Background:During the staged progression of chronic obstructive pulmonary disease (COPD), mitophagy homeostasis is disrupted and exhibits a typical dual role. Mitophagy is tightly regulated by ion channel-controlled mitochondrial membrane potential (ΔΨm) and may associate with mitochondrial permeability transition pore (mPTP) dynamics. However, this regulatory mechanism remains largely unknown, and the stage-specific requirements of mitophagy in COPD progression have yet to be established. Methods:This study proposed a novel theoretical framework from prior literature. Using public databases, we linked mPTP-related genes to COPD state transitions via differential analysis and Mendelian randomization (MR). Key biomarkers were validated through gene enrichment, functional annotation, immune infiltration, and single-cell RNA sequencing (scRNA-seq) to assess biological significance. Finally, molecular docking confirmed their potential roles. Results:We preliminarily aligned the "mitochondria-cell survival architecture" hypothesis with COPD progression. Compared with stable COPD (STCOPD), acute exacerbation of COPD (AECOPD) showed massive type II alveolar epithelial (AT2) cell death, hyperinflammation, increased energy demand, and impaired intercellular communication, consistent with activated ubiquitin-proteasome system (UPS), mitochondrial gene expression, macroautophagy initiation, and vesicle trafficking. Six biomarkers (including SPG7) were associated with AECOPD (AUC=0.705, 95% CI 0.554-0.705). SPG7 was positively correlated with AECOPD (OR=1.126, 95% CI 1.008-1.257), while the other five showed negative correlations. These markers were enriched in ion channel and G protein-coupled receptors (GPCRs) pathways. SPG7 expression paralleled energy demand and strongly interacted with AFG3L2 and PPIF, implicating it in mPTP regulation. Conclusion:This study preliminarily supports the mitochondria-cell survival hypothesis. Bioinformatic analysis suggests that mPTP-triggered mitochondrial flickering maintains mitochondrial quality control. Furthermore, transient mPTP opening via SPG7-mediated CypD activation may constitute an independent protective pathway, potentially involving unique SPG7-CypD modifications. However, non-significant colocalization limits study robustness, necessitating rigorous experimental validation of these predictions.

The aim is to empirically explore the relationship between the occurrence of affective distress and the fear transformation in cancer patients, and to analyze the theoretical implications of their development from multiple perspectives. Relevant studies on the transformation of affective distress into fear in cancer patients were retrieved from databases including CNKI (China National Knowledge Infrastructure), Wan Fang Data, SinoMed (China Biomedical Literature Database), PubMed, Embase, and others, up to July 12, 2025. Meta-analysis of the included studies was performed using R 4.4.1. ①A total of 27 studies were included in this research, covering 9 types of cancer and involving 14,011 participants. These included 24 cross-sectional studies, 2 cohort studies, and 1 case-control study. ②The meta-analysis revealed a significant association between the occurrence of fear and depressive emotions in cancer patients [1.63, 95

OBJECTIVE:To characterize sex- and age-specific changes in the comprehensive burden of major chronic respiratory diseases (CRDs) and their attributable risk factors among adults aged ≥55 years globally, regionally, and nationally from 1990 to 2021 using the Global Burden of Disease (GBD) 2021 database. METHODS:Utilizing the GBD 2021 database, we performed in-depth analyses and preliminary projections of global, regional, and national burden trends for chronic obstructive pulmonary disease (COPD), asthma, and interstitial lung disease & pulmonary sarcoidosis (ILD&PS) through multi-model approaches including but not limited to Age-Period-Cohort (APC) models, Joinpoint regression, and Bayesian Age-Period-Cohort (BAPC) modeling. RESULTS:The overall global CRD burden among adults ≥55 years declined from 1990 to 2021. However, the Corona Virus Disease 2019 (COVID-19) pandemic differentially altered asthma and COPD prevalence and incidence trends globally: low Socio-demographic Index (SDI) regions experienced an accelerated increase in prevalence, while high SDI regions showed a steeper rise in incidence. High mortality and disability-adjusted life years (DALYs) rates remained concentrated in low-middle SDI regions, notably Asia and North America. Consequently, prevalent CRD cases in this age group reached 223 million (95% UI 206.5-241.5) in 2021-accounting for half of all-age cases-with 18.47 million incident cases (95% UI 16.97-20.11), causing 4.15 million deaths (95% UI 3.76-4.58) and 83.67 million DALYs (95% UI 77.49-90.36). Air pollution, smoking, obesity, and chronic cold exposure persistently influenced COPD and asthma prevalence across regions and sexes. CONCLUSION:The pandemic shifted global CRD burden trends, particularly for asthma followed by COPD. Concurrent with global aging, burden trajectories across SDI levels raise concerns. As COVID-19 becomes endemic, older adults will experience impacts from recurrent viral infections, increasingly manifesting in coming years.

Asthma is a chronic airway disease characterized by Airway Remodeling (AR) and persistent inflammation, with Epithelial-Mesenchymal Transition (EMT) playing a crucial role in fibrosis and smooth muscle proliferation. The Transforming Growth Factor-Beta1 (TGFβ1)/Smad pathway is a key driver of EMT in asthma. Current treatments do not effectively prevent AR progression. Traditional Chinese Medicine, particularly the Xuanfei Pingchuan (XFPC) prescription, has shown potential in managing asthma, but its role in EMT regulation remains unclear. This study explored the role of "phlegm and stasis" in airway remodeling (AR) in asthma from the perspective of EMT and investigated the effects and underlying mechanisms of XFPC prescription on EMT in AR. In vitro, human bronchial epithelial (16HBE) cells were induced into EMT with TGFβ1 and treated with XFPC drug-containing serum, with EMT marker expression analyzed via RT-qPCR and Western blot. In vivo, an ovalbumin (OVA)-induced asthma model in Sprague Dawley rats was used to evaluate the effects of different XFPC doses through histopathology, immunofluorescence, and molecular analyses. Additionally, Smurf2 cDNA transfection was conducted to assess the role of Smurf2 in EMT regulation. The results confirmed that XFPC prescription suppressed the pathway of transforming-growth factor-beta1 (TGFβ1)-Smad by reducing Smad ubiquitination regulator 2 (Smurf2), Smad2, Smad3, TGFβ1 receptor (TβRI), N-cadherin, α-SMA, and Vimentin in terms of expressions at messenger ribonucleic acid (mRNA) and protein levels. However, XFPC prescription up-regulated expressions of SnoN and E-cadherin at protein and mRNA levels to inhibit EMT. The result also confirmed that XFPC prescription decreased the ubiquitination of Smad7. XFPC prescription could suppress AR in TGFβ1 induced 16HBE cells and OVA-sensitized animal models through TGFβ1/Smad pathway.

Background Qinggan Huoxue recipe (QGHXR), a traditional Chinese medicinal formula, has a protective effect against liver fibrosis. However, the underlying mechanisms remain unclear. Objective This study investigated the antifibrotic role of QGHXR and its underlying mechanisms. Methods The composition of QGHXR was determined using ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Female C57BL/6J mice were fed either a Lieber–DeCarli liquid diet or pair-fed control diet and intraperitoneally injected with CCl4 for 8 weeks (n = 8). In week 5, the mice were administered 100, 200, and 400 mg/kg QGHXR via oral gavage daily for 4 weeks. Results UPLC-MS result showed that QGHXR contained 45 compounds including salvianolic acid A, scutellarin, baicalin, rutin, and chai saponin D. QGHXR alleviated pathological alterations in the liver. The alanine aminotransferase (ALT) level was reduced to 44.88 ± 4.39 U/L, aspartate aminotransferase (AST) to 76.25 ± 4.17 U/L, alkaline phosphatase (ALP) to 60.75 ± 5.41 U/L, and acetaldehyde to 38.54 ± 1.01 U/L compared with that of the control group (ALT 72.38 ± 5.19 U/L, AST 119.63 ± 9.82 U/L, and ALP 98.63 ± 6.71 U/L and acetaldehyde 64.86 ± 4.70 U/L). QGHXR inhibited lipid overproduction and fibrotic gene expression. The serum concentration of chemokine C-X-C ligand 16 (CXCL16) was reduced to 62.83 ± 6.80 pg/ml compared with that of the control group (130.91 ± 13.72 pg/mL). QGHXR downregulated CXCL16 mRNA and protein expressions. Pharmacological CXCL16 treatment reversed the QGHXR-induced protective effects in ethanol plus CCl4 fed mice. QGHXR reduced CXCL16 levels (91.97 ± 5.86 pg/ml) in LPS-stimulated RAW264.7 cells compared with that of the control group (148.68 ± 8.62 pg/ml) and inhibited toll-like receptor 4 and nuclear factor-kappa B phosphorylation. Conclusions This study demonstrated that QGHXR mitigates experimental alcoholic liver fibrosis by CXCL16 inhibition, and may be considered a potential therapeutic agent for treating liver fibrosis.

KeChuanLiuWei‐Mixture (KCLW) is widely used as a Chinese medicine prescription to treat severe asthma. However, the underlying therapeutic mechanism of KCLW remains unclear. In this study, a network pharmacology method was used to identify the chemical constituents of KCLW by the TCMSP database and ultra‐performance liquid chromatography coupled with time‐of‐flight mass spectrometry. Differential expression identification, protein–protein interaction (PPI) network and functional enrichment analysis were used to screen key targets of KCLW for severe asthma. Our results confirmed that quercetin, luteolin, kaempferol, and wogonin are the most critical active ingredients in KCLW. Moreover, the 16 relevant severe asthma‐related targets of KCLW were obtained by overlapping the PPI networks of the KCLW putative targets and severe asthma‐related genes, among which the most important targets were IL‐6, NOS2, VEGFA, CXCL2, and PLAT. Functionally, the 16‐targets and their interacting differentially expressed genes were primarily related to biological functions and pathways related to immunity and inflammation, such as inflammatory response, T cell differentiation, Nrf2/HO‐1 signaling pathway, TGF‐β/Smad signaling pathway, and NF‐κB signaling pathway. KCLW inhibited inflammation in PDGF‐BB‐induced airway smooth muscle cells. In summary, this study demonstrates the active substance and potential therapeutic mechanism of KCLW in severe asthma, and offers a clinical direction for KCLW against severe asthma.

目的 采用网络药理学和分子对接技术探讨温阳抗寒汤治疗支气管哮喘的潜在作用机制.方法 基于中药系统药理学数据库与分析平台TCMSP获取温阳抗寒汤有效活性成分及其靶点,通过GeneCards、OMIM、PharmGKB、TTD、DrugBank数据库获取哮喘相关靶点,将药物靶点与疾病靶点映射得到温阳抗寒汤治疗支气管哮喘的预测靶点.使用Cytoscape软件绘制药物活性成分-靶点网络图,使用String数据库构建蛋白互作网络,使用R语言进行GO富集分析和KEGG通路富集分析,预测温阳抗寒汤治疗支气管哮喘的作用机制,使用AutoDockTools、Autodock vina、Pymol软件进行分子对接预测和部分对接结果可视化.结果 筛选得到温阳抗寒汤作用于支气管哮喘的有效活性成分115个,检索得到支气管哮喘相关的靶点4802个,温阳抗寒汤与支气管哮喘的交集靶点86个,关键有效成分包括槲皮素、山奈酚、木犀草素、汉黄芩素、黄芩苷、柚皮素等,涉及的核心靶点包括HIF1A、TP53、AKT1、ESR1等.通过GO分析(P<0.05)得到GO条目1866个,其中包括生物过程(BP)条目1672个,细胞组成(CC)43个,分子功能(MF)条目151个,涉及细胞外刺激的反应、对异型生物质刺激等.KEGG通路富集(P<0.05)得到通路149条,其中P53信号通路、IL-17信号通路、PI3K-Akt信号通路、TNF信号通路可能为治疗支气管哮喘的潜在信号通路.将涉及的核心靶点与中药活性成分进行分子对接,结果显示温阳抗寒汤的有效活性成分与选定的支气管哮喘的靶点均有较好的结合活性.结论 温阳抗寒汤主要通过HIF1A、TP53、AKT1、ESR1等靶点作用于P53信号通路、IL-17信号通路、PI3K-Akt信号通路、TNF信号通路等通过减轻气道炎症反应、抑制气道重塑等发挥治疗作用.

应用四君子汤合甘草泻心汤与针灸综合治疗顽固性恼人耳鸣反复发作1例.患者病程较长,既往中医辨证为脾肾两虚,采用内服中药与针灸治疗均未有明显改善.根据患者主症、次症和舌脉综合辨证为脾虚湿盛,寒热错杂证,治以健脾渗湿,寒热平调,方用四君子汤合甘草泻心汤加减,辅公孙、内关、足三里、丰隆、中脘、关元以健脾和胃,理气化痰,温补下元.患者耳鸣主症和脾胃兼证均改善后,治以益气和胃,健脾渗湿,开窍明耳,方用香砂六君子汤加减,辅太渊、太白、足三里、阴陵泉、关元针灸综合治疗以益气健脾,和胃渗湿,培元固本.患者耳鸣症状改善明显,自主选择终止治疗.

目的:探讨中医治未病理念对"血浊病"易发人群的临床干预效果.方法:选取2020年5月—2021年6月上海中医药大学附属龙华医院中医预防保健科调治的"血浊病"易发人群70例,随机分为观察组和对照组,各35例.对照组给予生活方式科普宣教,观察组在科普宣教基础上,给予中药调理方及耳穴贴压进行干预.比较干预前后两组病例的血脂、中医体质类型、体重指数、血糖、尿酸等指标.结果:对照组和观察组在血脂水平、血糖、尿酸等方面无明显变化,但观察组在中医体质类型的症候积分方面发生了明显改变,身体沉重、痰多、口中黏腻、大便黏滞不爽等症状得以改善,并显著优于对照组(P<0.05).结论:基于中医治未病理念对于"血浊病"易发人群的临床干预存在一定价值,值得在临床上推广和进一步探索.

目的 研究"邵氏保肺功"配合耳穴贴压对肺癌术后老年患者生活质量的影响.方法 选取符合纳入标准的肺癌术后老年患者96例,采用分层区组设计,将患者按自主意愿分入治疗组与对照组,剔除脱落病例后每组42例.治疗组采取"邵氏保肺功"功法锻炼共12周,对照组不进行功法锻炼.分别于入组时、干预12周后以及入组1年后对患者进行肺癌患者生活质量量表(FACT-L)、中医证候积分评估.结果 两组生活质量量表评分比较P<0.05,差异有统计学意义,治疗组在生活质量方面的改善优于对照组.两组中医证候评分比较P<0.05,差异有统计学意义,治疗组在中医证候评分的改善优于对照组.结论 邵氏保肺功可明显提高肺癌术后患者的生活质量,具有长期疗效,临床使用副作用少,治疗成本低,易于推广应用.

目的 探究麻黄加术汤在治疗间擦糜烂型足癣病中的作用.方法 1例患者经辨证论治结合相关文献论述,以麻黄加术汤加减,嘱其外用浸泡足趾,每天2次,疗程3周左右.结果 患者左足第4、5足趾间糜烂皮损均痊愈,趾间可见少许白色浸渍面,足底可见黄色浆痂,符合足癣疗效评定标准.结论 麻黄加术汤外用治疗寒湿蕴表型足癣病疗效显著,值得开展进一步临床研究.

曾学文老师认为,阴阳失调、气血运行失常、津液代谢紊乱导致心脏疾病,即整体失衡而发病.按照气血水厥的规律演变,心脏疾病后期病变波及多脏器,曾老师认为,心以气为根本,血为标象,阴为本体,阳为外用,神为安本,水为变证,厥为险证,邪为害物,依据气血水厥理论提出益气养心、活血通脉、滋阴温阳、安定心神、利水消肿、救厥固脱的治法,同时根据气血水厥的演变将心脏疾病辨证为心气虚证、心血瘀证、心水肿证、心厥脱证,分别给予益心气汤、活心血汤、利心水汤、救心厥汤治疗.

Background Dyslipidemia is a common comorbidity in elderly patients with postmenopausal osteoporosis (PMOP). Drynaria fortunei (Rhizoma drynariae) is well-known in traditional Chinese medicine for its ability to improve bone mineral density (BMD). However, whether and how Drynaria fortunei improves plasma lipid profiles in elderly PMOP patients remains unclear. Methods Eighty elderly female patients with concurrent PMOP and hyperlipemia were randomly assigned to Drynaria fortunei 2(n = 40) or control (n = 40) groups. The clinical efficacies of Drynaria fortunei were evaluated. At 0, 3-, 6-, 9-, and 12-month of follow-up, plasma levels of IL-1 beta, IL-18, TNF-alpha, IL-6, IL-8, and IL-10 were measured using ELISA, whereas PBMC levels of NLRP3, ASC, caspase-1, NF-kappa B, SIRT1, and Notch1 were measured using RT-qPCR. PBMC isolated from PMOP patients were cultured and treated with Drynaria fortunei to determine its influence on NLRP3 inflammasome and associated cytokines. Results Drynaria fortunei effectively improved patients' BMD and lipid profiles. IL-1 beta, IL-18, TNF-alpha, IL-6, IL-8 levels, as well as inflammasome-molecules of NLRP3, ASC, caspase-1, and NF-kappa B increased over time in the control group, but were significantly attenuated with Drynaria fortunei administration. In vitro, Drynaria fortunei suppressed NLRP3 inflammasome and associated cytokines by increasing SIRT1 or decreasing Notch1. Drynaria fortunei had inhibitory effects on NLRP3 inflammasome and Notch1 even when SIRT1 expression was suppressed. Conclusions Drynaria fortunei has been demonstrated to significantly improve lipid profiles for elderly PMOP patients. Drynaria fortunei may down-regulate Notch1 independently of SIRT1 to suppress NLRP3 inflammasome-mediated inflammation, thus improving plasma lipid profile.

目的 探讨高丽红参对虚证疲劳患者疲劳状态与免疫功能的影响及安全性分析.方法 选取2017年3月至2018年2月就诊于上海中医药大学附属龙华医院的180例虚证疲劳患者,按照随机数字表法分为A、B及C组,各60例,研究期间共有6名患者因不同原因脱落,揭盲后发现A组脱落4人,C组脱落2人,最后有效病例共174例(A、B、C组分别56、60、58例).所有患者均接受常规治疗(包括免疫抑制剂、安眠药、镇静剂等药物治疗及音乐疗法、运动疗法、心理疏导等非药物治疗),A组患者在常规治疗的基础上口服安慰剂胶囊(4粒/次,2次/d),B组患者在常规治疗的基础上口服红参参粉胶囊(2粒/次,高丽红参净含量为0.9 g,2次/d)和安慰剂胶囊(2粒/次,2次/d),C组患者在常规治疗的基础上口服红参参粉胶囊(4粒/次,高丽红参净含量为1.8 g,2次/d),3组患者用药疗程均为4周,用药后每周定期进行随访.比较3组患者治疗4周后的临床总有效率,各项主症疗效,治疗前与治疗2、3、4周后疲劳症状积分变化,治疗前与治疗4周后不同维度疲劳状态评分变化,治疗前与治疗4周后血清白细胞介素-2(IL-2)、肿瘤坏死因子-α(TNF-α)、可溶性白细胞介素2受体(sIL-2R)水平,以及治疗前和治疗2、3、4周后火(热)症状积分变化.结果 治疗4周后B、C组患者的临床治疗总有效率均显著高于A组(均P<0.05);治疗4周后C组患者精神不振和疲乏无力主症的治疗总有效率均显著高于A组,且C组患者疲乏无力主症的治疗总有效率显著高于B组(均P<0.05);与治疗前比,治疗1、2、3、4周后B、C组患者疲劳自评量表(FSAS)评分均呈显著降低趋势,且治疗2周后C组及治疗3、4周后B、C组患者均显著低于A组(均P<0.05);与治疗前比,治疗4周后3组患者躯体疲劳评分,B、C组患者精神疲劳、疲劳后果、疲劳对睡眠的反应、疲劳的情境性及C组患者疲劳的时间模式评分均显著降低,且治疗4周后B、C组患者躯体疲劳、精神疲劳、疲劳后果、疲劳对睡眠的反应及C组患者疲劳的情境性、疲劳的时间模式评分均显著低于A组,且C组患者疲劳的时间模式评分显著低于B组(均P<0.05);与治疗前比,治疗4周后A组患者血清TNF-α、IL-2水平均显著降低,C组患者血清TNF-α、IL-2水平均显著升高,且治疗4周后C组患者血清TNF-α水平显著高于A、B组,B、C组患者血清IL-2水平均显著高于A组(均P<0.05),但3组患者治疗前与治疗4周后组内及组间血清sIL-2R水平比较,差异均无统计学意义(均P>0.05);用药期间,3组患者火(热)证候积分均呈现下降趋势,但3组患者火(热)症状组间比较,差异均无统计学意义(均P>0.05).结论 中药高丽红参治疗虚证疲劳患者具有较好的治疗效果,有助于机体缓解躯体疲劳状态,同时可提高患者免疫功能,尤其是高剂量高丽红参治疗效果更为显著,且使用高丽红参治疗的安全性良好.

目的:观察化湿祛浊方联合耳穴疗法干预痰湿体质血脂异常易发人群的疗效,为中医治未病预防血脂异常提供依据.方法:选择痰湿体质血脂异常易发人群70例,将其随机分为观察组和对照组,每组各35例.对照组予以健康教育干预,观察组在对照组的基本上加用化湿祛浊方合耳穴干预.观察2组干预前后痰湿体质转化分,血脂指标[总胆固醇(TC)、三酰甘油(TG)],体质量指数(BMI)及腰臀比.结果:观察组干预后痰湿体质转化分较本组干预前明显改善(P＜0.01),且2组干预后痰湿体质转化分比较,差异有统计学意义(P＜0.05);而2组干预前后 TC、TG、BMI、腰臀比组内比较及干预后组间比较,差异均无统计学意义(P＞0.05).结论:化湿祛浊方联合耳穴疗法可以改善血脂异常易发人群的痰湿体质偏颇程度,有效降低血脂异常易发人群罹患高脂血症的风险.

目的:观察血脂异常患者体质类型分布与伴随疾病之间的相关性,为中医药对血脂异常患者辨证施治及疾病预后评估提供临床证据.方法:共收集565例血脂异常患者进行中医体质分析,同时观察其体质类型与血压、血糖、尿酸、体重指数的相关性.结果:565例血脂异常患者的主要体质类型分别是气虚质为191例(33.8％)、阴虚质176(31.2％)、血瘀质65例(11.5％).以中医体质为分组变量,临床数据为检验变量做K-W检验,结果显示中医体质分布在胆固醇、血糖及尿酸水平,有明显统计学差异,并且在胆固醇和血糖水平,中医体质类型以气郁质均数水平最高;在尿酸水平,以平和质均数水平最高.进一步两两比较,做相关性回归分析,发现特禀质与尿酸指标呈负相关.结论:血脂异常患者的体质类型多为偏颇体质,其中以气虚质、阴虚质、血瘀质为主;血脂异常患者中气郁质患者的血糖升高和尿酸升高者居多,血脂异常人群中特禀质和尿酸水平呈负相关.

目的:运用模糊数学方法分析慢性阻塞性肺疾病稳定期痰湿质患者脏腑辨证的分型,进一步探讨其与相关检测指标的相关性.方法:选取COPD稳定期痰湿质患者186例,基于模糊数学中的"择近原则"识别其脏腑证型并确定主要病位后,进一步统计与相关检测指标[呼吸困难指数(mMRC)、肺功能、BMI、吸烟指数、急性发作次数)的相关性.结果:①186例COPD稳定期痰湿质患者中,痰湿阻肺证84例(45.2％),湿困脾胃证64例(34.4％),痰阻心脉证38例(20.4％).②3种证型中呼吸困难指数mMRC严重程度,依次为痰阻心脉证>湿困脾胃证>痰湿阻肺证,差异具统计学意义(P<0.05).肺功能比较显示,FEV1/预计值％痰湿阻肺证>湿困脾胃证>痰阻心脉证,差异具统计学意义(P<0.05),FVC值痰阻心脉证较低,较另两组相差有统计学意义(P<0.05),FEV1/FVC％3组相差无统计学意义.BMI湿困脾胃证>痰湿阻肺证>痰阻心脉证,差异具统计学意义(P<0.05).痰阻心脉证患者吸烟指数、急性加重次数均较痰湿阻肺证、湿困脾胃证增加明显(P<0.05).结论:运用模糊数学方法能较全面地反映痰湿质COPD稳定期患者与脏腑辨证的相关性,随着病情的变化和进展,中医证候的理化检测指标随之变化.结合患者的偏颇体质和脏腑定位,更有针对性地进行辨证施治,更有利于COPD稳定期的个体化治疗.

目的 观察在西医常规治疗基础上,"邵氏保肺功"联合耳穴贴压治疗中重度慢性阻塞性肺疾病(COPD)稳定期患者的近远期疗效.方法 选取中重度COPD稳定期患者120例,按照随机数字表法分为观察组与对照组,各60例.对照组采用西医常规疗法,观察组在对照组基础上,加用"邵氏保肺功"联合耳穴贴压治疗.疗程均为12周.对比2组患者治疗前、治疗3个月后、治疗后1年的6分钟步行距离试验(6 MWT)、慢性阻塞性肺疾病评估测试(CAT)、肺功能指标(FEV1实测值/预计值％、FVC实测值).结果 治疗后1年观察组6MWT改善明显,与治疗前、治疗3个月后比较有统计学差异(P ＜ 0.05),且较对照组改善更明显(P＜ 0.05).治疗3个月后2组6 MWT与治疗前比较无统计学差异(P ＞ 0.05),对照组治疗后1年6 MWT与治疗前比较无统计学差异(P＞ 0.05):观察组治疗3个月后及随访1年后CAT评分与治疗前比较有统计学差异(P ＜ 0.05,P＜ 0.01);对照组治疗3个月后CAT评分与治疗前比较有统计学差异(P＜ 0.05),随访1年后与治疗前比较无统计学差异(P ＞ 0.05);2组CAT评分治疗3个月后比较有统计学差异(P ＜ 0.05),治疗后1年比较有显著差异(P ＜ 0.01).观察组治疗3个月后肺功能指标FEV1实测值/预计值％、FVC实测值均较治疗前无统计学差异(P ＞ 0.05),但FEV1实测值/预计值％在治疗后1年改善较明显(P＜ 0.05).对照组肺功能改善不明显.结论 邵氏保肺功联合耳穴贴压治疗中重度COPD患者,可提高患者运动耐量,减轻临床证候,改善肺功能,远期疗效更加显著.

"治未病"理论是中医学理论体系的不可或缺的组成部分,体现了中医预防和治疗疾病的先进理念.随着"治未病"理论的建设和发展,更广泛的临床应用,其社会意义、临床意义越来越受到关注.基于"治未病"理论基础的中医适宜技术在防治慢性阻塞性肺病中发挥了重要作用,多样的技术手段包括功法锻炼、中药内服、穴位贴敷、针刺、艾灸、食疗、精神调摄等,可个体化运用于患者,易于实施,收效明显,生命质量得到改善,不良反应及经济负担较小,值得进一步推广和实践.

立春是传统二十四节气中的第一个节气,是我国民间重要的传统节日之一.立春期间气温上升,日照趋于增多;雨水节气则雨量渐增,预示着冬季干冷天气即将结束.此时养生要顺应春季阳气生发的特点,注意保护阳气;雨水期间还要注意祛湿、保养脾胃;正值春节之时,更要科学养生,避免出现过节综合征,以健康的状态迎接新春.