Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.01.020
Tianshu Han , Wei Wei , Wenbo Jiang , Yiding Geng , Zijie Liu , Ruiming Yang , Chenrun Jin , Yating Lei , Xinyi Sun , Jiaxu Xu , Juan Chen , Changhao Sun
The concept of precision nutrition was first proposed almost a decade ago. Current research in precision nutrition primarily focuses on comprehending individualized variations in response to dietary intake, with little attention being given to other crucial aspects of precision nutrition. Moreover, there is a dearth of comprehensive review studies that portray the landscape and framework of precision nutrition. This review commences by tracing the historical trajectory of nutritional science, with the aim of dissecting the challenges encountered in nutrition science within the new era of disease profiles. This review also deconstructs the field of precision nutrition into four key components: the proposal of the theory for individualized nutritional requirement phenotypes; the establishment of precise methods for measuring dietary intake and evaluating nutritional status; the creation of multidimensional nutritional intervention strategies that address the aspects of what, how, and when to eat; and the construction of a pathway for the translation and integration of scientific research into healthcare practices, utilizing artificial intelligence and information platforms. Incorporating these four components, this review further discusses prospective avenues that warrant exploration to achieve the objective of enhancing health through precision nutrition.
{"title":"The Future Landscape and Framework of Precision Nutrition","authors":"Tianshu Han , Wei Wei , Wenbo Jiang , Yiding Geng , Zijie Liu , Ruiming Yang , Chenrun Jin , Yating Lei , Xinyi Sun , Jiaxu Xu , Juan Chen , Changhao Sun","doi":"10.1016/j.eng.2024.01.020","DOIUrl":"10.1016/j.eng.2024.01.020","url":null,"abstract":"<div><div>The concept of precision nutrition was first proposed almost a decade ago. Current research in precision nutrition primarily focuses on comprehending individualized variations in response to dietary intake, with little attention being given to other crucial aspects of precision nutrition. Moreover, there is a dearth of comprehensive review studies that portray the landscape and framework of precision nutrition. This review commences by tracing the historical trajectory of nutritional science, with the aim of dissecting the challenges encountered in nutrition science within the new era of disease profiles. This review also deconstructs the field of precision nutrition into four key components: the proposal of the theory for individualized nutritional requirement phenotypes; the establishment of precise methods for measuring dietary intake and evaluating nutritional status; the creation of multidimensional nutritional intervention strategies that address the aspects of <em>what, how, and when to eat</em>; and the construction of a pathway for the translation and integration of scientific research into healthcare practices, utilizing artificial intelligence and information platforms. Incorporating these four components, this review further discusses prospective avenues that warrant exploration to achieve the objective of enhancing health through precision nutrition.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 15-25"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140046940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.04.021
Yun Song , Hao Zhang , Huiyuan Guo , Xiaobin Wang
{"title":"Envisioning the Intersectionality and Synergy of Precision Nutrition and Engineering","authors":"Yun Song , Hao Zhang , Huiyuan Guo , Xiaobin Wang","doi":"10.1016/j.eng.2024.04.021","DOIUrl":"10.1016/j.eng.2024.04.021","url":null,"abstract":"","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 12-14"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141136276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2023.10.016
Xifan Wang , Pengjie Wang , Yixuan Li , Huiyuan Guo , Ran Wang , Siyuan Liu , Ju Qiu , Xiaoyu Wang , Yanling Hao , Yunyi Zhao , Haiping Liao , Zhongju Zou , Josephine Thinwa , Rong Liu
Inflammatory bowel disease (IBD) refers to a pair of prevalent conditions (Crohn’s disease and ulcerative colitis) distinguished by persistent inflammation of the large intestine. Procyanidin C1 (PCC1) is a naturally occurring substance derived from grape seeds that has demonstrated notable anti-inflammatory properties. This study examines the potential utility of PCC1 as a treatment for IBD and subsequently examines the host-cell- and microbiome-related mechanisms underlying the detected therapeutic benefits. Working with a classic dextran sodium sulfate (DSS)-induced mouse IBD model, we show that PCC1 protects the mucosal barrier and thereby confers strong protective effects against IBD. PCC1 pretreatment resulted in anti-inflammatory effects and protection against multiple pathological phenotypes in the IBD model mice, including reduced weight loss, lower disease activity index (DAI) totals, and enhanced colon size, as well as obviously beneficial effects on the mucosal barrier (e.g., barrier thickness and activity of mucus-degrading enzymes). We also analyzed the autophagy marker microtubule- associated protein1 light chain 3 (LC3) and found that the level of LC3 was significantly elevated in the intestinal epithelial cell samples of the PCC1-pretreatment group as compared with the non-model mice samples. PCC1 altered the fecal microbiome composition, which included elevating the abundance of Akkermansia muciniphila and Christensenella minuta. Fecal microbiome transplant (FMT) experiments showed that delivering a microbiome from PCC1-treated animals into PCC1-naïve animals conferred protection. Metabolic profiling revealed that both the PCC1-pretreatment and PCC1 FMT groups had elevated levels of the microbiota-derived metabolite valeric acid, and supplementation with this short-chain fatty acid (SCFA) also conferred strong protection against IBD. Finally, inhibitor experiments confirmed that the beneficial effects of valeric acid on the mucus layer are mediated by FOXO1 signaling in the goblet cells of the intestinal epithelium. Beyond showing that PCC1 confers anti-inflammatory effects and protection against IBD by altering the microbiome, our study demonstrates proof of principle for multiple straightforward interventions (PCC1, FMT, and valeric acid supplementation) for ameliorating mucosal barrier damage to treat IBD.
{"title":"Procyanidin C1 Modulates the Microbiome to Increase FOXO1 Signaling and Valeric Acid Levels to Protect the Mucosal Barrier in Inflammatory Bowel Disease","authors":"Xifan Wang , Pengjie Wang , Yixuan Li , Huiyuan Guo , Ran Wang , Siyuan Liu , Ju Qiu , Xiaoyu Wang , Yanling Hao , Yunyi Zhao , Haiping Liao , Zhongju Zou , Josephine Thinwa , Rong Liu","doi":"10.1016/j.eng.2023.10.016","DOIUrl":"10.1016/j.eng.2023.10.016","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) refers to a pair of prevalent conditions (Crohn’s disease and ulcerative colitis) distinguished by persistent inflammation of the large intestine. Procyanidin C1 (PCC1) is a naturally occurring substance derived from grape seeds that has demonstrated notable anti-inflammatory properties. This study examines the potential utility of PCC1 as a treatment for IBD and subsequently examines the host-cell- and microbiome-related mechanisms underlying the detected therapeutic benefits. Working with a classic dextran sodium sulfate (DSS)-induced mouse IBD model, we show that PCC1 protects the mucosal barrier and thereby confers strong protective effects against IBD. PCC1 pretreatment resulted in anti-inflammatory effects and protection against multiple pathological phenotypes in the IBD model mice, including reduced weight loss, lower disease activity index (DAI) totals, and enhanced colon size, as well as obviously beneficial effects on the mucosal barrier (e.g., barrier thickness and activity of mucus-degrading enzymes). We also analyzed the autophagy marker microtubule- associated protein1 light chain 3 (LC3) and found that the level of LC3 was significantly elevated in the intestinal epithelial cell samples of the PCC1-pretreatment group as compared with the non-model mice samples. PCC1 altered the fecal microbiome composition, which included elevating the abundance of <em>Akkermansia muciniphila</em> and <em>Christensenella minuta</em>. Fecal microbiome transplant (FMT) experiments showed that delivering a microbiome from PCC1-treated animals into PCC1-naïve animals conferred protection. Metabolic profiling revealed that both the PCC1-pretreatment and PCC1 FMT groups had elevated levels of the microbiota-derived metabolite valeric acid, and supplementation with this short-chain fatty acid (SCFA) also conferred strong protection against IBD. Finally, inhibitor experiments confirmed that the beneficial effects of valeric acid on the mucus layer are mediated by FOXO1 signaling in the goblet cells of the intestinal epithelium. Beyond showing that PCC1 confers anti-inflammatory effects and protection against IBD by altering the microbiome, our study demonstrates proof of principle for multiple straightforward interventions (PCC1, FMT, and valeric acid supplementation) for ameliorating mucosal barrier damage to treat IBD.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 108-120"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139822493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.08.014
Rui Quan , Chenhong Shi , Yanan Sun , Chengying Zhang , Ran Bi , Yiran Zhang , Xin Bi , Bin Liu , Ziheng Dong , Dekui Jin , Yixuan Li
Pulmonary fibrosis (PF) is a lethal lung disease that predominantly affects older adults; however, whether and how aging triggers fibrosis remains unclear. To pinpoint the predominant initiating factors of PF, we first analyzed single-cell RNA sequencing (scRNA-seq) data from the lung tissues of 45 normal donors and 51 PF patients and found that aging might serve as the primary catalyst for PF development. To further investigate the influence of aging on PF formation, we conducted a comprehensive and thorough study employing a natural aging mouse model. We found that dynamic alterations in the quantity and types of collagen fibers during aging-induced PF progression, especially in collagenous (Col) I, emerged as the predominant driver of PF. We then investigated the regulation of Col I synthesis during aging using primary alveolar type 2 (AT2) cells and A549 cells line through conditioned media and Transwell coculture, and found that secretions—particularly plasminogen activator inhibitor (PAI)-1—from aged AT2 cells promoted fibrosis and enhanced collagen type I alpha 1 (Col1al) production via the transforming growth factor (TGF)-β/small mother against decapentaplegic (Smad)2/3 pathway. Furthermore, scRNA-seq and a histological analysis of human lung tissue demonstrated a significant upregulation of SERPINE1 (the gene encoding PAI-1) and PAI-1 expression in both aging lung tissue and AT2 cells, which was consistent with our findings from animal experiments, providing additional evidence for the pivotal role of PAI-1 during aging and the development of PF. Our research demonstrates that PAI-1, a crucial factor secreted by aging AT2 cells, exerts a pivotal role in promoting the synthesis of Col1a1 in fibroblasts, subsequently leading to Col I deposition, and in driving the progression of PF by mediating the TGF-β/Smad2/3 pathway. Our findings offer critical evidence for the involvement of epithelial dysfunction in age-related PF and provides potential novel therapeutic targets for clinical intervention.
{"title":"PAI-1 Derived from Alveolar Type 2 Cells Drives Aging-Associated Pulmonary Fibrosis","authors":"Rui Quan , Chenhong Shi , Yanan Sun , Chengying Zhang , Ran Bi , Yiran Zhang , Xin Bi , Bin Liu , Ziheng Dong , Dekui Jin , Yixuan Li","doi":"10.1016/j.eng.2024.08.014","DOIUrl":"10.1016/j.eng.2024.08.014","url":null,"abstract":"<div><div>Pulmonary fibrosis (PF) is a lethal lung disease that predominantly affects older adults; however, whether and how aging triggers fibrosis remains unclear. To pinpoint the predominant initiating factors of PF, we first analyzed single-cell RNA sequencing (scRNA-seq) data from the lung tissues of 45 normal donors and 51 PF patients and found that aging might serve as the primary catalyst for PF development. To further investigate the influence of aging on PF formation, we conducted a comprehensive and thorough study employing a natural aging mouse model. We found that dynamic alterations in the quantity and types of collagen fibers during aging-induced PF progression, especially in collagenous (Col) I, emerged as the predominant driver of PF. We then investigated the regulation of Col I synthesis during aging using primary alveolar type 2 (AT2) cells and A549 cells line through conditioned media and Transwell coculture, and found that secretions—particularly plasminogen activator inhibitor (PAI)-1—from aged AT2 cells promoted fibrosis and enhanced collagen type I alpha 1 (Col1al) production via the transforming growth factor (TGF)-β/small mother against decapentaplegic (Smad)2/3 pathway. Furthermore, scRNA-seq and a histological analysis of human lung tissue demonstrated a significant upregulation of <em>SERPINE1</em> (the gene encoding PAI-1) and PAI-1 expression in both aging lung tissue and AT2 cells, which was consistent with our findings from animal experiments, providing additional evidence for the pivotal role of PAI-1 during aging and the development of PF. Our research demonstrates that PAI-1, a crucial factor secreted by aging AT2 cells, exerts a pivotal role in promoting the synthesis of Col1a1 in fibroblasts, subsequently leading to Col I deposition, and in driving the progression of PF by mediating the TGF-β/Smad2/3 pathway. Our findings offer critical evidence for the involvement of epithelial dysfunction in age-related PF and provides potential novel therapeutic targets for clinical intervention.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 74-87"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142701428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.05.015
Xu Chen , Zhiyong Du , Dongqing Guo , Jincheng Guo , Qianbin Sun , Tiantian Liu , Kun Hua , Chun Li , Yong Wang , Wei Wang
This investigation elucidates the spatiotemporal dynamics of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation following myocardial infarction (MI), a process that has not been fully characterized. We revealed early activation of the NLRP3 inflammasome in mice with MI and characterized its dynamic temporal expression. Notably, the knockout and inhibition of Nlrp3 expression were found to significantly mitigate infarct size and enhance cardiac function. Furthermore, our analysis of the spatial characteristics of inflammasome activation revealed predominant activation in macrophages and subsequent activation in fibroblasts on the third day post-MI. To elucidate the nexus between macrophage-associated NLRP3 inflammasome activation and myocardial fibrosis, we employed targeted metabolomics analyses of inflammatory oxylipins, small interfering RNA (siRNA) interference experiments, and various molecular assays. These findings revealed that macrophage-associated inflammasome activation facilitates the conversion of fibroblasts into myofibroblasts via the 15-hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE)-mediated small mother against decapentaplegic (Smad) pathway. Additionally, both mass spectrometry imaging (MSI) and targeted metabolomics analyses confirmed the significant increase in 15-HETE levels in mice with MI and in patients with MI and acute coronary syndrome (ACS). Our comprehensive dataset suggests that NLRP3 inflammasome activation in MI is characterized by distinct temporal and spatial patterns. These insights mark a significant advancement toward precise MI prevention and treatment strategies, particularly early myocardial fibrosis intervention.
{"title":"Activation of the Macrophage-Associated Inflammasome Exacerbates Myocardial Fibrosis Through the 15-HETE-Mediated Pathway in Acute Myocardial Infarction","authors":"Xu Chen , Zhiyong Du , Dongqing Guo , Jincheng Guo , Qianbin Sun , Tiantian Liu , Kun Hua , Chun Li , Yong Wang , Wei Wang","doi":"10.1016/j.eng.2024.05.015","DOIUrl":"10.1016/j.eng.2024.05.015","url":null,"abstract":"<div><div>This investigation elucidates the spatiotemporal dynamics of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation following myocardial infarction (MI), a process that has not been fully characterized. We revealed early activation of the NLRP3 inflammasome in mice with MI and characterized its dynamic temporal expression. Notably, the knockout and inhibition of <em>Nlrp3</em> expression were found to significantly mitigate infarct size and enhance cardiac function. Furthermore, our analysis of the spatial characteristics of inflammasome activation revealed predominant activation in macrophages and subsequent activation in fibroblasts on the third day post-MI. To elucidate the nexus between macrophage-associated NLRP3 inflammasome activation and myocardial fibrosis, we employed targeted metabolomics analyses of inflammatory oxylipins, small interfering RNA (siRNA) interference experiments, and various molecular assays. These findings revealed that macrophage-associated inflammasome activation facilitates the conversion of fibroblasts into myofibroblasts via the 15-hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE)-mediated small mother against decapentaplegic (Smad) pathway. Additionally, both mass spectrometry imaging (MSI) and targeted metabolomics analyses confirmed the significant increase in 15-HETE levels in mice with MI and in patients with MI and acute coronary syndrome (ACS). Our comprehensive dataset suggests that NLRP3 inflammasome activation in MI is characterized by distinct temporal and spatial patterns. These insights mark a significant advancement toward precise MI prevention and treatment strategies, particularly early myocardial fibrosis intervention.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 143-156"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141392634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.08.003
Junping Gu , Xiaoyu Qian , Yiwei Liu , Qinggong Wang , Yiyang Zhang , Xuan Ruan , Xiangjin Deng , Yaowen Lu , Jian Song , Hui Zhang , Yunning Dong , Mengmeng Wei , Wei Yao , Shuiqing Li , Weihua Wang , Zhigang Zou , Mengfei Yang
Facing the challenges of in-situ utilization of lunar regolith resources, applying an external electric field to manipulate lunar particles has become a promising method for space particle control, which mainly depends on the particle charging properties in the applied electric field. Using the surficial lunar regolith samples brought back from the Moon by the Chang’e-5 mission (CE5 LS), this work successively studied their charging properties, particle dynamics, and their collision damages to aerospace materials under the action of an external electric field in high-vacuum conditions. The results indicated that the charging process and electrostatic projection of lunar regolith particles under high-vacuum conditions were different from those under atmosphere conditions. The particle diameter range of CE5 LS used in the experiment is 27.7–139.0 μm. For electric field strength of 3–12 kV·cm−1, the charge obtained by CE5 LS is 4.8 × 10−15–4.7 × 10−13 C and the charge-to-mass ratio is 1.2 × 10−5–6.8 × 10−4 C·kg−1. The CE5 LS is easier to be negatively charged in an external electric field. Furthermore, significant damages were observed on the target impact surfaces, indicating severe influences of lunar regolith particles on aerospace materials. Our work contributes to a more comprehensive understanding of physical mechanisms controlling the lunar regolith shielding and utilization, and will inspire broad efforts to develop the lunar in-situ engineering solutions.
面对月球碎屑资源就地利用的挑战，应用外加电场操纵月球颗粒已成为一种前景广阔的空间颗粒控制方法，而这主要取决于颗粒在外加电场中的充电特性。本研究利用嫦娥五号任务（CE5 LS）从月球带回的表层月球碎屑样品，先后研究了其在高真空条件下外电场作用下的充电特性、颗粒动力学特性及其对航天材料的碰撞损伤。结果表明，在高真空条件下，月球碎屑颗粒的充电过程和静电投影与大气条件下不同。实验中使用的 CE5 LS 颗粒直径范围为 27.7-139.0 μm。在电场强度为 3-12 kV-cm-1 时，CE5 LS 获得的电荷为 4.8 × 10-15-4.7 × 10-13 C，电荷质量比为 1.2 × 10-5-6.8 × 10-4 C-kg-1。CE5 LS 在外部电场中更容易带负电。此外，在目标撞击表面观察到了明显的损伤，表明月球碎屑对航空航天材料的影响非常严重。我们的工作有助于更全面地了解控制月球渣岩屏蔽和利用的物理机制，并将激励人们广泛努力开发月球原位工程解决方案。
{"title":"Charging Properties and Particle Dynamics of Chang’e-5 Lunar Sample in an External Electric Field","authors":"Junping Gu , Xiaoyu Qian , Yiwei Liu , Qinggong Wang , Yiyang Zhang , Xuan Ruan , Xiangjin Deng , Yaowen Lu , Jian Song , Hui Zhang , Yunning Dong , Mengmeng Wei , Wei Yao , Shuiqing Li , Weihua Wang , Zhigang Zou , Mengfei Yang","doi":"10.1016/j.eng.2024.08.003","DOIUrl":"10.1016/j.eng.2024.08.003","url":null,"abstract":"<div><div>Facing the challenges of <em>in-situ</em> utilization of lunar regolith resources, applying an external electric field to manipulate lunar particles has become a promising method for space particle control, which mainly depends on the particle charging properties in the applied electric field. Using the surficial lunar regolith samples brought back from the Moon by the Chang’e-5 mission (CE5 LS), this work successively studied their charging properties, particle dynamics, and their collision damages to aerospace materials under the action of an external electric field in high-vacuum conditions. The results indicated that the charging process and electrostatic projection of lunar regolith particles under high-vacuum conditions were different from those under atmosphere conditions. The particle diameter range of CE5 LS used in the experiment is 27.7–139.0 μm. For electric field strength of 3–12 kV·cm<sup>−1</sup>, the charge obtained by CE5 LS is 4.8 × 10<sup>−15</sup>–4.7 × 10<sup>−13</sup> C and the charge-to-mass ratio is 1.2 × 10<sup>−5</sup>–6.8 × 10<sup>−4</sup> C·kg<sup>−1</sup>. The CE5 LS is easier to be negatively charged in an external electric field. Furthermore, significant damages were observed on the target impact surfaces, indicating severe influences of lunar regolith particles on aerospace materials. Our work contributes to a more comprehensive understanding of physical mechanisms controlling the lunar regolith shielding and utilization, and will inspire broad efforts to develop the lunar <em>in-situ</em> engineering solutions.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 267-277"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.09.008
Mark Peplow
{"title":"Hydrogen Hubs Arise in the United States","authors":"Mark Peplow","doi":"10.1016/j.eng.2024.09.008","DOIUrl":"10.1016/j.eng.2024.09.008","url":null,"abstract":"","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 3-5"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Susceptibility to pathogens in the elderly is heightened with age, largely because of immunosenescence. As an immune regulatory organ, bone marrow creates immune cells that move to other organs and tissues through the blood. Despite the significance of this process of this organ, there is limited research on changes in immune cell generation in the bone marrow and their effects on immunosenescence. In this study, the compositions of immune cells in bone marrow from young (three months) and old (24+ months) mice were compared by means of mass cytometry, with further validation obtained through the reanalysis of single-cell RNA sequencing data and cell sorting via flow cytometry. The effects of differential immune cells on immunosenescence in old mice were evaluated using the Clostridium difficile (C. difficile) infection model. Our results showed that aged mice presented with a reduction in bone trabeculae structure, which was accompanied by a notable increase in polymorphonuclear (PMN)-myeloid-derived suppressor cell (MDSC) abundance. Through bulk-seq and reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis, we identified differential genes associated with the immune response—specifically, the Th17 cell differentiation pathway. Furthermore, the increase in exported PMN-MDSCs to the large intestine resulted in increased gut permeability and inflammatory damage to the colon following C. difficile infection. After clearing the PMN-MDSCs in old mice using the anti-Gr-1 antibody, the symptoms induced by C. difficile were significantly relieved, as evidenced by an inhibited IL-17 pathway in the colon and reduced gut permeability. In conclusion, aging increases the number of PMN-MDSCs in both the generated bone marrow and the outputted intestine, which contributes to susceptibility to C. difficile infection. This study provides a novel target for anti-aging therapy for immunosenescence, which is beneficial for improving immune function in elders.
{"title":"PMN-MDSC: A Culprit Behind Immunosenescence and Increased Susceptibility to Clostridioides difficile Infection During Aging","authors":"Jianmin Wu , Ming Zhang , Hao Zhang , Mingxuan Sheng , Jiazeng Sun , Fang Wu , Haina Gao , Lishui Chen , Zhili Li , Qiyu Tian , Longjiao Zhu , Bing Fang","doi":"10.1016/j.eng.2024.06.014","DOIUrl":"10.1016/j.eng.2024.06.014","url":null,"abstract":"<div><div>Susceptibility to pathogens in the elderly is heightened with age, largely because of immunosenescence. As an immune regulatory organ, bone marrow creates immune cells that move to other organs and tissues through the blood. Despite the significance of this process of this organ, there is limited research on changes in immune cell generation in the bone marrow and their effects on immunosenescence. In this study, the compositions of immune cells in bone marrow from young (three months) and old (24+ months) mice were compared by means of mass cytometry, with further validation obtained through the reanalysis of single-cell RNA sequencing data and cell sorting via flow cytometry. The effects of differential immune cells on immunosenescence in old mice were evaluated using the <em>Clostridium difficile</em> (<em>C. difficile</em>) infection model. Our results showed that aged mice presented with a reduction in bone trabeculae structure, which was accompanied by a notable increase in polymorphonuclear (PMN)-myeloid-derived suppressor cell (MDSC) abundance. Through bulk-seq and reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis, we identified differential genes associated with the immune response—specifically, the Th17 cell differentiation pathway. Furthermore, the increase in exported PMN-MDSCs to the large intestine resulted in increased gut permeability and inflammatory damage to the colon following <em>C. difficile</em> infection. After clearing the PMN-MDSCs in old mice using the anti-Gr-1 antibody, the symptoms induced by <em>C. difficile</em> were significantly relieved, as evidenced by an inhibited IL-17 pathway in the colon and reduced gut permeability. In conclusion, aging increases the number of PMN-MDSCs in both the generated bone marrow and the outputted intestine, which contributes to susceptibility to <em>C. difficile</em> infection. This study provides a novel target for anti-aging therapy for immunosenescence, which is beneficial for improving immune function in elders.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 59-73"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141849696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01DOI: 10.1016/j.eng.2024.04.023
Xiang Wang , Di Zhang , Yogendra Pratap Singh , Miji Yeo , Guotao Deng , Jiaqi Lai , Fei Chen , Ibrahim T. Ozbolat , Yin Yu
Organ damage or failure arising from injury, disease, and aging poses challenges due to the body’s limited regenerative capabilities. Organ transplantation presents the issues of donor shortages and immune rejection risks, necessitating innovative solutions. The three-dimensional (3D) bioprinting of organs on demand offers promise in tissue engineering and regenerative medicine. In this review, we explore the state-of-the-art bioprinting technologies, with a focus on bioink and cell type selections. We follow with discussions on advances in the bioprinting of solid organs, such as the heart, liver, kidney, and pancreas, highlighting the importance of vascularization and cell integration. Finally, we provide insights into key challenges and future directions in the context of the clinical translation of bioprinted organs and their large-scale production.
{"title":"Progress in Organ Bioprinting for Regenerative Medicine","authors":"Xiang Wang , Di Zhang , Yogendra Pratap Singh , Miji Yeo , Guotao Deng , Jiaqi Lai , Fei Chen , Ibrahim T. Ozbolat , Yin Yu","doi":"10.1016/j.eng.2024.04.023","DOIUrl":"10.1016/j.eng.2024.04.023","url":null,"abstract":"<div><div>Organ damage or failure arising from injury, disease, and aging poses challenges due to the body’s limited regenerative capabilities. Organ transplantation presents the issues of donor shortages and immune rejection risks, necessitating innovative solutions. The three-dimensional (3D) bioprinting of organs on demand offers promise in tissue engineering and regenerative medicine. In this review, we explore the state-of-the-art bioprinting technologies, with a focus on bioink and cell type selections. We follow with discussions on advances in the bioprinting of solid organs, such as the heart, liver, kidney, and pancreas, highlighting the importance of vascularization and cell integration. Finally, we provide insights into key challenges and future directions in the context of the clinical translation of bioprinted organs and their large-scale production.</div></div>","PeriodicalId":11783,"journal":{"name":"Engineering","volume":"42 ","pages":"Pages 121-142"},"PeriodicalIF":10.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141389905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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