其他最新文献

{"title":"Targeting USP14 sensitizes glioma to radiotherapy through exacerbated reactive oxygen species accumulation.","authors":"Xinyu Liu, Lichen Shen, Yijun Lu, Zimeng Wang, Shuanghu Yuan, Hongcang Gu, Junchao Qian","doi":"10.4103/mgr.MEDGASRES-D-26-00027","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00027","url":null,"abstract":"<p><p>Radiotherapy is one of the most effective treatments for glioma, but therapeutic efficacy is strongly limited due to intrinsic radioresistance, which is closely linked to reactive oxygen species. This research was designed to elucidate the role and underlying mechanisms of the deubiquitinase ubiquitin-specific protease 14 (USP14) in reactive oxygen species Accumulation and radioresistance of glioma. Bioinformatics analysis demonstrated that upregulation of USP14 was associated with tumor progression, high levels of USP14 in glioma patients were correlated with a significantly poorer prognosis. Cytological experimental results demonstrated that radiotherapy could induce increased USP14 expression. Inhibition of USP14 disrupted intracellular protein homeostasis, leading to upregulation of endoplasmic reticulum stress-related proteins thereby exacerbating endoplasmic reticulum stress. This stress response further induced substantial reactive oxygen species generation and DNA damage accumulation, ultimately synergistically enhancing the tumoricidal effect of radiotherapy. In vivo, the combined application of b-AP15 (a USP14 inhibitor) and radiotherapy elicited potent antitumor effects, marked by significant suppression of tumor growth and increased apoptotic cell death. In summary, we reveal a new regulatory axis by which USP14 governs glioma radiosensitivity through reactive oxygen species-mediated DNA damage and apoptosis, providing a promising therapeutic target and strategy for reversing clinical radioresistance.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"79-88"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963631","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":"Ion Channels as Gatekeepers of Fertility: from Uterine Kir7.1 to Sperm CatSper.","authors":"Qingwei Niu, Polina V Lishko","doi":"10.1152/physiol.00015.2026","DOIUrl":"10.1152/physiol.00015.2026","url":null,"abstract":"<p><p>Ion channels coordinate diverse physiological functions through tightly regulated fluxes of Ca²⁺, K⁺, Na⁺, Cl^-, and H⁺ across both plasma and intracellular membranes. In the reproductive system, ion channels have emerged as key regulators of processes essential for reproductive success. They control epithelial transport and ciliary activity in the oviduct, regulate uterine smooth muscle contractility and receptivity, and orchestrate sperm capacitation, hyperactivation, acrosome reaction, and fertilization. These functions require precise spatial and temporal integration of environmental cues, including bioactive lipids, pH, temperature, and mechanical forces encountered throughout the reproductive tract. Dysregulation of ion channel activity has been increasingly linked to infertility, pregnancy complications, and other reproductive disorders. Recent advances in live-cell imaging, superresolution microscopy, electrophysiology, and cryo-electron microscopy have transformed our understanding of ion channel architecture, regulation, and organization within specialized membrane microdomains in reproductive tissues. In this review, we highlight recent discoveries of ion channels and their regulatory mechanisms specifically in reproductive tissues, with a focus on emerging roles of potassium channel Kir7.1 in uterine physiology and calcium channel CatSper in sperm motility, and discuss emerging questions that will guide future research in reproductive ion channel biology.</p>","PeriodicalId":520753,"journal":{"name":"Physiology (Bethesda, Md.)","volume":" ","pages":"0"},"PeriodicalIF":10.3,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13341003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148207641","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":"An End-to-End Pipeline to Generate Augmented Tactile Maps from Floor Plans.","authors":"Michelle Quach, James M Coughlan, Dragan Ahmetovic, Matteo Manzoni, Sergio Mascetti, Roberto Manduchi","doi":"10.1007/978-3-032-31308-9_58","DOIUrl":"10.1007/978-3-032-31308-9_58","url":null,"abstract":"<p><p>This paper presents an end-to-end pipeline for transforming indoor floor plans into accessible tactile maps enriched with audio annotations. The approach integrates SIM (Semantic Interior Mapology), which allows authors to trace floor plans and assign semantic labels to relevant spatial features (e.g., rooms, corridors, restrooms, and stairs), with CamIO, a camera-based web application that delivers spoken feedback when users point to interactive regions (hotspots) on a tactile graphic. A pilot study with two blind participants and a follow-up study with five additional participants showed that users could successfully complete room-finding and route-tracing tasks and appreciated the system's support for spatial understanding. Usability evaluation yielded a mean SUS score of 77, indicating good usability, while NASA-TLX results showed a relatively low perceived workload, supporting the effectiveness of the proposed solution. Results also highlighted areas for improvement, including lower latency and clearer interaction around doors and small hotspots.</p>","PeriodicalId":90476,"journal":{"name":"Computers helping people with special needs : ... International Conference, ICCHP ... : proceedings. International Conference on Computers Helping People with Special Needs","volume":"16867 ","pages":"485-492"},"PeriodicalIF":0.0,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714941","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":"Molecular Architecture of Temporal Variability Network Dysfunction in Bipolar Disorder.","authors":"Lin Jiang, Jiayu Ye, Yan Zhu, Shuqi Ma, Dezhong Yao, Zhen Yuan, Xuntai Ma, Peng Xu, Debo Dong, Fali Li","doi":"10.1142/S0129065727500043","DOIUrl":"10.1142/S0129065727500043","url":null,"abstract":"<p><p>Characterized by recurrent fluctuations in mood states, bipolar disorder (BD) is widely conceptualized as a disconnection syndrome associated with dysregulated brain dynamics. Nevertheless, the molecular mechanisms underlying this aberrant connectivity dynamics in BD remain elusive. Using resting-state electroencephalography (EEG) data from BD patients and healthy controls, this study first delineated the characteristic alterations in temporal variability of functional connectivity in BD and further elucidated their underlying molecular mechanisms and clinical relevance. Current findings revealed significantly reduced temporal variability within large-scale brain subnetworks, most notably in the dorsal attention, somatomotor, and visual networks. Importantly, these neurodynamic signatures effectively predicted the symptom severity in individuals with BD. Moreover, the spatial patterns of these dynamic alterations are associated with the expression of BD risk genes enriched in synaptic function and metabolic pathways, as well as with the spatial organizations of various neurotransmitter receptors, including CB1, mGluR5, H3, and MOR. Collectively, these results provide evidence for a multiscale pathophysiological framework that links genetic susceptibility and chemoarchitectural alterations to dynamic brain network instability, ultimately underpinning the core clinical manifestations in BD.</p>","PeriodicalId":94052,"journal":{"name":"International journal of neural systems","volume":" ","pages":"2750004"},"PeriodicalIF":6.4,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148674897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitric oxide and traumatic brain injury.","authors":"Dong Liang, Han Gao, Guoyuan Fan, Tianyu Zhang, Qibing Huang, Hai Yu, Zeli Zhang","doi":"10.4103/mgr.MEDGASRES-D-25-00357","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00357","url":null,"abstract":"<p><p>Dysregulation of the nitric oxide/nitric oxide synthase system is consistently observed in the aftermath of traumatic brain injury. It plays a pivotal yet paradoxical role in traumatic brain injury progression. Moreover, the modulation of the altered nitric oxide/nitric oxide synthase homeostasis via inhaled nitric oxide, nitric oxide donors, nitric oxide synthase inhibitors, and indirect methods such as mild hypothermia and medical gases in the brain, both during and after traumatic brain injury, can exert a significant impact on the clinical outcome. This review integrates current findings from preclinical studies and clinical trials to elucidate the dynamic contributions of nitric oxide to traumatic brain injury pathophysiology and to highlight emerging interventions targeting nitric oxide-related pathways. While physiological nitric oxide levels support cerebral blood flow and neuroprotection, excessive production via nitric oxide synthase isoforms (especially inducible nitric oxide synthase) drives secondary injury through cytotoxicity, edema, and blood-brain barrier disruption. Therapeutic strategies targeting nitric oxide pathways, including inhaled nitric oxide, nitric oxide donors, and specific nitric oxide synthase inhibitors like VAS203, show significant neuroprotective potential in preclinical models, though clinical translation remains limited.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"106-116"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942201","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":"Hyperbaric oxygen in the artificial intelligence era: integration and innovation.","authors":"Francisco Epelde","doi":"10.4103/mgr.MEDGASRES-D-25-00234","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00234","url":null,"abstract":"<p><p>Hyperbaric oxygen therapy is established for decompression illness, carbon monoxide poisoning, radiation-induced tissue injury, and diabetic foot ulcers. Interest in neurological and inflammatory indications is growing, yet outcomes are constrained by heterogeneous protocols, limited patient selection tools, and the absence of real-time physiological guidance. Artificial intelligence, including machine learning, explainable artificial intelligence, and digital twins, has transformed other clinical domains and could enable precision hyperbaric oxygen therapy. We searched PubMed, Scopus, Web of Science, and Google Scholar (January 2000-March 2025). Terms included \"hyperbaric oxygen therapy\" and (\"artificial intelligence\" OR \"machine learning\" OR \"deep learning\" OR \"digital twin\" OR \"biosensor*\"). English-language, peer-reviewed clinical, preclinical, or computational studies explicitly linking hyperbaric oxygen therapy with artificial intelligence or enabling technologies were eligible. Editorials without primary data, abstracts without full text, and non-peer-reviewed sources were excluded. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses-style flow-guided screening and selection. Fifty-three eligible studies (≥30% from 2022-2025) illustrate four convergent application areas: (1) protocol optimization using multicenter data, (2) biomarker-driven patient selection via multi-omics and imaging, (3) real-time adaptive control using biosensors, and (4) predictive safety analytics for oxygen toxicity and barotrauma. Exemplars from radiology, critical care, and cardiology demonstrate the feasibility of decision support, federated learning, and digital-twin simulations adaptable to hyperbaric oxygen therapy. Integrating artificial intelligence with hyperbaric oxygen therapy can shift practice from empirical protocols to patient-tailored, data-informed therapy. Priorities include hybrid clinical trials, interoperable registries, explainable and bias-aware models, and regulatory-aligned validation. With rigorous governance, artificial intelligence can improve efficacy, safety, and efficiency while advancing mechanistic understanding of hyperbaric oxygen therapy.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"301-305"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147988176","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":"Oxidative stress, aging, metabolism, SIRT1, and the gut microbiota: the neurocardiac basis of cognitive loss.","authors":"Kenneth Maiese","doi":"10.4103/mgr.MEDGASRES-D-26-00073","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00073","url":null,"abstract":"<p><p>Cardiovascular disease and cognitive loss have a neurocardiac basis. Poor vascular perfusion can impair cognitive function in both Alzheimer's disease and multiple sclerosis. However, a treatment gap exists because current approaches do not adequately address the shared underlying cellular mechanisms responsible for cognitive dysfunction in these conditions. Current treatments for cognitive impairment in diseases such as cardiovascular disease, Alzheimer's disease, multiple sclerosis, and diabetes often fail to fully address the shared underlying cellular mechanisms. Consequently, the prevailing precision treatment strategy, which focuses on managing symptoms and preventing disease progression, is insufficient. This highlights the urgent need for innovative approaches capable of targeting these common cellular pathways across these diverse conditions. Novel investigations into oxidative stress, cellular senescence, programmed cell death with apoptosis, ferroptosis, pyroptosis, and autophagy, cellular metabolism with apolipoprotein E and glucagon-like peptide-1 receptor agonism, silent mating type information regulation 2 homolog 1 ( Saccharomyces cerevisiae ), mitochondrial dynamics, and the gut microbiome offer the potential to address the risk factors and clinical treatments for cardiovascular disease and cognitive loss. These pathways are exquisitely dependent upon one another and require in-depth knowledge of the modulatory cellular mechanisms for effective translation to clinical care.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":" ","pages":"228-241"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148664094","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 in the occurrence and development of ischemic cerebrovascular disease.","authors":"Tatiana K Bogodvid, Dinara I Silantyeva, Viacheslav V Andrianov, Khalil L Gainutdinov","doi":"10.4103/mgr.MEDGASRES-D-25-00117","DOIUrl":"10.4103/mgr.MEDGASRES-D-25-00117","url":null,"abstract":"<p><p>Since nitric oxide is a chemically highly reactive free radical that can act as both an oxidizing agent and a reducing agent, it is assumed that it has diverse effects on biological tissues. Nitric oxide is fundamentally important for the regulation of immune, reproductive and neuromuscular system functions and is the main signaling molecule and effector that can dilate blood vessels and modulate energy metabolism. This review examines the key role of nitric oxide in the mechanisms underlying the response to hypoxia, as well as in the effects of factors induced by hypoxia. The available conflicting information allowed us to conclude that at present, there is no consensus about the role of endogenous nitric oxide in the processes occurring after ischemic cerebrovascular disease.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"95-105"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963580","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":"Molecular crosstalk between gas transmitters and catecholamine biosynthesis pathways: a narrative review.","authors":"Robert Dingley, Sujeenthar Tharmalingam, T C Tai","doi":"10.4103/mgr.MEDGASRES-D-26-00004","DOIUrl":"10.4103/mgr.MEDGASRES-D-26-00004","url":null,"abstract":"<p><p>Catecholamines, particularly the hormone and neurotransmitter epinephrine, are important regulators of blood pressure and cardiovascular function. The expression of genes encoding catecholamine biosynthetic enzymes is subject to strict transcriptional regulation through both hormonal and neuronal mechanisms. These genes are also regulated by hypoxia and reactive oxygen species. A class of small gaseous transmitters, known as gas transmitters, serve as potent regulators of blood pressure and hypoxic signaling; however, their roles in catecholamine biosynthesis remain poorly understood. This manuscript reviews the current state of catecholamine and gas transmitter research, particularly their interactions in relation to hypertension. Current evidence shows that the gas transmitters nitric oxide, carbon monoxide, and hydrogen sulfide modulate catecholamine biosynthesis and release through both shared and distinct mechanisms. This regulation is highly dependent on concentration, cellular context, and mode of delivery. Additionally, this review explores hypoxic signaling as a link between catecholamines and gas transmitters. Together, these findings highlight a complex and context-dependent regulatory signaling between gas transmitters and catecholamines. Further mechanistic studies investigating endogenous signaling are required to elucidate these interactions and their therapeutic potential.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"17 1","pages":"152-163"},"PeriodicalIF":4.2,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13667382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963588","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":"Dietary Modulation of CMA: Implications for Cancer Prevention and Therapy.","authors":"Cecilia Sanchez-Felipe, Esperanza Arias, Julio Madrigal-Matute","doi":"10.1152/physiol.00014.2026","DOIUrl":"10.1152/physiol.00014.2026","url":null,"abstract":"<p><p>Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation pathway that links nutrient availability to intracellular proteostasis through the targeted turnover of selective proteins. Through this selective control of protein quality, CMA participates in the regulation of metabolic adaptation, cellular homeostasis, and stress responses. CMA is highly responsive to nutritional cues, including caloric restriction (CR), fasting, and changes in macronutrient composition, positioning this pathway as a key mediator of cellular adaptation to metabolic stress. In cancer, CMA displays context-dependent functions that influence tumor metabolism, genomic stability, and survival under adverse microenvironmental conditions. These dual roles suggest that dietary modulation of CMA may shape tumor initiation and progression through effects on cellular proteostasis and metabolic plasticity. In this review, we summarize current knowledge on the molecular mechanisms by which nutritional signals regulate CMA and discuss the physiological implications of nutrition-driven CMA modulation for cancer prevention and therapy.</p>","PeriodicalId":520753,"journal":{"name":"Physiology (Bethesda, Md.)","volume":" ","pages":"0"},"PeriodicalIF":10.3,"publicationDate":"2027-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13587774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148498641","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}