Medical Gas Research最新文献

{"title":"Ambient particulate matter pollution and stroke burden.","authors":"Lu Jiang, Kuangyang Yu, Long Gu, Wenfeng Xiao, Wen Tan, Yong Jiang, Jianhua Peng","doi":"10.4103/mgr.MEDGASRES-D-25-00188","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00188","url":null,"abstract":"<p><p>As a major component of air pollution, ambient particulate matter pollution has rarely been studied with respect to its global stroke burden. This study aims to evaluate the global stroke incidence, mortality, and health inequalities related to ambient particulate matter pollution from 1990 to 2021. Utilizing the Global Burden of Disease Study 2021, we analyzed global stroke-related mortality, disability-adjusted life years, and their age-standardized rates. The estimated annual percentage change was calculated using a linear regression model. Health inequalities were measured using the concentration index and slope index of inequality. Between 1990 and 2021, global ambient particulate matter pollution-related stroke deaths and disability-adjusted life years increased by 107% and 101% respectively, yet age-standardized rates declined. China experienced the largest increases in deaths and disability-adjusted life years, Vietnam had the fastest rise in age-standardized mortality rates, the Russian Federation saw the steepest declines in deaths and disability-adjusted life years, and Estonia had the most rapid drop in age-standardized mortality rate. Middle socio-demographic index locations accounted for 46% of the global stroke burden, with age-standardized mortality rates and age-standardized disability-adjusted life years surpassing those in high socio-demographic index locations. From 1990 to 2021, age-standardized disability-adjusted life years rose in low-middle socio-demographic index locations but fell in high socio-demographic index locations. While the concentration index signaled an improvement in global inequality, the slope index of inequality in 2021 worsened compared with that in 1990. Between 1990 and 2021, the global burden of ambient particulate matter pollution-related stroke declined. However, substantial disparities persisted across different regions, sexes, and nations. For ongoing and future research efforts, priority should be given to high-risk populations and regions, while also developing innovative interventions to further reduce the incidence of ambient particulate matter pollution-related stroke and enhance patient outcomes.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"7-14"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection.","authors":"Yang Zhou, Yongliang Wu","doi":"10.4103/mgr.MEDGASRES-D-26-00008","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00008","url":null,"abstract":"<p><p>Parkinson's disease is strongly associated with mitochondrial dysfunction and impaired mitochondrial quality control, including defective mitophagy. Aerobic exercise is increasingly recognized as a safe and accessible intervention that can improve motor and non-motor outcomes in Parkinson's disease and may also engage mechanisms relevant to disease modification. In this review, we propose a context-dependent framework in which aerobic exercise reshapes nitric oxide signaling toward a more adaptive profile, characterized by relatively moderate, transient, and spatially restricted nitric oxide bioactivity, and we discuss how this shift may influence mitochondrial biogenesis, mitophagy initiation, and autophagic flux regulation. Rather than treating nitric oxide as uniformly protective or deleterious, we argue that its biological effects in Parkinson's disease depend on source, concentration, duration, subcellular localization, cellular target, and surrounding redox milieu. However, direct evidence that exercise-derived nitric oxide activates these pathways in Parkinson's disease-relevant neural tissue is still limited. We further highlight major translational gaps, including cell-type and brain-region heterogeneity, incomplete definition of exercise dose-response relationships, and the lack of validated in vivo biomarkers of neuronal mitophagy and nitric oxide dynamics in patients with Parkinson's disease. Overall, aerobic exercise is a plausible modulator of mitophagy-related pathways in Parkinson's disease, and nitric oxide is a credible contributor to this effect; however, the current evidence supports a multi-node, context-dependent model rather than a simple linear mechanism.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"129-138"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxygen, carbon dioxide, and nitric oxide: role in the pathophysiology of obstructive sleep apnea.","authors":"Antonio Fabozzi, Pasquale Tondo, Caterina Antonaglia, Alessia Steffanina, Donato Lacedonia, Marco Confalonieri, Matteo Bonini, Paolo Palange","doi":"10.4103/mgr.MEDGASRES-D-25-00224","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00224","url":null,"abstract":"<p><p>Obstructive sleep apnea is a prevalent sleep-related breathing disorder with recurrent episodes of upper airway collapse during sleep, leading to cyclic blood gas fluctuations. Oxygen, carbon dioxide, and nitric oxide play a crucial role in the pathophysiology. This narrative review aims to explore the role of gases in obstructive sleep apnea pathophysiology, focusing on the molecular pathways and effects of chronic intermittent hypoxia, intermittent hypercapnia, and nitric oxide dysregulation. Chronic intermittent hypoxia stimulates molecular pathways such as hypoxia-inducible factor-1α and inflammatory cascades such as nuclear factor kappa B, leading to oxidative stress, endothelial dysfunction, and sympathetic overactivation. Intermittent hypercapnia impacts on chemoreflex sensitivity, ventilatory instability, and autonomic function, with emerging evidence of both pathogenic and potentially beneficial effects. Nitric oxide, which modulates airway tone, vascular reactivity, and immune control, presents a reduced bioavailability in patients with obstructive sleep apnea. These three gas mediators contribute to the complex pathophysiology of obstructive sleep apnea and underlie the long-term cardiovascular, metabolic, and neurocognitive risks of obstructive sleep apnea. Appropriately prioritizing the relationship between these gases and the pathophysiology of obstructive sleep apnea contributes to a new understanding of the disease and new treatment approaches in the future.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"285-300"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic gases and the Nrf2/Keap1 pathway: direct thiol modification vs . indirect modulation.","authors":"Te Xiao, Chao Xia, Lisha Huang, Yanqi Li, Mengyu Liu, Pengxiang Zhao, Xuemei Ma, Fei Xie","doi":"10.4103/mgr.MEDGASRES-D-26-00086","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00086","url":null,"abstract":"<p><p>The nuclear factor erythroid 2-related factor 2/Kelch-like Ech-associated protein 1 (Nrf2/Keap1) pathway is a central homeostatic module that integrates oxidant, electrophilic, inflammatory, and metabolic signals into adaptive transcriptional programs. In parallel, nitric oxide (NO), hydrogen sulfide (H 2 S), and molecular hydrogen (H 2 ) have emerged as therapeutically relevant gaseous mediators with distinct chemical identities, tissue distribution profiles, and pharmacological constraints. This review re-examines these gases through a single organizing question: how can highly dissimilar small molecules converge on the same redox-defense hub? We compare the direct cysteine chemistry of NO and H 2 S with the mainly indirect actions proposed for H 2 , and we use the Nrf2/Keap1 axis as the mechanistic backbone for that comparison. NO and H 2 S are best understood as redox-active signaling gases capable of covalent protein modification, whereas H 2 appears to act largely by reshaping upstream oxidative events, mitochondrial electron leakage, membrane lipid oxidation products, and stress-responsive signaling states. Despite these differences, all three gases can feed into overlapping kinase pathways, mitochondrial quality-control networks, and cytoprotective gene programs. A second goal of this review is to move beyond single-gas narratives. We discuss the extent to which gas-gas crosstalk, especially between NO and H 2 S and the buffering role proposed for H 2 under severe oxidative stress, may create systems-level convergence rather than simple additive antioxidant effects. We argue that the most productive conceptual model is not \"one gas, one target\", but a context-dependent gas signaling network centered on Nrf2/Keap1, mitochondrial adaptation, and thiol chemistry. Finally, we assess the translational implications of this framework across ischemia-reperfusion injury, neurodegeneration, metabolic disease, and aging. We highlight the practical constraints that still limit clinical implementation, including dose windows, burst release, tissue targeting, biomarker selection, and the difficulty of tracking reversible cysteine modifications in vivo . By placing NO, H 2 S, and H 2 into one comparative redox framework, this review aims to clarify what is established, what remains inferential, and where future combination strategies may realistically emerge.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"261-267"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148819101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gas signaling molecule: a new research focus in the treatment of erectile dysfunction.","authors":"Xiaowei Dai, Zhenhuan Zhou","doi":"10.4103/mgr.MEDGASRES-D-25-00333","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00333","url":null,"abstract":"<p><p>Gas signaling molecules, including nitric oxide, carbon monoxide, and hydrogen sulfide, have recently gained attention in erectile dysfunction treatment research because of their roles in regulating blood vessel function, reducing oxidative stress, and protecting nerves and other cells. This article reviews how nitric oxide, carbon monoxide, and hydrogen sulfide are involved in the development of erectile dysfunction and their potential as treatments. The review focuses on how these gases improve blood vessel function, relax smooth muscles, repair nerve function, and reduce tissue scarring. Current research shows that methods of gas delivery, especially those using nanocarriers or prodrugs, greatly increase how well these gases are absorbed and where they act in the body. Early animal studies and initial clinical trials support the effectiveness of these gasotransmitters in treating various causes of erectile dysfunction, including diabetes, aging, and nerve damage. Although challenges remain in controlling the speed of delivery, determining the appropriate dosage, and tailoring treatment to individual patients, there is reason for optimism. The development of responsive delivery systems, combinations of multiple gases, and additional therapies for difficult cases suggests that gas signaling molecules could transform erectile dysfunction treatment.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"197-210"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of medical gases in prevention and treatment of electromagnetic radiation injury.","authors":"Yun Xing, Fengxu Chen, Gonggeng Liu, Shijun Bao, Xujian Zhang, Ziyi Guo, Zhaoyong Shou, Jiaming Guo","doi":"10.4103/mgr.MEDGASRES-D-26-00051","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00051","url":null,"abstract":"<p><p>The widespread proliferation of electromagnetic technologies in communications, healthcare, and daily life poses increasing risks of radiation-induced tissue injury. Mitigating these deleterious effects remains a formidable challenge. Recently, medical gases, including molecular hydrogen (H2), hydrogen sulfide (H2S), carbon monoxide (CO), nitric oxide (NO), and hyperbaric oxygen, have emerged as a promising therapeutic modality with radioprotective potential. These gases exert their effects through integrated, anti-inflammatory, anti-apoptotic, and mitochondrial-protective mechanisms. Specifically, the endogenous gasotransmitters (CO, NO, and H2S) modulate precise signaling networks, while the exogenous interventions (H2, and hyperbaric oxygen) function primarily through direct radical scavenging or the induction of hormetic stress responses. This review evaluates the research progress of these five medical gases in preventing and treating injuries across the electromagnetic spectrum. H2 possesses the broadest evidence base, particularly in radiofrequency and ultraviolet protection. H2S and CO demonstrate potent efficacy in addressing ultraviolet-induced skin and retinal damage. NO plays a dual role as both a cytoprotectant and a mediator of bystander effect propagation. Hyperbaric oxygen enhances systemic resilience through preconditioning. Delivery strategies have evolved from conventional inhalation and oral administration toward smart nanocarriers and stimuli-responsive donor systems. However, these platforms still face challenges in spatiotemporal control and long-term safety. Furthermore, broader limitations, including an uneven research distribution across electromagnetic wavebands, a scarcity of clinical trials, and the lack of non-invasive methods for real-time gas concentration monitoring, are comprehensively discussed.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"251-260"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xenon and modern anesthesiology: mechanism, clinical evidence and future development.","authors":"Maria Magdalena Teper, Wiktor Perz, Bartosz Palacz, Lena Merchel, Natalia Marianna Kubiś, Karol Seweryn Błąd","doi":"10.4103/mgr.MEDGASRES-D-25-00376","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00376","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"322-323"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147960093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical mechanisms underpinning impaired endogenous nitric oxide formation with the use of proton pump inhibitors.","authors":"Macario A Rebelo, Carla Fiama de Azevedo Medeiros, Heitor Moreno, Jose E Tanus-Santos","doi":"10.4103/mgr.MEDGASRES-D-25-00170","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00170","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"316-317"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147960135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breath, beyond blood: the role of gaseous biofluids in medical research.","authors":"Susmita Roy, Ronald Sroka, Kiran Sankar Maiti","doi":"10.4103/mgr.MEDGASRES-D-26-00055","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00055","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"326-327"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High levels of nitric oxide and peroxynitrite with protein nitration: a new therapeutic target for gliomas.","authors":"Ying Yang, Qi Zhang, Yuchen Ma, Serge Yannick Ouedraogo, Liang Chen, Xianquan Zhan","doi":"10.4103/mgr.MEDGASRES-D-25-00365","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00365","url":null,"abstract":"<p><p>The gap junction signaling pathway is a core hub mediating intercellular communication, which plays a vital role in maintaining tissue homeostasis, and its dysfunction is closely related to glioma. Nitroproteomics studies have shown that protein tyrosine nitration plays an important role in the progression of glioma, and gap junction is one of the significantly enriched nitroprotein signaling pathways in glioma; proteoformics reveals that nitration can produce various proteoforms of related proteins, which have different functional states in different subtypes of glioma, suggesting that nitration may alter the functional states of related proteins in gap junction pathways. When levels of nitric oxide and peroxynitrite (ONOO-) rise, they induce the tyrosine nitration of key proteins in the gap junction pathway; this nitration not only interferes with the function of the gap junction pathway, but also affects other gap junction-linked signaling networks. Forming an attack network on the gap junction pathway through multi-pathway cross-regulation has great potential for therapeutic strategies targeting the gap junction pathway. We recommend in-depth studies of the gap junction signaling pathway and potential drugs targeting gap junction signals, including drugs that target gap junction communication activators, nitration inhibitors, and drugs that directly target specific nitroproteins, combined with conventional chemotherapy or immune checkpoint inhibitors, as well as the construction of personalized medical frameworks as important future research directions.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"117-128"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}