Obesity and diabetes represent two prevalent metabolic challenges intricately linked to poor dietary habits and a sedentary lifestyle. The escalating incidence of both conditions in recent years has approached epidemic proportions, with concomitant associations observed in individuals with excessive body weight, including hypertension and cancer. In response to this growing health concern, treatment approaches such as food therapy are deemed necessary. A pivotal aspect in managing these conditions is the careful selection of an appropriate diet to facilitate effective weight loss while minimizing potential adverse effects. Consequently, the ketogenic diet (KD) has garnered attention and support in the treatment of obesity and diabetes. This review aims to discern the potential advantages and risks associated with the utilization of a low-carbohydrate diet in Type 2 diabetic patients. It is well-established that dietary choices significantly impact the health of diabetic patients, and therefore, adopting an appropriate diet is crucial. The KD has demonstrated positive effects on blood sugar levels and glycosylated hemoglobin (HbA1c) levels, concurrently contributing to a reduction in insulin requirements during medication therapy. Furthermore, short-term experiments have revealed a positive association between nutrition choices and weight management. Beneficial improvements have been noted in the lipid profiles, including high-density lipoprotein, low-density lipoprotein, HbA1c, and triglyceride levels. For individuals grappling with diabetes or obesity, a low-carbohydrate diet emerges as a genuine and potentially beneficial therapy option. This review provides a comprehensive overview of the key concepts influencing the treatment of obesity and Type 2 diabetic patients through low-carbohydrate diets.
{"title":"Efficacy of ketogenic and low-carbohydrate diets in the management of Type 2 diabetes: A narrative review","authors":"Sabrina Zaman, Tamsel Ahammed, Md. Nazmul Haque, Md. Enamul Huque","doi":"10.36922/gtm.1361","DOIUrl":"https://doi.org/10.36922/gtm.1361","url":null,"abstract":"Obesity and diabetes represent two prevalent metabolic challenges intricately linked to poor dietary habits and a sedentary lifestyle. The escalating incidence of both conditions in recent years has approached epidemic proportions, with concomitant associations observed in individuals with excessive body weight, including hypertension and cancer. In response to this growing health concern, treatment approaches such as food therapy are deemed necessary. A pivotal aspect in managing these conditions is the careful selection of an appropriate diet to facilitate effective weight loss while minimizing potential adverse effects. Consequently, the ketogenic diet (KD) has garnered attention and support in the treatment of obesity and diabetes. This review aims to discern the potential advantages and risks associated with the utilization of a low-carbohydrate diet in Type 2 diabetic patients. It is well-established that dietary choices significantly impact the health of diabetic patients, and therefore, adopting an appropriate diet is crucial. The KD has demonstrated positive effects on blood sugar levels and glycosylated hemoglobin (HbA1c) levels, concurrently contributing to a reduction in insulin requirements during medication therapy. Furthermore, short-term experiments have revealed a positive association between nutrition choices and weight management. Beneficial improvements have been noted in the lipid profiles, including high-density lipoprotein, low-density lipoprotein, HbA1c, and triglyceride levels. For individuals grappling with diabetes or obesity, a low-carbohydrate diet emerges as a genuine and potentially beneficial therapy option. This review provides a comprehensive overview of the key concepts influencing the treatment of obesity and Type 2 diabetic patients through low-carbohydrate diets.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"36 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138972792","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}
Carpal tunnel syndrome (CTS) is the most commonly diagnosed peripheral neuropathy, with a prevalence of 1 – 16% within the general population. If left untreated, it can lead to permanent dysfunctionality and disability. This study aimed to determine the outcomes and complications associated with open carpal tunnel release surgery (OCTR), compare the presentation of CTS symptoms before and after the operation, and investigate the factors contributing to post-operative complications. To achieve these objectives, a case series design was employed, and the study was conducted at the Department of Orthopedics and Traumatology in Zliten Teaching Hospital, Libya, from January 2016 to December 2018. A total of 256 patients who had opted to undergo OCTR of the transverse carpal ligament during the preoperative stage were enrolled and prospectively followed up for 2 years. The post-operative follow-up analysis revealed a statistically significant reduction in symptoms such as dull aching discomfort in the hand and forearm, as well as paresthesia and numbness when compared to the pre-operative period (10.2% vs. 90.5%; P < 0.0001). However, there were no significant differences in clumsiness (18.8% vs. 25.8%; P = 0.256) or thenar muscle atrophy (1.6% vs. 5.0%; P = 0.194). The majority of the patients (90.6%) expressed high levels of satisfaction with the procedure, reporting no recurrence of symptoms. In contrast, only 9.4% of patients experienced post-operative complications. The study findings revealed no significant correlation between post-operative complications and body mass index (P = 0.194). Nonetheless, a statistically significant association was observed between the severity of nerve conduction and post-operative complications (P = 0.011). In summary, the open release of the transverse carpal ligament resulted in positive surgical outcomes.
腕管综合征(Carpal tunnel syndrome, CTS)是最常见的周围神经病变，患病率为1 &在普通人群中占16%如果不及时治疗，可能会导致永久性功能障碍和残疾。本研究旨在确定开放式腕管松解手术(OCTR)的预后和并发症，比较术前和术后CTS症状的表现，并探讨导致术后并发症的因素。为了实现这些目标，采用了病例系列设计，并于2016年1月至2018年12月在利比亚Zliten教学医院骨科和创伤科进行了研究。共纳入256例术前选择行腕横韧带OCTR的患者，并进行了2年的前瞻性随访。术后随访分析显示，与术前相比，手部和前臂钝痛不适、感觉异常和麻木等症状有统计学意义的减少(10.2% vs. 90.5%;P & lt;0.0001)。然而，笨拙性没有显著差异(18.8% vs. 25.8%;P = 0.256)或鱼际肌萎缩(1.6% vs. 5.0%;P = 0.194)。大多数患者(90.6%)对手术表示高度满意，无症状复发。相比之下，只有9.4%的患者出现了术后并发症。研究结果显示，术后并发症与体重指数无显著相关性(P = 0.194)。然而，神经传导的严重程度与术后并发症之间存在统计学意义上的相关性(P = 0.011)。综上所述，腕横韧带的开放释放获得了积极的手术结果。
{"title":"Surgical outcome of open carpal tunnel release: A 2-year case series study at Zliten Teaching Hospital, Libya","authors":"Mohamed Gwila, Mostafa Ebshina, Syeda Humayra, Moniruddin Chowdhury","doi":"10.36922/gtm.1019","DOIUrl":"https://doi.org/10.36922/gtm.1019","url":null,"abstract":"Carpal tunnel syndrome (CTS) is the most commonly diagnosed peripheral neuropathy, with a prevalence of 1 &ndash; 16% within the general population. If left untreated, it can lead to permanent dysfunctionality and disability. This study aimed to determine the outcomes and complications associated with open carpal tunnel release surgery (OCTR), compare the presentation of CTS symptoms before and after the operation, and investigate the factors contributing to post-operative complications. To achieve these objectives, a case series design was employed, and the study was conducted at the Department of Orthopedics and Traumatology in Zliten Teaching Hospital, Libya, from January 2016 to December 2018. A total of 256 patients who had opted to undergo OCTR of the transverse carpal ligament during the preoperative stage were enrolled and prospectively followed up for 2 years. The post-operative follow-up analysis revealed a statistically significant reduction in symptoms such as dull aching discomfort in the hand and forearm, as well as paresthesia and numbness when compared to the pre-operative period (10.2% vs. 90.5%; P < 0.0001). However, there were no significant differences in clumsiness (18.8% vs. 25.8%; P = 0.256) or thenar muscle atrophy (1.6% vs. 5.0%; P = 0.194). The majority of the patients (90.6%) expressed high levels of satisfaction with the procedure, reporting no recurrence of symptoms. In contrast, only 9.4% of patients experienced post-operative complications. The study findings revealed no significant correlation between post-operative complications and body mass index (P = 0.194). Nonetheless, a statistically significant association was observed between the severity of nerve conduction and post-operative complications (P = 0.011). In summary, the open release of the transverse carpal ligament resulted in positive surgical outcomes.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135634390","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}
Parkinson’s disease (PD) is a common neurodegenerative disease that primarily affects the elderly, significantly impacting patients’ health and quality of life. While most genetic studies on PD have focused on single nucleotide polymorphisms, the effects of other forms of genomic variation in PD are yet to be fully elucidated. Transposable elements (TEs) are one of the main sources of human genome structural variation, with known associations with many human diseases. However, their potential connection to PD remains unclear. In this study, we investigated non-reference TE polymorphisms in three independent PD cohorts and explored their associations with both PD risk and progression. Our findings revealed that one non-reference TE is associated with the risk of PD, while two TEs are associated with disease progression. Furthermore, through expression quantitative trait locus (eQTL) analysis, we identified 18 cis TE-eQTLs in an interaction model and 290 cis TE-eQTLs in a non-interaction model. Several non-reference TE polymorphisms are correlated with specific PD-gene expression patterns in trans. These results indicate the feasibility of delving into the genetics of PD through the study of complex genomic variations. Advances in genomics research have the potential to deepen our understanding of this disease and pave the way for further translational medicine research in PD.
{"title":"Genome-wide analysis identifies non-reference transposable element polymorphisms associated with Parkinson’s disease","authors":"Hao Wu, Junfeng Luo, Ganqiang Liu","doi":"10.36922/gtm.1583","DOIUrl":"https://doi.org/10.36922/gtm.1583","url":null,"abstract":"Parkinson&rsquo;s disease (PD) is a common neurodegenerative disease that primarily affects the elderly, significantly impacting patients&rsquo; health and quality of life. While most genetic studies on PD have focused on single nucleotide polymorphisms, the effects of other forms of genomic variation in PD are yet to be fully elucidated. Transposable elements (TEs) are one of the main sources of human genome structural variation, with known associations with many human diseases. However, their potential connection to PD remains unclear. In this study, we investigated non-reference TE polymorphisms in three independent PD cohorts and explored their associations with both PD risk and progression. Our findings revealed that one non-reference TE is associated with the risk of PD, while two TEs are associated with disease progression. Furthermore, through expression quantitative trait locus (eQTL) analysis, we identified 18 cis TE-eQTLs in an interaction model and 290 cis TE-eQTLs in a non-interaction model. Several non-reference TE polymorphisms are correlated with specific PD-gene expression patterns in trans. These results indicate the feasibility of delving into the genetics of PD through the study of complex genomic variations. Advances in genomics research have the potential to deepen our understanding of this disease and pave the way for further translational medicine research in PD.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136112632","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}
During cancer progression, bromodomain and extra-terminal (BET) families regulate chromatin and recruit enzymes that are associated with chromatin regulation to control gene expression. The bromodomain-containing protein 4 (BRD4) plays an important role in DNA damage repair, nuclear factor kappa B (NFκB) signaling, interaction with c-Myc, and transcription regulation of genes essential in carcinogenesis, as well as links transcription at enhancers and genes to regulate enhancer transcription. The colocalization of BRD4 with enhancer and promoter-proximal gene regions enables the elongation activation at enhancer genes. The inactivation of BRD4 has been demonstrated to inhibit cancer development, corroborating BRD4 as a promising therapeutic target. In addition, small-molecule inhibitors targetting functional domains of BRD4 are under investigation for their potential therapeutic applications in cancer and other diseases. This review presents an overview of BRD4 function and its dysfunction in cancer progression, as well as discusses how the potential of BRD4 as a therapeutic target.
在癌症进展过程中，溴结构域和外端(BET)家族调控染色质并招募与染色质调控相关的酶来控制基因表达。含溴结构域蛋白4 (BRD4)在DNA损伤修复、核因子kappa B (NFκB)信号转导、与c-Myc的相互作用、致癌必需基因的转录调控等方面发挥重要作用，并连接增强子和基因的转录，调控增强子转录。BRD4与增强子和启动子近端基因区域的共定位使增强子基因的延伸激活成为可能。BRD4的失活已被证明可以抑制癌症的发展，证实BRD4是一个有希望的治疗靶点。此外，靶向BRD4功能域的小分子抑制剂正在研究其在癌症和其他疾病中的潜在治疗应用。本文综述了BRD4的功能及其在癌症进展中的功能障碍，并讨论了BRD4作为治疗靶点的潜力。
{"title":"Essential roles of BRD4 in cancer: DNA damage, transcription regulation, and signal transduction","authors":"Sylvia Y. Sun","doi":"10.36922/gtm.1442","DOIUrl":"https://doi.org/10.36922/gtm.1442","url":null,"abstract":"During cancer progression, bromodomain and extra-terminal (BET) families regulate chromatin and recruit enzymes that are associated with chromatin regulation to control gene expression. The bromodomain-containing protein 4 (BRD4) plays an important role in DNA damage repair, nuclear factor kappa B (NF&kappa;B) signaling, interaction with c-Myc, and transcription regulation of genes essential in carcinogenesis, as well as links transcription at enhancers and genes to regulate enhancer transcription. The colocalization of BRD4 with enhancer and promoter-proximal gene regions enables the elongation activation at enhancer genes. The inactivation of BRD4 has been demonstrated to inhibit cancer development, corroborating BRD4 as a promising therapeutic target. In addition, small-molecule inhibitors targetting functional domains of BRD4 are under investigation for their potential therapeutic applications in cancer and other diseases. This review presents an overview of BRD4 function and its dysfunction in cancer progression, as well as discusses how the potential of BRD4 as a therapeutic target.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135296117","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}
Severe adverse events, including autoimmune diseases, have been noted in some individuals following vaccination. It is still unknown whether a subset of these autoimmune disease adverse events (ADAE) is triggered by the immunization and is not background chance occurrences. Only a small fraction of adverse events experienced by vaccinees has been reported to the Vaccine Adverse Event Reporting System (VAERS) database. In this study, ADAEs within VAERS are examined. The frequency of autoimmune disease adverse reactions reported immediately following vaccination was compared to the background population adverse event frequency. The frequency of immediate-onset autoimmune diseases, extracted from VAERS, arisen after vaccination was found to exceed the expected background occurrences. Vaccinees who receive a second COVID-19 mRNA vaccination dose 3 weeks after the first dose appear to experience an increased number of ADAE. Furthermore, human papillomavirus (HPV), hepatitis A, and hepatitis B vaccines exhibit distinctive patterns of associations with autoimmune diseases. The potential role of vaccine aluminum adjuvant, included in these vaccines, cannot be ruled out as contributing to ADAE. VAERS data illustrate immediate onset correlations for multiple autoimmune diseases across various vaccines. Autoimmune diseases immediate temporal onset associations that occur following COVID-19 mRNA and adenoviral vaccinations are predicted to occur with similar frequencies for all mRNA and adenoviral vaccines and therapeutics. Taken together, removal of aluminum adjuvants from HPV, hepatitis A, and hepatitis B vaccines, among others, should be considered in the effort to reduce the occurrence of immediate-onset autoimmune diseases.
{"title":"Immediate onset signatures of autoimmune diseases after vaccination","authors":"Darrell O. Ricke","doi":"10.36922/gtm.1455","DOIUrl":"https://doi.org/10.36922/gtm.1455","url":null,"abstract":"Severe adverse events, including autoimmune diseases, have been noted in some individuals following vaccination. It is still unknown whether a subset of these autoimmune disease adverse events (ADAE) is triggered by the immunization and is not background chance occurrences. Only a small fraction of adverse events experienced by vaccinees has been reported to the Vaccine Adverse Event Reporting System (VAERS) database. In this study, ADAEs within VAERS are examined. The frequency of autoimmune disease adverse reactions reported immediately following vaccination was compared to the background population adverse event frequency. The frequency of immediate-onset autoimmune diseases, extracted from VAERS, arisen after vaccination was found to exceed the expected background occurrences. Vaccinees who receive a second COVID-19 mRNA vaccination dose 3 weeks after the first dose appear to experience an increased number of ADAE. Furthermore, human papillomavirus (HPV), hepatitis A, and hepatitis B vaccines exhibit distinctive patterns of associations with autoimmune diseases. The potential role of vaccine aluminum adjuvant, included in these vaccines, cannot be ruled out as contributing to ADAE. VAERS data illustrate immediate onset correlations for multiple autoimmune diseases across various vaccines. Autoimmune diseases immediate temporal onset associations that occur following COVID-19 mRNA and adenoviral vaccinations are predicted to occur with similar frequencies for all mRNA and adenoviral vaccines and therapeutics. Taken together, removal of aluminum adjuvants from HPV, hepatitis A, and hepatitis B vaccines, among others, should be considered in the effort to reduce the occurrence of immediate-onset autoimmune diseases.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135131694","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}
Lacosamide is a third-generation anticonvulsant used in the treatment of epilepsy. While therapeutic levels for various patient subpopulations are still under investigation to achieve optimal responses, therapeutic drug monitoring has been proven to be useful in improving patient management. To ensure the reliability of results, it is essential to establish a reliable quantitative method. Thus, the aim of this study was to develop and validate a simple and feasible method for quantifying lacosamide in human plasma, with the specific aim of facilitating drug monitoring purposes. A high-performance liquid chromatography method with ultraviolet detection was developed for the quantification of lacosamide in human plasma. Analyte recovery was achieved through ethyl acetate extraction, with propranolol serving as the internal standard. A C18 column and a mobile phase consisting of 10 mM phosphate buffer and acetonitrile (70:30 v/v, pH = 3.5) were employed. Validation parameters included specificity, linearity, repeatability, precision, accuracy, sensitivity, and stability. The method exhibited linearity within the range of 2.5 – 30 μg/ml (R2 = 0.997), with a limit of quantitation of 2.29 μg/ml. The average recovery percentage was 100.2%, and it proved to be accurate, precise, and specific. In plasma samples, the drug content remained stable for 72 h at 4°C, 1 month at −20°C, and 2 years at −80°C. The post-processed sample remained stable for 1 week under all tested conditions. Due to its simplicity, short analysis time, sensitivity, and cost-effectiveness, the proposed analytical method proves to be useful for therapeutic monitoring and pharmacokinetic studies of lacosamide.
{"title":"A simple, fast, and cost-effective high-performance liquid chromatography-ultraviolet validated method to quantify lacosamide in therapeutic drug monitoring","authors":"Ángeles Gloria Rodríguez-Basso, María Cecilia Kravetz, María Sylvia Viola, Florencia Ayelén Fernández, Nicolás Martín Barrionuevo, Damián Consalvo, Mariano Núñez, Guillermo Federico Bramuglia","doi":"10.36922/gtm.1265","DOIUrl":"https://doi.org/10.36922/gtm.1265","url":null,"abstract":"Lacosamide is a third-generation anticonvulsant used in the treatment of epilepsy. While therapeutic levels for various patient subpopulations are still under investigation to achieve optimal responses, therapeutic drug monitoring has been proven to be useful in improving patient management. To ensure the reliability of results, it is essential to establish a reliable quantitative method. Thus, the aim of this study was to develop and validate a simple and feasible method for quantifying lacosamide in human plasma, with the specific aim of facilitating drug monitoring purposes. A high-performance liquid chromatography method with ultraviolet detection was developed for the quantification of lacosamide in human plasma. Analyte recovery was achieved through ethyl acetate extraction, with propranolol serving as the internal standard. A C18 column and a mobile phase consisting of 10 mM phosphate buffer and acetonitrile (70:30 v/v, pH = 3.5) were employed. Validation parameters included specificity, linearity, repeatability, precision, accuracy, sensitivity, and stability. The method exhibited linearity within the range of 2.5 &ndash; 30 &mu;g/ml (R2 = 0.997), with a limit of quantitation of 2.29 &mu;g/ml. The average recovery percentage was 100.2%, and it proved to be accurate, precise, and specific. In plasma samples, the drug content remained stable for 72 h at 4&deg;C, 1 month at &minus;20&deg;C, and 2 years at &minus;80&deg;C. The post-processed sample remained stable for 1 week under all tested conditions. Due to its simplicity, short analysis time, sensitivity, and cost-effectiveness, the proposed analytical method proves to be useful for therapeutic monitoring and pharmacokinetic studies of lacosamide.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"35 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135719304","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}
In this study, we investigated the incidence of venous thromboembolism (VTE), related risk factors for VTE, and the effect of VTE on overall survival in patients with non-small-cell lung cancer harboring epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) gene mutations. The study included patients older than 18 years of age who were diagnosed with histologically proven locally advanced or advanced-stage adenocarcinoma and were followed in our center between January 2014 and December 2019. These patients were divided into two groups: one comprising mutation-positive individuals and the other mutation-negative individuals. We examined factors influencing the occurrence of VTE, assessed the incidence of VTE, and compared the differences in overall survival. Univariate Cox regression analysis revealed that the independent predictors of VTE were the number of metastases (Hazard ratio [HR]: 3.784; 95% confidence interval [CI]: 2.198 – 6.515; P < 0.001) and the presence of EGFR exon 21 mutations (HR: 2.386; 95% CI: 1.276 – 4.462; P = 0.006). However, in multivariate analysis, only the number of comorbidities was associated with an increased risk for VTE (HR: 3.462; 95% CI: 1.977 – 6.060; P < 0.001). It is essential to consider the risk of VTE development in patients with EGFR exon 21 mutation-positive lung adenocarcinoma. Physicians should be vigilant in terms of screening, prophylaxis, and follow-up for underlying VTE in these patients.
{"title":"Thromboembolism risk in patients diagnosed with EGFR- and ALK-mutant lung adenocarcinoma","authors":"Suna Kavurgacı, Yasemin Söyler, Pınar Akın Kabalak, Derya Kızılgöz, Ülkü Yılmaz","doi":"10.36922/gtm.1027","DOIUrl":"https://doi.org/10.36922/gtm.1027","url":null,"abstract":"In this study, we investigated the incidence of venous thromboembolism (VTE), related risk factors for VTE, and the effect of VTE on overall survival in patients with non-small-cell lung cancer harboring epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) gene mutations. The study included patients older than 18 years of age who were diagnosed with histologically proven locally advanced or advanced-stage adenocarcinoma and were followed in our center between January 2014 and December 2019. These patients were divided into two groups: one comprising mutation-positive individuals and the other mutation-negative individuals. We examined factors influencing the occurrence of VTE, assessed the incidence of VTE, and compared the differences in overall survival. Univariate Cox regression analysis revealed that the independent predictors of VTE were the number of metastases (Hazard ratio [HR]: 3.784; 95% confidence interval [CI]: 2.198 &ndash; 6.515; P < 0.001) and the presence of EGFR exon 21 mutations (HR: 2.386; 95% CI: 1.276 &ndash; 4.462; P = 0.006). However, in multivariate analysis, only the number of comorbidities was associated with an increased risk for VTE (HR: 3.462; 95% CI: 1.977 &ndash; 6.060; P < 0.001). It is essential to consider the risk of VTE development in patients with EGFR exon 21 mutation-positive lung adenocarcinoma. Physicians should be vigilant in terms of screening, prophylaxis, and follow-up for underlying VTE in these patients.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"31 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135825992","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}
Efforts have been made to employ the nuclear magnetic resonance (NMR)-biochemical correlation concept or a combination of MR imaging (MRI) and MR spectroscopy (MRS) as an established diagnostic tool for medical practice in clinical settings. Recent reviews and meta-analyses indicate the great possibility of using integrated multimodal multiparametric MRI and MRS for deep learning (DL) of soft-tissue pathophysiology, enabling improved decision-making and disease progression monitoring in precision medicine. Recent guidelines and clinical trials suggest the need for DL of the biophysical and biochemical nature of the brain, breast, prostate, liver, and heart tissue from digital spectromics analysis, along with other molecular imaging modalities. The current opinions, based on recent recommendations, available literature on evidence-based MR spectromics, clinical trials, and meta-analyses on high-resolution MRI and MRS suggest that utilizing MRI and MRS signals as theranostic biomarkers for various soft tissues can demonstrate NMR-biochemical correlation and employ MRI with MRS as adjunct real-time tools, generating robust, and fast tissue digital images with metabolic screening. The integration of DL features can aid in evaluating patient disease diagnosis and therapy within a clinical setting, considering the available medical practices and their limitations.
{"title":"Nuclear magnetic resonance-biochemical correlation toward deep learning of theranosis and precision medicine","authors":"Rakesh Sharma, A. Trivedi","doi":"10.36922/gtm.337","DOIUrl":"https://doi.org/10.36922/gtm.337","url":null,"abstract":"Efforts have been made to employ the nuclear magnetic resonance (NMR)-biochemical correlation concept or a combination of MR imaging (MRI) and MR spectroscopy (MRS) as an established diagnostic tool for medical practice in clinical settings. Recent reviews and meta-analyses indicate the great possibility of using integrated multimodal multiparametric MRI and MRS for deep learning (DL) of soft-tissue pathophysiology, enabling improved decision-making and disease progression monitoring in precision medicine. Recent guidelines and clinical trials suggest the need for DL of the biophysical and biochemical nature of the brain, breast, prostate, liver, and heart tissue from digital spectromics analysis, along with other molecular imaging modalities. The current opinions, based on recent recommendations, available literature on evidence-based MR spectromics, clinical trials, and meta-analyses on high-resolution MRI and MRS suggest that utilizing MRI and MRS signals as theranostic biomarkers for various soft tissues can demonstrate NMR-biochemical correlation and employ MRI with MRS as adjunct real-time tools, generating robust, and fast tissue digital images with metabolic screening. The integration of DL features can aid in evaluating patient disease diagnosis and therapy within a clinical setting, considering the available medical practices and their limitations.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"285 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76861407","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}
Guoshen Zhong, Yanhua Shi, L. Kong, Kaixuan Lv, Lichun Zhang, Mei Yang, Na Tian, Nana Yang
Acute lung injury (ALI) results from excessive inflammation and disruption of the alveolar-capillary barrier, leading to acute respiratory distress syndrome. Hydrogen, known as a reducing substance, has been commonly used in preclinical trials of ALI. The present paper aims to summarize the effects of hydrogen on animal models of ALI and the possible antioxidant and anti-inflammation mechanisms of hydrogen. We conducted a thorough search of the relevant literature on PubMed, EMBASE, Web of Science, and CNKI. Data retrieved from 20 studies were analyzed to assess the beneficial effects of hydrogen therapy on ALI animal models. To evaluate the effects of hydrogen, commonly assessed outcome indicators include wet-to-dry ratio (W/D), arterial oxygen partial pressure (PaO2), malondialdehyde (MDA), superoxide dismutase (SOD), and tumor necrosis factor-alpha (TNF-α). The results demonstrate that hydrogen reduces pulmonary edema (W/D: 95% CI = −0.98 – −0.85, P < 0.001), mitigates hypoxia (PaO2: 95% CI = 6.08 – 22.30, P < 0.001), represses lipid peroxidation (MDA: 95% CI = −2.12 – −1.06, P < 0.001), scavenges free radicals (SOD: 95% CI = 10.12 – 30.07, P < 0.001), and inhibits inflammatory response (TNF-α: 95% CI = −5.52 – −1.72, P < 0.001). The subgroup analysis showed significant differences between interventions (MDA: P < 0.05; TNF-α: P < 0.05; SOD: P < 0.001). The meta-regression suggests that species may cause heterogeneity (P < 0.05). These results suggest the potential of using hydrogen in clinical trials. Different interventions with hydrogen can affect metabolic transport and distribution in vivo. Further studies should be conducted to validate and confirm these findings.
急性肺损伤(ALI)是由于过度炎症和肺泡-毛细血管屏障的破坏，导致急性呼吸窘迫综合征。氢是一种还原性物质，常用于急性脑损伤的临床前试验。本文就氢对ALI动物模型的影响及其可能的抗氧化和抗炎机制进行综述。我们在PubMed、EMBASE、Web of Science和CNKI上进行了相关文献的全面检索。我们分析了20项研究的数据，以评估氢疗法对ALI动物模型的有益作用。为了评估氢的影响，通常评估的结局指标包括干湿比(W/D)、动脉氧分压(PaO2)、丙二醛(MDA)、超氧化物歧化酶(SOD)和肿瘤坏死因子-α (TNF-α)。结果表明，氢可以减轻肺水肿(W/D: 95% CI = - 0.98 - - 0.85, P < 0.001)，减轻缺氧(PaO2: 95% CI = 6.08 - 22.30, P < 0.001)，抑制脂质过氧化(MDA: 95% CI = - 2.12 - - 1.06, P < 0.001)，清除自由基(SOD: 95% CI = 10.12 - 30.07, P < 0.001)，抑制炎症反应(TNF-α: 95% CI = - 5.52 - - 1.72, P < 0.001)。亚组分析显示干预间差异有统计学意义(MDA: P < 0.05;Tnf -α: p < 0.05;Sod: p < 0.001)。meta回归分析显示物种可能导致异质性(P < 0.05)。这些结果表明在临床试验中使用氢气的潜力。不同的氢干预可以影响体内代谢运输和分布。应该进行进一步的研究来验证和确认这些发现。
{"title":"Inhibiting oxidative stress and inflammation in acute lung injury using hydrogen: A preclinical systematic review and meta-analysis","authors":"Guoshen Zhong, Yanhua Shi, L. Kong, Kaixuan Lv, Lichun Zhang, Mei Yang, Na Tian, Nana Yang","doi":"10.36922/gtm.0379","DOIUrl":"https://doi.org/10.36922/gtm.0379","url":null,"abstract":"Acute lung injury (ALI) results from excessive inflammation and disruption of the alveolar-capillary barrier, leading to acute respiratory distress syndrome. Hydrogen, known as a reducing substance, has been commonly used in preclinical trials of ALI. The present paper aims to summarize the effects of hydrogen on animal models of ALI and the possible antioxidant and anti-inflammation mechanisms of hydrogen. We conducted a thorough search of the relevant literature on PubMed, EMBASE, Web of Science, and CNKI. Data retrieved from 20 studies were analyzed to assess the beneficial effects of hydrogen therapy on ALI animal models. To evaluate the effects of hydrogen, commonly assessed outcome indicators include wet-to-dry ratio (W/D), arterial oxygen partial pressure (PaO2), malondialdehyde (MDA), superoxide dismutase (SOD), and tumor necrosis factor-alpha (TNF-α). The results demonstrate that hydrogen reduces pulmonary edema (W/D: 95% CI = −0.98 – −0.85, P < 0.001), mitigates hypoxia (PaO2: 95% CI = 6.08 – 22.30, P < 0.001), represses lipid peroxidation (MDA: 95% CI = −2.12 – −1.06, P < 0.001), scavenges free radicals (SOD: 95% CI = 10.12 – 30.07, P < 0.001), and inhibits inflammatory response (TNF-α: 95% CI = −5.52 – −1.72, P < 0.001). The subgroup analysis showed significant differences between interventions (MDA: P < 0.05; TNF-α: P < 0.05; SOD: P < 0.001). The meta-regression suggests that species may cause heterogeneity (P < 0.05). These results suggest the potential of using hydrogen in clinical trials. Different interventions with hydrogen can affect metabolic transport and distribution in vivo. Further studies should be conducted to validate and confirm these findings.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85911409","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}
Deepyaman Das, C. Munshi, Kalpesh Jas, Sourish Pramanik
Research into the pathophysiology of Alzheimer’s disease (AD) and Parkinson’s disease (PD) has spanned decades, unraveling deregulated signaling cascades in these diseases. Recently, the discovery of the link between ferroptosis and neurodegeneration has opened new avenues for neurodegenerative disease research. Despite this, the key players in the ferroptotic pathway potentially governing the progression of neurodegenerative disease remain unidentified. Thus, in the present study, we reconstructed two protein–protein interaction networks (PPINs) for AD and PD with their respective differentially expressed genes from post-mortem tissues and identified 21 highly connected clusters within the AD PPIN and 17 clusters within the PD PPIN. Then, we identified 8 ferroptotic transcription factors (FerrTFs) that regulate hub genes from the 7 deregulated clusters of AD and 6 FerrTFs from the 4 deregulated clusters of PD. Functional enrichment analysis of these clusters revealed impairment in important neurological functions. Finally, we identified 681 drugs with potential therapeutic effects against the 8 FerrTFs associated with AD and 633 drugs against the 6 FerrTFs linked to PD. In addition, 126 and 114 miRNAs might silence 7 and 5 FerrTFs against AD and PD, respectively. This exploratory study identifies potential markers of ferroptosis that could exacerbate these neurodegenerative diseases and also suggests possible therapeutic measures against them.
{"title":"Demystifying the influence of ferroptosis on Alzheimer’s and Parkinson’s diseases: A network and systems biology approach","authors":"Deepyaman Das, C. Munshi, Kalpesh Jas, Sourish Pramanik","doi":"10.36922/gtm.0318","DOIUrl":"https://doi.org/10.36922/gtm.0318","url":null,"abstract":"Research into the pathophysiology of Alzheimer’s disease (AD) and Parkinson’s disease (PD) has spanned decades, unraveling deregulated signaling cascades in these diseases. Recently, the discovery of the link between ferroptosis and neurodegeneration has opened new avenues for neurodegenerative disease research. Despite this, the key players in the ferroptotic pathway potentially governing the progression of neurodegenerative disease remain unidentified. Thus, in the present study, we reconstructed two protein–protein interaction networks (PPINs) for AD and PD with their respective differentially expressed genes from post-mortem tissues and identified 21 highly connected clusters within the AD PPIN and 17 clusters within the PD PPIN. Then, we identified 8 ferroptotic transcription factors (FerrTFs) that regulate hub genes from the 7 deregulated clusters of AD and 6 FerrTFs from the 4 deregulated clusters of PD. Functional enrichment analysis of these clusters revealed impairment in important neurological functions. Finally, we identified 681 drugs with potential therapeutic effects against the 8 FerrTFs associated with AD and 633 drugs against the 6 FerrTFs linked to PD. In addition, 126 and 114 miRNAs might silence 7 and 5 FerrTFs against AD and PD, respectively. This exploratory study identifies potential markers of ferroptosis that could exacerbate these neurodegenerative diseases and also suggests possible therapeutic measures against them.","PeriodicalId":73176,"journal":{"name":"Global translational medicine","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80119535","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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