Larissa Gomes Sartori, Roger Burgo de Souza, Daniel Prado Campos, Paulo Broniera Júnior, José Jair Alves Mendes Junior, Eddy Krueger
In response to the challenge of spinal cord injury (SCI) rehabilitation, this study aimed to investigate the effect of applying a non-invasive interface of surface neuroelectrical signals and functional electrical stimulation (sNES-sFES) with a static magnetic field on the motor outcome of the quadriceps femoris muscle in an individual with a complete SCI. The participant, who had a complete SCI in the chronic stage, was evaluated before (pre) and after nine (post) interventions using surface electromyography (sEMG). In addition, spasticity (modified Ashworth scale [MAS]) was observed in all sessions. Moreover, the user learning curve process (classifier percentage and correct success of the sFES hits) was evaluated. In general, we observed: (i) No voluntary muscle contraction (pre- and post-root mean square of sEMG = 0%) improvement; (ii) spasticity decrease (average one point in MAS); (iii) gradual improvement in the user learning effect on the interface, reaching 84% in classifier accuracy and a maximum percentage of correct sFES activation of 53%. In conclusion, no improvement in voluntary muscular contraction was observed within 9 weeks of the intervention (1 session/day; 1 h/week). However, our study demonstrates the safety and feasibility of our methodology for future research involving continuous physical rehabilitation training and the implementation of assistive technology.
{"title":"Ineffective voluntary motor improvement through non-invasive BCI-FES with static magnetic field in complete spinal cord injury: A pilot study","authors":"Larissa Gomes Sartori, Roger Burgo de Souza, Daniel Prado Campos, Paulo Broniera Júnior, José Jair Alves Mendes Junior, Eddy Krueger","doi":"10.36922/gtm.2285","DOIUrl":"https://doi.org/10.36922/gtm.2285","url":null,"abstract":"In response to the challenge of spinal cord injury (SCI) rehabilitation, this study aimed to investigate the effect of applying a non-invasive interface of surface neuroelectrical signals and functional electrical stimulation (sNES-sFES) with a static magnetic field on the motor outcome of the quadriceps femoris muscle in an individual with a complete SCI. The participant, who had a complete SCI in the chronic stage, was evaluated before (pre) and after nine (post) interventions using surface electromyography (sEMG). In addition, spasticity (modified Ashworth scale [MAS]) was observed in all sessions. Moreover, the user learning curve process (classifier percentage and correct success of the sFES hits) was evaluated. In general, we observed: (i) No voluntary muscle contraction (pre- and post-root mean square of sEMG = 0%) improvement; (ii) spasticity decrease (average one point in MAS); (iii) gradual improvement in the user learning effect on the interface, reaching 84% in classifier accuracy and a maximum percentage of correct sFES activation of 53%. In conclusion, no improvement in voluntary muscular contraction was observed within 9 weeks of the intervention (1 session/day; 1 h/week). However, our study demonstrates the safety and feasibility of our methodology for future research involving continuous physical rehabilitation training and the implementation of assistive technology.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":" 18","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140387405","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}
This paper reports on a 55-year-old woman presenting with left lower quadrant and groin pain that posed a significant diagnostic challenge. She had a history of obesity and stage 1B endometrial carcinoma treated with surgery and radiation 1-year prior. Despite several unsuccessful biopsy attempts and unclear imaging findings, she was ultimately diagnosed with a pelvic sidewall abscess secondary to a bowel microperforation, a rare late complication of radiation related to adhesions, weakened bowel, and peristalsis. Her condition was successfully treated with drainage and antibiotics. It is widely known that patients with endometrial cancer and comorbid obesity often experience diagnostic delay, weight stigma, and other barriers and thus deserve careful attention and continued advocacy.
{"title":"You’re a pain in my side! Abscess and microperforation as a complication of therapy from early-stage endometrial cancer: A case report","authors":"Jennifer McCall, Jena Hall, Elena Park","doi":"10.36922/gtm.2114","DOIUrl":"https://doi.org/10.36922/gtm.2114","url":null,"abstract":"This paper reports on a 55-year-old woman presenting with left lower quadrant and groin pain that posed a significant diagnostic challenge. She had a history of obesity and stage 1B endometrial carcinoma treated with surgery and radiation 1-year prior. Despite several unsuccessful biopsy attempts and unclear imaging findings, she was ultimately diagnosed with a pelvic sidewall abscess secondary to a bowel microperforation, a rare late complication of radiation related to adhesions, weakened bowel, and peristalsis. Her condition was successfully treated with drainage and antibiotics. It is widely known that patients with endometrial cancer and comorbid obesity often experience diagnostic delay, weight stigma, and other barriers and thus deserve careful attention and continued advocacy.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"95 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140228213","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 COVID-19 pandemic outbreak has profoundly challenged global public health over the last couple of years. Throughout this period, numerous mutant strains of SARS-CoV-2 have emerged, presenting diverse pathophysiology and immune response challenges for infected individuals. Among these, variant of concern strains, including Alpha (B.1.1.7), Delta (B.1.617.2), and Omicron (B.1.1.529), has garnered the most significant attention for their role in causing epidemiological dynamics, ultimately leading to elevated infectivity and significant mortality rates. This review aims to provide a comparative analysis of the immune-pathophysiological mechanisms associated with these aforementioned strains of SARS-CoV-2.
{"title":"Comparative analysis of immune responses in humans infected with Alpha, Delta, and Omicron strains of SARS-CoV-2","authors":"Mihieka Bose, C. Munshi","doi":"10.36922/gtm.2228","DOIUrl":"https://doi.org/10.36922/gtm.2228","url":null,"abstract":"The COVID-19 pandemic outbreak has profoundly challenged global public health over the last couple of years. Throughout this period, numerous mutant strains of SARS-CoV-2 have emerged, presenting diverse pathophysiology and immune response challenges for infected individuals. Among these, variant of concern strains, including Alpha (B.1.1.7), Delta (B.1.617.2), and Omicron (B.1.1.529), has garnered the most significant attention for their role in causing epidemiological dynamics, ultimately leading to elevated infectivity and significant mortality rates. This review aims to provide a comparative analysis of the immune-pathophysiological mechanisms associated with these aforementioned strains of SARS-CoV-2.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"7 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140230633","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}
C. Munshi, Tithi Paul, Kalpesh Jas, Mihieka Bose, Shelley Bhattacharya
Ferroptosis is a regulated cell death pathophysiologically associated with the depletion of the antioxidant system due to iron overload, which results in excess lipid peroxidation. Mitochondria are crucial organelles known for their prominent involvement in various cellular metabolic activities and cell death processes. While our understanding of ferroptotic signaling pathways is advancing, further investigation into the intricate relationship between mitochondrial bio-process and this mode of cell death is necessary to identify effective biomedical therapeutic options targeting this organelle. However, the direct involvement of mitochondria in ferroptosis has remained a topic of debate due to the limited availability of concrete information to date. This review aims to elucidate the pathophysiological perspectives of mitochondria during ferroptotic cell death.
{"title":"Mitochondrial involvement in ferroptotic cell death","authors":"C. Munshi, Tithi Paul, Kalpesh Jas, Mihieka Bose, Shelley Bhattacharya","doi":"10.36922/gtm.2208","DOIUrl":"https://doi.org/10.36922/gtm.2208","url":null,"abstract":"Ferroptosis is a regulated cell death pathophysiologically associated with the depletion of the antioxidant system due to iron overload, which results in excess lipid peroxidation. Mitochondria are crucial organelles known for their prominent involvement in various cellular metabolic activities and cell death processes. While our understanding of ferroptotic signaling pathways is advancing, further investigation into the intricate relationship between mitochondrial bio-process and this mode of cell death is necessary to identify effective biomedical therapeutic options targeting this organelle. However, the direct involvement of mitochondria in ferroptosis has remained a topic of debate due to the limited availability of concrete information to date. This review aims to elucidate the pathophysiological perspectives of mitochondria during ferroptotic cell death.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"43 33","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140231398","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}
Drug discovery relies on high-throughput screening (HTS) methods incorporating both target- and cell-based assays. This comprehensive review delves into the challenges and benefits associated with these assays within the context of HTS. The strategies for developing screening assays, spanning both primary and secondary screens for target identification, are discussed. Furthermore, we review the methods of identifying the most efficacious drugs through these approaches for the treatment of cancer in detail. While various drugs have been identified for cancer treatment, there remains a pressing need for more relevant phenotypic assays. These assays aim to produce the desired disease phenotype, with a specific emphasis on highlighting targets rather than off-targets. The ultimate goal is to pave the way for innovative drug development strategies that can effectively treat cancer patients, thereby reducing the mortality rate.
{"title":"Challenges and advancements in high-throughput screening strategies for cancer therapeutics","authors":"Ruchi Roy, Sunil Kumar Singh, Nashrah Ahmad, Sweta Misra","doi":"10.36922/gtm.2448","DOIUrl":"https://doi.org/10.36922/gtm.2448","url":null,"abstract":"Drug discovery relies on high-throughput screening (HTS) methods incorporating both target- and cell-based assays. This comprehensive review delves into the challenges and benefits associated with these assays within the context of HTS. The strategies for developing screening assays, spanning both primary and secondary screens for target identification, are discussed. Furthermore, we review the methods of identifying the most efficacious drugs through these approaches for the treatment of cancer in detail. While various drugs have been identified for cancer treatment, there remains a pressing need for more relevant phenotypic assays. These assays aim to produce the desired disease phenotype, with a specific emphasis on highlighting targets rather than off-targets. The ultimate goal is to pave the way for innovative drug development strategies that can effectively treat cancer patients, thereby reducing the mortality rate.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"103 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140395730","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}
{"title":"A message from the Editor-in-Chief, Prof. Lemin Zheng","authors":"Lemin Zheng","doi":"10.36922/gtm.2365","DOIUrl":"https://doi.org/10.36922/gtm.2365","url":null,"abstract":"<jats:p />","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":" 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139145163","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}
Cardiac fibrosis, a significant pathological alteration following myocardial infarction (MI), remains enigmatic with respect to the role of cardiac endothelial cells (ECs). To elucidate the proteomic shifts in cardiac ECs accompanying MI-induced cardiac fibrosis, a standard MI mice model was established through ligation of the left anterior descending branch. Following 14 days of effective modeling, we isolated primary ECs from the hearts of both sham and MI models utilizing the CD31 microbeads sorting technique. Quantitative proteomics and bioinformatics methodologies, including tandem mass spectrometry, were employed to discern proteomic alterations in the primary endothelial cells of the experimental groups. Comprehensive analyses, including Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, functional enrichment analysis, and functional enrichment cluster analysis, revealed an up-regulation of proteins associated with extracellular matrix-receptor interaction pathway in cardiac fibrosis post-MI. Subsequent Western blot analysis confirmed the up-regulation of specific proteins involved in this pathway, namely collagen type VI alpha 2 (Col6α2), vitronectin (Vtn), and integrin beta (Itgβ). We conclude that the expression levels of Col6α2, Vtn, and Itgβ in primary ECs during the early stage of cardiac fibrosis, 14 days post-MI, were significantly elevated compared to the sham group (P < 0.05). This observation suggests that ECM-receptor interaction could potentially influence the progression of cardiac fibrosis following MI.
心脏纤维化是心肌梗死（MI）后的一种重要病理改变，但心脏内皮细胞（ECs）的作用仍是一个谜。为了阐明心肌梗死诱发心脏纤维化后心脏内皮细胞蛋白质组的变化，我们通过结扎左前降支建立了标准的心肌梗死小鼠模型。经过 14 天的有效建模后，我们利用 CD31 微珠分选技术从假性和 MI 模型的心脏中分离出了原发性心 ECs。我们采用定量蛋白质组学和生物信息学方法（包括串联质谱法）来鉴别实验组原代内皮细胞的蛋白质组学变化。基因本体分析、京都基因和基因组百科全书（KEGG）分析、功能富集分析和功能富集聚类分析等综合分析表明，在心肌梗死后的心脏纤维化中，与细胞外基质-受体相互作用通路相关的蛋白质上调。随后的 Western 印迹分析证实了参与该通路的特定蛋白的上调，即Ⅵ型胶原α2（Col6α2）、玻璃连蛋白（Vtn）和整合素β（Itgβ）。我们得出结论：与假组相比，在心肌梗死后 14 天的心脏纤维化早期，原发性心肌中 Col6α2、Vtn 和 Itgβ 的表达水平显著升高（P < 0.05）。这一观察结果表明，ECM 与受体的相互作用可能会影响心肌梗死后心脏纤维化的进展。
{"title":"Quantitative proteomic analysis reveals regulatory networks of extracellular matrix receptor interaction pathways in endothelial cells after myocardial infarction","authors":"Xuan Wu, Jiageng Cai, Peng Wang, Lingyun Zu","doi":"10.36922/gtm.2217","DOIUrl":"https://doi.org/10.36922/gtm.2217","url":null,"abstract":"Cardiac fibrosis, a significant pathological alteration following myocardial infarction (MI), remains enigmatic with respect to the role of cardiac endothelial cells (ECs). To elucidate the proteomic shifts in cardiac ECs accompanying MI-induced cardiac fibrosis, a standard MI mice model was established through ligation of the left anterior descending branch. Following 14 days of effective modeling, we isolated primary ECs from the hearts of both sham and MI models utilizing the CD31 microbeads sorting technique. Quantitative proteomics and bioinformatics methodologies, including tandem mass spectrometry, were employed to discern proteomic alterations in the primary endothelial cells of the experimental groups. Comprehensive analyses, including Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, functional enrichment analysis, and functional enrichment cluster analysis, revealed an up-regulation of proteins associated with extracellular matrix-receptor interaction pathway in cardiac fibrosis post-MI. Subsequent Western blot analysis confirmed the up-regulation of specific proteins involved in this pathway, namely collagen type VI alpha 2 (Col6α2), vitronectin (Vtn), and integrin beta (Itgβ). We conclude that the expression levels of Col6α2, Vtn, and Itgβ in primary ECs during the early stage of cardiac fibrosis, 14 days post-MI, were significantly elevated compared to the sham group (P < 0.05). This observation suggests that ECM-receptor interaction could potentially influence the progression of cardiac fibrosis following MI.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":" 35","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139144788","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}
A. Tahanovich, M. Kauhanka, Zhanna A. Rutkovskaya, Ekaterina A. Khotko, O. V. Gotko, Violetta I . Prokhorova
Lung cancer, the leading cause of cancer-related mortality, predominantly exists as non-small cell lung cancer, accounting for approximately 85% of cases and comprising adenocarcinoma, squamous cell carcinoma (SCC), and large cell carcinoma as the three most prevalent histological subtypes. This study focused on investigating pre- and post-operative concentrations of SCC antigen in blood serum, as well as the percentage of CXCR2-containing lymphocytes and CD44v6-containing monocytes in blood cell populations among patients with Stages I–II squamous cell lung cancer (SCLC) within 1 year after tumor resection. The primary objective was to assess their potential for predicting relapse. The study cohort comprised 57 patients (32 men and 25 women) with newly diagnosed squamous cell lung cancer (21 at stage I and 36 at stage II). Following tumor resection, categorized as R0 in terms of surgical intervention, all parameters were examined before surgery and at 3 weeks, 3 months, and 6 months postoperatively. Analysis revealed that the probability of relapse could be accurately predicted, ranging from 68.4% to 89.5%, based on differences in SCC antigen concentration, the percentage of lymphocytes with CXCR2, and monocytes with the CD44v6 receptor during various post-operative intervals. Subsequent regression analysis and the formulation of a combined model incorporating the above-mentioned parameters led to an enhanced predictive value for tumor recurrence, reaching 96.5% accuracy (with specificity at 95.6% and sensitivity at 100%). These results indicate the potential utility of the combined model as an additional marker for predicting postoperative relapse in patients with Stage I–II SCLC.
{"title":"Prognostic evaluation of relapse based on squamous cell carcinoma antigen, CXCR2, and CD44V6 blood levels in patients with Stage I–II squamous cell lung cancer","authors":"A. Tahanovich, M. Kauhanka, Zhanna A. Rutkovskaya, Ekaterina A. Khotko, O. V. Gotko, Violetta I . Prokhorova","doi":"10.36922/gtm.2209","DOIUrl":"https://doi.org/10.36922/gtm.2209","url":null,"abstract":"Lung cancer, the leading cause of cancer-related mortality, predominantly exists as non-small cell lung cancer, accounting for approximately 85% of cases and comprising adenocarcinoma, squamous cell carcinoma (SCC), and large cell carcinoma as the three most prevalent histological subtypes. This study focused on investigating pre- and post-operative concentrations of SCC antigen in blood serum, as well as the percentage of CXCR2-containing lymphocytes and CD44v6-containing monocytes in blood cell populations among patients with Stages I–II squamous cell lung cancer (SCLC) within 1 year after tumor resection. The primary objective was to assess their potential for predicting relapse. The study cohort comprised 57 patients (32 men and 25 women) with newly diagnosed squamous cell lung cancer (21 at stage I and 36 at stage II). Following tumor resection, categorized as R0 in terms of surgical intervention, all parameters were examined before surgery and at 3 weeks, 3 months, and 6 months postoperatively. Analysis revealed that the probability of relapse could be accurately predicted, ranging from 68.4% to 89.5%, based on differences in SCC antigen concentration, the percentage of lymphocytes with CXCR2, and monocytes with the CD44v6 receptor during various post-operative intervals. Subsequent regression analysis and the formulation of a combined model incorporating the above-mentioned parameters led to an enhanced predictive value for tumor recurrence, reaching 96.5% accuracy (with specificity at 95.6% and sensitivity at 100%). These results indicate the potential utility of the combined model as an additional marker for predicting postoperative relapse in patients with Stage I–II SCLC.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"145 3‐9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139149347","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}
Atherosclerosis and coronary artery disease are the main causes of impairment and cardiac death, placing a significant burden on our health-care system. This review focuses on elucidating the involvement of various epigenetic mechanisms in the genesis and progression of cardiovascular diseases (CVDs), particularly chronic CVDs. The deregulation of epigenetic mechanisms plays a crucial role in the progression of CVDs, prompting exploration into novel preventive approaches. Advancements in molecular procedures, network-based approaches, and data analysis have identified new targets in CVDs, permitting the utilization of individualized epigenetic factors for personalized diagnosis and treatment. While promising for improving diagnostic and prognostic assessments, the clinical implementation of epigenetic biomarkers lags behind. Multicenter clinical documentation in a large sample population is crucial to confidently ascertain the clinical utility of specific epigenetic biomarkers. Of particular interest is the interplay between epigenetics and the conflict between the gene-based reductionist theory and the holistic principle of systems biology (SB). The holistic principle analyzes the structural organization and regulation of biological networks, influencing the genesis and progression of complex cardiac diseases like CVDs. This review emphasizes the complexity of CVDs, elucidates the interrelationship between disease networks and epigenetic mechanisms, and highlights the importance of the holistic principle of SB, coupled with artificial intelligence, in clarifying this interrelationship. The constant and uninterrupted epigenetic impact holds immense potential for advancing our understanding of disease progression and treatment across cells and tissues. Despite these advancements, the full integration of the epigenetic impact into medical practice remains incomplete, with limited utilization in clinical applications. Nevertheless, it is likely that in the near future, the epigenetic regulation of gene expression, with its lifelong and extended effects on health, will become an integral part of everyday clinical practice.
{"title":"Epigenetic perspective on atherosclerotic cardiovascular diseases: The holistic principle of systems biology and epigenetic reasoning","authors":"K. Lourida, George E. Louridas","doi":"10.36922/gtm.1868","DOIUrl":"https://doi.org/10.36922/gtm.1868","url":null,"abstract":"Atherosclerosis and coronary artery disease are the main causes of impairment and cardiac death, placing a significant burden on our health-care system. This review focuses on elucidating the involvement of various epigenetic mechanisms in the genesis and progression of cardiovascular diseases (CVDs), particularly chronic CVDs. The deregulation of epigenetic mechanisms plays a crucial role in the progression of CVDs, prompting exploration into novel preventive approaches. Advancements in molecular procedures, network-based approaches, and data analysis have identified new targets in CVDs, permitting the utilization of individualized epigenetic factors for personalized diagnosis and treatment. While promising for improving diagnostic and prognostic assessments, the clinical implementation of epigenetic biomarkers lags behind. Multicenter clinical documentation in a large sample population is crucial to confidently ascertain the clinical utility of specific epigenetic biomarkers. Of particular interest is the interplay between epigenetics and the conflict between the gene-based reductionist theory and the holistic principle of systems biology (SB). The holistic principle analyzes the structural organization and regulation of biological networks, influencing the genesis and progression of complex cardiac diseases like CVDs. This review emphasizes the complexity of CVDs, elucidates the interrelationship between disease networks and epigenetic mechanisms, and highlights the importance of the holistic principle of SB, coupled with artificial intelligence, in clarifying this interrelationship. The constant and uninterrupted epigenetic impact holds immense potential for advancing our understanding of disease progression and treatment across cells and tissues. Despite these advancements, the full integration of the epigenetic impact into medical practice remains incomplete, with limited utilization in clinical applications. Nevertheless, it is likely that in the near future, the epigenetic regulation of gene expression, with its lifelong and extended effects on health, will become an integral part of everyday clinical practice.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"226 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139152715","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}
Tainara Tavares Menchete, Rodolfo Silva Bertoli, Amanda Aguiar Loureiro, Ana Carolina Japur de Sá Rosa-e-Silva, Fabiola Dach, J. Troncon, Debora Aiesha Leite Cantelli, Lúcia Alves da Silva Lara
Persistent genital arousal disorder (PGAD) is a pathological condition characterized by intrusive, unwanted, and distressing symptoms related to spontaneous and prolonged sensations of genital arousal in the absence of sexual desire or stimulation that may compromise the individual’s quality of life. Here, we report the case of a woman who suffered from PGAD probably associated with multiple alterations in the spinal column and Tarlov cyst, which caused the compression of nerve roots and the abnormal sensitivity of the genital region.
{"title":"Management of persistent genital arousal disorder: A case report","authors":"Tainara Tavares Menchete, Rodolfo Silva Bertoli, Amanda Aguiar Loureiro, Ana Carolina Japur de Sá Rosa-e-Silva, Fabiola Dach, J. Troncon, Debora Aiesha Leite Cantelli, Lúcia Alves da Silva Lara","doi":"10.36922/gtm.2341","DOIUrl":"https://doi.org/10.36922/gtm.2341","url":null,"abstract":"Persistent genital arousal disorder (PGAD) is a pathological condition characterized by intrusive, unwanted, and distressing symptoms related to spontaneous and prolonged sensations of genital arousal in the absence of sexual desire or stimulation that may compromise the individual’s quality of life. Here, we report the case of a woman who suffered from PGAD probably associated with multiple alterations in the spinal column and Tarlov cyst, which caused the compression of nerve roots and the abnormal sensitivity of the genital region.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"76 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139155804","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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