Pub Date : 2024-04-22DOI: 10.37349/emed.2024.00218
Hassib Narchi, Priyadharshini Yuvaraju, Junu A. George, Richard L. Jayaraj, Radhakrishnan Subramanian
Aim: Hypoglycemia occurs in the neonatal period but the exact pathophysiology of the resulting brain injury at the cellular level is not well known. Therefore, a neonatal murine model was developed with insulin-induced hypoglycemia, to analyze the in-vitro effects of hypoglycemia on brain nucleotides and adenylate energy charge (AEC) throughout the first ten days of life. Methods: Newly born BALB/c pups between one and ten days of age were used. In each age group, six pups were subjected to insulin-induced hypoglycemia and six others served as controls. In both groups, immediately after euthanasia, brain tissues were collected. The in-vitro effects of hypoglycemia on brain nucleotides [adenosine monophosphate (AMP), adenosine diphosphate (ADP), and adenosine triphosphate (ATP)] were analyzed using liquid chromatography with tandem mass spectrometry (LC-MS/MS) as well on AEC. Results: In the controls, the cellular AEC steadily decreased with age by at least 50% over the 10-day study period (P < 0.05) except in the parietal tissue (P = 0.30) where it remained stable throughout that period. The most marked decrease was observed in the occipital tissue (P < 0.001). In the hypoglycemic mice, AEC in both the parietal and occipital tissues decreased significantly more than in the controls, more rapidly and pronounced between day 2 and 5 in the occipital tissue, reaching very low levels from day 5 onward. Except in the occipital tissue, none of the adenine nucleotides on its own, including ATP, reflected the cellular AEC. Conclusions: Over the first ten days of life, hypoglycemia progressively depleted cellular AEC in the brain, unlike cellular ATP concentration which did not appropriately reflect cellular energy.
{"title":"Cellular adenylate energy charge and adenine nucleotides in brain tissue during hypoglycemia in newly born BALB/c mice pups","authors":"Hassib Narchi, Priyadharshini Yuvaraju, Junu A. George, Richard L. Jayaraj, Radhakrishnan Subramanian","doi":"10.37349/emed.2024.00218","DOIUrl":"https://doi.org/10.37349/emed.2024.00218","url":null,"abstract":"Aim: Hypoglycemia occurs in the neonatal period but the exact pathophysiology of the resulting brain injury at the cellular level is not well known. Therefore, a neonatal murine model was developed with insulin-induced hypoglycemia, to analyze the in-vitro effects of hypoglycemia on brain nucleotides and adenylate energy charge (AEC) throughout the first ten days of life. Methods: Newly born BALB/c pups between one and ten days of age were used. In each age group, six pups were subjected to insulin-induced hypoglycemia and six others served as controls. In both groups, immediately after euthanasia, brain tissues were collected. The in-vitro effects of hypoglycemia on brain nucleotides [adenosine monophosphate (AMP), adenosine diphosphate (ADP), and adenosine triphosphate (ATP)] were analyzed using liquid chromatography with tandem mass spectrometry (LC-MS/MS) as well on AEC. Results: In the controls, the cellular AEC steadily decreased with age by at least 50% over the 10-day study period (P < 0.05) except in the parietal tissue (P = 0.30) where it remained stable throughout that period. The most marked decrease was observed in the occipital tissue (P < 0.001). In the hypoglycemic mice, AEC in both the parietal and occipital tissues decreased significantly more than in the controls, more rapidly and pronounced between day 2 and 5 in the occipital tissue, reaching very low levels from day 5 onward. Except in the occipital tissue, none of the adenine nucleotides on its own, including ATP, reflected the cellular AEC. Conclusions: Over the first ten days of life, hypoglycemia progressively depleted cellular AEC in the brain, unlike cellular ATP concentration which did not appropriately reflect cellular energy.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"99 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140676732","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 : 2024-04-12DOI: 10.37349/emed.2024.00216
Yixuan Wang, Jinghan Huang, T. F. Ang, Yibo Zhu, Q. Tao, Jesse B. Mez, M. Alosco, Gerald V. Denis, A. Belkina, A. Gurnani, Mark Ross, Bin Gong, Jingyan Han, Kathryn L. Lunetta, T. Stein, Rhoda Au, Lindsay A. Farrer, Xiaoling Zhang, Wei Qiao Qiu
Aim: Endothelial dysfunction has been associated with both cerebrovascular pathology and Alzheimer’s disease (AD). However, the connection between circulating endothelial cells and the risk of AD remains uncertain. The objective was to leverage data from the Framingham Heart Study to investigate various circulating endothelial subtypes and their potential correlations with the risk of AD. Methods: The study conducted data analyses using Cox proportional hazard regression and linear regression methods. Additionally, genome-wide association study (GWAS) was carried out to further explore the data. Results: Among the eleven distinct circulating endothelial subtypes, only circulating endothelial progenitor cells (EPCs) expressing CD34+CD133+ were found to be negatively and dose-dependently associated with reduced AD risk. This association persisted even after adjusting for age, sex, years of education, apolipoprotein E (APOE) ε4 status, and various vascular diseases. Particularly noteworthy was the significant association observed in individuals with hypertension and cerebral microbleeds. Consistently, positive associations were identified between CD34+CD133+ EPCs and specific brain regions, such as higher proportions of circulating CD34+CD133+ cells correlating with increased volumes of white matter and the hippocampus. Additionally, a GWAS study unveiled that CD34+CD133+ cells influenced AD risk specifically in individuals with homozygous genotypes for variants in two stem cell-related genes: kirre like nephrin family adhesion molecule 3 (KIRREL3, rs580382 CC and rs4144611 TT) and exocyst complex component 6B (EXOC6B, rs61619102 CC). Conclusions: The findings suggest that circulating CD34+CD133+ EPCs possess a protective effect and may offer a new therapeutic avenue for AD, especially in individuals with vascular pathology and those carrying specific genotypes of KIRREL3 and EXOC6B genes.
目的：内皮功能障碍与脑血管病变和阿尔茨海默病（AD）有关。然而，循环内皮细胞与阿尔茨海默病风险之间的联系仍不确定。我们的目的是利用弗雷明汉心脏研究的数据，研究各种循环内皮细胞亚型及其与阿尔茨海默病风险的潜在相关性。研究方法研究采用 Cox 比例危险回归和线性回归方法进行数据分析。此外，还进行了全基因组关联研究（GWAS）以进一步探索数据。研究结果在11种不同的循环内皮亚型中，只有表达CD34+CD133+的循环内皮祖细胞（EPCs）与AD风险的降低呈剂量依赖性的负相关。即使在调整了年龄、性别、受教育年限、载脂蛋白E（APOE）ε4状态和各种血管疾病后，这种关联依然存在。尤其值得注意的是，在高血压和脑微小出血患者中观察到了显著的相关性。同样，CD34+CD133+ EPCs 与特定脑区之间也发现了正相关，如循环 CD34+CD133+ 细胞比例越高，白质和海马体积越大。此外，一项GWAS研究揭示，CD34+CD133+细胞对AD风险的影响尤其体现在两个干细胞相关基因变异的同源基因型个体中：Kirre like nephrin family adhesion molecule 3（KIRREL3，rs580382 CC和rs4144611 TT）和exocyst complex component 6B（EXOC6B，rs61619102 CC）。结论研究结果表明，循环 CD34+CD133+ EPCs 具有保护作用，可为 AD 提供新的治疗途径，尤其是对血管病变患者和携带 KIRREL3 和 EXOC6B 基因特定基因型的患者。
{"title":"The association between circulating CD34+CD133+ endothelial progenitor cells and reduced risk of Alzheimer’s disease in the Framingham Heart Study","authors":"Yixuan Wang, Jinghan Huang, T. F. Ang, Yibo Zhu, Q. Tao, Jesse B. Mez, M. Alosco, Gerald V. Denis, A. Belkina, A. Gurnani, Mark Ross, Bin Gong, Jingyan Han, Kathryn L. Lunetta, T. Stein, Rhoda Au, Lindsay A. Farrer, Xiaoling Zhang, Wei Qiao Qiu","doi":"10.37349/emed.2024.00216","DOIUrl":"https://doi.org/10.37349/emed.2024.00216","url":null,"abstract":"Aim: Endothelial dysfunction has been associated with both cerebrovascular pathology and Alzheimer’s disease (AD). However, the connection between circulating endothelial cells and the risk of AD remains uncertain. The objective was to leverage data from the Framingham Heart Study to investigate various circulating endothelial subtypes and their potential correlations with the risk of AD. Methods: The study conducted data analyses using Cox proportional hazard regression and linear regression methods. Additionally, genome-wide association study (GWAS) was carried out to further explore the data. Results: Among the eleven distinct circulating endothelial subtypes, only circulating endothelial progenitor cells (EPCs) expressing CD34+CD133+ were found to be negatively and dose-dependently associated with reduced AD risk. This association persisted even after adjusting for age, sex, years of education, apolipoprotein E (APOE) ε4 status, and various vascular diseases. Particularly noteworthy was the significant association observed in individuals with hypertension and cerebral microbleeds. Consistently, positive associations were identified between CD34+CD133+ EPCs and specific brain regions, such as higher proportions of circulating CD34+CD133+ cells correlating with increased volumes of white matter and the hippocampus. Additionally, a GWAS study unveiled that CD34+CD133+ cells influenced AD risk specifically in individuals with homozygous genotypes for variants in two stem cell-related genes: kirre like nephrin family adhesion molecule 3 (KIRREL3, rs580382 CC and rs4144611 TT) and exocyst complex component 6B (EXOC6B, rs61619102 CC). Conclusions: The findings suggest that circulating CD34+CD133+ EPCs possess a protective effect and may offer a new therapeutic avenue for AD, especially in individuals with vascular pathology and those carrying specific genotypes of KIRREL3 and EXOC6B genes.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"8 24","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140710579","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 : 2024-04-08DOI: 10.37349/emed.2024.00213
K. Sak
Over the past few decades, it has become clear that an excessive activity of matrix metalloproteinases (MMPs) can accelerate the progression and fatal outcomes of several serious age-related diseases, including atherosclerotic coronary heart disorders and various types of malignancies. These proteolytic enzymes mediate the degradation and remodeling of the extracellular matrix through cleaving its various components, thereby affecting many critical functions of surrounding cells and intercellular communication. Consequently, the low expression levels of MMPs can be important in the prevention and treatment of such chronic life-threatening pathologies, contributing to the better quality of life and longer life expectancy. In this review article, the pathogenic proteolytic roles of MMPs are examined in more detail, especially in the cases of heart attack and stroke as well as cancer invasion and metastasis, showing that these enzymes can be considered not only as diagnostic and prognostic biomarkers but also as important therapeutic targets in the fight against many age- and lifestyle-related serious disorders. The identification and development of suppressing agents with a selective activity towards specific MMPs have, however, still remained a complex and complicated challenge, in which natural plant-derived compounds are increasingly recognized as promising leads for the new-generation inhibitors.
{"title":"The low expression of matrix metalloproteinases: a key to longevity?","authors":"K. Sak","doi":"10.37349/emed.2024.00213","DOIUrl":"https://doi.org/10.37349/emed.2024.00213","url":null,"abstract":"Over the past few decades, it has become clear that an excessive activity of matrix metalloproteinases (MMPs) can accelerate the progression and fatal outcomes of several serious age-related diseases, including atherosclerotic coronary heart disorders and various types of malignancies. These proteolytic enzymes mediate the degradation and remodeling of the extracellular matrix through cleaving its various components, thereby affecting many critical functions of surrounding cells and intercellular communication. Consequently, the low expression levels of MMPs can be important in the prevention and treatment of such chronic life-threatening pathologies, contributing to the better quality of life and longer life expectancy. In this review article, the pathogenic proteolytic roles of MMPs are examined in more detail, especially in the cases of heart attack and stroke as well as cancer invasion and metastasis, showing that these enzymes can be considered not only as diagnostic and prognostic biomarkers but also as important therapeutic targets in the fight against many age- and lifestyle-related serious disorders. The identification and development of suppressing agents with a selective activity towards specific MMPs have, however, still remained a complex and complicated challenge, in which natural plant-derived compounds are increasingly recognized as promising leads for the new-generation inhibitors.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140728975","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 : 2024-01-01Epub Date: 2024-04-11DOI: 10.37349/emed.2024.00215
Leonard A Jason, Sarah Ngonmedje
Aim: It is unclear if individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with family histories of ME/CFS differ from those with ME/CFS without this family history. To explore this issue, quantitative data from patients with ME/CFS and controls were collected, and we examined those with and without family histories of ME/CFS.
Methods: The samples included 400 patients with ME/CFS, and a non-ME/CFS chronic illness control group of 241 patients with multiple sclerosis (MS) and 173 with post-polio syndrome (PPS).
Results: Confirming findings from prior studies, those with ME/CFS were more likely to have family members with ME/CFS than controls. We found family histories of ME/CFS were significantly higher (18%) among the ME/CFS group than the non-ME/CFS controls (3.9%). In addition, patients with ME/CFS who had family histories of ME/CFS were more likely to have gastrointestinal symptoms than those with ME/CFS without those family histories.
Conclusions: Given the recent reports of gastrointestinal difficulties among those with ME/CFS, our findings might represent one predisposing factor for the emergence of ME/CFS.
{"title":"The influence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) family history on patients with ME/CFS.","authors":"Leonard A Jason, Sarah Ngonmedje","doi":"10.37349/emed.2024.00215","DOIUrl":"10.37349/emed.2024.00215","url":null,"abstract":"<p><strong>Aim: </strong>It is unclear if individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with family histories of ME/CFS differ from those with ME/CFS without this family history. To explore this issue, quantitative data from patients with ME/CFS and controls were collected, and we examined those with and without family histories of ME/CFS.</p><p><strong>Methods: </strong>The samples included 400 patients with ME/CFS, and a non-ME/CFS chronic illness control group of 241 patients with multiple sclerosis (MS) and 173 with post-polio syndrome (PPS).</p><p><strong>Results: </strong>Confirming findings from prior studies, those with ME/CFS were more likely to have family members with ME/CFS than controls. We found family histories of ME/CFS were significantly higher (18%) among the ME/CFS group than the non-ME/CFS controls (3.9%). In addition, patients with ME/CFS who had family histories of ME/CFS were more likely to have gastrointestinal symptoms than those with ME/CFS without those family histories.</p><p><strong>Conclusions: </strong>Given the recent reports of gastrointestinal difficulties among those with ME/CFS, our findings might represent one predisposing factor for the emergence of ME/CFS.</p>","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"5 2","pages":"185-192"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585118","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}
Pub Date : 2023-12-29DOI: 10.37349/emed.2023.00196
D. Coradini, Federico Ambrogi
Aim: Cholesterol is an essential component of cell membranes and serves as a precursor for several bioactive molecules, including steroid hormones and isoprenoids. Generally supplied by the bloodstream, the de novo cholesterol biosynthesis is activated in response to an increased cell requirement due to normal tissue remodeling or tumor proliferation. In estrogen receptor (ER)-positive breast cancers, cholesterol biosynthesis may promote and sustain tumor growth and concur with the failure of the treatment with aromatase inhibitors. Methods: In this study, the comparison of gene compared the expression involved in cholesterol biosynthesis was conducted in ER-positive tumors that were responsive and nonresponsive to letrozole; besides, an exploration of their association with genes implicated in estrogen production, the Hippo pathway, and cell cycle control was performed. Results: In responsive tumors, letrozole significantly decreased the expression of five genes [acetyl-coenzyme A (CoA) acetyltransferase 2 (ACAT2), 3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), and squalene epoxidase (SQLE)] crucial for the biosynthetic process. Conversely, in nonresponsive tumors, these genes were unaffected by letrozole but associated with several genes involved in estrogens production [cytochrome P450 family 19 subfamily A member 1 (CYP19A1), hydroxysteroid 17-beta dehydrogenase 2 (HSD17B2), and sulfotransferase family 1A member 1 (SULT1A1)], cell cycle [control cyclin dependent kinase 4 (CDK4) and CDK6], and Hippo pathway [Yes1 associated transcriptional regulator (YAP1) and baculoviral inhibitor of apoptosis (IAP) repeat containing 5 (BIRC5)]. Conclusions: The findings corroborated the notion that the dysregulation of the mevalonate pathway may contribute to the resistance to letrozole and supported the use of statins to contrast this metabolic dysfunction.
{"title":"Cholesterol de novo biosynthesis: a promising target to overcome the resistance to aromatase inhibitors in postmenopausal patients with estrogen receptor-positive breast cancer","authors":"D. Coradini, Federico Ambrogi","doi":"10.37349/emed.2023.00196","DOIUrl":"https://doi.org/10.37349/emed.2023.00196","url":null,"abstract":"Aim: Cholesterol is an essential component of cell membranes and serves as a precursor for several bioactive molecules, including steroid hormones and isoprenoids. Generally supplied by the bloodstream, the de novo cholesterol biosynthesis is activated in response to an increased cell requirement due to normal tissue remodeling or tumor proliferation. In estrogen receptor (ER)-positive breast cancers, cholesterol biosynthesis may promote and sustain tumor growth and concur with the failure of the treatment with aromatase inhibitors. Methods: In this study, the comparison of gene compared the expression involved in cholesterol biosynthesis was conducted in ER-positive tumors that were responsive and nonresponsive to letrozole; besides, an exploration of their association with genes implicated in estrogen production, the Hippo pathway, and cell cycle control was performed. Results: In responsive tumors, letrozole significantly decreased the expression of five genes [acetyl-coenzyme A (CoA) acetyltransferase 2 (ACAT2), 3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), and squalene epoxidase (SQLE)] crucial for the biosynthetic process. Conversely, in nonresponsive tumors, these genes were unaffected by letrozole but associated with several genes involved in estrogens production [cytochrome P450 family 19 subfamily A member 1 (CYP19A1), hydroxysteroid 17-beta dehydrogenase 2 (HSD17B2), and sulfotransferase family 1A member 1 (SULT1A1)], cell cycle [control cyclin dependent kinase 4 (CDK4) and CDK6], and Hippo pathway [Yes1 associated transcriptional regulator (YAP1) and baculoviral inhibitor of apoptosis (IAP) repeat containing 5 (BIRC5)]. Conclusions: The findings corroborated the notion that the dysregulation of the mevalonate pathway may contribute to the resistance to letrozole and supported the use of statins to contrast this metabolic dysfunction.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" 5","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139143278","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 : 2023-12-29DOI: 10.37349/emed.2023.00198
Freda N. Gonot-Schoupinsky
Gelotology (the study of laughter) has it seems mainly evaded the attention of longevity scientists, positive biologists, and geroscientists. However, the potential of laughter to result in immediate improved affect, increase overall well-being, reduce cortisol levels, benefit the immune system, and support cardiovascular health, to name only a few of its possible effects, renders it of high interest as an anti-aging strategy. As an intervention, laughter has, at least theoretically, the potential to slow the process of aging, and to ameliorate its lived experience. What makes laughter particularly attractive is that it is accessible to all, is very low risk, and is inherently, for most people, enjoyable. Ten years ago, lifestyle medics first proposed that laughter be prescribed in primary care. They pointed to its efficacy in general patient care, geriatrics, rheumatology, critical care, oncology, rehabilitation, psychiatry, home care, palliative care, terminal care, and hospice care. Nevertheless, laughter prescription has been slow to take off. It is therefore of interest to contemplate why, how, and to what effect, laughter can be harnessed to improve people’s lives. Quality research is recommended to uncover the secrets of laughter, its dynamic effects on the body, if, and how, it may impact longevity, and how it can best be used to promote successful and active aging.
{"title":"From positive psychology to positive biology: laughter and longevity","authors":"Freda N. Gonot-Schoupinsky","doi":"10.37349/emed.2023.00198","DOIUrl":"https://doi.org/10.37349/emed.2023.00198","url":null,"abstract":"Gelotology (the study of laughter) has it seems mainly evaded the attention of longevity scientists, positive biologists, and geroscientists. However, the potential of laughter to result in immediate improved affect, increase overall well-being, reduce cortisol levels, benefit the immune system, and support cardiovascular health, to name only a few of its possible effects, renders it of high interest as an anti-aging strategy. As an intervention, laughter has, at least theoretically, the potential to slow the process of aging, and to ameliorate its lived experience. What makes laughter particularly attractive is that it is accessible to all, is very low risk, and is inherently, for most people, enjoyable. Ten years ago, lifestyle medics first proposed that laughter be prescribed in primary care. They pointed to its efficacy in general patient care, geriatrics, rheumatology, critical care, oncology, rehabilitation, psychiatry, home care, palliative care, terminal care, and hospice care. Nevertheless, laughter prescription has been slow to take off. It is therefore of interest to contemplate why, how, and to what effect, laughter can be harnessed to improve people’s lives. Quality research is recommended to uncover the secrets of laughter, its dynamic effects on the body, if, and how, it may impact longevity, and how it can best be used to promote successful and active aging.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"113 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139146887","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}
Cancer cure with immunotherapy is an innovative step towards cancer treatment with better survivability, but it is mostly dependent on the response of the patient’s immune system to the immunotherapeutic approach. This descriptive review article emphasizes the conventional and advanced treatment modalities currently available for breast cancer management. This review also highlights the clinical management of breast cancer concerning immune response especially to unravel the prospects for manipulation of immune cells: such as lymphocytes, including T-cells, T-regulatory cells and natural killer cells, and others like macrophages, dendritic cells, and the panel of interleukins or interferons released by them which has made a significant impact on breast cancer research. In addition, an effort was made to emphasize the different clinical trials and their future implication for the reduction of breast cancer cases. Overall, an attempt has been made to shed light on the possibilities of immunotherapeutics in breast cancer care, as well as the role of immune response in the incidence, aggressiveness, and survival of breast cancer.
利用免疫疗法治愈癌症是提高癌症治疗存活率的创新举措，但这主要取决于患者的免疫系统对免疫疗法的反应。这篇描述性综述文章强调了目前可用于乳腺癌治疗的常规和先进治疗方法。这篇综述还强调了与免疫反应有关的乳腺癌临床治疗，特别是揭示了操纵免疫细胞的前景：如淋巴细胞，包括 T 细胞、T 调节细胞和自然杀伤细胞，以及其他如巨噬细胞、树突状细胞和它们释放的白细胞介素或干扰素，这对乳腺癌研究产生了重大影响。此外，还努力强调不同的临床试验及其对减少乳腺癌病例的未来影响。总之，我们试图揭示免疫疗法在乳腺癌治疗中的可能性，以及免疫反应在乳腺癌发病率、侵袭性和存活率中的作用。
{"title":"The differential effect of the immune system in breast cancer","authors":"Banashree Bondhopadhyay, Showket Hussain, Vishakha Kasherwal","doi":"10.37349/emed.2023.00197","DOIUrl":"https://doi.org/10.37349/emed.2023.00197","url":null,"abstract":"Cancer cure with immunotherapy is an innovative step towards cancer treatment with better survivability, but it is mostly dependent on the response of the patient’s immune system to the immunotherapeutic approach. This descriptive review article emphasizes the conventional and advanced treatment modalities currently available for breast cancer management. This review also highlights the clinical management of breast cancer concerning immune response especially to unravel the prospects for manipulation of immune cells: such as lymphocytes, including T-cells, T-regulatory cells and natural killer cells, and others like macrophages, dendritic cells, and the panel of interleukins or interferons released by them which has made a significant impact on breast cancer research. In addition, an effort was made to emphasize the different clinical trials and their future implication for the reduction of breast cancer cases. Overall, an attempt has been made to shed light on the possibilities of immunotherapeutics in breast cancer care, as well as the role of immune response in the incidence, aggressiveness, and survival of breast cancer.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"19 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139147908","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 integration of three-dimensional (3D) printing techniques into the domains of biomedical research and personalized medicine highlights the evolving paradigm shifts within contemporary healthcare. This technological advancement signifies potential breakthroughs in patient-specific therapeutic interventions and innovations. This systematic review offers a critical assessment of the existing literature, elucidating the present status, inherent challenges, and prospective avenues of 3D printing in augmenting biomedical applications and formulating tailored medical strategies. Based on an exhaustive literature analysis comprising empirical studies, case studies, and extensive reviews from the past decade, pivotal sectors including tissue engineering, prosthetic development, drug delivery systems, and customized medical apparatuses are delineated. The advent of 3D printing provides precision in the fabrication of patient-centric implants, bio-structures, and devices, thereby mitigating associated risks. Concurrently, it facilitates the ideation of individualized drug delivery paradigms to optimize therapeutic outcomes. Notwithstanding these advancements, issues concerning material biocompatibility, regulatory compliance, and the economic implications of avant-garde printing techniques persist. To fully harness the transformative potential of 3D printing in healthcare, collaborative endeavors amongst academicians, clinicians, industrial entities, and regulatory bodies are paramount. With continued research and innovation, 3D printing is poised to redefine the trajectories of biomedical science and patient-centric care. The paper aims to justify the research objective of whether to what extent the integration of 3D printing technology in biomedicine enhances patient-specific treatment and contributes to improved healthcare outcomes.
将三维（3D）打印技术融入生物医学研究和个性化医疗领域，凸显了当代医疗保健领域不断发展的范式转变。这一技术进步标志着在针对患者的治疗干预和创新方面可能取得突破。这篇系统性综述对现有文献进行了批判性评估，阐明了 3D 打印在增强生物医学应用和制定定制医疗策略方面的现状、固有挑战和前景。基于详尽的文献分析，包括过去十年的实证研究、案例研究和大量综述，对组织工程、假肢开发、给药系统和定制医疗器械等关键领域进行了划分。三维打印技术的出现为制造以患者为中心的植入物、生物结构和设备提供了精确度，从而降低了相关风险。同时，3D 打印技术还促进了个性化给药模式的构思，以优化治疗效果。尽管取得了这些进步，但有关材料生物兼容性、监管合规性以及前卫打印技术的经济影响等问题依然存在。要充分利用 3D 打印技术在医疗保健领域的变革潜力，学术界、临床医生、工业实体和监管机构之间的合作至关重要。随着研究和创新的不断深入，3D 打印技术有望重新定义生物医学科学和以患者为中心的医疗服务的发展轨迹。本文旨在论证以下研究目标：3D 打印技术与生物医学的结合是否能在多大程度上增强针对患者的治疗，并有助于改善医疗效果。
{"title":"3D printing in biomedicine: advancing personalized care through additive manufacturing","authors":"K. Pathak, Riya Saikia, Aparoop Das, Dibyajyoti Das, Md Ariful Islam, Pallab Pramanik, Abhishek Parasar, PARTHA PROTIM BORTHAKUR, Pranjal Sarmah, Madhurjya Saikia, Barbie Borthakur","doi":"10.37349/emed.2023.00200","DOIUrl":"https://doi.org/10.37349/emed.2023.00200","url":null,"abstract":"The integration of three-dimensional (3D) printing techniques into the domains of biomedical research and personalized medicine highlights the evolving paradigm shifts within contemporary healthcare. This technological advancement signifies potential breakthroughs in patient-specific therapeutic interventions and innovations. This systematic review offers a critical assessment of the existing literature, elucidating the present status, inherent challenges, and prospective avenues of 3D printing in augmenting biomedical applications and formulating tailored medical strategies. Based on an exhaustive literature analysis comprising empirical studies, case studies, and extensive reviews from the past decade, pivotal sectors including tissue engineering, prosthetic development, drug delivery systems, and customized medical apparatuses are delineated. The advent of 3D printing provides precision in the fabrication of patient-centric implants, bio-structures, and devices, thereby mitigating associated risks. Concurrently, it facilitates the ideation of individualized drug delivery paradigms to optimize therapeutic outcomes. Notwithstanding these advancements, issues concerning material biocompatibility, regulatory compliance, and the economic implications of avant-garde printing techniques persist. To fully harness the transformative potential of 3D printing in healthcare, collaborative endeavors amongst academicians, clinicians, industrial entities, and regulatory bodies are paramount. With continued research and innovation, 3D printing is poised to redefine the trajectories of biomedical science and patient-centric care. The paper aims to justify the research objective of whether to what extent the integration of 3D printing technology in biomedicine enhances patient-specific treatment and contributes to improved healthcare outcomes.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139142204","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 : 2023-12-29DOI: 10.37349/emed.2023.00199
Silvia Siragusa, Giulia Natali, A. Nogara, Marcello Trevisani, C. Lagrasta, Silvia Pontis
Chronic obstructive pulmonary disease (COPD) is an inflammatory lung pathology characterized by persistent airflow limitation and is the third leading cause of death globally. COPD pathophysiology includes both environmental and host risk factors and the presence of comorbidities contributes to its harmful outcome. Cardiovascular disease (CVD) is closely related to COPD and their coexistence is associated with worse outcomes than either condition alone. COPD impairs the cardiovascular system favoring mostly endothelial dysfunction that is a significant COPD prognostic factor at different stages of the disease. The mechanisms promoting endothelial dysfunction in the systemic and/or pulmonary circulation of COPD patients are different and include systemic inflammation, alteration of adhesion and pro-inflammatory molecules, oxidative stress, cellular senescence, and apoptosis. Nevertheless, the role of endothelium in the onset and progression of COPD and CVD is not yet fully understood. Hence, the purpose of this narrative review is to analyze the literature and provide evidence supporting the importance of endothelial dysfunction in COPD.
{"title":"The role of pulmonary vascular endothelium in chronic obstructive pulmonary disease (COPD): Does endothelium play a role in the onset and progression of COPD?","authors":"Silvia Siragusa, Giulia Natali, A. Nogara, Marcello Trevisani, C. Lagrasta, Silvia Pontis","doi":"10.37349/emed.2023.00199","DOIUrl":"https://doi.org/10.37349/emed.2023.00199","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is an inflammatory lung pathology characterized by persistent airflow limitation and is the third leading cause of death globally. COPD pathophysiology includes both environmental and host risk factors and the presence of comorbidities contributes to its harmful outcome. Cardiovascular disease (CVD) is closely related to COPD and their coexistence is associated with worse outcomes than either condition alone. COPD impairs the cardiovascular system favoring mostly endothelial dysfunction that is a significant COPD prognostic factor at different stages of the disease. The mechanisms promoting endothelial dysfunction in the systemic and/or pulmonary circulation of COPD patients are different and include systemic inflammation, alteration of adhesion and pro-inflammatory molecules, oxidative stress, cellular senescence, and apoptosis. Nevertheless, the role of endothelium in the onset and progression of COPD and CVD is not yet fully understood. Hence, the purpose of this narrative review is to analyze the literature and provide evidence supporting the importance of endothelial dysfunction in COPD.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":"5 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139147427","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 : 2023-12-29DOI: 10.37349/emed.2023.00195
Zhanglan Fang, Hao Yang, Yi Long, Dongyun Xu, Benyu Su, Chao Xu, Huguang Yang, Feng Xu, Ling Luo
Aim: Respiratory failure is common after esophagectomy for esophageal cancer (EC). This study aimed to identify the risk factors associated with postoperative respiratory failure following esophagectomy for EC. Methods: A single-center observational study from China was conducted on 262 patients with EC who underwent thoracoscopic esophagectomy between April 2014 and June 2016. The patients were divided into two groups: group I (respiratory failure) and group II (without respiratory failure). Demographic and perioperative variables, tumor-related factors, surgical factors, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, and clinical course were compared between the groups. Univariable and multivariable logistic regression analyses were performed to assess the risk factors of postoperative respiratory failure after esophagectomy. Results: Among the 262 patients, 24 (9.2%) developed respiratory failure. Univariable analysis revealed several risk factors, including age, smoking, comorbidities, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), forced vital capacity (FVC), FVC percentage (FVC%), urine volume during surgery, and APACHE II score. Multivariable analysis showed that age, comorbidities of diabetes mellitus (DM), FVC%, urine volume during surgery, and APACHE II score were independent predictors of respiratory failure. Specifically, elderly patients (> 65 years) with comorbidities of DM, lower FVC%, higher urine volume during surgery, and elevated APACHE II score were found to be more susceptible to respiratory failure, resulting in prolonged hospitalization and increased healthcare burden. These findings emphasize the importance of considering these factors in the management and care of patients at risk of respiratory failure. Conclusions: As a common complication following esophagectomy for EC. Respiratory failure is significantly associated with age, comorbidities of DM, FVC%, urine volume during surgery, and APACHE II score in the dataset. The findings will contribute to the evaluation of the risk of respiratory failure and guide early intervention strategies in clinical decision-making.
目的：食管癌（EC）食管切除术后呼吸衰竭很常见。本研究旨在确定食管癌食管切除术后呼吸衰竭的相关风险因素。方法：一项来自中国的单中心观察性研究对2014年4月至2016年6月期间接受胸腔镜食管切除术的262例食管癌患者进行了研究。患者分为两组：I组（呼吸衰竭）和II组（无呼吸衰竭）。比较了两组患者的人口统计学和围手术期变量、肿瘤相关因素、手术因素、急性生理学和慢性健康评估 II（APACHE II）评分以及临床病程。进行单变量和多变量逻辑回归分析，以评估食管切除术后呼吸衰竭的风险因素。结果262 名患者中有 24 人（9.2%）出现呼吸衰竭。单变量分析显示了几个风险因素，包括年龄、吸烟、合并症、氧分压（PO2）、二氧化碳分压（PCO2）、强迫生命容量（FVC）、FVC 百分比（FVC%）、术中尿量和 APACHE II 评分。多变量分析显示，年龄、糖尿病（DM）合并症、FVC%、术中尿量和 APACHE II 评分是呼吸衰竭的独立预测因素。具体来说，合并有 DM、FVC% 较低、术中尿量较多、APACHE II 评分较高的老年患者（65 岁以上）更容易出现呼吸衰竭，导致住院时间延长和医疗负担加重。这些发现强调了在管理和护理有呼吸衰竭风险的患者时考虑这些因素的重要性。结论：呼吸衰竭是食管切除术后常见的并发症。在数据集中，呼吸衰竭与年龄、DM合并症、FVC%、术中尿量和APACHE II评分明显相关。研究结果将有助于评估呼吸衰竭的风险，并指导临床决策中的早期干预策略。
{"title":"Risk factors associated with postoperative respiratory failure after esophagectomy for esophageal cancer","authors":"Zhanglan Fang, Hao Yang, Yi Long, Dongyun Xu, Benyu Su, Chao Xu, Huguang Yang, Feng Xu, Ling Luo","doi":"10.37349/emed.2023.00195","DOIUrl":"https://doi.org/10.37349/emed.2023.00195","url":null,"abstract":"Aim: Respiratory failure is common after esophagectomy for esophageal cancer (EC). This study aimed to identify the risk factors associated with postoperative respiratory failure following esophagectomy for EC. Methods: A single-center observational study from China was conducted on 262 patients with EC who underwent thoracoscopic esophagectomy between April 2014 and June 2016. The patients were divided into two groups: group I (respiratory failure) and group II (without respiratory failure). Demographic and perioperative variables, tumor-related factors, surgical factors, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, and clinical course were compared between the groups. Univariable and multivariable logistic regression analyses were performed to assess the risk factors of postoperative respiratory failure after esophagectomy. Results: Among the 262 patients, 24 (9.2%) developed respiratory failure. Univariable analysis revealed several risk factors, including age, smoking, comorbidities, partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), forced vital capacity (FVC), FVC percentage (FVC%), urine volume during surgery, and APACHE II score. Multivariable analysis showed that age, comorbidities of diabetes mellitus (DM), FVC%, urine volume during surgery, and APACHE II score were independent predictors of respiratory failure. Specifically, elderly patients (> 65 years) with comorbidities of DM, lower FVC%, higher urine volume during surgery, and elevated APACHE II score were found to be more susceptible to respiratory failure, resulting in prolonged hospitalization and increased healthcare burden. These findings emphasize the importance of considering these factors in the management and care of patients at risk of respiratory failure. Conclusions: As a common complication following esophagectomy for EC. Respiratory failure is significantly associated with age, comorbidities of DM, FVC%, urine volume during surgery, and APACHE II score in the dataset. The findings will contribute to the evaluation of the risk of respiratory failure and guide early intervention strategies in clinical decision-making.","PeriodicalId":72999,"journal":{"name":"Exploration of medicine","volume":" 13","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139143045","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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