Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, tau hyperphosphorylation, and chronic neuroinflammation. While neuroinflammation-mediated by microglial and astrocyte activation-has long been considered a secondary response to Aβ pathology, emerging evidence positions it as a primary driver of cognitive decline. Notably, the gut microbiota, through the microbiota-gut-brain axis (MGBA), is crucial in modulating neuroinflammation. Dysbiosis disrupts gut barrier integrity, promotes systemic inflammation, and exacerbates neuroinflammatory responses, thereby accelerating AD progression. Recent advances reveal that gut microbiota-derived metabolites (e.g., short-chain fatty acids, lipopolysaccharides) directly influence microglial activation and Aβ aggregation. These findings have opened new therapeutic possibilities, with microbiota-targeted approaches such as probiotics, prebiotics, and fecal microbiota transplantation demonstrating promising neuroprotective effects in preclinical studies by reducing neuroinflammation and preserving cognitive function. However, translating these findings into clinical applications requires further validation through randomized controlled trials. This review summarizes the current understanding of gut microbiota-driven neuroinflammation in AD, from molecular mechanisms to potential therapeutic strategies. Targeting the MGBA represents a paradigm shift in AD management, emphasizing the modulation of neuroinflammation and pathological progression through gut microbiota interventions. The discussion also addresses existing research challenges and outlines future directions to advance this promising field.

BACKGROUND:Several observational studies have revealed that different neurotrophic factors (NTFs) are associated with delirium, yet the direction and magnitude of the causal association remain poorly understood. Herein, we performed a two-sample Mendelian randomization (MR) analysis to investigate the causal relationship between these factors and delirium. METHODS:GWAS data for delirium were sourced from the FINN10 database; GWAS data for risk factors (protein kinase C-binding protein NELL1, neurotrophin-3, neurotrophin-4, brain-derived neurotrophic factor levels, nerve growth factor, ciliary neurotrophic factor, and glial cell-derived neurotrophic factor levels) were from the IEU Open GWAS. Inverse-variance weighted (IVW) was used as a primary analysis. MR-Egger, weighted median (WM), and weighted model were applied to validate the robustness of the results. The MR-Egger regression method was used to explore the presence of horizontal pleiotropy, and the MR pleiotropy residual sum, and outlier (MR-PRESSO) method was applied to detect potential outliers. Cochran's Q test assessed heterogeneity among instrumental variables (IVs). The leave-one-out (LOO) method was used to enhance the precision and veracity of our findings. RESULTS:IVW analyses revealed no association between risk factors and delirium. MR Egger, WM, and the weighted mode approach further confirmed these data. MR-Egger regression analysis confirmed the absence of directional pleiotropy in our analysis. Heterogeneity and sensitivity analyses showed reliable results. CONCLUSION:No association between other factors and delirium was identified; however, further research is needed to determine if these results apply to other races. Also, advances in molecular biology and epigenetics may shed light on this topic.

Antimicrobial resistance (AMR) has become a major and escalating global health threat, undermining the effectiveness of current antibiotic and antimicrobial therapies. The rise of multidrug-resistant bacteria has led to increasingly difficult-to-treat infections, resulting in higher morbidity, mortality, and healthcare costs. Tackling this crisis requires the development of novel antimicrobial agents, optimization of current therapeutic strategies, and global initiatives in infection surveillance and control. Recent studies highlight the crucial role of the human gut microbiota in defending against AMR pathogens. A balanced microbiota protects the body through mechanisms such as colonization resistance, positioning it as a key ally in the fight against AMR. In contrast, gut dysbiosis disrupts this defense, thereby facilitating the persistence, colonization, and dissemination of resistant pathogens. This review will explore how gut microbiota influence drug-resistant bacterial infections, its involvement in various types of AMR-related infections, and the potential for novel microbiota-targeted therapies, such as fecal microbiota transplantation, prebiotics, probiotics, phage therapy. Elucidating the interactions between gut microbiota and AMR pathogens will provide critical insights for developing novel therapeutic strategies to prevent and treat AMR infections. While previous reviews have focused on the general impact of the microbiota on human health, this review will specifically look at the latest research on the interactions between the gut microbiota and the evolution and spread of AMR, highlighting potential therapeutic strategies.

Antimicrobial resistance (AMR) poses a global health threat, particularly in critically ill patients with multidrug-resistant organism (MDRO) colonization or infection. While evidence suggests the gut microbiota plays a critical role in MDRO colonization and infection, its specific characteristics and the host immune response remain poorly understood. This case–control study compared 88 MDRO-infected patients, 100 MDRO-colonized patients, and 86 healthy controls, using 16S rRNA sequencing and cytokine profiling. MDRO cohorts exhibited profound gut dysbiosis, including reduced gut microbial diversity and distinct community structures, reduced beneficial bacteria (e.g., Bacteroides, Faecalibacterium, Roseburia, Prevotella), and expansion of pathobionts—resident microbes with pathogenic potential (e.g., Enterococcus, Klebsiella, Escherichia-Shigella). Enterotype analysis revealed a shift from a Bacteroides-dominated to one Enterococcus-dominated microbiota in both colonized and infected patients compared to controls. Serum cytokine profiling indicated immune dysfunction in MDRO-associated patients. Correlation analysis showed that beneficial genera were negatively correlated with pro-inflammatory cytokines (IL-1ra, IL-2, IL-7, TNF-α, and IFN-γ) and positively associated with anti-inflammatory markers, while pathobionts exhibited the opposite trend. Several key differential genera, such as Enterococcus and Klebsiella, either individually or in combination, have been identified as key discriminators of MDRO status. Functional predictions through PiCRUSt observed disruptions in carbohydrate and lipid metabolism in the MDRO cohorts. Overall, MDRO colonization and infection lead to gut dysbiosis and immune dysfunction, with microbiota-immune interactions playing a crucial role in disease progression, suggesting the gut microbiota as a potential diagnostic and therapeutic target for AMR.

Non-small cell lung cancer (NSCLC) is the most common malignancy worldwide, with a high death rate. Long noncoding RNA (LncRNA) NKX2-1 antisense RNA 1 (NKX2-1-AS1) has been reported to be an oncogene in lung tumorigenesis. However, the precise mechanism of NKX2-1-AS1 underlying NSCLC progression is blurry. The intention of our research was to probe the potential mechanism of NKX2-1-AS1 underlying NSCLC. NKX2-1-AS1 expression and relevant downstream gene expression were measured using RT-qPCR. Cell proliferation and apoptosis were determined by MTT assay, EdU assay along with flow cytometry analysis. Cell migratory and invasive abilities were inspected by transwell assay. Western blot and immunofluorescence staining were utilized to assess the levels of epithelial-mesenchymal transition (EMT)-related proteins. RNA pull-down together with luciferase reporter assays were performed to verify the interaction between NKX2-1-AS1 and its downstream RNAs. Xenograft tumor-bearing mouse models were built to analyze tumor growth in vivo. The results suggested that NKX2-1-AS1 was upregulated in NSCLC patient tissues and cell lines. NKX2-1-AS1 deficiency suppressed cell proliferation, migration, invasion and EMT while elevated apoptosis. NKX2-1-AS1 bound to miR-589-5p, and NME/NM23 nucleoside diphosphate kinase 1 (NME1) was targeted by miR-589-5p in NSCLC cells. Additionally, NKX2-1-AS1 accelerated the progression of NSCLC by regulating miR-589-5p/NME1 axis. NKX2-1-AS1 knockdown repressed tumor growth in vivo. In conclusion, NKX2-1-AS1 accelerated the NSCLC progression through interacting with miR-589-5p for NME1 upregulation, which may provide clues for NSCLC targeting therapy.

The purpose of this study was to explore the value of resting-state magnetic resonance imaging (MRI) based on the brain extraction tool (BET) algorithm in evaluating the cranial nerve function of patients with delirium in intensive care unit (ICU). A total of 100 patients with delirium in hospital were studied, and 20 healthy volunteers were used as control. All the subjects were examined by MRI, and the images were analyzed by the BET algorithm, and the convolution neural network (CNN) algorithm was introduced for comparison. The application effects of the two algorithms were analyzed, and the differences of brain nerve function between delirium patients and normal people were explored. The results showed that the root mean square error, high frequency error norm, and structural similarity of the BET algorithm were 70.4%, 71.5%, and 0.92, respectively, which were significantly higher than those of the CNN algorithm (P < 0.05). Compared with normal people, the ReHo values of pontine, hippocampus (right), cerebellum (left), midbrain, and basal ganglia in delirium patients were significantly higher. ReHo values of frontal gyrus, middle frontal gyrus, left inferior frontal gyrus, parietal lobe, and temporal lobe and anisotropy scores (FA) of cerebellums (left), frontal lobe, temporal lobe (left), corpus callosum, and hippocampus (left) decreased significantly. The average diffusivity (MD) of medial frontal lobe, superior temporal gyrus (right), the first half of cingulate gyrus, bilateral insula, and caudate nucleus (left) increased significantly (P < 0.05). MRI based on the deep learning algorithm can effectively improve the image quality, which is valuable in evaluating the brain nerve function of delirium patients. Abnormal brain structure damage and abnormal function can be used to help diagnose delirium.

目的 探讨涤痰通腑、益气活血方灌肠辅助治疗慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)合并呼吸衰竭的临床效果.方法 回顾性选取2020年7月至2022年7月丽水市第二人医院收治的COPD合并呼吸衰竭患者103例为研究对象,根据治疗方法不同将其分为参照组(n=51)和灌肠组(n=52).两组患者均接受无创正压通气治疗,灌肠组患者辅以涤痰通腑、益气活血方灌肠治疗,比较两组患者的临床症状评分、动脉血气指标、肺功能、炎症因子及并发症发生情况.结果 治疗后,灌肠组患者的临床症状评分、动脉血二氧化碳分压、第1秒用力呼气容积(forced expiratory volume in one second,FEV1)、用力肺活量(forced vital capacity,FVC)、FEV1/FVC、C 反应蛋白、降钙素原均显著低于参照组,动脉血氧分压显著高于参照组(P＜0.05);灌肠组患者的并发症总发生率、气管插管率均低于参照组,机械通气时间短于参照组,撤机成功率高于参照组(P＜0.05);两组患者的病死率比较差异无统计学意义(P＞0.05).结论 涤痰通腑、益气活血方灌肠辅助治疗COPD合并呼吸衰竭可改善患者的临床症状、动脉血气指标与肺功能,下调炎症因子,提升呼吸机治疗效果并减少相关并发症的发生.

Objective:To investigate the clinical effects of moxifloxacin combined with biapenem on controlling inflammatory responses and improving immune function in older adult patients with severe pneumonia.Methods:120 older adult patients with severe pneumonia, who received treatment in the Second People's Hospital of Lishui from February 2017 to March 2020, were included in this study. They were randomly assigned to receive either biapenem (control group, n = 55) or moxifloxacin combined with biapenem (observation group, n = 65) for 7 days. Inflammatory response control, immune function improvement, and adverse reactions were assessed in each group after treatment. Results:After treatment, levels of interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP) and procalcitonin (PCT) in the observation group were (24.51 ± 4.24) ng/L, (12.51 ± 3.15) mg/L and (4.62 ± 1.05) μg/L, respectively, which were significantly lower than those in the control group [(48.74 ± 4.67) ng/L, (26.80 ± 4.24) mg/L, (8.92 ± 1.10) μg/L, t = 29.77, 21.14, 21.87, all P < 0.001). The proportion of CD 3+ and CD 4+ cells and CD 4+ / CD 8+ ratio in the observation group were (63.27 ± 3.72)%, (39.97 ± 2.18)%, 1.79 ± 0.16, respectively, which were significantly higher than those in the control group [(55.58 ± 2.28)%, (35.18 ± 2.62)%, 1.41 ± 0.15, t = 17.08, 10.93, 13.34, all P < 0.001). Total effective rate was significantly higher in the observation group than in the control group [96.92% (63/65) vs. 83.64% (46/55), χ2 = 6.32, P < 0.05]. There was no significant difference in the incidence of adverse reactions between observation and control groups [10.77% (7/65) vs. 9.09% (5/55), χ2 = 0.09, P > 0.05]. Conclusion:Moxifloxacin combined with biapenem based on routine treatment for severe pneumonia in older adult patients can greatly strengthen anti-inflammatory effects, improve immune function, and enhance clinical efficacy without increasing adverse drug reactions.

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases without effective pharmacological intervention. Liensinine (LIEN), a plant-derived isoquinoline alkaloid, exerts key roles in regulating various cellular processes. However, its potential on NAFLD progression has not been reported. In the study, we attempted to explore the regulatory effects of LIEN on fatty liver, and the underlying molecular mechanisms. Our in vitro experiments showed that LIEN treatments significantly reduced the lipid deposition in palmitate acid (PA)-treated cells by improving AMP-activated protein kinase (AMPK) activation. Additionally, excessive reactive oxygen species (ROS) generation was also strongly down-regulated by LIEN in cells upon PA stimulation through enhancing nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation. Moreover, PA-triggered inflammatory response was markedly restrained by LIEN via the blockage of TGF-β-activating kinase 1/nuclear factor-κB (TAK1/NF-κB) signaling. Intriguingly, we further found that LIEN-prohibited ROS production, lipid disorder and inflammation were largely dependent on AMPK activation through repressing TAK1. Consistently, our in vivo experiments confirmed that LIEN treatments efficiently improved the metabolic disorder, insulin resistance, dyslipidemia in high fat diet (HFD)-fed mice. Furthermore, HFD-triggered oxidative stress and inflammation in liver were greatly meliorated by LIEN administration by mediating Nrf2 and TAK1 signaling pathways, respectively. Collectively, all these findings demonstrated that LIEN exerted anti-dyslipidemia, anti-oxidant and anti-inflammatory effects to alleviate NAFLD progression mainly through modulating TAK1/AMPK signaling, and thus could be considered as a promising therapeutic strategy.

Alzheimer’s disease (AD) is the most common age-related progressive neurodegenerative disease, characterized by a decline in cognitive function and neuronal loss, and is caused by several factors. Numerous clinical and experimental studies have suggested the involvement of gut microbiota dysbiosis in patients with AD. The altered gut microbiota can influence brain function and behavior through the microbiota–gut–brain axis via various pathways such as increased amyloid-β deposits and tau phosphorylation, neuroinflammation, metabolic dysfunctions, and chronic oxidative stress. With no current effective therapy to cure AD, gut microbiota modulation may be a promising therapeutic option to prevent or delay the onset of AD or counteract its progression. Our present review summarizes the alterations in the gut microbiota in patients with AD, the pathogenetic roles and mechanisms of gut microbiota in AD, and gut microbiota–targeted therapies for AD. Understanding the roles and mechanisms between gut microbiota and AD will help decipher the pathogenesis of AD from novel perspectives and shed light on novel therapeutic strategies for AD.

目的:观察米桑胶囊对ICU老年患者肠道菌群、营养指标及临床预后的影响。方法:前瞻性选取2017年9月至2019年9月丽水市第二人民医院收治的入住ICU的老年患者，采用随机数字表法分为对照组和观察组各60例，对照组予肠内营养混悬液治疗，观察组在对照组基础上加用米桑胶囊。5 d为一疗程。采集粪便样本分析肠道菌群，胃肠道症状分级评分量表(GSRS)评价胃肠道症状，比较两组营养状况[血清白蛋白(Alb)、血红蛋白(Hb)、上臂三头肌肌围(MAMC)]、治疗情况(脱机时间、ICU住院时间)，记录并发症和死亡率。结果:治疗后，对照组各菌群数量无显著改变( P>0.05)；观察组葡萄球菌、肠杆菌数量显著降低，乳杆菌、双歧杆菌显著增加，GSRS评分和Alb、Hb、MAMC降低( P<0.05)；治疗后，组间相比，观察组肠杆菌、乳杆菌、双歧杆菌数量，GSRS评分和Alb、Hb、MAMC均优于对照组( P<0.05)。观察组呼吸机撤机及ICU住院时间分别为(2.6±0.3)d和(6.6±0.8)d，均少于对照组的(3.0±0.3)d和(7.6±1.3)d( P<0.05)；并发症发生率为20.0%，明显低于对照组的53.3%( P<0.05)；两组死亡率相近( P>0.05)。 结论:米桑胶囊可调节ICU老年患者肠道菌群失衡，改善营养指标和临床预后。

This article has been retracted by the authors.

Increasing evidence suggests that gut dysbiosis plays vital roles in a variety of gut–brain disorders, such as Alzheimer's disease (AD). However, alterations of the gut microbiota as well as their correlations with cognitive scores and host immunity have remained unclear in well-controlled trials on Chinese AD patients. In this study, samples from 100 AD patients, and 71 age- and gender-matched, cognitively normal controls were obtained to explore the structural and functional alterations of the fecal microbiota targeting the V3–V4 region of the 16S rRNA gene by MiSeq sequencing, and to analyze their associations with clinical characteristics. Our data demonstrated a remarkably reduction in the bacterial diversity and alterations in the taxonomic composition of the fecal microbiota of the AD patients. Interestingly, the abundant butyrate-producing genera such as Faecalibacterium decreased significantly, where this was positively correlated with such clinical indicators as the MMSE, WAIS, and Barthel scores in the AD patients. On the contrary, abundant lactate-producing genera, such as Bifidobacterium , increased prominently, and were inversely correlated with these indicators. This shift in the gut dysbiosis of the microbiota, from being butyrate producers to lactate producers, contributed to immune disturbances in the host that could be used as non-invasive biomarkers to distinguish the controls from the AD patients. Moreover, several predicted functional modules, including the biosynthesis and the metabolism of fatty acids, that were altered in the microbiota of the AD patients could be utilized by the bacteria to produce immunomodulatory metabolites. Our study established the structural and functional dysbiosis of fecal microbiota in AD patients, and the results suggest the potential for use of gut bacteria for the early, non-invasive diagnosis of AD, personalized treatment, and the development of tailor-made probiotics designed for Chinese AD patients.

Purpose: To investigate the neuroprotective effect of the natural flavonoid rhoifolin in rats with streptozotocin (STZ)-induced (AD). Methods: Morris water-maze and novel object recognition tests were carried out to estimate the effect of rhoifolin on memory and cognition. Histopathological analysis was made to observe thickness of hippocampal CA1 pyramidal layer. Analysis of oxidative stress markers was performed to estimate the effect of rhoifolin on oxidative stress in the hippocampus and frontal cortex. Results: Morris water maze and novel object recognition tests showed a significant improvement in the memory, cognition and spatial learning in rhoifolin treated AD animals (p < 0.05). Moreover, rhoifolin treatment resulted in a significant increase in the CA1 pyramidal layer of AD animals indicating its neuroprotective properties (p < 0.05). The increase in the hippocampal CA1 area further validated the reversal of cognitive dysfunctions caused by STZ treatment. Furthermore, analysis of oxidative stress markers SOD, CAT, GPX, GRX, and MDA showed a significant improvement in the oxidative stress in the hippocampus and frontal cortex (p < 0.05). Conclusion: The present study is the first report to demonstrate the effect of plant flavonoid, rhoifolin on STZ-induced AD in rat model. Rhoifolin improves spatial learning, cognition, and memory in STZ-treated rat model. Therefore, rhoifolin may be a promising therapeutic agent for the management of AD.

Gut bacterial dysbiosis plays a vital role in the development of Alzheimer’s disease (AD). However, our understanding of alterations to the gut fungal microbiota and their correlations with host immunity in AD is still limited. Samples were obtained from 88 Chinese patients with AD, and 65 age- and gender-matched, cognitively normal controls. Using these samples, we investigated the fungal microbiota targeting internal transcribed spacer 2 (ITS2) rRNA genes using MiSeq sequencing, and analyzed their associations with the host immune response. Our data demonstrated unaltered fungal diversity but altered taxonomic composition of the fecal fungal microbiota in the AD patients. The analysis of the fungal microbiota was performed using 6,585,557 high-quality reads (2,932,482 reads from the controls and 3,653,075 from the AD patients), with an average of 43,042 reads per sample. We found that several key differential fungi such as Candida tropicalis and Schizophyllum commune were enriched in the AD patients, while Rhodotorula mucilaginosa decreased significantly. Interestingly, C. tropicalis and S. commune were positively correlated with IP-10 and TNF-α levels. In contrast, C. tropicalis was negatively correlated with IL-8 and IFN-γ levels, and R. mucilaginosa was negatively correlated with TNF-α level. PiCRUSt analysis revealed that lipoic acid metabolism, starch and sucrose metabolism were significantly decreased in the AD fungal microbiota. This study is the first to demonstrate fecal fungal dysbiosis in stable AD patients at a deeper level, and to identify the key differential fungi involved in regulating host systemic immunity. The analysis of the fungal microbiota in AD performed here may provide novel insights into the etiopathogenesis of AD and pave the way for improved diagnosis and treatment of AD.

目的:观察冠心宁片治疗冠心病合并抑郁症的效果.方法:将冠心病合并抑郁症患者100例随机分为对照组和观察组,每组50例;对照组给予冠心痛常规治疗方案进行治疗,观察组在对照组的基础上加用冠心宁片治疗,观察比较2组治疗前后血清C-反应蛋白(CRP)、同型半胱氨酸(HCY)水平,汉密尔顿抑郁量表(HAMD)评分、抑郁自评量表(SDS)评分、西雅图心绞痛量表(SAQ)评分,评价2组心电图临床疗效、抑郁症临床疗效及不良反应情况.结果:治疗后,2组抑郁症临床疗效、心电图临床疗效比较,经秩和检验,差异均有统计学意义(P＜0.05),观察组疗效优于对照组.治疗后,2组患者HAMD、SDS评分均较治疗前降低(P＜0.05),SAQ评分较治疗前升高(P＜0.05);且观察组上述各项评分改善均优于对照组(P＜0.05).治疗后,2组血清CRP、HCY水平均较治疗前降低(P＜0.05);且观察组CRP、HCY水平均低于对照组(P＜0.05).治疗过程中,2组肝功能损伤、肾功能损伤、恶心、呕吐、皮疹、发热等不良反应率比较,差异均无统计学意义(P＞0.05).结论:冠心宁片治疗冠心痛合并抑郁症,可有效改善患者心脏及抑郁症状,提高临床疗效,且安全性良好.

Objective:To investigate the effects of ulinastatin combined with meropenem on immune function, interleukin 2(IL-2), interleukin 4(IL-4), interleukin-6(IL-6), interleukin 10(IL-10) and tumor necrosis factor (TNF-) levels in elderly patients with severe infection.Methods:From January 2016 to June 2018, 60 elderly patients with severe infections admitted to the Second People's Hospital of Lishui were randomly divided into control group(30 cases) and observation group(30 cases). The patients in the control group were treated with meropenem, while the patients in the observation group were treated with ulinastatin on the basis of the control group.Both two groups were treated for 14 days.The therapeutic effects, changes of T lymphocyte subsets, IL-2, IL-4, IL-6, IL-10 and TNF-levels, recovery time of gastrointestinal function and occurrence of systemic inflammatory response syndrome(SIRS) before and after treatment were compared between the two groups.Results:The total effective rate of the observation group(93.33%) was higher than that of the control group(66.67%)(χ 2=6.667, P<0.05). After treatment, CD 3+ [(64.38±3.19)%], CD 4+ [(40.39±2.35)%]and CD 4+/CD 8+ (1.65±0.19) in the observation group were higher than those in the control group[(58.94±3.56)%, (35.47±2.87)% and (1.34±0.14)]( t=6.233, 7.265, 3.834, all P<0.05). The serum levels of IL-2[(126.87±17.49)ng/L], IL-4[(8.98±2.14)g/L], IL-6[(176.89±23.1)ng/L], IL-10[(37.94±12.56)ng/L] and TNF-α[(163.45±17.96)ng/L]in the observation group were lower than those in the control group[(343.27±28.56)ng/L, (19.65±4.56) g/L, (346.37±38.98)ng/L, (83.21±18.56)ng/L and (254.37±23.45)ng/L]( t=35.392, 10.602, 20.476, 11.064, 16.860, all P<0.05). The recovery time of gastrointestinal function in the observation group[(5.31±1.29)d] was shorter than that in the control group[(6.97±1.43)d]( t=4.721, P<0.05), while the incidence of SIRS(13.33%) was lower than that in the control group(43.33%)(χ 2=6.648, P<0.05). Conclusion:Ulinastatin combined with meropenem is effective in the treatment of elderly patients with severe infection.It can improve the immune function of the patients, reduce the levels of IL-2, IL-4, IL-6, IL-10 and TNF-, and alleviate the inflammatory reaction.It is worthy of clinical reference.

目的 探讨基于云端锻炼控制系统(EXBC)的可穿戴设备计步器对稳定期慢性阻塞性肺疾病(COPD)患者生活质量的影响.方法 选取2019年1～12月在丽水市第二人民医院呼吸科就诊的110例稳定期COPD患者,随机分成对照组(50例)与研究组(60例),对照组予以常规肺功能康复训练,研究组在常规肺功能康复治疗的基础上增加计步器监督步行,干预9个月后观察两组患者肺功能指标、6 min步行距离(6MWT)、生活质量变化,并记录两组锻炼依从性、急性发作的次数.结果 干预后两组FVC、FEV1占预计值、MMEF、PEF均较干预前增高(P<0.05),且干预后研究组上述指标均明显高于对照组,差异有统计学意义(P<0.05);两组6MWT均增高,CAT评分均降低,差异有统计学意义(P<0.05),且研究组6MWT、CAT评分改变幅度大于对照组(P<0.05),研究组观察期间急性发作次数较对照组明显减少(P<0.05);干预期间研究组锻炼依从性为100.00％,明显高于对照组(90.00％),差异有统计学意义(P<0.05).结论 基于EXBC的计步器可显著改善稳定期COPD患者的肺功能和生活质量,提高其体力活动能力和锻炼依从性,值得临床推广应用.

目的 探究云端锻炼控制系统对稳定期COPD患者锻炼依从性与生活质量的影响.方法 采用前瞻性研究方法,选择丽水市第二人民医院2017年6月～2019年5月收治的COPD患者160例为研究对象,采用随机数字表法进行随机分组,对照组与研究组各80例.患者病情进入稳定期后,对照组开展常规锻炼;研究组在对照组基础上增加云端锻炼控制系统监督步行,对两组患者进行随访3个月,比较两组患者肺功能(FEV1、PEF、FVC)、生活质量(CAT)、步行情况(6MWD)、锻炼依从性、急性发作次数及呼吸困难程度(mMRC).结果 两组患者出院时FEV1、PEF、FVC评分比较,差异无统计学意义(P>0.05),3个月后研究组各指标水平明显高于对照组,差异有统计学意义(P<0.05);两组患者出院时CAT、6MWD、mMRC数据比较,差异无统计学意义(P>0.05),3个月后研究组CAT、mMRC评分明显低于对照组,6MWD数据明显高于对照组,差异有统计学意义(P<0.05);研究组3个月后锻炼依从性97.50％明显高于对照组的78.75％(P<0.05);研究组患者3个月内COPD急性发作次数明显低于对照组(P<0.05).结论 云端锻炼控制系统能够提升稳定期COPD患者运动锻炼依从性,改善其肺功能,降低呼吸困难程度,提升生活质量,值得应用与推广.

目的 观察布地奈德联合博利康尼治疗慢性阻塞性肺疾病急性加重期的临床疗效.方法 选择2017年12月～2018年12月我院住院治疗的慢性阻塞性肺疾病患者80例,随机分为观察组和对照组,各40例,对照组予布地奈德雾化液1 mg+生理盐水3 mL,每天2次雾化吸入;观察组在对照组基础上加用博利康尼雾化液1 mg联合布地奈德雾化液1 mg+生理盐水3 mL雾化吸入,每天2次,6d为一个疗程.治疗后对比分析两组的临床疗效及肺功能各项指标的变化情况.结果 观察组患者治疗后的总有效率达97.2％,显著高于对照组的75.0％,两组比较差异具有显著性(P＜0.05).观察组患者治疗后的FEV1、PEF及FEV1/FVC分别为(1.93±0.27)L,(3.81+1.16)L/s、(90.43±12.65),均较治疗前明显提高,且观察组患者治疗后的FEV1、PEF及FEV1/FVC水平分别显著高于对照组,两组比较差异具有显著性(P＜0.05).结论 布地奈德联合博利康尼治疗慢性阻塞性肺疾病急性加重期疗效确切,能明显改善患者的肺功能,从而缓解患者的临床症状,提高生活质量,改善预后.