When people ascend to a high altitude (HA), the body’s oxygen (O2) sensing mechanisms can sense perturbation in partial pressure and trigger adaptive responses. Rapid ascending to HA without ample time for acclimatization culminates in high-altitude illnesses, which can derail the body functioning of lowlanders moving to HA. High-altitude native populations have undergone positive natural selection to efficiently overcome the challenges of chronic hypobaric hypoxia (HH) and thus offer a unique model to understand physiological and genetic adaptations at high altitudes. In addition, evolutionary shreds of evidence propose that sulfur belonging to the same periodic table family can mimic oxygen to bypass its metabolic oxygen demand and modulate energy production.Intriguingly, our group has identified a strong association between diminished hydrogen sulfide (H2S)levels and HH-induced pathological responses. We have recently presented experimental evidence of cysteine deficit, which functionally regulates both lowered levels of endogenous H2S and HH-induced neuropathological responses. In this review, we sought to understand the role of H2S and the transsulfuration pathway at HA.
当人们上升到高海拔地区（HA）时，身体的氧气（O2）感应机制会感知到分压的扰动，并引发适应性反应。在没有充分适应时间的情况下快速上升到高海拔地区，最终会导致高海拔疾病，这可能会破坏低地移居到高海拔地区的人的身体机能。高海拔地区的原生种群经历了积极的自然选择，有效地克服了长期低压缺氧（HH）的挑战，因此为了解高海拔地区的生理和遗传适应性提供了一个独特的模型。此外，进化方面的一些证据表明，同属元素周期表家族的硫可以模拟氧，绕过氧的代谢需氧量，调节能量的产生。我们最近提出了半胱氨酸缺乏的实验证据，半胱氨酸对内源性 H2S 水平降低和 HH 诱导的神经病理反应都有功能调节作用。在本综述中，我们试图了解 H2S 和转硫化途径在 HA 中的作用。
{"title":"Emerging Evidence for Association of Transsulfuration Pathway with Hypoxia Responses","authors":"Neha Jain, Manish Sharma","doi":"10.14429/dlsj.9.19478","DOIUrl":"https://doi.org/10.14429/dlsj.9.19478","url":null,"abstract":"When people ascend to a high altitude (HA), the body’s oxygen (O2) sensing mechanisms can sense perturbation in partial pressure and trigger adaptive responses. Rapid ascending to HA without ample time for acclimatization culminates in high-altitude illnesses, which can derail the body functioning of lowlanders moving to HA. High-altitude native populations have undergone positive natural selection to efficiently overcome the challenges of chronic hypobaric hypoxia (HH) and thus offer a unique model to understand physiological and genetic adaptations at high altitudes. In addition, evolutionary shreds of evidence propose that sulfur belonging to the same periodic table family can mimic oxygen to bypass its metabolic oxygen demand and modulate energy production.Intriguingly, our group has identified a strong association between diminished hydrogen sulfide (H2S)levels and HH-induced pathological responses. We have recently presented experimental evidence of cysteine deficit, which functionally regulates both lowered levels of endogenous H2S and HH-induced neuropathological responses. In this review, we sought to understand the role of H2S and the transsulfuration pathway at HA.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140524523","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}
Hypobaric hypoxia occurs at high altitudes where barometric pressure is low causing insufficient supply of oxygen leading to many high-altitude illnesses like acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE) etc.Medications have been applied to treat and prevent injuries caused by HBH, showing anti-inflammatory, anti-edemagenic, and antioxidant properties. AMS symptoms, such as headache, nausea, weariness, usually go away in 1-2 days. HACE causes brain swelling, elevated intracranial pressure, resulting in confusion, stupor, ataxia, and death.Acetazolamide, dexamethasone, nifedipine are the drugs used for treatment acting oncarbonic anhydrase enzyme, calcium channels.Acetazolamide increases arterial partial pressure of oxygen.Nifedipine relaxes vascular smooth muscles and increases blood flow. Some drugscause side effects also like dizziness, diuresis, nausea, malaise, etc. Hence, a new drug search is needed to find more targeted and fewer side effects for faster relief and better health at high altitudes.
{"title":"Potential Candidate Molecules of Past and Present for Combating High Altitude Hypoxia Induced Maladies","authors":"Shweta Kushwaha, Deepika Saraswat","doi":"10.14429/dlsj.9.19443","DOIUrl":"https://doi.org/10.14429/dlsj.9.19443","url":null,"abstract":"Hypobaric hypoxia occurs at high altitudes where barometric pressure is low causing insufficient supply of oxygen leading to many high-altitude illnesses like acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE) etc.Medications have been applied to treat and prevent injuries caused by HBH, showing anti-inflammatory, anti-edemagenic, and antioxidant properties. AMS symptoms, such as headache, nausea, weariness, usually go away in 1-2 days. HACE causes brain swelling, elevated intracranial pressure, resulting in confusion, stupor, ataxia, and death.Acetazolamide, dexamethasone, nifedipine are the drugs used for treatment acting oncarbonic anhydrase enzyme, calcium channels.Acetazolamide increases arterial partial pressure of oxygen.Nifedipine relaxes vascular smooth muscles and increases blood flow. Some drugscause side effects also like dizziness, diuresis, nausea, malaise, etc. Hence, a new drug search is needed to find more targeted and fewer side effects for faster relief and better health at high altitudes.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140521621","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}
Systematic human expeditions to very high (≥ 3500 meters) and extreme altitudes (≥ 5500 meters) have documented marked changes in human physiology. However, only a handful of studies have reported lowlander transcriptome alterations at extreme altitudes. In this study, we compared the lowlander transcriptomes available in the literature for Chinese mountaineers (n=4, 3 males and 1 female)inthe Himalayas (Mount Xixabangma base camp, 5600 meters) and French mountaineers (n=8, all males) at Andes (La Rinconada, Peru, 5100 meters). We sought to find out significantly alteredpathways, gene networks, andtranscription factors (TFs) for each data set. We observed profound upregulation of GATA1 in the Himalaya transcriptome data set (+ 1.38-fold) in comparison tothe Andes data set (-1.36-fold). Core transcriptome analysis revealed that GATA1 upregulated erythropoiesis genes like KLF1, HBD, HBG, EPB42, ALAS2, and AHSP in the Himalayan dataset in contrast to the Andean data set.We also observed contrasting expression profiles ofKLF1 in the Himalayas (+1.22-fold) and Andes (-1.15-fold)for lowlander populations and differential expression regulation of its downstream target genes like AHSP, ALAS2, SLC4A1, EPB42,HBG2, andHBB.We also observed upregulation of SP1 (+ 2.46-fold) in the Himalayan transcriptome as compared to the Andean transcriptome which also regulates erythropoiesis genes along with GATA1. Our results indicate profound upregulation of erythropoiesis-promotingTFs and genes in Chinese mountaineers at extreme altitudes in contrast to French mountaineers at similar altitudes. Though our present analysis does not provide possible reasons for the observed differences inhypoxia-responsive erythropoiesis gene signatures, it certainly highlights ethnicity-dependenttranscriptome level variations in lowlanders at extreme altitudes.
{"title":"Comparative Analysis of Low Lander Transcriptomes at Himalayas and Andes Reveals Differential Regulation of Erythropoiesis at Extreme Altitude","authors":"Vandana Sharma, N. Sethy","doi":"10.14429/dlsj.9.19454","DOIUrl":"https://doi.org/10.14429/dlsj.9.19454","url":null,"abstract":"Systematic human expeditions to very high (≥ 3500 meters) and extreme altitudes (≥ 5500 meters) have documented marked changes in human physiology. However, only a handful of studies have reported lowlander transcriptome alterations at extreme altitudes. In this study, we compared the lowlander transcriptomes available in the literature for Chinese mountaineers (n=4, 3 males and 1 female)inthe Himalayas (Mount Xixabangma base camp, 5600 meters) and French mountaineers (n=8, all males) at Andes (La Rinconada, Peru, 5100 meters). We sought to find out significantly alteredpathways, gene networks, andtranscription factors (TFs) for each data set. We observed profound upregulation of GATA1 in the Himalaya transcriptome data set (+ 1.38-fold) in comparison tothe Andes data set (-1.36-fold). Core transcriptome analysis revealed that GATA1 upregulated erythropoiesis genes like KLF1, HBD, HBG, EPB42, ALAS2, and AHSP in the Himalayan dataset in contrast to the Andean data set.We also observed contrasting expression profiles ofKLF1 in the Himalayas (+1.22-fold) and Andes (-1.15-fold)for lowlander populations and differential expression regulation of its downstream target genes like AHSP, ALAS2, SLC4A1, EPB42,HBG2, andHBB.We also observed upregulation of SP1 (+ 2.46-fold) in the Himalayan transcriptome as compared to the Andean transcriptome which also regulates erythropoiesis genes along with GATA1. Our results indicate profound upregulation of erythropoiesis-promotingTFs and genes in Chinese mountaineers at extreme altitudes in contrast to French mountaineers at similar altitudes. Though our present analysis does not provide possible reasons for the observed differences inhypoxia-responsive erythropoiesis gene signatures, it certainly highlights ethnicity-dependenttranscriptome level variations in lowlanders at extreme altitudes.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140523137","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 autophagy process plays a cytoprotective role and ensures the healthy survival of a cell. The role of autophagy has been implicated in various diseases, making it an essential candidate for therapeutic interventions. Beclin 1, a candidate autophagy protein, plays a critical role during autophagy initiation and maturation by interacting with various other autophagy proteins. Beclin1 has been reported to be involved in various human diseases. This study uses a computational approach to study the effect of non-coding region single nucleotide polymorphisms (SNPs) of gene encoding beclin1. RegulomeDB, SNP2TFBS, and PROMO ALLGEN were used to predict the effect of promoter region variants on transcription factor binding sites. SNPs located within 3'UTR were analyzed by miRdSNP, PolymiRTS Database 3.0, miRNASNP-V3, MicroSNIPER, and miRmap. Nine promoter region variants that alter the transcription factor binding sites and 4 variants in 3'UTR were identified that either create a new target site for miRNA or disrupt an existing one. The functional analysis of these identified SNPs could be done experimentally to unravel their relation with a particular disease and the genetic predisposition of human subjects for a disease.
{"title":"Computational Investigation of Regulatory Region SNPs of Autophagy Gene BECN1","authors":"Sargeet Kaur, Jitendraa Vashistt, H. Changotra","doi":"10.14429/dlsj.9.19452","DOIUrl":"https://doi.org/10.14429/dlsj.9.19452","url":null,"abstract":"The autophagy process plays a cytoprotective role and ensures the healthy survival of a cell. The role of autophagy has been implicated in various diseases, making it an essential candidate for therapeutic interventions. Beclin 1, a candidate autophagy protein, plays a critical role during autophagy initiation and maturation by interacting with various other autophagy proteins. Beclin1 has been reported to be involved in various human diseases. This study uses a computational approach to study the effect of non-coding region single nucleotide polymorphisms (SNPs) of gene encoding beclin1. RegulomeDB, SNP2TFBS, and PROMO ALLGEN were used to predict the effect of promoter region variants on transcription factor binding sites. SNPs located within 3'UTR were analyzed by miRdSNP, PolymiRTS Database 3.0, miRNASNP-V3, MicroSNIPER, and miRmap. Nine promoter region variants that alter the transcription factor binding sites and 4 variants in 3'UTR were identified that either create a new target site for miRNA or disrupt an existing one. The functional analysis of these identified SNPs could be done experimentally to unravel their relation with a particular disease and the genetic predisposition of human subjects for a disease.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140527304","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}
Dolly Sharma, Anu Kumari, Manisha Kumari, Ramesh C. Meena
Protein SUMOylation is a reversible and well knownpost-translational modificationprocess of the cells. It may change a protein's cellular location, interactions, and possible structural shape before it develops to carry out its basic functions.Also, it decides the binding of transcription factors and DNA binding proteins tochromatin in addition to various cis and trans regulatory factors. Alterations in protein SUMOylation have been linked with a variety of disorders and developmental anomalies.Tentative approaches to identify SUMO binding sites are challenging due todynamic nature of the SUMOylation processand various critical lab experimentswhich are involved very high cost.Therefore, the computational methodologies may guide the experimental identification of SUMOylation sites and provide insights for improving comprehensionofSUMOylation mechanism in the cells.In this study, we identify the SUMO binding sites in transcription factors that are actively involved and have crucial roles in cardiac development andpathophysiology of the heart.A list of important transcription factors was preparedfrom thehuman transcription factor database.The GPS-SUMO, SUMO plot, and JASSA web serverswere used for the prediction of SUMO binding sites in cardiac transcription factors.We identified the SUMOylation of several novel, previously uncharacterized SUMO targetsthat are actively involved in thecardiovascular system.Thus, the present study may help to uncoverthe significance ofSUMO modificationin cardiac development and illnesses which creates a fresh avenue for future studies ontarget-specific SUMOylation for identification of novel therapeutic targets andmanagement strategies forhypoxia-induced cardiovascular disorders.
{"title":"SUMO Sites Prediction in Human Transcription Factors Involved in Hypoxia induced Cardiac Illnesses","authors":"Dolly Sharma, Anu Kumari, Manisha Kumari, Ramesh C. Meena","doi":"10.14429/dlsj.9.19455","DOIUrl":"https://doi.org/10.14429/dlsj.9.19455","url":null,"abstract":"Protein SUMOylation is a reversible and well knownpost-translational modificationprocess of the cells. It may change a protein's cellular location, interactions, and possible structural shape before it develops to carry out its basic functions.Also, it decides the binding of transcription factors and DNA binding proteins tochromatin in addition to various cis and trans regulatory factors. Alterations in protein SUMOylation have been linked with a variety of disorders and developmental anomalies.Tentative approaches to identify SUMO binding sites are challenging due todynamic nature of the SUMOylation processand various critical lab experimentswhich are involved very high cost.Therefore, the computational methodologies may guide the experimental identification of SUMOylation sites and provide insights for improving comprehensionofSUMOylation mechanism in the cells.In this study, we identify the SUMO binding sites in transcription factors that are actively involved and have crucial roles in cardiac development andpathophysiology of the heart.A list of important transcription factors was preparedfrom thehuman transcription factor database.The GPS-SUMO, SUMO plot, and JASSA web serverswere used for the prediction of SUMO binding sites in cardiac transcription factors.We identified the SUMOylation of several novel, previously uncharacterized SUMO targetsthat are actively involved in thecardiovascular system.Thus, the present study may help to uncoverthe significance ofSUMO modificationin cardiac development and illnesses which creates a fresh avenue for future studies ontarget-specific SUMOylation for identification of novel therapeutic targets andmanagement strategies forhypoxia-induced cardiovascular disorders.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140520790","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}
Nilanjana Ghosh, Swati Srivastava, B. Kumari, I. Garg
DNA methylation being one of the chief controllers of gene expression has not only been the reason behind the initiation of a plethora of diseases like Cancer, Alzheimer’s disease, Parkinson’s disease, etc. Still, it is an active contributor to the pathophysiology of several cardiovascular diseases like coronary artery disease (CAD), Atherosclerosis, Stroke, Cardiomyopathy, etc. The role of nuclear DNA methylation in VTE has been studied earlier, but the comparison of methylation in both nuclear genes and mitochondrial genes in high altitude VTE (HA-VTE) and sea level VTE (SL-VTE) patients has not been studied in depth. Through this present study, DNA methylation patterns of mitochondrial encoded as well as nuclear-encoded mitochondrial genes of five high-altitude VTE patients and five sea-level VTE patients have been obtained. On comparing HA-VTE vs. SL-VTE methylation, one hundred and twenty hypermethylated genes and one hundred and thirty-eight hypomethylated genes were observed. Post gene enrichment and ontology study, the TCA cycle and NADH dehydrogenase were found to be the highly enriched pathways in both the study groups. Protein-protein interaction network using STRING pointed out the enriched pathway of L-2-hydroxyglutaric acid when both the gene sets were enriched. These results show the crucial role of mitochondrial DNA methylation in the pathophysiology of thrombosis and show great potential to study the role of mitochondria in thrombosis.
DNA 甲基化是基因表达的主要控制者之一，它不仅是引发癌症、阿尔茨海默病、帕金森病等多种疾病的原因。它还是冠状动脉疾病（CAD）、动脉粥样硬化、中风、心肌病等多种心血管疾病病理生理学的积极贡献者。核 DNA 甲基化在 VTE 中的作用早前已有研究，但对高海拔 VTE（HA-VTE）和海平面 VTE（SL-VTE）患者的核基因和线粒体基因的甲基化比较还没有深入研究。本研究获得了五名高海拔 VTE 患者和五名海平面 VTE 患者线粒体编码基因和核编码基因的 DNA 甲基化模式。在比较 HA-VTE 与 SL-VTE 的甲基化情况时，观察到 120 个高甲基化基因和 138 个低甲基化基因。经过基因富集和本体研究，发现 TCA 循环和 NADH 脱氢酶是两个研究组中富集程度较高的通路。使用 STRING 的蛋白质-蛋白质相互作用网络指出，当两个基因组都被富集时，L-2-羟基戊二酸的途径也被富集。这些结果表明线粒体DNA甲基化在血栓形成的病理生理学中起着至关重要的作用，并显示出研究线粒体在血栓形成中的作用的巨大潜力。
{"title":"Altered Mitochondrial DNA Methylation Patterns in Thrombosis","authors":"Nilanjana Ghosh, Swati Srivastava, B. Kumari, I. Garg","doi":"10.14429/dlsj.9.19447","DOIUrl":"https://doi.org/10.14429/dlsj.9.19447","url":null,"abstract":"DNA methylation being one of the chief controllers of gene expression has not only been the reason behind the initiation of a plethora of diseases like Cancer, Alzheimer’s disease, Parkinson’s disease, etc. Still, it is an active contributor to the pathophysiology of several cardiovascular diseases like coronary artery disease (CAD), Atherosclerosis, Stroke, Cardiomyopathy, etc. The role of nuclear DNA methylation in VTE has been studied earlier, but the comparison of methylation in both nuclear genes and mitochondrial genes in high altitude VTE (HA-VTE) and sea level VTE (SL-VTE) patients has not been studied in depth. Through this present study, DNA methylation patterns of mitochondrial encoded as well as nuclear-encoded mitochondrial genes of five high-altitude VTE patients and five sea-level VTE patients have been obtained. On comparing HA-VTE vs. SL-VTE methylation, one hundred and twenty hypermethylated genes and one hundred and thirty-eight hypomethylated genes were observed. Post gene enrichment and ontology study, the TCA cycle and NADH dehydrogenase were found to be the highly enriched pathways in both the study groups. Protein-protein interaction network using STRING pointed out the enriched pathway of L-2-hydroxyglutaric acid when both the gene sets were enriched. These results show the crucial role of mitochondrial DNA methylation in the pathophysiology of thrombosis and show great potential to study the role of mitochondria in thrombosis.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140519415","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}
Ashok Priyadarshi, Gaurav K. Keshri, Asheesh Gupta
Combat and soft tissue traumatic injuries pose unique challenges in terms of their severity, complexity, and thus need for the exploration of rapid, novel therapeutic interventions. Traditionally, combat injuries have been managed through invasive surgical procedures associated with potential complications and prolonged recovery times. However, advancements in non-invasive treatment modalities have opened up new possibilities for managing combat injuries more effectively and efficiently. The present article aims to provide a comprehensive overview of non-invasive, drug-free, biophysical therapeutic approaches for combat and external traumatic injuries, focusing on their benefits, efficacy, and potential applications. The non-invasive nature and favourable safety profile of photobiomodulation therapy (PBMT) make it an attractive option for combat injury management. The evidence on underlying mechanistic insights supports the efficacy of PBMT in promoting tissue repair, reducing pain, inflammation, oxidative stress, and facilitating functional recovery. In conclusion, the present review highlights the significant potential of non-invasive PBMT using dual/multi-wavelength light energy as a valuable therapeutic approach for traumatic soft tissue and combat injuries and extensively explores associated mechanistic insights. Further research on combination therapies using potential pharmacological agents in conjunction with PBMT, with optimal irradiation protocols and other energy-based healing modalities will favour the translation of potential non-invasive healing intervention for combat and traumatic injuries in clinical applications.
{"title":"Multi Targeted Non Invasive Photoceutical Therapeutic Approach for Combat and Traumatic Soft Tissue Injuries","authors":"Ashok Priyadarshi, Gaurav K. Keshri, Asheesh Gupta","doi":"10.14429/dlsj.9.19442","DOIUrl":"https://doi.org/10.14429/dlsj.9.19442","url":null,"abstract":"Combat and soft tissue traumatic injuries pose unique challenges in terms of their severity, complexity, and thus need for the exploration of rapid, novel therapeutic interventions. Traditionally, combat injuries have been managed through invasive surgical procedures associated with potential complications and prolonged recovery times. However, advancements in non-invasive treatment modalities have opened up new possibilities for managing combat injuries more effectively and efficiently. The present article aims to provide a comprehensive overview of non-invasive, drug-free, biophysical therapeutic approaches for combat and external traumatic injuries, focusing on their benefits, efficacy, and potential applications. The non-invasive nature and favourable safety profile of photobiomodulation therapy (PBMT) make it an attractive option for combat injury management. The evidence on underlying mechanistic insights supports the efficacy of PBMT in promoting tissue repair, reducing pain, inflammation, oxidative stress, and facilitating functional recovery. In conclusion, the present review highlights the significant potential of non-invasive PBMT using dual/multi-wavelength light energy as a valuable therapeutic approach for traumatic soft tissue and combat injuries and extensively explores associated mechanistic insights. Further research on combination therapies using potential pharmacological agents in conjunction with PBMT, with optimal irradiation protocols and other energy-based healing modalities will favour the translation of potential non-invasive healing intervention for combat and traumatic injuries in clinical applications.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140523309","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}
Many people visit and stay at high altitude due to adventure or occupation. The high-altitude environment comprises many factors alien to sea residents and detrimental to physical and mental health. Myokines are peptides and cytokines secreted from muscles and have a prime role in regulating skeletal muscle growth and myo-degradation. Therefore, the present study investigated the function of myokines in regulating muscle mass during acute and chronic high-altitude exposure. The study was conducted on Indian healthy subjects (n=29) who were distributed into three groups: Control (sea level (SL; n=15), acute high altitude stayed subjects (stayed at high altitude for less than ten days (AHA; n=7); chronic high altitude stayed subjects (stayed at high altitude for 15 days to 3 months (CHA; n=7). Acute exposure to high altitude leads to an increase in myostatin levels, indicating enhanced myo-degradation. Irisin levels were also increased in AHA group compared to SL group, depicting inclined myogenesis. However, CHA group showed an increase in myostatin levels but a non-significant change in irisin content in relation to SL group, suggesting enhanced myo-degradation. These findings generated a unique role of myokines, including myostatin and irisin, in managing skeletal muscle health with reference to high altitude.
{"title":"A Pilot Study Investigating the Impact of High Altitude on Myostatin and Irisin Levels","authors":"Richa Rathor, G. Suryakumar, Somnath Singh","doi":"10.14429/dlsj.9.19449","DOIUrl":"https://doi.org/10.14429/dlsj.9.19449","url":null,"abstract":"Many people visit and stay at high altitude due to adventure or occupation. The high-altitude environment comprises many factors alien to sea residents and detrimental to physical and mental health. Myokines are peptides and cytokines secreted from muscles and have a prime role in regulating skeletal muscle growth and myo-degradation. Therefore, the present study investigated the function of myokines in regulating muscle mass during acute and chronic high-altitude exposure. The study was conducted on Indian healthy subjects (n=29) who were distributed into three groups: Control (sea level (SL; n=15), acute high altitude stayed subjects (stayed at high altitude for less than ten days (AHA; n=7); chronic high altitude stayed subjects (stayed at high altitude for 15 days to 3 months (CHA; n=7). Acute exposure to high altitude leads to an increase in myostatin levels, indicating enhanced myo-degradation. Irisin levels were also increased in AHA group compared to SL group, depicting inclined myogenesis. However, CHA group showed an increase in myostatin levels but a non-significant change in irisin content in relation to SL group, suggesting enhanced myo-degradation. These findings generated a unique role of myokines, including myostatin and irisin, in managing skeletal muscle health with reference to high altitude. ","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140525726","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}
High altitude regions above 2,700 meters pose unique physiological challenges to travellers, including hypoxia caused by decreased oxygen levels. Gastrointestinal issues such as nausea, vomiting, and anorexia are common in high altitude sojourners. The gastrointestinal barrier is composed of epithelial cells connected with tight junctions, desmosomes, and covered with a thick layer of mucous. The mucosal and immunological barriers work together to regulate intestinal homeostasis and prevent harmful pathogens from entering the system. Any damage to the gastrointestinal barrier can lead to an increase in permeability which can cause harmful microbial toxins and unwanted substances to enter the bloodstream, triggering an inflammatory response. External factors such as hypoxia and intense physical workouts at high altitude can disrupt the barrier and lead to inflammation and microbial dysbiosis, which changes the normal population of gut microbiota and can cause gastrointestinal discomfort. This review aims to examine the effects of these external factors on the gastrointestinal barrier and highlights the importance of therapeutic and dietary interventions to manage high altitude induced mucosal barrier dysfunction and restore immunological homeostasis of the gut.
{"title":"External Factors Affecting Gastrointestinal Barrier and Mucosal Immunity at High Altitude","authors":"Jyotsana Bakshi, Somnath Singh, K. Mishra","doi":"10.14429/dlsj.9.19448","DOIUrl":"https://doi.org/10.14429/dlsj.9.19448","url":null,"abstract":"High altitude regions above 2,700 meters pose unique physiological challenges to travellers, including hypoxia caused by decreased oxygen levels. Gastrointestinal issues such as nausea, vomiting, and anorexia are common in high altitude sojourners. The gastrointestinal barrier is composed of epithelial cells connected with tight junctions, desmosomes, and covered with a thick layer of mucous. The mucosal and immunological barriers work together to regulate intestinal homeostasis and prevent harmful pathogens from entering the system. Any damage to the gastrointestinal barrier can lead to an increase in permeability which can cause harmful microbial toxins and unwanted substances to enter the bloodstream, triggering an inflammatory response. External factors such as hypoxia and intense physical workouts at high altitude can disrupt the barrier and lead to inflammation and microbial dysbiosis, which changes the normal population of gut microbiota and can cause gastrointestinal discomfort. This review aims to examine the effects of these external factors on the gastrointestinal barrier and highlights the importance of therapeutic and dietary interventions to manage high altitude induced mucosal barrier dysfunction and restore immunological homeostasis of the gut.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140524966","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}
Mohd Adnan Siddiqui, Upasna Gupta, Mohammed Haris Siddiqui, Afzal Azim, Neeraj Sinha
High altitude diseases and sepsis may seem distinct at first glance, but there are underlying physiological similarities that lie in their responses to hypoxia, tissue dysfunction, inflammation, and multi-organ failure conditions. Understanding these commonalities can help medical professionals draw parallels between them and apply relevant knowledge to improve patient care and treatment.In this direction,a literature review of metabolomics-based studies has been done for high-altitude diseases and sepsis, and the panel of common disease-related metabolic markers and associated pathways areunraveled. Themetabolic pathways found dysregulated in both conditions are amino acid metabolism, lipid metabolism, energy metabolism, inflammatory response-related metabolism, bile acid metabolism, and purine and pyrimidine metabolism.
{"title":"Metabolomics Unraveling the Biochemical Insight of High Altitude Diseases and Sepsis A Narrative Review","authors":"Mohd Adnan Siddiqui, Upasna Gupta, Mohammed Haris Siddiqui, Afzal Azim, Neeraj Sinha","doi":"10.14429/dlsj.9.19441","DOIUrl":"https://doi.org/10.14429/dlsj.9.19441","url":null,"abstract":"High altitude diseases and sepsis may seem distinct at first glance, but there are underlying physiological similarities that lie in their responses to hypoxia, tissue dysfunction, inflammation, and multi-organ failure conditions. Understanding these commonalities can help medical professionals draw parallels between them and apply relevant knowledge to improve patient care and treatment.In this direction,a literature review of metabolomics-based studies has been done for high-altitude diseases and sepsis, and the panel of common disease-related metabolic markers and associated pathways areunraveled. Themetabolic pathways found dysregulated in both conditions are amino acid metabolism, lipid metabolism, energy metabolism, inflammatory response-related metabolism, bile acid metabolism, and purine and pyrimidine metabolism.","PeriodicalId":36557,"journal":{"name":"Defence Life Science Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140522537","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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