Deep peripheral nerve regeneration is hindered by inflammatory infection, neurotrophic factor deficiency, and slow axonal growth kinetics. Although multifunctional nerve guidance conduits (NGCs) have been developed, achieving spatiotemporally precise neuromodulation within deeply located neural tissues remains a significant challenge. Herein, we developed a nerve conduit fabricated with a gut metabolite indole-3-propionic acid (IPA)-functionalized and polydopamine-coated Au nanorod clusters (AuNR@PDA-IPA (API)) loaded on a parallel fiber film of PLGA, exhibiting NIR-II-responsiveness for spatiotemporally precise neuromodulation. API nanoclusters convert deep-penetrating NIR-II light (1064 nm wavelength) into deeply localized heat (∼42-43 °C), which noninvasively activates the transient receptor potential vanilloid 1 (TRPV1) channel in Schwann cells (SCs). This activation triggers Ca2+ influx and membrane depolarization, promoting neurotrophic expression. Concurrently, NIR-II irradiation directly modulated the release of neuroprotective IPA from the API platform through an on-off switching mechanism. Meanwhile, IPA combined with PDA potently scavenged reactive oxygen species (ROS), suppressed NF-κB activation, and promoted M2 polarization of macrophages, thereby reshaping the neuroregenerative microenvironment. The in vitro and in vivo results demonstrate that API-functionalized conduit enhances VEGF-driven angiogenesis and activates SCs to upregulate the expression of neurotrophic factors (BDNF, NGF) and glial-specific proteins (S100, GFAPs). By orchestrated tripartite regulation of the "anti-inflammatory-angiogenic-neuroregenerative" system, the conduit enabled robust axonal regrowth, remyelination, and functional recovery in peripheral nerve defects, offering a transformative strategy for the repair of deeply located neural tissues. This work presents a noninvasive bioelectronic paradigm that merges spatiotemporal photothermal neuromodulation with immune metabolic reprogramming for precision neural reconstruction.

ABSTRACT:Conventional medical sensors primarily function as passive transducers and often struggle to maintain accuracy and stability under complex physiological conditions. Their limited capacity for local data processing, adaptive compensation, and real-time interaction also constrains continuous monitoring and individualized clinical decision-making. The convergence of microelectronics, materials science, wireless communication, and artificial intelligence (AI) has therefore accelerated the development of intelligent medical sensors that integrate sensing, processing, communication, and decision-support functions. This review summarizes recent advances and remaining challenges in this field. We examine the technical architectures and core functions of next-generation sensors, including self-compensation, self-calibration, self-diagnosis, and bidirectional data interaction, and compare four major technological platforms: flexible wearable sensors, optical fiber sensors, electrochemical sensors, and functional nucleic acid and molecularly imprinted biosensors. We further discuss signal-transduction, anti-interference, and data-transmission mechanisms; advances in flexible materials, micro/nano-fabrication, multimodal integration, and AI-enabled signal processing; and applications in physiological monitoring, biomarker detection, chronic disease management, wearable therapy, interventional support, and extreme environments. Despite rapid progress, clinical translation remains limited by data security and privacy risks, insufficient standardization and regulatory alignment, long-term stability and biocompatibility concerns, and uneven validation maturity across technologies. Future development should prioritize clinically driven design, staged and technology-specific validation, multimodal and low-power integration, and coordinated regulatory and manufacturing strategies to support reliable, scalable, and patient-centered implementation.

Heat stress (HS) is an increasingly prevalent environmental and exertional challenge. In severe cases, HS may progress to heatstroke, a life-threatening clinical syndrome characterized by severe hyperthermia, systemic inflammation, and multi-organ dysfunction. This review synthesizes evidence from laboratory rodent models and suggests that gut microbiota dysbiosis may act as a mediator and amplifier of HS-induced pathology. Across diverse rodent models, HS remodels the gut microbiota by reducing microbial diversity. These compositional changes are accompanied by decreased short-chain fatty acids, altered bile acid profiles, and increased lipopolysaccharide burden, although the specific metabolites affected vary across models. Causal evidence from fecal microbiota transplantation and gnotobiotic experiments supports microbiota-dependent amplification of intestinal barrier failure, hepatic inflammation, and neuroinflammation. In contrast, evidence for the gut-reproductive, gut-kidney, gut-heart, gut-muscle, and gut-adipose axes remains predominantly associative or derived from interventional correlations without formal causality testing. Targeting the gut-organ axis through probiotics, prebiotics, antioxidants, or functional amino acids offers promising but largely preclinical adjunctive strategies, with rapid cooling and supportive care remaining the foundation of heatstroke management. Future research should prioritize temporally resolved human studies, multi-omics integration, and causal validation to define the translational potential of microbiome-directed interventions.

Inspired by the geometric characteristics of bamboo with exceptional mechanical properties, this research proposes a novel bionic variable cross-section (VCS) strut design and applies to alumina ceramic lattices fabricated by stereolithography additive manufacturing technology. The mechanical behavior of ceramic lattices with different relative densities and structural parameters are studied by quasi-static uniaxial compression tests and finite element (FE) analysis. The results indicate that bionic design has effectively enhanced the mechanical properties of ceramic lattices. Compared to the conventional structures, the compressive strength and energy absorption of the ceramic lattices with variable cross-section are increased by up to 47.2% and 50.2% respectively. Furthermore, comprehensive parametric analysis indicates that the performance of ceramic lattices can be customized through tailored structural parameters, with the compressive strength enhanced by up to 46.3%. This study provides a novel approach for the structural design and mechanical performance regulation of ceramic lattice.

Lysine lactylation (Kla) is a metabolite-sensing post-translational modification that bridges cellular metabolism to protein function. Here, we discover that heat stress triggers anaerobic glycolysis and lactate accumulation in brain microvascular endothelial cells. We find that plasma lactate inversely correlates with Glasgow Coma Scale scores in heat stroke patients and predicts poor outcomes. Mechanistically, AARS1 catalyzes the transfer of lactate to HSP90β at lysine 275 (K275). Critically, the lactylation of HSP90β disrupts its interaction with apoptotic protease-activating factor 1 (APAF-1). This modification compromises the protective function of HSP90β, liberating APAF-1 to activate the mitochondrial apoptosis pathway, resulting in blood-brain barrier (BBB) injury. Functional validation reveals that decreasing lactate production or inhibiting AARS1 confers protection. These findings establish HSP90β K275 lactylation as a metabolic switch that modulates protective mechanisms during heat stress-induced cerebrovascular injury. Collectively, our study provides insights into heat stress pathogenesis and identifies potential therapeutic targets for heat-related brain damage.

As an important tool for the surgical treatment of pelvic floor dysfunction, the safety of mesh must be guaranteed. Although the short-term curative effect of most synthetic mesh is satisfactory, complications often occur due to its material. Planting stem cells on mesh through specific methods may resolve the problems of mesh with poor biocompatibility or an uncontrollable rate o degradation. Based on recent research, this paper summarizes the research progress of stem cells composited with common mesh materials, such as polypropylene, polylactic acid and acellular matrix.

Natural background radiation is a pervasive element affecting biological organisms. However, the consequences of its absence are not well comprehended. This study investigates the effects of ultra-low background radiation on head and neck tumor cells using the China Jinping Underground Laboratory (CJPL), which effectively shields cosmic rays. Our results demonstrate that ultra-low background radiation significantly suppresses tumor cell proliferation and migration. Moreover, mitochondrial dysfunction is characterized by reduced membrane potential, impaired oxidative phosphorylation, and increased oxidative stress. Through RNA sequencing, the ATM gene is identified as a pivotal regulator in this process. Furthermore, the downregulation of ATM under ultra-low background radiation results in decreased expression of PGC-1α, NRF-1, and TFAM, all of which are associated with mitochondrial function. In contrast, the overexpression of ATM or TFAM partially ameliorates the inhibition of tumor cell behavior and mitochondrial function induced by ultra-low background radiation. Collectively, these findings demonstrate that ultra-low background radiation inhibits tumor cell behavior through mitochondrial dysfunction mediated by ATM downregulation, providing valuable insights into the potential therapeutic applications and molecular targets of ultra-low background radiation.

Heat acclimation (HA) is an evolutionarily conserved trait that enhances tolerance to novel stressors by inducing heat shock proteins (HSPs). However, the molecular mechanisms underlying this phenomenon remain elusive. In this study, we established a HA mouse model through intermittent heat stimulation. Subsequently, this model was evaluated using an array of physiological and histological assessments. In vitro, HA cell model with mouse brain microvascular endothelial cells (bEnd.3) was established and analyzed for cell viability and apoptosis markers. We investigated HA-mediated heat and hypoxia tolerance mechanisms using HIF-1α and HSP70 inhibitors and siRNA. Our results demonstrated that HA enhances the tolerance of bEnd.3 cells and mice to both heat and hypoxia, Mechanistically, HA upregulated the expression of HIF-1α and HSP70. However, inhibition of HIF-1α or HSP70 partially attenuated HA-induced tolerance to heat and hypoxia. Additionally, HA significantly decreased the ubiquitination levels of HIF-1α, whereas inhibition of HSP70 increased its ubiquitination. HA also substantially enhanced the interaction between HIF-1α and HSP70. In conclusion, our findings indicate that HA enhances tolerance to heat and hypoxia by stabilizing HIF-1α through increased interaction with HSP70. This discovery elucidates a novel mechanism of cellular protection conferred by HA and provides new strategies and potential targets for human adaptation to extreme environments.

Objective:To investigate the effects of low background radiation environments in deep underground settings on the biological behavior of NP69 human nasopharyngeal epithelial cells (NP69 cells) and the underlying molecular mechanisms. Methods:A parallel control experimental design was adopted and NP69 cells were synchronously cultured in settings of three underground depths at the China in situ Deep-Underground Facility & Life Observatory (DeUFO)-ground level (DeUFO-0 m), 1000 m underground (DeUFO-1000 m), and 1500 m underground (DeUFO-1500 m). Changes in cell proliferation and migration capabilities were assessed using the Cell Counting Kit-8 (CCK-8) assay and scratch assay, respectively. High-throughput RNA sequencing (RNA-Seq) was performed to identify differentially expressed genes (DEGs). Functional annotation and pathway enrichment analysis of the DEGs were performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Results:CCK-8 assay revealed that, after 72 h of culture, the absorbance value of the DeUFO-0 m group was 1.35 times and 1.27 times those of the those of the DeUFO-1000 m and DeUFO-1500 m groups, respectively (both P < 0.0001). After 96 h of culture, the absorbance value of the DeUFO-0 m group was 1.52 times and 1.41 times those of the DeUFO-1000 m and DeUFO-1500 m groups, respectively (both P < 0.0001). Colony formation assays revealed that the number of cell colonies in the DeUFO-0 m group was 1.59 times and 1.27 times those in the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.001). The scratch assay revealed that the 36-hour wound healing rate of the DeUFO-0 m group was 2.22 times and 4.00 times those of the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.0001). Transwell assays revealed that the number of migrating cells in the DeUFO-0 m group was 2.08 times and 2.56 times those in the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.0001). Transcriptome sequencing analysis revealed consistent upregulation of CELF2, CELF4, CGB8, GRHL2, and DMRTA2 genes in the DeUFO-1000 m and DeUFO-1500 m groups. Pathway enrichment analysis indicated significant enrichment of extracellular matrix (ECM) remodeling-associated pathways and gene expression regulation pathways in the experimental groups (false discovery rate [FDR] < 0.05). Conclusion:The low background radiation environment in deep underground settings suppresses the proliferation and migration activities of NP69 cells by mediating ECM remodeling and post-transcriptional regulatory mechanisms through the regulation of target genes such as the CELF family. This study provides experimental evidence for establishing a dose-response relationship between environmental radiation and cellular effects.

Objectives: Recently, pre-/post-operative Local Estrogen Therapy (LET) has shown effectiveness in alleviating Pelvic Organ Prolapse (POP) symptoms in clinical therapy. However, there is a lack of scientific evidence to support these claims. Therefore, we aimed to explore the anti-senescence effects and mechanisms of 17[3-estradiol (E2) on POP-derived fibroblasts. Methods: The primary fibroblast cells were isolated and cultured from the surgical samples of postmenopausal women clinically diagnosed with pelvic organ prolapse (POP) at stages III-IV (quantified using the POP-Q system) and without any other treatment within 6 months. (n = 12, age 50-75). Colorimetric Cell Counting Kit (CCK-8) assay and Senescence-Associated-[3-Galactosidase (SA-[3-Gal) staining were used to test the cell proliferative capacity and the senescence rate. Western blotting (WB) was used to detect the expression of Collagen Type I (COL-I), Collagen Type III (COL-III), Cyclin-dependent kinase 4 inhibitor A (p16INK4a), Cyclin-dependent kinase inhibitor 1A (p21), Tumor Protein 53 (p53), Sirtuin 1 (SIRT-1) and Microtubule-associated protein 1A/1B-light chain 3-I/II (LC3I/II) protein. A transmission Electron Microscope (TEM) was used to observe the ultrastructure of fibroblasts. Results: The results showed that E2 significantly promoted the proliferation of fibroblasts derived from POP and reduced the staining rate of SA-[3-Gal. It markedly enhanced the extracellular matrix proteins COL-I and COL-III, accompanied by inhibition of the senescent maker p16INK4a. Additionally, our results improved the cells' autophagy and metabolic activity. Additionally, our results indicate the anti-senescence mechanism of E2 through the mediated SIRT-1/p53/p21 axis pathway. Conclusion: We provide preliminary evidence for the anti-aging effects and mechanisms of E2 on POP, hoping to provide a theoretical basis for estrogen against POP senescence and guide the clinical application and local administration of estrogen in POP treatment.

Mild photothermal therapy (PTT) in the near-infrared II region (NIR-II) window provides an effective and safe modality for nasopharyngeal carcinoma treatment, based on its superior tissue penetration and clinical suitability. However, its effectiveness is compromised by the overexpression of heat shock proteins (HSPs) with enhanced tumor resistance to heat. In this study, Au-polydopamine blackspheres (AuPBs) are synthesized and functionalized with the HSP70 inhibitors VER-155008 (AuPB-VER) via pi-pi stacking interactions, achieving enhanced photothermal conversion efficiency and controlled drug release. In vitro and organoid studies demonstrate the significant tumor-inhibitory effects of AuPB-VER treatment at a mild 40 degrees C PTT. Remarkably, AuPB-VER achieves complete tumor eradication at just 40 degrees C in vivo, indicating that AuPB-VER could effectively overcome heat resistance in deep tissues, enhancing the therapeutic efficacy of mild PTT and minimizing damage to surrounding tissues. These findings pave the way for a promising clinical approach to treating advanced or recurrent nasopharyngeal carcinoma.

Current dural repair biomaterials cannot meet the multifunctional requirement for effective repair. Photothermal therapy (PTT) is a promising solution to promote nerve repair, and control inflammation by mild localized heating. PDA-coated AuNCs were incorporated into a PAM/Alg hydrogel, achieving double crosslinking through PAM cross-linking network, and ionic bonds between Ca2+ and Alg, and the PAM/Alg/AuNCs hydrogel prepared by the optimal parameters, exhibited the enhanced mechanical flexibility and photothermal conversion efficiency, and then was applied in the repair of dural and brain injury under second near-infrared (NIR-II) irradiation. The low-temperature photothermal under NIR-II effect not only boosts fibroblast proliferation and macrophage polarization towards the anti-inflammatory M2 phenotype, but also stimulates angiogenesis and higher expression of two neurotrophic factors, inhibiting brain scarring by reduced the expression of GFAP, IBA-1, TNF-alpha, and COX-2, thereby improving dural repair and functional recovery, while minimizing inflammation and aiding in the concurrent repair of brain damage accompanied by dural defects, and a primary mechanism of functionalized composite hydrogel under NIR-II for promoting concurrent repair of dural and slight brain injects was also discussed. Meanwhile, the cerebrospinal fluid leakage in rats was successfully identified by MRI technology and a MRI detection system for evaluating cerebrospinal fluid leakage in rats were established.

The efficacy of electrical stimulation facilitating peripheral nerve regeneration is evidenced extensively, while the associated secondary damage resulting from repeated electrode invasion and indiscriminate stimulation is inevitable. Here, we present an optogenetics strategy that utilizes upconversion nanoparticles (UCNPs) to convert deeply penetrating near-infrared excitation into blue emission, which activates an adeno-associated virus-encoding ChR2 photoresponsive ion channel on cell membranes. The induced Ca2+ flux, similar to the ion flux in the electrical stimulation approach, efficiently regulates viability and proliferation, secretion of nerve growth factor, and neural function of RSC96 cells. Furthermore, deep near-infrared excitation is harnessed to stimulate autologous Schwann cells in situ via a UCNP-composited scaffold, which enhances nerve sprouting and myelination, consequently promoting functional recovery, electrophysiological restoration, and reinnervation of damaged nerves. This developed postoperatively noninvasive optogenetics strategy presents a novel, minimally traumatic, and enduring therapeutic stimulus to effectively promote peripheral nerve repair.

Heat acclimation (HA) is found to help decrease the incidence of heat-related illnesses such as heat syncope and exertional heat stroke. However, the response of vascular endothelial cells to HA remain to be elucidated. In this study, mouse brain microvascular endothelial cells (bEnd.3), human umbilical vein endothelial cells (HUVEC), and human aortic endothelial cells (HAEC) were selected. The cells were first subjected to HA at 40 ℃ for 2 h per day for 3 days, and then subjected to heat stress at 43 ℃ for 2 h or 4 h. After heat stress, HA-pretreated cells showed a significant increase in cell viability, cell integrity, a decrease in the proportion of S phase cells, cell apoptosis, and cytoskeletal shrinkage compared with the cells without HA pretreatment. Additionally, the expression of VEGF, ICAM-1, iNOS and EPO in HA-pretreated cells significantly increased. We also presented evidence that HA upregulated HSP70 and bcl-2, while downregulated p-p53 and bax. Notably, the suppression of HSP70 expression attenuated the protective role of heat acclimation. Furthermore, HA mitigated injuries in vital organs of mice exposed to heat stress. Conclusively, these findings indicated the HA can increase the vitality of vascular endothelial cells after heat stress, partially restore the function of vascular endothelial cells, and this protective effect may be related to the upregulation of HSP70 expression.

Typical symptoms of acute myocardial infarction (AMI) and acute aortic dissection (AAD) are similar chest pain, leading to higher clinical misdiagnosis rate, evenly the mortality rate of patients. In this work, ZrO2@PEI-QDs nanospheres with higher fluorescence were prepared by sequential electrostatic adsorption of branched PEI chains and CdSe/ZnS-COOH QDs on hollow ZrO2 nanospheres. Three multi-channel LFIA strips (on sST2 and cTnI, cTnI and h-FABP, HMGB1 and sST2, respectively) based on ZrO2@PEI-QDs for rapid and correct distinguishing of AMI and ADD were constructed. Their visual limit of detection (vLOD for sST2 and cTnI, cTnI and h-FABP, HMGB1 and sST2) within 10 15min reached 0.075 and 0.1ng/mL, 0.1 and 1ng/mL, 1 and 0.1ng/mL, respectively, which were all lower than the normal level of healthy people. Compared with previous studies, ZrO2 surface adsorbs more QDs, the fluorescence intensity was increased by about 2.84 times, and vLODs of three strips based on the quantitative fluorescence analysis were also increased by up to one orders of magnitude. The test results of five clinical serum samples indicated that three multi-channel LFIA strips could quantitatively detect four biomarkers of chest pain, and successfully distinguish AMI patients from AAD patients. These results indicated that this set of multi-channel LFIA strips could become an effective tool for the early and accurate detection or distinguish of ADD and AMI.

IntroductionExtreme heat events caused by occupational exposure and heat waves are becoming more common. However, the molecular changes underlying the response to heat exposure in humans remain to be elucidated.MethodsThis study used longitudinal multi-omics profiling to assess the impact of acute heat exposure (50°C for 30 min) in 24 subjects from a mine rescue team. Intravenous blood samples were collected before acute heat exposure (baseline) and at 5 min, 30 min, 1 h, and 24 h after acute heat exposure (recovery). In-depth multi-omics profiling was performed on each sample, including plasma proteomics (untargeted) and metabolomics (untargeted).ResultsAfter data curation and annotation, the final dataset contained 2,473 analytes, including 478 proteins and 1995 metabolites. Time-series analysis unveiled an orchestrated molecular choreography of changes involving the immune response, coagulation, acid–base balance, oxidative stress, cytoskeleton, and energy metabolism. Further analysis through protein–protein interactions and network analysis revealed potential regulators of acute heat exposure. Moreover, novel blood-based analytes that predicted change in cardiopulmonary function after acute heat exposure were identified.ConclusionThis study provided a comprehensive investigation of the dynamic molecular changes that underlie the complex physiological processes that occur in human males who undergo heat exposure. Our findings will help health impact assessment of extreme high temperature and inspire future mechanistic and clinical studies.

Recently,with the rapid growth of the global population and the exhaustion of resources,exploration activities in extreme environments such as the polar regions,the outer space,the deep sea,the deep underground and highlands are becoming increasingly more frequent.This in-depth exploration of the external environment and the consequent dramatic changes in lifestyles impact on sleep,a basic life activity of humans,in ways that cannot be overlooked.the basic life activity of human beings.Sleep,a basic life activity and the result of the evolution of organisms to adapt to their environment,is closely associated with sleep homeostasis and endogenous rhythms.However,external environmental changes and lifestyle shifts in extreme environments have had a significant impact on the patterns and the quality of sleep in humans.Furthermore,this impact can lead to many physiological and psychological problems,posing a great threat to human health.In this review,we delved into the specific effects of different extreme natural environments and enclosed environments on sleep,elaborating on how these environments alter the patterns and the quality of sleep in humans.In addition,we summarized the changes in human sleep under extreme environments to help gain a better understanding of the mechanisms by which these specific environments impact human sleep.It is expected that this review will provide a solid theoretical foundation for optimizing long-term survival strategies in extreme environments and help humans adapt to and overcome the challenges posed by extreme environments more effectively.

Abstract Occupational exposure to extreme high temperatures and the increasing global temperatures necessitates a deeper understanding of the impact of heat exposure on human health. However, the molecular mechanisms underlying the response of monocytes and neutrophils to heat exposure in occupational population remain to be fully elucidated. This study used longitudinal transcriptome to assess the impact of acute heat exposure (50°C for 30 min) in 10 subjects from a mine rescue team before acute heat exposure (baseline) and at 5 min, 30 min, 1 h, and 24 h after acute heat exposure (recovery). The time‐series analysis revealed a coordinated molecular choreography of changes involving inflammation, coagulation, extracellular matrix, and energy metabolism. Importantly, the study characterized the inflammatory signature associated with heat exposure in monocytes and neutrophils, as evidenced by the rapid activation of the inflammation‐related transcriptome following heat exposure. Additionally, we pinpointed potential regulators, such as NR4A1, FOSL1, EGR3, and ATF3. In summary, the study suggested that the initial response to heat stress in monocytes and neutrophils from mine rescue team member was primarily characterized by a pro‐inflammatory stress response, which could potentially lead to the development of inflammation and ultimately result in a systemic inflammatory response in heatstroke.

Near infrared second region (NIR II) is applied in deep tissue imaging and tumor therapy. TRPV1 ion channels in cell membrane are widely distributed in nerve tissue, and opened with thermal stimulation, inducing Ca 2 + influx. Gold-polydopamine (PDA) blackspheres (AuPBs) with good NIR II absorption and photothermal conversion were prepared by self-oxidation - reduction of dopamine and chlorauric acid, and then loaded on PLLA-SF parallel films (PSPF), which were then curved into nerve scaffolds (PSPF@AuPBs). After this scaffold implantation in sciatic nerve injury site (a depth of more than 1 cm under the skin), PDA in AuPBs relieved inflammatory response in injury site, leading to higher VEGF expression and new -vessels formation; furthermore, TRPV1 ion channels in Schwann cells (SCs) were periodically opened under NIR II irradiation to achieve effect of Ca 2 + influx, activating SCs to highly express BDNF and NGF, and then promoting arrangement and myelination of SCs, nerve regeneration and functional recovery. These results suggested that our fabricated PSPF@AuPBs, as an effective NIR II adsorption platform, could provide a good photothermal conversion therapy to improve deep tissue regeneration.

目的 观察瑞马唑仑用于高原老年患者无痛胃镜诊疗的临床效果.方法 接受无痛胃镜检查的老年患者192例,随机数字表法分为观察组和对照组各96例,对照组给予丙泊酚干预,观察组给予瑞马唑仑干预.比较两组患者不同时点的呼吸频率,麻醉前后的应激反应指标变化,以及苏醒时间、药品不良反应发生率.结果 观察组胃镜进镜前和胃镜检查结束时的呼吸频率均低于对照组(P＜0.05).置入胃镜时,观察组患者的血糖、肾上腺素、皮质醇水平较麻醉前明显升高,但低于同期对照组(P＜0.05).观察组的苏醒时间较对照组短(P＜0.05),药品不良反应发生率也明显低于对照组(P＜0.05).结论 瑞马唑仑在高原老年患者无痛胃镜诊疗中的临床应用效果好.