BackgroundIn aviation and aerospace missions, personnel and astronauts are subjected to brief episodes of +Gz acceleration, resulting in overload stress that adversely affects the cardiovascular, respiratory, and nervous systems. This mechanical stress disrupts hemodynamic balance, tissue oxygenation, and physiological homeostasis. Increasing evidence links this stressor to hepatic injury; as the primary organ for drug metabolism, liver dysfunction may alter the expression and activity of drug-metabolizing enzymes and the pharmacokinetic profiles of circadian rhythm-regulating medications, such as modafinil. This study systematically evaluates the effects of repeated brief + Gz exposure on hepatic drug-metabolizing enzymes and modafinil pharmacokinetics using a murine model.MethodsA mouse model was established using a 7-day continuous +15 Gz exposure regimen. The anti-fatigue effect of modafinil under + Gz and sleep deprivation conditions was assessed using the Morris water maze. Modafinil plasma concentration was analyzed by ultra-high-performance liquid chromatography (UHPLC) to determine pharmacokinetic parameters. Transcriptomic sequencing, RT-qPCR, Western blot, and enzyme activity assays were employed to comprehensively evaluate the expression of hepatic drug metabolism-related genes and the expression/activity of the key enzyme Cyp3a11.Results+Gz exposure impaired spatial learning and memory in mice, showing a synergistic negative effect with 24-h sleep deprivation. Modafinil intervention significantly ameliorated these cognitive deficits, indicating retained anti-fatigue efficacy under acceleration stress. +Gz exposure induced mild hepatic dysfunction (elevated ALT/AST). Pharmacokinetic analysis revealed a reduced peak plasma concentration (Cmax), along with significantly prolonged mean residence time (MRT) and elimination half-life (t1/2z) of modafinil in the +Gz group, characterizing a pattern of “delayed absorption-impaired clearance”. Transcriptomic analysis showed that + Gz exposure significantly downregulated the transporter Slc17a9 and Ugt2b37, while upregulating Slc25a34/Slc25a47, Abcg5/Abcg8, and the metabolizing enzymes Cyp2b10 and Cyp2c38. Modafinil partially reversed these alterations. The key finding was that + Gz exposure did not alter the mRNA or protein expression levels of Cyp3a11, the principal enzyme responsible for modafinil metabolism, but significantly suppressed its enzymatic activity.ConclusionBrief repeated + Gz stress reprograms the hepatic drug-metabolizing gene expression profile, potentially affecting the metabolism of various drugs in the unique conditions of aerospace environments. Importantly, it functionally inhibits the activity of the key metabolic enzyme Cyp3a11, without altering its expression, resulting in characteristic changes in modafinil pharmacokinetics.

This study aimed to elucidate the dynamic impact of acute hypobaric hypoxia (HH) on the pharmacokinetics of modafinil (MOD) and its association with liver injury and regulation of the key metabolizing enzyme Cyp3a11. A mouse model combining acute HH (simulating 5000 m) with 24 hours sleep deprivation was established. MOD was administered by gavage. Assessments included the Morris water maze test, high-performance liquid chromatography pharmacokinetic analysis, serum alanine aminotransferase/aspartate aminotransferase measurement, hepatic H&E staining, and analysis of Cyp3a11 expression via quantitative reverse transcription polymerase chain reaction, Western blot, and immunohistochemistry assays. HH exacerbated cognitive deficits, which were ameliorated by MOD. It induced biphasic pharmacokinetic alterations: accelerated absorption (higher early plasma concentration) but impeded elimination (increased area under the plasma concentration-time curve, prolonged mean residence time, and decreased apparent clearance). These changes correlated with time-dependent liver responses: after 1 hour HH, alanine aminotransferase/aspartate aminotransferase transiently decreased with compensatory Cyp3a11 upregulation but no significant histopathological damage; after 24 hours HH, progressive liver injury (inflammation, vacuolation, and necrosis) developed alongside significant suppression of Cyp3a11 expression. While MOD retains cognitive-enhancing efficacy under HH, its pharmacokinetics are markedly altered. The shift from accelerated absorption to delayed elimination is closely associated with HH-induced biphasic regulation of hepatic Cyp3a11 and progressive liver injury, indicating a need for optimized dosing strategies in HH scenarios. SIGNIFICANCE STATEMENT: This study reveals how high-altitude hypoxia alters modafinil's pharmacokinetics and efficacy via hepatic Cyp3a11 regulation, offering critical insights for optimizing drug use in hypobaric hypoxia environments.

Quercetin is a flavonoid commonly found in various fruits, vegetables, and grains. Studies have demonstrated that quercetin may help protect neuronal cells from damage caused by neurotoxins associated with Parkinson’s disease, however, the underlying mechanism remains unclear. The current study aimed to investigate the neuroprotective effects of quercetin in MPTP-induced Parkinson’s disease mouse models and elucidate its mechanistic role in modulating the PI3K/Akt/GSK-3β signaling pathway. Male C57BL/6 mice were divided into control, MPTP, quercetin, and MPTP + quercetin groups. The protective effects of quercetin on Parkinson’s disease in mice were evaluated using animal behaviour analysis, histopathological examination, and immunofluorescence staining. Subsequently, network pharmacology was utilized to determine the primary target sites of quercetin in Parkinson’s disease. Finally, western blotting and molecular docking techniques were applied to validate the identified targets. Quercetin significantly improved motor deficits in MPTP mice, reduced neuronal atrophy, and preserved TH+ dopaminergic neurons. Western blotting analysis revealed quercetin upregulated anti-inflammatory IL-10 (p < 0.01) and TGF-β (p < 0.01) while suppressing pro-inflammatory IL-1β (p < 0.01) and iNOS (p < 0.01). It activated the PI3K/Akt/GSK-3β pathway by increasing phosphorylation of PI3K (p < 0.01), Akt (p < 0.01), and GSK-3β (p < 0.01). Quercetin also elevated anti-apoptotic Bcl-2 (p < 0.01) and reduced pro-apoptotic Bax (p < 0.01) and Caspase-9 (p < 0.01). Molecular docking confirmed strong binding between quercetin and PI3K/Akt/GSK-3β (binding energies: −6.44 to −5.24 kcal/mol). Quercetin alleviates Parkinson’s disease pathology by inhibiting neuroinflammation, reducing apoptosis, and activating the PI3K/Akt/GSK-3β pathway. These findings underscore its potential as a multi-target therapeutic agent for Parkinson’s disease.

We evaluated the effect of acute hypobaric hypoxia (AHH) on the heart of early-stage spontaneously hypertensive male rats (SHRs). The rats were classified into a control (ground level; similar to 400 m altitude) group and an SHR-AHH experimental group placed in an animal hypobaric chamber at a simulated altitude of 5500 m for 24 hours (24h). RNA-Seq analysis of the hearts showed that differentially expressed genes (DEGs) were primarily associated with cellular processes, binding, and cell parts. KEGG enrichment analysis revealed that the DEGs were linked to the NOD-like receptor signaling pathway, MAPK signaling pathway, and metabolic pathways. Protein-protein interaction network analysis revealed that 165 DEGs were implicated in energy metabolism. Subsequently, we performed validation experiments to show that 8 DEGs were closely associated with energy metabolism. Among these genes, Ccna2, Cdc20, Prc1, Kif11, Kif20a, Ube2c, and Melk exhibited downregulated expression, while Cenpa exhibited upregulated expression. Collectively, these results indicated that energy metabolism-associated gene expression in the heart was altered in early-stage hypertension upon AHH exposure.

We evaluated the effect of acute hypobaric hypoxia (AHH) on the heart of early-stage spontaneously hypertensive male rats (SHRs). The rats were classified into a control (ground level; ~400 m altitude) group and an SHR-AHH experimental group placed in an animal hypobaric chamber at a simulated altitude of 5500 m for 24 hours (24h).RNA-Seq analysis of the hearts showed that differentially expressed genes (DEGs) were primarily associated with cellular processes, binding, and cell parts. KEGG enrichment analysis revealed that the DEGs were linked to the NOD-like receptor signaling pathway, MAPK signaling pathway, and metabolic pathways. Protein-protein interaction network analysis revealed that 165 DEGs were implicated in energy metabolism. Subsequently, we performed validation experiments to show that 8 DEGs were closely associated with energy metabolism. Among these genes, Ccna2, Cdc20, Prc1, Kif11, Kif20a, Ube2c, and Melk exhibited downregulated expression, while Cenpa exhibited upregulated expression.Collectively, these results indicated that energy metabolism-associated gene expression in the heart was altered in early-stage hypertension upon AHH exposure.

Objective: This study investigates the effects of acute hypobaric hypoxia (HH) on the anti-fatigue properties of pitolisant and explores the underlying mechanisms. The aim is to provide a theoretical basis for expanding its clinical indications and optimizing its use in individuals exposed to HH conditions. Methods: The anti-fatigue effects of pitolisant were evaluated using the water maze, novel object recognition, and rotating rod tests. Drug concentrations and dopamine levels were analyzed using High-Performance Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (HPLC-MS/MS). Additionally, gene and protein expression levels of P-glycoprotein (P-gp) and organic cation transporter 1 (OCT1) were assessed to explore the mechanisms by which HH affects pitolisant's pharmacodynamics. Results: A 40 mg/kg dose of pitolisant significantly improved learning, memory, cognitive, and motor functions in sleep-deprived mice under HH conditions (P < 0.05). Pharmacokinetic analysis revealed a reduction in pitolisant concentration in the brain under HH conditions. Furthermore, OCT1 protein expression decreased after 1 h and 1 day of HH exposure (P < 0.05), while P-gp expression decreased after 1 h (P < 0.05). Conclusion: HH possibly reduced pitolisant's brain concentration and efficacy by altering the expression of OCT1 and P-gp transporters. A 40 mg/kg dose was necessary for an effective anti-fatigue response. Pitolisant shows potential for supporting circadian rhythm regulation in shift workers and individuals suffering from jet lag. When used under HH conditions, adjusting the dose and frequency may be necessary due to altered pharmacokinetics.

The relationship between circadian rhythm disorders and the development of various diseases appears to be significant, with limited current interventions available. Research literature suggests that hypoxia may influence the expression of clock genes and the shifting of rhythm phases. However, the precise mechanisms underlying the modulation of circadian rhythm through circulating exosomes by hypoxia preconditioning remain unclear. In this study, the mice were exposed to hypobaric conditions, simulating an altitude of 5000 m, for 1 h daily over the course of 1 week in order to achieve hypoxia preconditioning. Compared to the control group, no significant alteration was observed in the concentration, modal size, and mean size of circulating exosomes in hypoxia preconditioning mice. Exosomes derived from hypoxia preconditioning effectively suppressed the expression of Per1, Clock, and Bmal1 in NIH 3T3 cells. The miRNA sequencing analysis revealed miR-34b-3p as a potential regulator of the Clock, resulting in the downregulation of clock gene expression and subsequent promotion of proliferation and migration in NIH 3T3 cells. This study elucidated a novel mechanism of hypoxia preconditioning in the regulation of circadian rhythm, proposing that exosomal miR-34b-3p functions as an unrecognized molecule entity involved in the modulation of circadian rhythm. These findings offer a new avenue for developing protective strategies and therapeutic targets for circadian rhythm disorders.

Aim High-altitude cardiac injury is a prevalent form of tissue damage resulting from hypobaric hypoxia (HH). MICU1 is a critical modulator of mitochondrial calcium uptake, with significant implications for the regulation of mitochondrial redox homeostasis. This study sought to examine the impact of MICU1 and elucidate the underlying mechanism in myocardial exposed to HH. Methods Loss-and gain-of-function approaches were used to investigate the role of MICU1 in cardiac response to HH. In vitro, the function of MICU1 in the primary neonatal rat cardiomyocytes under hypoxia was examined. Results We observed that MICU1 was downregulated in hearts exposed to HH, contributing to myocardial apoptosis. In vitro experiments demonstrated that MICU1 knockdown exacerbated hypoxic cardiomyocyte injury, as evidenced by an increase in apoptotic cells and a decrease in mitochondrial membrane potential. Conversely, overexpression of MICU1 in mice significantly mitigated myocardial injury, leading to enhanced cardiac function and reduced myocardial hypertrophy and fibrosis in hypobaric hypoxic mice, consistent with the in vitro findings. Further investigations revealed that overexpression of MICU1 inhibited apoptosis by augmenting mitochondrial Ca2+ uptake and subsequently enhancing the activity of tricarboxylic acid cycle (TCA) related enzymes. Lastly, our results suggest that hypoxia-induced downregulation of MICU1 is mediated by the reduction of MAZ expression in primary neonatal rat cardiomyocytes. Conclusion Our results suggest that MICU1 plays an important role in myocardial protection subjected to HH, suggesting that enhancing the expression or activity of MICU1 may be a potential pharmacological target to ameliorate myocardial injury at high altitude.

如何早期有效筛查冠心病一直是航空医学面临的主要问题之一.笔者就目前外军常用冠心病早期筛查手段及策略进行分析,并与我军筛查体系进行比较,发现基于CT的冠状动脉钙化积分对未来心血管事件的风险预测优于功能学检查,指出利用风险分层算法对飞行人员进行差异性筛选可以显著提升筛查体系的效能,并强调了基于CT的血流储备分数和心肌核磁共振新筛查技术在飞行人员冠心病早期筛查中的应用前景.

目的 分析国内外军事航空医学研究热点及研究前沿.方法 用CiteSpace软件分别对中国知网及科学网两个数据库2002年1月1日至2022年10月31日收录的国内外军事航空医学研究论文进行可视化分析,内容包括发文国家、机构、作者和高频关键词等.结果 共纳入588篇中文文献及874篇英文文献.中文文献2002年发文量最多,2003-2020年发文量波动性缓慢上升,2021年发文量陡增至53篇.英文文献发文量从2002-2019年整体波动式呈上升趋势,2019年达到高峰为72篇,2020-2022年发文量逐年下降.我国共549位作者发表军事航空医学中文论文;共有612位作者发表军事航空医学的英文论文.通过对中文文献进行聚类分析,得出排名前10的论文主题为:合格鉴定、医学鉴定、体格检查、诊断、高血压、疾病谱、加速度、眩晕、治疗和危险因素;通过对英文文献进行聚类分析,得出排名前10的论文主题为:injury、performance、symptoms、risk factors、brain、fatigue、post-traumatic stress、neck pain、exposure、aging.中文文献突现词包括加速度、身体耐力、抗荷服、航天医学、疗养院等;英文文献突现词包括alertness、pilot、population、risk factor、neck pain.结论 我国与国外军事航空医学研究热点并不完全相同,我国目前以航空医学鉴定标准更新细化及飞行人员体格检查为主,国外以战后创伤治疗及改善飞行人员机能为主.

Objective: To investigate the protective effect and its possible mechanism of A-kinase anchored protein 1 (AKAP1) on the myocardial injury induced by highland hypobaric hypoxia. Methods: From January 2021 to May 2022, male C57BL/6 SPF grade mice were divided into wild type control (WT) group and highland hypobaric hypoxia (HH) group with 6 mice in each group. HH group simulated 6000 m altitude with low pressure oxygen chamber for 4 weeks to build the model. Primary myocardial cells of SD rats were divided into normoxia control group and hypoxia experimental group (n=3). Cell models were constructed in a three-gas hypoxia incubator with 1% oxygen concentration for 24 h. AKAP1 protein and mRNA expression in myocardial tissue and cells were detected by western blotting, immunohistochemistry and quantitative real-time polymerase chain reaction (qPCR). After myocardial point injection of the AKAP1 or the control adenovirus, the mice were divided into 3 groups (n=6) : WT group, highland hypobaric hypoxia overexpression control group (HH+Ad-Ctrl group) and highland hypobaric hypoxia overexpression experimental group (HH+Ad-AKAP1 group). The cardiac function of mice was detected by noninvasive M-type ultrasonic cardiomotive, myocardial fibrosis was detected by Masson and Sirius Red staining, and cardiomyocyte hypertrophy was detected by wheat germ agglutinin. After the expression of AKAP1 in primary cardiomyocytes was downregulated by siRNA and upregulated by adenovirus, the cells were divided into three groups (n=3) : normoxia control group, hypoxia interference control group (hypoxia+siCtrl group), hypoxia AKAP1 knockdown group (hypoxia+siAKAP1 group) ; normoxia control group, hypoxia overexpression control group (hypoxia+Ad-Ctrl group), hypoxia AKAP1 overexpression group (hypoxia+Ad-AKAP1 group). Apoptosis was detected by flow cytometry, AKAP1, apoptosis-related protein and mRNA expression levels were detected by western blotting and qPCR, mitochondrial membrane potential was detected by JC-1 staining, and mitochondrial reactive oxygen specie (ROS) level was detected by MitoSOX. Results: The expression of AKAP1 in cardiac muscle of HH group was lower than that in the WT group, and the expression of AKAP1 in hypoxia experimental group was lower than that in normoxia control group (P<0.01). Compared with WT group, the left ventricular ejection fraction and fraction shortening of left ventricle in HH+Ad-Ctrl group were decreased (P<0.01), myocardial fibrosis and hypertrophy were aggravated (P<0.01), and the expression of B-cell lymphoma-2 (BCL-2) was decreased, the expressions of BCL-2-associated X protein (BAX), Caspase 3 and Caspase 9 were increased (P<0.01). After AKAP1 overexpression, compared with HH+Ad-Ctrl group, the left ventricular ejection fraction and left ventricular fraction shortening were increased in HH+Ad-AKAP1 group (P<0.01), myocardial fibrosis and hypertrophy were reduced (P<0.01), and the expression of BCL-2 was increased, the expressions of BAX, Caspase 3 and Caspase 9 were decreased (P<0.01). Compared with normoxia control group, the expression of BCL-2 in hypoxia+siCtrl group was decreased, the expressions of BAX, Caspase 3, Caspase 9 were increased, the apoptosis level was increased (P<0.01), the mitochondrial membrane potential was decreased and the production of ROS was increased (P<0.01). After AKAP1 knockdown, compared with hypoxia+siCtrl group, the expression of BCL-2 in hypoxia+siAKAP1 group was decreased, the expressions of BAX, Caspase 3, Caspase 9 were increased, the apoptosis level was increased (P<0.01), mitochondrial membrane potential was decreased, and the production of ROS was increased (P<0.01). After AKAP1 overexpression, compared with hypoxia+Ad-Ctrl group, the expression of BCL-2 in hypoxia+Ad-AKAP1 group was increased, the expressions of BAX, Caspase 3 and Caspase 9 were decreased (P<0.05), the apoptosis level was decreased (P<0.01), and the mitochondrial membrane potential was enhanced, and the production of ROS was decreased (P<0.01) . Conclusion: The downregulation of AKAP1 in cardiomyocytes under highland hypobaric hypoxia may lead to the decrease of mitochondrial membrane potential and the increase of ROS generation, leading to the apoptosis of cardiomyocytes, and thus aggravating the myocardial injury at highland hypobaric hypoxia.

Introduction: Culturing cerebrovascular smooth muscle cells (CVSMCs) in vitro can provide a model for studying many cerebrovascular diseases. This study describes a convenient and efficient method to obtain mouse CVSMCs by enzyme digestion. Methods: Mouse circle of Willis was isolated, digested, and cultured with platelet-derived growth factor-BB (PDGF-BB) to promote CVSMC growth, and CVSMCs were identified by morphology, immunofluorescence analysis, and flow cytometry. The effect of PDGF-BB on vascular smooth muscle cell (VSMC) proliferation was evaluated by cell counting kit (CCK)-8 assay, morphological observations, Western blotting, and flow cytometry. Results: CVSMCs cultured in a PDGF-BB-free culture medium had a typical peak-to-valley growth pattern after approximately 14 days. Immunofluorescence staining and flow cytometry detected strong positive expression of the cell type-specific markers alpha-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain 11 (SMMHC), smooth muscle protein 22 (SM22), calponin, and desmin. In the CCK-8 assay and Western blotting, cells incubated with PDGF-BB had significantly enhanced proliferation compared to those without PDGF-BB. Conclusion: We obtained highly purified VSMCs from the mouse circle of Willis using simple methods, providing experimental materials for studying the pathogenesis and treatment of neurovascular diseases in vitro. Moreover, the experimental efficiency improved with PDGF-BB, shortening the cell cultivation period.

We evaluated the effect of acute hypobaric hypoxia (AHH) on the hippocampal region of the brain in early-stage spontaneously hypertensive male rats. The rats were classified into a control (ground level; ~ 400 m altitude) group and an AHH experimental group placed in an animal hypobaric chamber at a simulated altitude of 5500 m for 24 h. RNA-Seq analysis of the brains and hippocampi showed that differentially expressed genes (DEGs) were primarily associated with ossification, fibrillar collagen trimer, and platelet-derived growth factor binding. The DEGs were classified into functional categories including general function prediction, translation, ribosomal structure and biogenesis, replication, recombination, and repair. Pathway enrichment analysis revealed that the DEGs were primarily associated with relaxin signaling, PI3K-Akt signaling, and amoebiasis pathways. Protein–protein interaction network analysis indicated that 48 DEGs were involved in both inflammation and energy metabolism. Further, we performed validation experiments to show that nine DEGs were closely associated with inflammation and energy metabolism, of which two ( Vegfa and Angpt2 ) and seven ( Acta2, Nfkbia, Col1a1, Edn1, Itga1, Ngfr , and Sgk1 ) genes showed up and downregulated expression, respectively. Collectively, these results indicated that inflammation and energy metabolism-associated gene expression in the hippocampus was altered in early-stage hypertension upon AHH exposure.

临床实习是医学专业本科学员获得岗位胜任力的关键环节.航空航天医学专业及相关医学岗位任职需求具有特殊性,对本科学员临床实习的教学管理工作提出了更高要求.该研究在介绍航空航天医学专业本科学员临床实习教学特殊性的基础上,通过分析空军军医大学在该专业本科学员临床实习教学管理中存在的问题,探讨改进措施,以提高临床实习教学水平及本科学员的岗位胜任力.

消化道溃疡(peptic ulcer,PU)主要指发生于胃和十二指肠的慢性溃疡,是一种由酸性胃液及蛋白酶对黏膜自身消化作用所致的多发病、常见病[1].幽门螺杆菌(H.pylori)感染、吸烟、应激以及胃十二指肠黏膜防御功能降低等都容易诱发PU的发生.飞行人员作为航空兵部队的战斗核心,一旦罹患PU,轻者会出现腹部疼痛、腹胀等不适症状,直接影响飞行状态,严重的可能发生消化道出血、穿孔,进而引发严重的飞行安全事故.飞行人员常受到低气压缺氧、过载和噪声等特殊的航空环境影响,加之其在飞行过程中身心常处于应激状态,导致飞行人员PU的发病有其自身的特点.因此,全面了解飞行人员PU的病因、临床特点、防治措施以及航空医学诊疗原则,对于飞行人员PU的精准化和有效性防治具有重要意义.

BACKGROUND:Myocardial microvascular injury is the key event in early diabetic heart disease. The injury of myocardial microvascular endothelial cells (CMECs) is the main cause and trigger of myocardial microvascular disease. Mitochondrial calcium homeostasis plays an important role in maintaining the normal function, survival and death of endothelial cells. Considering that mitochondrial calcium uptake 1 (MICU1) is a key molecule in mitochondrial calcium regulation, this study aimed to investigate the role of MICU1 in CMECs and explore its underlying mechanisms.METHODS:To examine the role of endothelial MICU1 in diabetic cardiomyopathy (DCM), we used endothelial-specific MICU1ecKO mice to establish a diabetic mouse model and evaluate the cardiac function. In addition, MICU1 overexpression was conducted by injecting adeno-associated virus 9 carrying MICU1 (AAV9-MICU1). Transcriptome sequencing technology was used to explore underlying molecular mechanisms.RESULTS:Here, we found that MICU1 expression is decreased in CMECs of diabetic mice. Moreover, we demonstrated that endothelial cell MICU1 knockout exacerbated the levels of cardiac hypertrophy and interstitial myocardial fibrosis and led to a further reduction in left ventricular function in diabetic mice. Notably, we found that AAV9-MICU1 specifically upregulated the expression of MICU1 in CMECs of diabetic mice, which inhibited nitrification stress, inflammatory reaction, and apoptosis of the CMECs, ameliorated myocardial hypertrophy and fibrosis, and promoted cardiac function. Further mechanistic analysis suggested that MICU1 deficiency result in excessive mitochondrial calcium uptake and homeostasis imbalance which caused nitrification stress-induced endothelial damage and inflammation that disrupted myocardial microvascular endothelial barrier function and ultimately promoted DCM progression.CONCLUSIONS:Our findings demonstrate that MICU1 expression was downregulated in the CMECs of diabetic mice. Overexpression of endothelial MICU1 reduced nitrification stress induced apoptosis and inflammation by inhibiting mitochondrial calcium uptake, which improved myocardial microvascular function and inhibited DCM progression. Our findings suggest that endothelial MICU1 is a molecular intervention target for the potential treatment of DCM.

航空医疗救援是借助航空器作为交通工具,运用医学手段救助受困对象的活动,在救灾救援任务中发挥着举足轻重的作用.本文主要探讨了航空医疗救援活动中,航空特殊环境的特点及可能带来的危害;常见危重疾病的机上救治和护理要点.这有助于减少因医疗操作不当造成的损伤,从而使航空医疗救援活动安全、有序、高效地展开.

Adv. Sci. 2021, 8, 2002794 DOI: 10.1002/advs.202002794 In the original published article, the previous forward and reverse primers of Cidea in Table S1 (Supporting Information) were reversed. Now these two primers of Cidea have been exchanged. Please find the correct Table S1 below. The authors apologize for any inconvenience caused.

高原低氧习服是指进入高原后机体产生一系列生理改变以确保能在低氧环境中更好地生活,其对高原人群身心健康至关重要.然而如何快速习服高原低氧环境、减少高原低氧对机体损伤至今仍不清楚.了解高原低氧损伤发生、发展机制,寻找精准预测高原低氧损伤发生的靶点,研发高效预防和治疗高原低氧损伤的措施迫在眉睫.该文就高原低氧损伤发生机制、高原低氧损伤易感性靶点、促进高原低氧习服措施进行综述,旨在为高原医学快速发展提供参考,为构建对高原低氧损伤的充分认识、早期预警、有效预防和快速治疗于一体的诊防治新策略提供新思路.

哌托生特作为一种组胺H3受体拮抗剂/反向激动剂,其明确的促觉醒作用以及低药物依赖性使其迅速成为欧美治疗成人发作性睡病的一线用药.本文通过总结组胺H3受体分布及作用特点,阐明了哌托生特的作用靶点及其产生的相关效应;并通过总结哌托生特的药物化学特点以及将其与常见抗疲劳药物成瘾性之间进行对比,展望了哌托生特在特殊环境/条件下的应用潜能.本文为哌托生特在我国特殊环境/条件下,如军事、轮班、紧急任务等方面的合理化应用提供了理论依据.