In recent years, aortic aneurysms (AAs) have attracted increasing attention due to their asymptomatic onset and high mortality. In clinic, surgery and anti-hypertensive or lipid-lowering medicine is usually applied in the treatments of AA. However, AA is prone to relapse and sudden rupture may happen. Therefore, more effective prevention and treatment methods are urgently needed. Stem cells are believed to play a crucial role in vascular formation and regeneration of damaged tissues during vascular disease progression. With the development of single-cell RNA sequencing analysis, many populations of stem cells have been discovered in AA tissues. Recent studies have demonstrated that they may participate in the occurrence or development of AAs. Besides, there is a prospect in clinical treatment for AAs when regenerative medicine with stem cells comes into the picture. This review mainly discusses the latest findings on the crucial roles of stem cells in AAs as well as their potential therapeutic strategies of stem cells, which provides some references for the prevention, diagnosis, and treatment of AAs. Further studies are needed to explore the novel application of stem cell therapies for AAs.
{"title":"Role of stem cells in aortic aneurysm","authors":"Zheng-hua Wang, Yu Yin, Yuge Zhang, Aijuan Qu, Bao-qi Yu","doi":"10.36922/gtm.v2i1.241","DOIUrl":"https://doi.org/10.36922/gtm.v2i1.241","url":null,"abstract":"In recent years, aortic aneurysms (AAs) have attracted increasing attention due to their asymptomatic onset and high mortality. In clinic, surgery and anti-hypertensive or lipid-lowering medicine is usually applied in the treatments of AA. However, AA is prone to relapse and sudden rupture may happen. Therefore, more effective prevention and treatment methods are urgently needed. Stem cells are believed to play a crucial role in vascular formation and regeneration of damaged tissues during vascular disease progression. With the development of single-cell RNA sequencing analysis, many populations of stem cells have been discovered in AA tissues. Recent studies have demonstrated that they may participate in the occurrence or development of AAs. Besides, there is a prospect in clinical treatment for AAs when regenerative medicine with stem cells comes into the picture. This review mainly discusses the latest findings on the crucial roles of stem cells in AAs as well as their potential therapeutic strategies of stem cells, which provides some references for the prevention, diagnosis, and treatment of AAs. Further studies are needed to explore the novel application of stem cell therapies for AAs.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80081243","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}
Human T-lymphotropic virus Type 1 (HTLV-1) is a viral infectious agent that may cause chronic infection of T lymphocytes. HTLV-1 infection is related to multiple human diseases, including adult T-cell leukemia, which is a neoplastic growth of HTLV-1-infected T cells, and neoplastic inflammatory conditions such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), Sjögren’s syndrome, polymyositis uveitis, and bronchoalveolitis. T regulatory cells (Tregs), also known as regulatory T cells, and T helper 17 (Th17) cells, a distinct subset of cluster differentiation T cells with interleukin-17 as their major cytokine, orchestrate the pathogenesis of anti-inflammatory and inflammatory responses in HTLV-1-mediated diseases. In this review, we aim to evaluate the immune responses of Tregs as anti-inflammatory cells and Th17 cells as inflammatory cells in HTLV-1 infection.
{"title":"Inflammatory and anti-inflammatory responses inhuman T-lymphotropic virus Type 1 infection","authors":"Elnaz Sadat Hosseini, E. Abdollahi, N. Saghafi","doi":"10.36922/gtm.v2i1.67","DOIUrl":"https://doi.org/10.36922/gtm.v2i1.67","url":null,"abstract":"Human T-lymphotropic virus Type 1 (HTLV-1) is a viral infectious agent that may cause chronic infection of T lymphocytes. HTLV-1 infection is related to multiple human diseases, including adult T-cell leukemia, which is a neoplastic growth of HTLV-1-infected T cells, and neoplastic inflammatory conditions such as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), Sjögren’s syndrome, polymyositis uveitis, and bronchoalveolitis. T regulatory cells (Tregs), also known as regulatory T cells, and T helper 17 (Th17) cells, a distinct subset of cluster differentiation T cells with interleukin-17 as their major cytokine, orchestrate the pathogenesis of anti-inflammatory and inflammatory responses in HTLV-1-mediated diseases. In this review, we aim to evaluate the immune responses of Tregs as anti-inflammatory cells and Th17 cells as inflammatory cells in HTLV-1 infection.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89429050","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}
Cardiometabolic diseases (CMDs), which cause 31% of all global deaths, are one of the greatest public health challenges. Mineralocorticoid receptor (MR), as a key nuclear transcription factor, is an important drug target for the treatment of CMDs. It is known that MR is expressed in almost all tissues and organs involved in cardiovascular homeostasis, including immune tissue, adipose tissue, brain, heart, kidney, and blood vessels. In the pathophysiology of CMDs, MR exerts different functions in different tissues and cells. This review summarizes the roles of MR in various cell types and discusses the molecular mechanisms through which MR exerts it functions in CMDs.
{"title":"The The multifaceted functions of mineralocorticoid receptor in cardiometabolic disease","authors":"Jian-Yong Sun, Yong-Li Wang, Hong Zhu, S. Duan","doi":"10.36922/gtm.v2i1.229","DOIUrl":"https://doi.org/10.36922/gtm.v2i1.229","url":null,"abstract":"Cardiometabolic diseases (CMDs), which cause 31% of all global deaths, are one of the greatest public health challenges. Mineralocorticoid receptor (MR), as a key nuclear transcription factor, is an important drug target for the treatment of CMDs. It is known that MR is expressed in almost all tissues and organs involved in cardiovascular homeostasis, including immune tissue, adipose tissue, brain, heart, kidney, and blood vessels. In the pathophysiology of CMDs, MR exerts different functions in different tissues and cells. This review summarizes the roles of MR in various cell types and discusses the molecular mechanisms through which MR exerts it functions in CMDs.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"51 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76440179","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}
Resveratrol is a naturally occurring polyphenolic compound that is thought to have vasculoprotective properties. Its observed effects are proposed, in part, to be mediated through the induction of endothelial Krϋppel-like factor 2 (KLF2) expression. KLF2 is a nuclear transcription factor that is highly expressed within the vascular endothelium. Studies from our laboratory and others have shown that this protein mediates vascular function through its transactivation domain, and its targeted expression promotes vascular health, notably by acting as an important positive regulator of endothelial barrier function. In this study, we demonstrate that resveratrol possesses endothelial barrier protective effects dependent on the presence of KLF2, with several key endothelial tight junction proteins expressed in a KLF2-dependent manner. Collectively, our findings identify KLF2 as essential for resveratrol-mediated endothelial barrier protection, thus further implicating KLF2 as a critical vasculoprotective factor.
{"title":"The vasculoprotective effects of resveratrol are mediated via Kruppel-like factor 2 dependent protection of endothelial barrier function","authors":"Xianming Zhou, Lily Lin, Hong Shi","doi":"10.36922/gtm.v2i1.218","DOIUrl":"https://doi.org/10.36922/gtm.v2i1.218","url":null,"abstract":"Resveratrol is a naturally occurring polyphenolic compound that is thought to have vasculoprotective properties. Its observed effects are proposed, in part, to be mediated through the induction of endothelial Krϋppel-like factor 2 (KLF2) expression. KLF2 is a nuclear transcription factor that is highly expressed within the vascular endothelium. Studies from our laboratory and others have shown that this protein mediates vascular function through its transactivation domain, and its targeted expression promotes vascular health, notably by acting as an important positive regulator of endothelial barrier function. In this study, we demonstrate that resveratrol possesses endothelial barrier protective effects dependent on the presence of KLF2, with several key endothelial tight junction proteins expressed in a KLF2-dependent manner. Collectively, our findings identify KLF2 as essential for resveratrol-mediated endothelial barrier protection, thus further implicating KLF2 as a critical vasculoprotective factor.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91134402","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}
S. Malyutina, V. Maximov, O. Chervova, P. Orlov, V. Voloshin, A. Ryabikov, M. Voevoda, T. Nikitenko
In this study, we evaluated the association of blood leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNA-CN) with the risk of incident colorectal cancer (CRC). We studied and followed-up a cohort of Russian men and women (aged 45 – 69 years, n = 9360, 54% female) from the HAPIEE study for 15 years. Using the nested case-control design, we selected cases with incident CRC among those free from any baseline cancer (n = 146) and sex- and age-stratified controls among those free from baseline cancer and cardiovascular disease and alive at the end of the follow-up (n = 799). We employed multivariable-adjusted logistic regression to estimate the odds ratios (ORs) of CRC per 1 decile of LTL or mtDNA-CN. We observed an inverse association of LTL and mtDNA-CN baseline values with the 15-year risk of incident CRC. Carriers of shorter telomeres had an increased 15-year risk of incident CRC with adjusted OR 3.2 (95% CI: 2.56 – 3.87, P < 0.001) per 1 decile decrease in LTL, independent of baseline age, sex, smoking, body mass index, blood pressure, lipid levels, and education. Similarly, lower mtDNA-CN was associated with the higher risk of incident CRC with adjusted OR 1.7 (95% CI: 1.12 – 1.89, P < 0.001) per 1 decile decrease in mtDNA-CN, independent of the aforementioned factors. Using the modified values of LTL and mtDNA-CN adjusted for multiple factors and their interactions with a case–control status, the ORs of CRC were 2.53 and 1.52 per 1 decile decrease in adjusted baseline LTL and mtDNA-CN, respectively. In conclusion, LTL and mtDNA-CN were independent inverse predictors of the 15-year risk of CRC in the Russian cohort. These findings highlight the relevance for subsequent research to exploit the mechanisms through which LTL and mtDNA-CN may reflect human health.
{"title":"Leukocyte telomere length and mitochondrial DNA copy number association with colorectal cancer risk in an aging population","authors":"S. Malyutina, V. Maximov, O. Chervova, P. Orlov, V. Voloshin, A. Ryabikov, M. Voevoda, T. Nikitenko","doi":"10.36922/gtm.v2i1.184","DOIUrl":"https://doi.org/10.36922/gtm.v2i1.184","url":null,"abstract":"In this study, we evaluated the association of blood leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNA-CN) with the risk of incident colorectal cancer (CRC). We studied and followed-up a cohort of Russian men and women (aged 45 – 69 years, n = 9360, 54% female) from the HAPIEE study for 15 years. Using the nested case-control design, we selected cases with incident CRC among those free from any baseline cancer (n = 146) and sex- and age-stratified controls among those free from baseline cancer and cardiovascular disease and alive at the end of the follow-up (n = 799). We employed multivariable-adjusted logistic regression to estimate the odds ratios (ORs) of CRC per 1 decile of LTL or mtDNA-CN. We observed an inverse association of LTL and mtDNA-CN baseline values with the 15-year risk of incident CRC. Carriers of shorter telomeres had an increased 15-year risk of incident CRC with adjusted OR 3.2 (95% CI: 2.56 – 3.87, P < 0.001) per 1 decile decrease in LTL, independent of baseline age, sex, smoking, body mass index, blood pressure, lipid levels, and education. Similarly, lower mtDNA-CN was associated with the higher risk of incident CRC with adjusted OR 1.7 (95% CI: 1.12 – 1.89, P < 0.001) per 1 decile decrease in mtDNA-CN, independent of the aforementioned factors. Using the modified values of LTL and mtDNA-CN adjusted for multiple factors and their interactions with a case–control status, the ORs of CRC were 2.53 and 1.52 per 1 decile decrease in adjusted baseline LTL and mtDNA-CN, respectively. In conclusion, LTL and mtDNA-CN were independent inverse predictors of the 15-year risk of CRC in the Russian cohort. These findings highlight the relevance for subsequent research to exploit the mechanisms through which LTL and mtDNA-CN may reflect human health.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86682634","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}
Dien Ye, Congqing Wu, Lei Cai, Deborah A Howatt, Ching-Ling Liang, Yuriko Katsumata, Adam E Mullick, Ryan E Temel, A H Jan Danser, Alan Daugherty, Hong S Lu
Hepatocyte-derived angiotensinogen (AGT) is the precursor of angiotensin II (AngII). We determined the effects of hepatocyte-specific (N-acetylgalactosamine-conjugated) antisense oligonucleotides targeting AGT (GalNAc AGT ASO) on AngII-mediated blood pressure (BP) regulation and atherosclerosis and compared its effects with losartan, an AngII type 1 (AT1) receptor blocker, in hypercholesterolemic mice. Eight-week-old male low-density lipoprotein (LDL) receptor deficient mice were administered vehicle or GalNAc AGT ASO (1, 2.5, or 5 mg/kg) subcutaneously beginning 2 weeks before the initiation of Western diet feeding. All mice were fed Western diet for 12 weeks. Their systolic BP was monitored by the tail-cuff technique, and the atherosclerotic lesion area was measured by an en face method. Although the effects of all 3 doses of GalNAc AGT ASO on plasma AGT concentrations were similar, GalNAc AGT ASO reduced BP and atherosclerotic lesion size in a dose-dependent manner. Subsequently, we compared the effects of GalNAc AGT ASO (5 mg/kg) with losartan (15 mg/kg/day). Compared to losartan, GalNAc AGT ASO led to more profound increases in plasma renin and reduction in BP but had similar effects on atherosclerosis. Remarkably, GalNAc AGT ASO also reduced liver steatosis, which was not observed in losartan-treated mice. In conclusion, the BP increase and atherosclerosis development in hypercholesterolemic mice are dependent on AngII generated from hepatic AGT. Deleting hepatic AGT improves diet-induced liver steatosis, and this occurs in an AT1 receptor-independent manner.
{"title":"Antisense oligonucleotides targeting hepatic angiotensinogen reduce atherosclerosis and liver steatosis in hypercholesterolemic mice.","authors":"Dien Ye, Congqing Wu, Lei Cai, Deborah A Howatt, Ching-Ling Liang, Yuriko Katsumata, Adam E Mullick, Ryan E Temel, A H Jan Danser, Alan Daugherty, Hong S Lu","doi":"10.36922/gtm.288","DOIUrl":"https://doi.org/10.36922/gtm.288","url":null,"abstract":"<p><p>Hepatocyte-derived angiotensinogen (AGT) is the precursor of angiotensin II (AngII). We determined the effects of hepatocyte-specific (<i>N</i>-acetylgalactosamine-conjugated) antisense oligonucleotides targeting AGT (GalNAc AGT ASO) on AngII-mediated blood pressure (BP) regulation and atherosclerosis and compared its effects with losartan, an AngII type 1 (AT1) receptor blocker, in hypercholesterolemic mice. Eight-week-old male low-density lipoprotein (LDL) receptor deficient mice were administered vehicle or GalNAc AGT ASO (1, 2.5, or 5 mg/kg) subcutaneously beginning 2 weeks before the initiation of Western diet feeding. All mice were fed Western diet for 12 weeks. Their systolic BP was monitored by the tail-cuff technique, and the atherosclerotic lesion area was measured by an <i>en face</i> method. Although the effects of all 3 doses of GalNAc AGT ASO on plasma AGT concentrations were similar, GalNAc AGT ASO reduced BP and atherosclerotic lesion size in a dose-dependent manner. Subsequently, we compared the effects of GalNAc AGT ASO (5 mg/kg) with losartan (15 mg/kg/day). Compared to losartan, GalNAc AGT ASO led to more profound increases in plasma renin and reduction in BP but had similar effects on atherosclerosis. Remarkably, GalNAc AGT ASO also reduced liver steatosis, which was not observed in losartan-treated mice. In conclusion, the BP increase and atherosclerosis development in hypercholesterolemic mice are dependent on AngII generated from hepatic AGT. Deleting hepatic AGT improves diet-induced liver steatosis, and this occurs in an AT1 receptor-independent manner.</p>","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10249463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9622254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inaugural editorial: A new platform dedicated to promote bench-to-bedside translation","authors":"Lemin Zheng","doi":"10.36922/gtm.v1i2.315","DOIUrl":"https://doi.org/10.36922/gtm.v1i2.315","url":null,"abstract":"<jats:p>N/A</jats:p>","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79205483","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}
The most important clinical features of aortic dissection (AD) are its acute onset, rapid progress, and high fatality rate. The exact pathogenesis of AD is unclear, and the focus of current research on the mechanism of AD has been primarily on hypertension and changes in metalloproteinases, among which leptin plays an important role. The purpose of this study is to evaluate the effect of leptin on AD. We conducted a computerized literature search on animal studies related to leptin and dissecting aortic aneurysm in PubMed, EMBASE, Cochrane Library, MEDLINE, and other databases from their inception to present. Meta-analysis was conducted to compare the changes in aortic diameter, aortic dilatation, and the incidence of AD in mice under the local intervention of leptin or leptin antagonist (LepA). A total of four studies were included, involving five batches of animal experiments. According to the results of the meta-analysis, the increase in local leptin content led to the enlargement of aortic diameter (relative risk [RR] = 0.18; 95% confidence interval [CI]: 0.09 – 0.27; P < 0.0001) and increased aortic dilatation (RR = 0.11; 95% CI: 0.01 – 0.22; P < 0.0001). This meta-analysis showed that local leptin administration increased the aortic diameter and aortic dilatation. However, due to high heterogeneity between the results, it is difficult to draw a clear conclusion on the effect of leptin on AD.
{"title":"Effect of leptin on aortic dissection","authors":"Ling Chen, Y. Xi, Fan Xu, L. Chen","doi":"10.36922/gtm.v1i2.85","DOIUrl":"https://doi.org/10.36922/gtm.v1i2.85","url":null,"abstract":"The most important clinical features of aortic dissection (AD) are its acute onset, rapid progress, and high fatality rate. The exact pathogenesis of AD is unclear, and the focus of current research on the mechanism of AD has been primarily on hypertension and changes in metalloproteinases, among which leptin plays an important role. The purpose of this study is to evaluate the effect of leptin on AD. We conducted a computerized literature search on animal studies related to leptin and dissecting aortic aneurysm in PubMed, EMBASE, Cochrane Library, MEDLINE, and other databases from their inception to present. Meta-analysis was conducted to compare the changes in aortic diameter, aortic dilatation, and the incidence of AD in mice under the local intervention of leptin or leptin antagonist (LepA). A total of four studies were included, involving five batches of animal experiments. According to the results of the meta-analysis, the increase in local leptin content led to the enlargement of aortic diameter (relative risk [RR] = 0.18; 95% confidence interval [CI]: 0.09 – 0.27; P < 0.0001) and increased aortic dilatation (RR = 0.11; 95% CI: 0.01 – 0.22; P < 0.0001). This meta-analysis showed that local leptin administration increased the aortic diameter and aortic dilatation. However, due to high heterogeneity between the results, it is difficult to draw a clear conclusion on the effect of leptin on AD.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"103 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80651835","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}
Jinyang Wang, Lei Zhu, Po Yang, P. Li, Jihong Wang, Huating Li, Bin Sheng
This paper presents a survey on the development and major advances of artificial intelligence assisted robotics for therapeutic tasks by concentrating on the current challenges emerging from the clinical application process and the research efforts mitigating the problems. In this survey, we search Nature, Science, Cell and other websites with high influence by using keywords (i.e., artificial assisted medical robots), categorized research works over the past three decades based on therapeutic applications, and discussed the latest development and bottleneck problems of each subtopic finally. Specifically, we first present a chronology of the artificial intelligence assisted techniques developed for medical therapeutic tasks over the past three decades and then classify them according to the principles of the algorithm and its corresponding type of medical therapeutic tasks. The artificial intelligence technologies in the chronology evolve from classic machine learning statistical methods of the early nineties to data driven deep learning methods. Then a taxonomy of the artificial intelligence technologies assisted therapeutic tasks in the past three decades is described according to the therapeutic task types and hot topics of the knotty problems. One prosperous trend has been abstracted from the interpretation of our taxonomy and the most highly cited research papers using certain search criteria with Nature and Cell databases, which undergoes revolutionary development of artificial intelligence and closer integration with clinical therapeutic tasks. The trend is unprecedent and more comprehensive Human-Robot Interaction, which benefits sophisticated telesurgery and microsurgery by being capable of facilitating Surgeons with higher imaging accuracy and human-like tactile sensation. Our survey discusses the current grand challenges and future trends of artificial intelligence assisted therapeutic tasks for the convenience of clinical research and applications. We hope this survey would help bridging the gap between entrepreneurial translation and research.
{"title":"State-of-the-Art: A Taxonomy of AI-Assisted Robotics for Medical Therapies and Applications","authors":"Jinyang Wang, Lei Zhu, Po Yang, P. Li, Jihong Wang, Huating Li, Bin Sheng","doi":"10.36922/gtm.v1i2.176","DOIUrl":"https://doi.org/10.36922/gtm.v1i2.176","url":null,"abstract":"This paper presents a survey on the development and major advances of artificial intelligence assisted robotics for therapeutic tasks by concentrating on the current challenges emerging from the clinical application process and the research efforts mitigating the problems. In this survey, we search Nature, Science, Cell and other websites with high influence by using keywords (i.e., artificial assisted medical robots), categorized research works over the past three decades based on therapeutic applications, and discussed the latest development and bottleneck problems of each subtopic finally. Specifically, we first present a chronology of the artificial intelligence assisted techniques developed for medical therapeutic tasks over the past three decades and then classify them according to the principles of the algorithm and its corresponding type of medical therapeutic tasks. The artificial intelligence technologies in the chronology evolve from classic machine learning statistical methods of the early nineties to data driven deep learning methods. Then a taxonomy of the artificial intelligence technologies assisted therapeutic tasks in the past three decades is described according to the therapeutic task types and hot topics of the knotty problems. One prosperous trend has been abstracted from the interpretation of our taxonomy and the most highly cited research papers using certain search criteria with Nature and Cell databases, which undergoes revolutionary development of artificial intelligence and closer integration with clinical therapeutic tasks. The trend is unprecedent and more comprehensive Human-Robot Interaction, which benefits sophisticated telesurgery and microsurgery by being capable of facilitating Surgeons with higher imaging accuracy and human-like tactile sensation. Our survey discusses the current grand challenges and future trends of artificial intelligence assisted therapeutic tasks for the convenience of clinical research and applications. We hope this survey would help bridging the gap between entrepreneurial translation and research.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83945431","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}
Sh.R. Zulkarneev, R. Zulkarneev, G. Korytina, Irshat A. Gibadullin, A. M. Avzaletdinov, Z. Niu, Jiayu Guo, Y. G. Aznabaeva, G. Nurtdinova, N. Zagidullin
Idiopathic pulmonary fibrosis (IPF) is the most common form of fibrosis of internal organs. The etiology and pathogenesis of IPF are still not well understood. However, a growing line of evidence shows that both genetic and non-genetic factors contribute to IPF development. The release of pro-inflammatory cytokines activates the immune cells. The enhanced synthesis of interleukins and cytokines, especially transforming growth factor β1 leads to the proliferation of fibroblasts, increased extracellular matrix formation, and epithelial-mesenchymal transformation of the lung tissue. These pathological changes could lead to fibrosis. Polymorphisms of genes responsible for the function of mucociliary clearance (MUC5B), telomerases (TERT, TERC), as well as signaling pathway related-genes such as Sonic hedgehog, Wnt, and some other genes are also risk factors for IPF development. Epigenetic regulatory mechanisms, such as methylation and acetylation of DNA and histones, may also influence the development and progression of this disease. At present, the role of non-coding RNAs, in particular long non-coding RNAs (lncRNA) in the development of fibrotic processes, is actively studied. LncRNA is an RNA that is longer than 200 base pairs and does not code for any proteins. LncRNAs perform various functions in the cell, from nuclear compartmentation to epigenetic regulation of gene expression and post-translational modification of proteins. In this review, we present the important aspects in the pathogenesis of IPF.
{"title":"Genetic and non-genetic risk factors of idiopathic pulmonary fibrosis: A review","authors":"Sh.R. Zulkarneev, R. Zulkarneev, G. Korytina, Irshat A. Gibadullin, A. M. Avzaletdinov, Z. Niu, Jiayu Guo, Y. G. Aznabaeva, G. Nurtdinova, N. Zagidullin","doi":"10.36922/gtm.v1i2.107","DOIUrl":"https://doi.org/10.36922/gtm.v1i2.107","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is the most common form of fibrosis of internal organs. The etiology and pathogenesis of IPF are still not well understood. However, a growing line of evidence shows that both genetic and non-genetic factors contribute to IPF development. The release of pro-inflammatory cytokines activates the immune cells. The enhanced synthesis of interleukins and cytokines, especially transforming growth factor β1 leads to the proliferation of fibroblasts, increased extracellular matrix formation, and epithelial-mesenchymal transformation of the lung tissue. These pathological changes could lead to fibrosis. Polymorphisms of genes responsible for the function of mucociliary clearance (MUC5B), telomerases (TERT, TERC), as well as signaling pathway related-genes such as Sonic hedgehog, Wnt, and some other genes are also risk factors for IPF development. Epigenetic regulatory mechanisms, such as methylation and acetylation of DNA and histones, may also influence the development and progression of this disease. At present, the role of non-coding RNAs, in particular long non-coding RNAs (lncRNA) in the development of fibrotic processes, is actively studied. LncRNA is an RNA that is longer than 200 base pairs and does not code for any proteins. LncRNAs perform various functions in the cell, from nuclear compartmentation to epigenetic regulation of gene expression and post-translational modification of proteins. In this review, we present the important aspects in the pathogenesis of IPF.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"134 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86300092","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}
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