。结果 IBD、UC 和 CD 可能对 GP 有因果影响(IBD,逆方差加权 [IVW] OR = 1.05,95% CI = 1.00-1.10,P = 0.03;UC,IVW OR = 1.05,95% CI = 1.00-1.11,P = 0.03;CD,加权中位数 OR = 1.06,95% CI = 1.00-1.13,P = 0.04;简单模式 OR = 1.15,95% CI = 1.02-1.31,P = 0.03)。散点图、森林图和漏斗图显示了 IBD 与 GP 之间的显著关系,并证实了模型的稳健性。在敏感性测试中,本研究未发现水平多向性或异质性。结论 本研究发现 IBD(UC 和 CD)与 GP 之间可能存在因果关系,值得在临床实践中加以考虑。
{"title":"Causal relationship between inflammatory bowel disease and gingivitis or periodontal disease: A two-sample Mendelian randomized analysis","authors":"Yi-Chao Ma, Wen-Qi Li, Chen Wei, Fei Wang, Yiqun Liao, Bin Zhao, Yuji Chen, Qi Zhao, Jie Qiu, Dong Tang","doi":"10.1097/JN9.0000000000000010","DOIUrl":"https://doi.org/10.1097/JN9.0000000000000010","url":null,"abstract":"Abstract Background Observational studies have shown that inflammatory bowel disease (IBD), such as ulcerative colitis (UC) and Crohn disease (CD), is associated with gingivitis and periodontal disease (GP). This study aims to investigate whether there is a causal relationship between IBD and GP. Methods This study assessed the causal relationship between IBD and GP through a two-sample Mendelian randomization (MR) study. The required data were obtained through the IEU OpenGWAS project. Instrumental variable screening and the MR and sensitivity analyses were performed using the “TwoSampleMR” R package. Results IBD, UC, and CD may have a causal effect on GP (IBD, inverse variance weighting [IVW] OR = 1.05, 95% CI = 1.00–1.10, P = 0.03; UC, IVW OR = 1.05, 95% CI = 1.00–1.11, P = 0.03; CD, weighted median OR = 1.06, 95% CI = 1.00–1.13, P = 0.04; simple mode OR = 1.15, 95% CI = 1.02–1.31, P = 0.03). Scatterplots, forest plots, and funnel plots showed a significant relationship between IBD and GP and confirmed the robustness of the model. In sensitivity testing, no horizontal pleiotropy or heterogeneity was found in this study. Conclusions This study found a possible causal relationship between IBD (UC and CD) and GP, which deserves to be considered in clinical practice.","PeriodicalId":101772,"journal":{"name":"Journal of Nutritional Oncology","volume":"5 1","pages":"107 - 114"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139371912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1097/JN9.0000000000000011
Shou-Mei Yang, Xiao-Dan Zhang, Huai-Xing Ma, Dan Wu, Xing Liu, Hao-Bin Yu, Shi-Wei Li, Wen-Jun Gao, Wei-Wei Liu, Su-Yi Li
Abstract Objective This is a retrospective observational cohort study. The objective of this retrospective observational cohort study was to evaluate the value of the combined serum d-lactic acid, diamine oxidase (DAO), and endotoxin levels to predict intestinal barrier impairment and gut-derived infection (GDI) in cancer patients. Methods Cancer patients receiving chemotherapy or palliative care treatment at our hospital were enrolled in the study. The serum concentrations of DAO, d-lactic acid, and endotoxin were determined using the intestinal barrier function biochemical index analysis system. The patients' infection information came from the hospital's Medicom Prescription Automatic Screening System and the medical records. Three hundred fifty-three cancer patients were included in the study (53.8% female, 73.7% cancer stage IV, 27.8% had bowel obstruction). Results The total incidence of GDI was 33.4% (118/353). The median length of hospital stay was 16 days for patients with GDI, compared with 7 days for patients without GDI (P < 0.001). The media hospitalization costs were ¥27,362.35 for patients with GDI compared with ¥11,614.08 for patients without GDI (P < 0.001). The serum concentrations of DAO, d-lactic acid, and endotoxin were significantly higher in patients with GDI. As malignant bowel obstruction (MBO) worsened, the concentrations of DAO, d-lactic acid, and endotoxin increased. Multivariate logistic regression models revealed that the DAO, endotoxin, IL-6, and C-reactive protein levels were significantly associated with an increased risk of GDI. In addition, we also found a fivefold increased risk of infection in patients with MBO compared with those without bowel obstruction (OR = 6.210, P < 0.001). All of the areas under the receiver operating characteristic curve (AUCs) for DAO, d-lactate, and endotoxin to predict GDI were <0.7 (AUC = 0.648, P < 0.001; AUC = 0.624, P < 0.01; AUC = 0.620, P < 0.01, respectively). However, when the parameters were combined (DAO + d-lactate + endotoxin), the predictive power increased significantly (AUC = 0.797, P < 0.001). Moreover, combining these intestinal barrier indicators and the presence of MBO had better power to predict GDI than either alone (AUC = 0.837, P < 0.001). Conclusions Combining the serum DAO, d-lactic acid, and endotoxin levels was a better predictor of GDI than any of the indicators alone, and combining these with the diagnosis of MBO could further improve the efficacy for predicting GDI.
{"title":"Value of combining the serum d-lactate, diamine oxidase, and endotoxin levels to predict gut-derived infections in cancer patients","authors":"Shou-Mei Yang, Xiao-Dan Zhang, Huai-Xing Ma, Dan Wu, Xing Liu, Hao-Bin Yu, Shi-Wei Li, Wen-Jun Gao, Wei-Wei Liu, Su-Yi Li","doi":"10.1097/JN9.0000000000000011","DOIUrl":"https://doi.org/10.1097/JN9.0000000000000011","url":null,"abstract":"Abstract Objective This is a retrospective observational cohort study. The objective of this retrospective observational cohort study was to evaluate the value of the combined serum d-lactic acid, diamine oxidase (DAO), and endotoxin levels to predict intestinal barrier impairment and gut-derived infection (GDI) in cancer patients. Methods Cancer patients receiving chemotherapy or palliative care treatment at our hospital were enrolled in the study. The serum concentrations of DAO, d-lactic acid, and endotoxin were determined using the intestinal barrier function biochemical index analysis system. The patients' infection information came from the hospital's Medicom Prescription Automatic Screening System and the medical records. Three hundred fifty-three cancer patients were included in the study (53.8% female, 73.7% cancer stage IV, 27.8% had bowel obstruction). Results The total incidence of GDI was 33.4% (118/353). The median length of hospital stay was 16 days for patients with GDI, compared with 7 days for patients without GDI (P < 0.001). The media hospitalization costs were ¥27,362.35 for patients with GDI compared with ¥11,614.08 for patients without GDI (P < 0.001). The serum concentrations of DAO, d-lactic acid, and endotoxin were significantly higher in patients with GDI. As malignant bowel obstruction (MBO) worsened, the concentrations of DAO, d-lactic acid, and endotoxin increased. Multivariate logistic regression models revealed that the DAO, endotoxin, IL-6, and C-reactive protein levels were significantly associated with an increased risk of GDI. In addition, we also found a fivefold increased risk of infection in patients with MBO compared with those without bowel obstruction (OR = 6.210, P < 0.001). All of the areas under the receiver operating characteristic curve (AUCs) for DAO, d-lactate, and endotoxin to predict GDI were <0.7 (AUC = 0.648, P < 0.001; AUC = 0.624, P < 0.01; AUC = 0.620, P < 0.01, respectively). However, when the parameters were combined (DAO + d-lactate + endotoxin), the predictive power increased significantly (AUC = 0.797, P < 0.001). Moreover, combining these intestinal barrier indicators and the presence of MBO had better power to predict GDI than either alone (AUC = 0.837, P < 0.001). Conclusions Combining the serum DAO, d-lactic acid, and endotoxin levels was a better predictor of GDI than any of the indicators alone, and combining these with the diagnosis of MBO could further improve the efficacy for predicting GDI.","PeriodicalId":101772,"journal":{"name":"Journal of Nutritional Oncology","volume":"3 1","pages":"101 - 106"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139371902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1097/JN9.0000000000000015
Yu-Jia Zhai, Pei-Yao Si, Ming-Li Liu, Lan Huang
Abstract Cancer is one of the most common causes of morbidity and mortality worldwide. The high demand for specific nutrients and the sensitivity to nutritional deficiencies are newly recognized features of cancer cells. Dietary interventions can suppress tumor demand for particular nutrients and alter certain nutrients to target a tumor's metabolic vulnerability. Cyclic fasting or fasting-mimicking diets (FMDs) are popular approaches that can reduce nutrient intake over a specific period. Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells. Furthermore, FMDs potentiate the sensitivity of tumors to conventional cancer treatments and limit adverse events. Recent findings also highlight the potential value of FMDs in boosting antitumor immune surveillance. However, clinical trials regarding the impact of FMDs on cancer patients remain limited and controversial. Here, we provide the latest information on the effects of FMDs on cancer progression and treatment, focusing on future clinical applications.
{"title":"The emerging role of fasting-mimicking diets in cancer treatment","authors":"Yu-Jia Zhai, Pei-Yao Si, Ming-Li Liu, Lan Huang","doi":"10.1097/JN9.0000000000000015","DOIUrl":"https://doi.org/10.1097/JN9.0000000000000015","url":null,"abstract":"Abstract Cancer is one of the most common causes of morbidity and mortality worldwide. The high demand for specific nutrients and the sensitivity to nutritional deficiencies are newly recognized features of cancer cells. Dietary interventions can suppress tumor demand for particular nutrients and alter certain nutrients to target a tumor's metabolic vulnerability. Cyclic fasting or fasting-mimicking diets (FMDs) are popular approaches that can reduce nutrient intake over a specific period. Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells. Furthermore, FMDs potentiate the sensitivity of tumors to conventional cancer treatments and limit adverse events. Recent findings also highlight the potential value of FMDs in boosting antitumor immune surveillance. However, clinical trials regarding the impact of FMDs on cancer patients remain limited and controversial. Here, we provide the latest information on the effects of FMDs on cancer progression and treatment, focusing on future clinical applications.","PeriodicalId":101772,"journal":{"name":"Journal of Nutritional Oncology","volume":"178 1","pages":"66 - 70"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139371566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1097/JN9.0000000000000009
Pengning Gao, Chuanlin Wang, Jia-Li Xu, Shan-Ling Liu, Lan Zhou
Abstract Selenium is an essential nutrient closely related to redox homeostasis in the body. A redox imbalance will adversely affect the microenvironment inside and outside the cell, leading to cell death. Various types of cell death have been discovered in recent years, but the role(s) of selenium and the associated mechanism(s) of action require further elaboration. We review the roles and mechanisms of action of selenium in cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis. Under normal conditions, selenium inhibits cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis by downregulating the nuclear factor κB pathway, upregulating antiapoptotic proteins, decreasing oxidative stress, increasing antioxidant enzyme activity, enhancing the mTOR pathway, and downregulating the NLRP3/caspase-1 pathway, thereby helping to maintain the normal physiological functions of cells. On the other hand, selenium deficiency leads to activation of the PI3K/AKT and Notch/Hes1 pathways, causing a significant increase in the level of oxidative stress in the organism, resulting in cell necrosis, apoptosis, and pyroptosis. In the case of malignancy, the in vivo metabolite of inorganic selenium, hydrogen selenide, plays an antitumor role by inducing apoptosis and ferroptosis in tumor cells because of its high redox activity. In conclusion, an adequate level of selenium in the body is essential for maintaining normal cellular physiological functions and reducing fibrotic alterations. Furthermore, the in vivo metabolites of inorganic selenium may have some clinical value in antitumor therapy.
{"title":"Role of selenium in cell death","authors":"Pengning Gao, Chuanlin Wang, Jia-Li Xu, Shan-Ling Liu, Lan Zhou","doi":"10.1097/JN9.0000000000000009","DOIUrl":"https://doi.org/10.1097/JN9.0000000000000009","url":null,"abstract":"Abstract Selenium is an essential nutrient closely related to redox homeostasis in the body. A redox imbalance will adversely affect the microenvironment inside and outside the cell, leading to cell death. Various types of cell death have been discovered in recent years, but the role(s) of selenium and the associated mechanism(s) of action require further elaboration. We review the roles and mechanisms of action of selenium in cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis. Under normal conditions, selenium inhibits cell necrosis, apoptosis, ferroptosis, autophagy, and pyroptosis by downregulating the nuclear factor κB pathway, upregulating antiapoptotic proteins, decreasing oxidative stress, increasing antioxidant enzyme activity, enhancing the mTOR pathway, and downregulating the NLRP3/caspase-1 pathway, thereby helping to maintain the normal physiological functions of cells. On the other hand, selenium deficiency leads to activation of the PI3K/AKT and Notch/Hes1 pathways, causing a significant increase in the level of oxidative stress in the organism, resulting in cell necrosis, apoptosis, and pyroptosis. In the case of malignancy, the in vivo metabolite of inorganic selenium, hydrogen selenide, plays an antitumor role by inducing apoptosis and ferroptosis in tumor cells because of its high redox activity. In conclusion, an adequate level of selenium in the body is essential for maintaining normal cellular physiological functions and reducing fibrotic alterations. Furthermore, the in vivo metabolites of inorganic selenium may have some clinical value in antitumor therapy.","PeriodicalId":101772,"journal":{"name":"Journal of Nutritional Oncology","volume":"312 1","pages":"94 - 100"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139371773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-01DOI: 10.1097/JN9.0000000000000013
Fei-Fei Guo, Jue Huang, Fei Chen, Jiuwei Cui
Abstract Multiple pulmonary ground-glass nodules (GGNs), a typical clinical manifestation of multiple primary lung cancers (MPLCs), are of great significance for the early screening, diagnosis, and accurate treatment of lung cancer. Thus, the recent increase in the detection rate of multiple pulmonary GGNs has attracted much attention. However, compared with the more widely studied single GGNs, evaluating GGNs is more challenging because of the uncertainty of the etiology, difficult differential diagnosis, and lack of optimal management standards and guidelines. Most current solutions for multiple GGNs are based on the management experiences and principles of a single GGN. Therefore, it is necessary to obtain better understanding of multiple GGNs and to optimize the diagnostic methods and treatments. Both the existing challenges and potential of new methods for diagnosing and treating multiple pulmonary GGNs are reviewed and discussed in this article, with the aim of providing a reference for the clinical management of this highly prevalent condition.
{"title":"Multiple pulmonary ground-glass nodules: Challenges and advances","authors":"Fei-Fei Guo, Jue Huang, Fei Chen, Jiuwei Cui","doi":"10.1097/JN9.0000000000000013","DOIUrl":"https://doi.org/10.1097/JN9.0000000000000013","url":null,"abstract":"Abstract Multiple pulmonary ground-glass nodules (GGNs), a typical clinical manifestation of multiple primary lung cancers (MPLCs), are of great significance for the early screening, diagnosis, and accurate treatment of lung cancer. Thus, the recent increase in the detection rate of multiple pulmonary GGNs has attracted much attention. However, compared with the more widely studied single GGNs, evaluating GGNs is more challenging because of the uncertainty of the etiology, difficult differential diagnosis, and lack of optimal management standards and guidelines. Most current solutions for multiple GGNs are based on the management experiences and principles of a single GGN. Therefore, it is necessary to obtain better understanding of multiple GGNs and to optimize the diagnostic methods and treatments. Both the existing challenges and potential of new methods for diagnosing and treating multiple pulmonary GGNs are reviewed and discussed in this article, with the aim of providing a reference for the clinical management of this highly prevalent condition.","PeriodicalId":101772,"journal":{"name":"Journal of Nutritional Oncology","volume":"157 1","pages":"85 - 93"},"PeriodicalIF":0.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139371939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}