Hou Huang, Jiaming Yu, Xianlong Li, Ming Ling, Chaobao Zhang, Yongqian Fan
Background
Osteoporosis is a foremost public health challenge, especially with the global aging population. Both frailty and osteoporosis share many risk factors, although the relationship between them remains partially explored. This study aims to explore the correlation between varying frailty statuses and osteoporosis incidence.
Methods
Participants from the 2017–2018 NHANES were classified into three groups: frailty, prefrailty, and robust, based on the frailty phenotype. The correlation between frailty and osteoporosis prevalence was assessed using weighted multivariate logistic regression models. Causal relationship was verified by Mendelian randomization using frailty data from the U.K. Biobank and osteoporosis data from the FinnGen database. Proteomic analysis including associated protein screening and functional enrichments was performed based on data from the Icelandic cohort.
Results
The study group comprised 1814 participants. An increased incidence of osteoporosis was observed in older age and lower body mass index populations. A significant frailty–osteoporosis correlation (odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.14–1.64; p = 0.001) was indicated both in the crude model and after adjustments (OR: 1.23; 95% CI: 1.01–1.51; p = 0.039). The inverse variance weighting method observed a potential effect of frailty on osteoporosis risk (β/SE, 0.209/0.099; OR: 1.233; 95% CI: 1.014–1.499; p = 0.036). Thirteen frailty–osteoporosis-associated proteins were found, and proteomic enrichment indicated oxidative stress-related pathways as a hypothesis-generating mechanism of frailty-mediated osteoporosis.
Conclusions
Our findings suggest a potential causal association between frailty and osteoporosis, with risk exacerbating with the progression of frailty severity. Frailty potentially impacts the progression of osteoporosis through response to oxidative stress.
骨质疏松症是一个重要的公共卫生挑战，特别是随着全球人口老龄化。虚弱和骨质疏松都有许多共同的危险因素，尽管它们之间的关系仍有待部分探索。本研究旨在探讨不同虚弱状态与骨质疏松发病率之间的关系。方法根据脆弱表型，将2017-2018年NHANES的参与者分为虚弱、脆弱和健壮三组。使用加权多变量logistic回归模型评估虚弱和骨质疏松患病率之间的相关性。因果关系通过孟德尔随机化验证，使用来自英国生物银行的脆弱性数据和来自FinnGen数据库的骨质疏松症数据。蛋白质组学分析，包括相关蛋白质筛选和功能富集，基于冰岛队列的数据进行。结果研究组共纳入1814名受试者。骨质疏松症的发病率在老年和低体重指数人群中增加。在原始模型和调整后的模型中，虚弱与骨质疏松均存在显著相关性（优势比[OR]: 1.37； 95%可信区间[CI]: 1.14-1.64; p = 0.001） （OR: 1.23; 95% CI: 1.01-1.51; p = 0.039）。反方差加权法观察到虚弱对骨质疏松风险的潜在影响（β/SE, 0.209/0.099; OR: 1.233; 95% CI: 1.014-1.499; p = 0.036）。13个脆弱骨质疏松相关蛋白被发现，蛋白质组学富集表明氧化应激相关途径是脆弱介导的骨质疏松的假设产生机制。结论：我们的研究结果表明，虚弱和骨质疏松之间存在潜在的因果关系，并且随着虚弱严重程度的进展，风险加剧。虚弱可能通过对氧化应激的反应影响骨质疏松症的进展。
{"title":"Frailty Promotes Osteoporosis Development via Oxidative Stress: Evidence From Multicohort and Proteomic Analyses","authors":"Hou Huang, Jiaming Yu, Xianlong Li, Ming Ling, Chaobao Zhang, Yongqian Fan","doi":"10.1155/ijcp/6662987","DOIUrl":"https://doi.org/10.1155/ijcp/6662987","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Osteoporosis is a foremost public health challenge, especially with the global aging population. Both frailty and osteoporosis share many risk factors, although the relationship between them remains partially explored. This study aims to explore the correlation between varying frailty statuses and osteoporosis incidence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Participants from the 2017–2018 NHANES were classified into three groups: frailty, prefrailty, and robust, based on the frailty phenotype. The correlation between frailty and osteoporosis prevalence was assessed using weighted multivariate logistic regression models. Causal relationship was verified by Mendelian randomization using frailty data from the U.K. Biobank and osteoporosis data from the FinnGen database. Proteomic analysis including associated protein screening and functional enrichments was performed based on data from the Icelandic cohort.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study group comprised 1814 participants. An increased incidence of osteoporosis was observed in older age and lower body mass index populations. A significant frailty–osteoporosis correlation (odds ratio [OR]: 1.37; 95% confidence interval [CI]: 1.14–1.64; <i>p</i> = 0.001) was indicated both in the crude model and after adjustments (OR: 1.23; 95% CI: 1.01–1.51; <i>p</i> = 0.039). The inverse variance weighting method observed a potential effect of frailty on osteoporosis risk (β/SE, 0.209/0.099; OR: 1.233; 95% CI: 1.014–1.499; <i>p</i> = 0.036). Thirteen frailty–osteoporosis-associated proteins were found, and proteomic enrichment indicated oxidative stress-related pathways as a hypothesis-generating mechanism of frailty-mediated osteoporosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings suggest a potential causal association between frailty and osteoporosis, with risk exacerbating with the progression of frailty severity. Frailty potentially impacts the progression of osteoporosis through response to oxidative stress.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/6662987","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145887388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammed Alnaggar, Mueataz A. Mahyoub, Wen Cheng, Weiwei Huang, Yalin Xu, Shengzhou Wang, Ting Chen, Jamal Alshorman
Background
Diarrhea constitutes a significant complication among colorectal cancer (CRC) patients undergoing cytotoxic chemotherapy, impacting both their quality of life and treatment adherence. We aimed to assess the safety and efficacy of fecal microbiota transplantation (FMT) in severe chemotherapy-induced diarrhea (CID) among patients with CRC.
Materials and Methods
We conducted an open-label, single-arm trial involving 20 patients with CRC experiencing severe CID (grade 2 or 3) as defined by the Common Terminology Criteria for Adverse Events (CTCAE) Version 5.0, in whom conventional standard antidiarrheal treatments were ineffective. Patients received a single course of orally administered FMT capsules, with a protocol allowing for a repeat course at a 2-week interval if needed. Each course consisted of 90 capsules (10 capsules three times daily on Days 1, 2, and 3), delivering approximately 180 × 1010 colony-forming units (CFU) of bacteria. Patients were monitored for 12 weeks. The primary endpoint was the proportion of patients achieving a sustained clinical response (diarrhea reduced to less than six unformed bowel movements per day). Secondary endpoints included changes in gut microbiome composition and immune cell populations. Genomic analysis (16S rRNA gene sequencing) and immune cell phenotyping (flow cytometry) were performed on samples collected before and after FMT.
Results
The overall response rate, characterized by the improvement of diarrhea to less than six unformed bowel movements per day following one or more FMT procedures over a minimum period of 12 weeks, was noted in 85% (17/20) of patients (95% confidence interval [CI], [62.1%, 96.8%]). Genomic analysis demonstrated significant improvements in gut microbiome diversity after FMT. Moreover, it revealed significant alterations in immune cell populations post-FMT. Specifically, we observed a statistically significant increase in CD19+ B cells (p = 0.0001), CD3+ CD8+ T cytotoxic cells (p = 0.0010), and natural killer (NK) cells (p = 0.0002) following FMT treatment. No significant adverse events were reported.
Conclusions
These preliminary results suggest that FMT is a safe and potentially effective therapeutic approach for managing severe CID in the CRC patient population.
{"title":"Assessing the Safety and Efficacy of Fecal Microbiota Transplantation for Severe Chemotherapy-Induced Diarrhea in Colorectal Cancer Patients: A Single-Arm Clinical Trial","authors":"Mohammed Alnaggar, Mueataz A. Mahyoub, Wen Cheng, Weiwei Huang, Yalin Xu, Shengzhou Wang, Ting Chen, Jamal Alshorman","doi":"10.1155/ijcp/8052716","DOIUrl":"https://doi.org/10.1155/ijcp/8052716","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Diarrhea constitutes a significant complication among colorectal cancer (CRC) patients undergoing cytotoxic chemotherapy, impacting both their quality of life and treatment adherence. We aimed to assess the safety and efficacy of fecal microbiota transplantation (FMT) in severe chemotherapy-induced diarrhea (CID) among patients with CRC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>We conducted an open-label, single-arm trial involving 20 patients with CRC experiencing severe CID (grade 2 or 3) as defined by the Common Terminology Criteria for Adverse Events (CTCAE) Version 5.0, in whom conventional standard antidiarrheal treatments were ineffective. Patients received a single course of orally administered FMT capsules, with a protocol allowing for a repeat course at a 2-week interval if needed. Each course consisted of 90 capsules (10 capsules three times daily on Days 1, 2, and 3), delivering approximately 180 × 10<sup>10</sup> colony-forming units (CFU) of bacteria. Patients were monitored for 12 weeks. The primary endpoint was the proportion of patients achieving a sustained clinical response (diarrhea reduced to less than six unformed bowel movements per day). Secondary endpoints included changes in gut microbiome composition and immune cell populations. Genomic analysis (16S rRNA gene sequencing) and immune cell phenotyping (flow cytometry) were performed on samples collected before and after FMT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The overall response rate, characterized by the improvement of diarrhea to less than six unformed bowel movements per day following one or more FMT procedures over a minimum period of 12 weeks, was noted in 85% (17/20) of patients (95% confidence interval [CI], [62.1%, 96.8%]). Genomic analysis demonstrated significant improvements in gut microbiome diversity after FMT. Moreover, it revealed significant alterations in immune cell populations post-FMT. Specifically, we observed a statistically significant increase in CD19+ B cells (<i>p</i> = 0.0001), CD3+ CD8+ T cytotoxic cells (<i>p</i> = 0.0010), and natural killer (NK) cells (<i>p</i> = 0.0002) following FMT treatment. No significant adverse events were reported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These preliminary results suggest that FMT is a safe and potentially effective therapeutic approach for managing severe CID in the CRC patient population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/8052716","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145887387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<div> <section> <h3> Background</h3> <p>Given the high recurrence rate of kidney stone disease (KSD), surgical interventions alone are not an optimal solution. Antibody-mediated immune responses and mitochondrial dysfunction influence the risk and prognosis of KSD; however, the exact causal mechanisms underlying these relationships remain unclear. Investigating these causal relationships is crucial for improving treatment and prevention strategies.</p> </section> <section> <h3> Methods</h3> <p>This study utilized summary-level genome-wide association study data to perform a two-sample Mendelian randomization (MR) analysis. A total of 46 antibody-mediated immune responses from 13 pathogens and mitochondrial DNA copy number (mtDNA-CN), an indicator of mitochondrial function, were analyzed in KSD. Causal effects were estimated with up to 10 MR methods, primarily inverse-variance weighting (IVW) and the Wald ratio. Sensitivity analyses, including assessments of pleiotropy, heterogeneity, and leave-one-out analysis, were supplemented by causal analysis using summary effect estimates (CAUSE) to ensure robust results.</p> </section> <section> <h3> Results</h3> <p>After false discovery rate (FDR) correction, significant causal associations were observed between genetically predicted antihuman herpesvirus 6 (HHV-6) IgG seropositivity (odds ratio [OR] = 1.481, 95% confidence interval (CI) 1.133–1.935, <i>p</i> = 4.01 × 10<sup>−3</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.047) and HHV-6 IE1B antibody levels (OR = 2.024, 95% CI 1.455–2.817, <i>p</i> = 2.87 × 10<sup>−5</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 6.74 × 10<sup>−4</sup>) with increased KSD risk, as well as <i>Chlamydia trachomatis</i> tarp-D F2 antibody levels (OR = 0.912, 95% CI 0.861–0.966, <i>p</i> = 1.58 × 10<sup>−3</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.025) and human herpesvirus 7 (HHV-7) U14 antibody levels (OR = 0.694, 95% CI 0.593–0.813, <i>p</i> = 5.96 × 10<sup>−6</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 2.80 × 10<sup>−4</sup>) with reduced KSD risk. Additionally, suggestive evidence was identified for three other antibody-mediated immune responses. Reverse analysis indicated a potential causal relationship between KSD and lower mtDNA-CN levels (<i>β</i> = −0.012, 95% CI −0.024 to −0.0002, <i>p</i> = 0.045, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.539). Multiple sensitivity analyses confirmed the robustness of these findings.</p> </section> <section> <h3> Conclusion</h3> <p>This study demonstrates causal links between specific immune responses,
背景考虑到肾结石疾病（KSD）的高复发率，单纯的手术干预并不是最佳的解决方案。抗体介导的免疫反应和线粒体功能障碍影响KSD的风险和预后然而，这些关系背后的确切因果机制尚不清楚。调查这些因果关系对于改善治疗和预防策略至关重要。方法本研究利用汇总水平的全基因组关联研究数据进行双样本孟德尔随机化（MR）分析。分析了13种病原菌46种抗体介导的免疫应答和线粒体DNA拷贝数（mtDNA-CN）（线粒体功能指标）。因果效应估计有多达10个MR方法，主要是反方差加权（IVW）和沃尔德比。敏感性分析，包括评估多效性、异质性和遗漏分析，辅以因果分析，使用总结效应估计（CAUSE）来确保可靠的结果。结果经错误发现率（FDR）校正后，基因预测抗人疱疹病毒6 (HHV-6) IgG血清阳性（比值比[OR] = 1.481, 95%可信区间（CI） 1.133-1.935, p = 4.01 × 10−3,PFDR = 0.047）和HHV-6 IE1B抗体水平（OR = 2.024, 95% CI 1.455-2.817, p = 2.87 × 10−5,PFDR = 6.74 × 10−4）与KSD风险增加存在显著的因果关系。沙眼衣原体tarp-D F2抗体水平（OR = 0.912, 95% CI 0.861-0.966, p = 1.58 × 10−3,PFDR = 0.025）和人疱疹病毒7 (HHV-7) U14抗体水平（OR = 0.694, 95% CI 0.593-0.813, p = 5.96 × 10−6,PFDR = 2.80 × 10−4）与KSD风险降低有关。此外，还发现了其他三种抗体介导的免疫反应的暗示性证据。反向分析表明，KSD与mtDNA-CN水平降低之间存在潜在的因果关系（β = - 0.012, 95% CI = - 0.024 ~ - 0.0002, p = 0.045, PFDR = 0.539）。多重敏感性分析证实了这些发现的稳健性。结论本研究表明特异性免疫应答、mtDNA-CN和KSD之间存在因果关系，强调了免疫调节和线粒体功能障碍的作用。这些发现为预防和个性化治疗提供了新的目标。
{"title":"Exploring the Causal Relationship Between Mitochondrial DNA Copy Number, Antibody-Mediated Immune Response, and Risk of Kidney Stone Disease: A Mendelian Randomization Study","authors":"Wenqiong Chen, Yan Qian","doi":"10.1155/ijcp/7114145","DOIUrl":"https://doi.org/10.1155/ijcp/7114145","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Given the high recurrence rate of kidney stone disease (KSD), surgical interventions alone are not an optimal solution. Antibody-mediated immune responses and mitochondrial dysfunction influence the risk and prognosis of KSD; however, the exact causal mechanisms underlying these relationships remain unclear. Investigating these causal relationships is crucial for improving treatment and prevention strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study utilized summary-level genome-wide association study data to perform a two-sample Mendelian randomization (MR) analysis. A total of 46 antibody-mediated immune responses from 13 pathogens and mitochondrial DNA copy number (mtDNA-CN), an indicator of mitochondrial function, were analyzed in KSD. Causal effects were estimated with up to 10 MR methods, primarily inverse-variance weighting (IVW) and the Wald ratio. Sensitivity analyses, including assessments of pleiotropy, heterogeneity, and leave-one-out analysis, were supplemented by causal analysis using summary effect estimates (CAUSE) to ensure robust results.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After false discovery rate (FDR) correction, significant causal associations were observed between genetically predicted antihuman herpesvirus 6 (HHV-6) IgG seropositivity (odds ratio [OR] = 1.481, 95% confidence interval (CI) 1.133–1.935, <i>p</i> = 4.01 × 10<sup>−3</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.047) and HHV-6 IE1B antibody levels (OR = 2.024, 95% CI 1.455–2.817, <i>p</i> = 2.87 × 10<sup>−5</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 6.74 × 10<sup>−4</sup>) with increased KSD risk, as well as <i>Chlamydia trachomatis</i> tarp-D F2 antibody levels (OR = 0.912, 95% CI 0.861–0.966, <i>p</i> = 1.58 × 10<sup>−3</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.025) and human herpesvirus 7 (HHV-7) U14 antibody levels (OR = 0.694, 95% CI 0.593–0.813, <i>p</i> = 5.96 × 10<sup>−6</sup>, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 2.80 × 10<sup>−4</sup>) with reduced KSD risk. Additionally, suggestive evidence was identified for three other antibody-mediated immune responses. Reverse analysis indicated a potential causal relationship between KSD and lower mtDNA-CN levels (<i>β</i> = −0.012, 95% CI −0.024 to −0.0002, <i>p</i> = 0.045, <i>P</i><sub><i>F</i><i>D</i><i>R</i></sub> = 0.539). Multiple sensitivity analyses confirmed the robustness of these findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study demonstrates causal links between specific immune responses,","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/7114145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145887340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenqiang Guo, Shifeng Guo, Kang Yang, Hua Huang, Jia Chen, Zhihui Huang, Qing Hong, Leizhen Xia, Jialv Huang, Tao Luo, Lin Xu, Houyang Chen
Background
Congenital bilateral absence of the vas deferens (CBAVD) is one of the causes of male infertility.
Objective
The study aims to analyze the genetic screening results and assisted reproductive outcomes of CBAVD patients, providing a reference for improving the genetic mutation profile and assisted reproductive outcomes in the Chinese population.
Methods
CFTR and ADGRG2 genes were screened and sequenced in 26 CBAVD patients using high-throughput sequencing to summarize and assess assisted reproduction outcomes.
Results
Among the 26 CBAVD patients, 76.9% (20/26) had one or more reportable CFTR mutations. In addition to the IVS9-5T mutation, 23 different CFTR mutations were detected in these 26 patients, with 6 mutations found to be harmful through bioinformatics analysis. No new CFTR mutations or ADGRG2 mutations were found. The sperm of all 26 patients was obtained through surgical procedures, with a fertilization rate of 74.9%, cleavage rate of 92.8%, available embryo rate of 55.1%, high-quality embryo rate of 22.4%, implantation rate of 36.7%, clinical pregnancy rate of 47.1%, and live birth rate of 32.3%.
Conclusions
CBAVD patients can reproduce offspring through assisted reproductive techniques, and no statistically significant differences in assisted reproduction outcomes were found in patients with CBAVD with or without reportable CFTR mutations.
{"title":"Genetic Analysis and Assisted Reproductive Outcomes in Patients With CBAVD in China: A Retrospective Study","authors":"Wenqiang Guo, Shifeng Guo, Kang Yang, Hua Huang, Jia Chen, Zhihui Huang, Qing Hong, Leizhen Xia, Jialv Huang, Tao Luo, Lin Xu, Houyang Chen","doi":"10.1155/ijcp/9919699","DOIUrl":"https://doi.org/10.1155/ijcp/9919699","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Congenital bilateral absence of the vas deferens (CBAVD) is one of the causes of male infertility.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The study aims to analyze the genetic screening results and assisted reproductive outcomes of CBAVD patients, providing a reference for improving the genetic mutation profile and assisted reproductive outcomes in the Chinese population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>CFTR and ADGRG2 genes were screened and sequenced in 26 CBAVD patients using high-throughput sequencing to summarize and assess assisted reproduction outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the 26 CBAVD patients, 76.9% (20/26) had one or more reportable CFTR mutations. In addition to the IVS9-5T mutation, 23 different CFTR mutations were detected in these 26 patients, with 6 mutations found to be harmful through bioinformatics analysis. No new CFTR mutations or ADGRG2 mutations were found. The sperm of all 26 patients was obtained through surgical procedures, with a fertilization rate of 74.9%, cleavage rate of 92.8%, available embryo rate of 55.1%, high-quality embryo rate of 22.4%, implantation rate of 36.7%, clinical pregnancy rate of 47.1%, and live birth rate of 32.3%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>CBAVD patients can reproduce offspring through assisted reproductive techniques, and no statistically significant differences in assisted reproduction outcomes were found in patients with CBAVD with or without reportable CFTR mutations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/9919699","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145887386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study investigates the causal relationship between cathepsins and myocardial infarction (MI) through bidirectional Mendelian randomization (MR) analysis and examines cathepsin G (CTSG) in relation to various cancers using pan-cancer analysis.
Methods
We used data from the FinnGen database (28,546 MI cases and 378,019 controls) and 3301 participants from the INTERVAL study. The inverse variance weighted (IVW) method assessed the causal effect between exposure and outcome. MR-Egger regression, weighted median, simple mode, and weighted mode analyses were used for validation. Pan-cancer data were obtained from the UCSC database to explore CTSG expression across 39 tumor types.
Results
Among nine cathepsins, only elevated CTSG was linked to a higher likelihood of MI (IVW p = 0.0062, OR = 1.0576, 95% CI = 1.0160–1.1009). No significant causal effect was found between MI and CTSG levels. Pan-cancer analysis revealed CTSG downregulation in 16 tumor types, with significant expression differences in lung and colon cancers. High CTSG expression correlated with poor prognosis in stomach and bladder cancers, while low expression was linked to worse prognosis in sarcoma and other tumors. CTSG expression varied across tumor stages in multiple cancers.
Conclusion
Elevated CTSG is a potential risk factor for MI. Our findings suggest CTSG as a novel biomarker for MI prognosis and highlight its potential role in cancer prognosis and stage differentiation.
目的通过双向孟德尔随机化（MR）分析探讨组织蛋白酶（cathepsin G）与心肌梗死（MI）的因果关系，并通过泛癌症分析探讨组织蛋白酶G （CTSG）与各种癌症的关系。方法我们使用FinnGen数据库的数据（28,546例MI病例和378,019例对照）和来自INTERVAL研究的3301名参与者。反方差加权（IVW）方法评估暴露与结果之间的因果关系。采用MR-Egger回归、加权中位数、简单模式和加权模式分析进行验证。从UCSC数据库中获得泛癌数据，以探索39种肿瘤类型中的CTSG表达。结果在9种组织蛋白酶中，只有CTSG升高与心肌梗死的可能性升高有关（IVW p = 0.0062, OR = 1.0576, 95% CI = 1.0160-1.1009）。心肌梗死和CTSG水平之间没有明显的因果关系。泛癌分析显示，CTSG在16种肿瘤类型中下调，在肺癌和结肠癌中表达差异显著。CTSG在胃癌和膀胱癌中高表达与预后差相关，而在肉瘤等肿瘤中低表达与预后差相关。CTSG在不同肿瘤分期中的表达不同。结论CTSG升高是心肌梗死的潜在危险因素，提示CTSG是心肌梗死预后的一种新的生物标志物，在肿瘤预后和分期分化中具有潜在作用。
{"title":"The Causal Role of Cathepsin G in Myocardial Infarction and Its Prognostic Value Across Cancers: A Mendelian Randomization and Pan-Cancer Study","authors":"Yanwei Wang, Xue Yan, Pin Wang, Ning Hu, Lu Xu","doi":"10.1155/ijcp/4265666","DOIUrl":"https://doi.org/10.1155/ijcp/4265666","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the causal relationship between cathepsins and myocardial infarction (MI) through bidirectional Mendelian randomization (MR) analysis and examines cathepsin G (CTSG) in relation to various cancers using pan-cancer analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used data from the FinnGen database (28,546 MI cases and 378,019 controls) and 3301 participants from the INTERVAL study. The inverse variance weighted (IVW) method assessed the causal effect between exposure and outcome. MR-Egger regression, weighted median, simple mode, and weighted mode analyses were used for validation. Pan-cancer data were obtained from the UCSC database to explore CTSG expression across 39 tumor types.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among nine cathepsins, only elevated CTSG was linked to a higher likelihood of MI (IVW <i>p</i> = 0.0062, OR = 1.0576, 95% CI = 1.0160–1.1009). No significant causal effect was found between MI and CTSG levels. Pan-cancer analysis revealed CTSG downregulation in 16 tumor types, with significant expression differences in lung and colon cancers. High CTSG expression correlated with poor prognosis in stomach and bladder cancers, while low expression was linked to worse prognosis in sarcoma and other tumors. CTSG expression varied across tumor stages in multiple cancers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Elevated CTSG is a potential risk factor for MI. Our findings suggest CTSG as a novel biomarker for MI prognosis and highlight its potential role in cancer prognosis and stage differentiation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/4265666","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145887254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ali Yosefianjazi, Hourieh Ansari, Ali Hajigholami, Alirezamansouri
Background and Objective
Cancer-related fatigue (CRF) is recognized as one of the most common side effects of cancer and its treatment and can affect the quality of life of individuals. Studies have shown that there is an inseparable link between CRF and inflammation. Selenium, known as an antioxidant and anti-inflammatory agent, reduces the production of inflammatory markers as well as the accumulation of free oxygen radicals. Therefore, a decrease in selenium levels leads to increased inflammation and, consequently, greater fatigue. This study aimed to determine the level of selenium and its relationship with CRF.
Methodology
A total of 70 patients who met the entry criteria for the study were examined after the level of fatigue was determined through the Multidimensional Fatigue Inventory (MFI) questionnaire, and the selenium content in the serum was measured by atomic absorption spectrophotometry.
Findings
In this study, 70 cancer patients who underwent chemotherapy, including 32 men and 38 women, were examined. The total fatigue score measured through the MFI questionnaire was 57.82 ± 10.42, and the level of selenium in the blood of the patients was 77.75 ± 19.24 μg/L.
Conclusion
The results of this study demonstrated that there was a significant negative correlation between selenium levels and CRF (p < 0.001, r = −0.524), indicating that with decreasing selenium levels, the amount of CRF increased. These results vary depending on the type of cancer.
{"title":"Determining the Selenium Level in Patients With Cancer-Related Fatigue (2023)","authors":"Ali Yosefianjazi, Hourieh Ansari, Ali Hajigholami, Alirezamansouri","doi":"10.1155/ijcp/9394802","DOIUrl":"https://doi.org/10.1155/ijcp/9394802","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Objective</h3>\u0000 \u0000 <p>Cancer-related fatigue (CRF) is recognized as one of the most common side effects of cancer and its treatment and can affect the quality of life of individuals. Studies have shown that there is an inseparable link between CRF and inflammation. Selenium, known as an antioxidant and anti-inflammatory agent, reduces the production of inflammatory markers as well as the accumulation of free oxygen radicals. Therefore, a decrease in selenium levels leads to increased inflammation and, consequently, greater fatigue. This study aimed to determine the level of selenium and its relationship with CRF.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methodology</h3>\u0000 \u0000 <p>A total of 70 patients who met the entry criteria for the study were examined after the level of fatigue was determined through the Multidimensional Fatigue Inventory (MFI) questionnaire, and the selenium content in the serum was measured by atomic absorption spectrophotometry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Findings</h3>\u0000 \u0000 <p>In this study, 70 cancer patients who underwent chemotherapy, including 32 men and 38 women, were examined. The total fatigue score measured through the MFI questionnaire was 57.82 ± 10.42, and the level of selenium in the blood of the patients was 77.75 ± 19.24 μg/L.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The results of this study demonstrated that there was a significant negative correlation between selenium levels and CRF (<i>p</i> < 0.001, <i>r</i> = −0.524), indicating that with decreasing selenium levels, the amount of CRF increased. These results vary depending on the type of cancer.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/9394802","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The occurrence of hypokalemia during the management of diabetic ketoacidosis (DKA) remains high, even with the availability of comprehensive potassium replacement guidelines for its treatment. This study aims to assess the predictive value of pH-adjusted potassium (pHK) as a biomarker for the development of hypokalemia in patients treated for DKA.
Methods
We conducted a retrospective analysis of 126 hospitalized patients diagnosed with DKA. Patients were categorized based on their lowest serum potassium levels during treatment into two groups: DKA hypokalemia group and normal serum potassium group. Demographic and clinical parameters, including glycated hemoglobin (HbA1c), admission blood glucose, admission serum potassium, pHK, arterial blood pH(pH), bicarbonate(HCO3−), hospital stay, and hospitalization costs, were compared between groups. Influencing factors of DKA hypokalemia were analyzed to identify predictors of its occurrence during treatment.
Results
The DKA hypokalemia group exhibited significantly lower arterial blood pH, HCO3−, and pHK levels compared with the normal serum potassium group (p < 0.01). Conversely, HbA1c, hospital stay, and hospitalization costs were higher in the hypokalemia group (p < 0.01 or p < 0.05). The incidence of hypokalemia was markedly higher in patients with low admission pHK compared with those with normal or high pHK (p < 0.01). Binary logistic regression identified HCO3− and pHK as independent risk factors for DKA hypokalemia (β = −0.13, −0.83, p < 0.01). The receiver operating characteristic (ROC) curve analysis indicated that both HCO3− and pHK had an area under the curve of 0.74 for predicting the development of hypokalemia during DKA treatment (p < 0.01).
Conclusion
pHK level is a predictive marker for the risk of hypokalemia and correlates with the severity of acidosis.
{"title":"Investigation of pH-Adjusted Potassium for Predicting Hypokalemia During the Management of Diabetic Ketoacidosis","authors":"Congqing Miao, DeChuan Lu, Jingjing Liu, Xin Sun, Yue Zhao, Peng Du, Yingzi Chen","doi":"10.1155/ijcp/3240512","DOIUrl":"https://doi.org/10.1155/ijcp/3240512","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>The occurrence of hypokalemia during the management of diabetic ketoacidosis (DKA) remains high, even with the availability of comprehensive potassium replacement guidelines for its treatment. This study aims to assess the predictive value of pH-adjusted potassium (pHK) as a biomarker for the development of hypokalemia in patients treated for DKA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a retrospective analysis of 126 hospitalized patients diagnosed with DKA. Patients were categorized based on their lowest serum potassium levels during treatment into two groups: DKA hypokalemia group and normal serum potassium group. Demographic and clinical parameters, including glycated hemoglobin (HbA1c), admission blood glucose, admission serum potassium, pHK, arterial blood pH(pH), bicarbonate(HCO3<sup>−</sup>), hospital stay, and hospitalization costs, were compared between groups. Influencing factors of DKA hypokalemia were analyzed to identify predictors of its occurrence during treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The DKA hypokalemia group exhibited significantly lower arterial blood pH, HCO3<sup>−</sup>, and pHK levels compared with the normal serum potassium group (<i>p</i> < 0.01). Conversely, HbA1c, hospital stay, and hospitalization costs were higher in the hypokalemia group (<i>p</i> < 0.01 or <i>p</i> < 0.05). The incidence of hypokalemia was markedly higher in patients with low admission pHK compared with those with normal or high pHK (<i>p</i> < 0.01). Binary logistic regression identified HCO3<sup>−</sup> and pHK as independent risk factors for DKA hypokalemia (<i>β</i> = −0.13, −0.83, <i>p</i> < 0.01). The receiver operating characteristic (ROC) curve analysis indicated that both HCO3<sup>−</sup> and pHK had an area under the curve of 0.74 for predicting the development of hypokalemia during DKA treatment (<i>p</i> < 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>pHK level is a predictive marker for the risk of hypokalemia and correlates with the severity of acidosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/3240512","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yang Zheng, Liang Chen, Lu Liu, Qixin Hao, Linlin Guo, Zhaorui Wang, Shaowei Ma, Hui Xie
Background
Lactylation, a novel post-translational modification of proteins, has been shown to promote tumor growth and inhibit the antitumor response of the tumor microenvironment (TME) in various ways. However, the complex mechanism of this modification in gastric cancer, particularly nonhistone lactylation and its interplay with tumor metabolism and immune escape, remains enigmatic.
Methods
Using single-cell RNA sequencing data and the AddModuleScore algorithm, we screened for lactylation-related genes at the single-cell level. We then integrated 10 machine learning algorithms and 101 combinations of these to construct a lactylation-related gene signature (LRS) model. The results were validated in the GEO dataset. Ultimately, we identified genes with prognostic predictive value, forming three gene feature profiles. We further analyzed the associations between lactylation-related gene risk scores and clinical features, mutation profiles, biological functions, immune cell infiltration, and immunotherapy response. For the core genes, we explored in-depth biological mechanisms through bioinformatics analysis and in vitro experiments.
Results
We identified 119 lactylation-related genes at the single-cell level. Utilizing a computational framework with 101 combinations of machine learning algorithms, we successfully constructed a risk prediction model that includes three lactylation-associated genes. This model showed excellent performance in prognosis prediction and clinical translation. The study also found significant differences in clinical features, biological functions, immune cell infiltration, immune checkpoint expression, and immunotherapy response among patients in different risk groups.
Conclusions
The LRS model demonstrates significant potential for improving the management of gastric cancer patients and enhancing treatment outcomes, particularly in the areas of immunotherapy and immune escape. This discovery highlights the clinical importance of overall lactic acidification in gastric cancer and provides a foundation for mechanistic studies and targeted therapeutic strategies.
{"title":"Construction of Lactylation-Related Gene Signature at the Single-Cell Level and Its Application in Prognostic Prediction and Immune Escape Mechanism in Gastric Cancer","authors":"Yang Zheng, Liang Chen, Lu Liu, Qixin Hao, Linlin Guo, Zhaorui Wang, Shaowei Ma, Hui Xie","doi":"10.1155/ijcp/1954934","DOIUrl":"https://doi.org/10.1155/ijcp/1954934","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Lactylation, a novel post-translational modification of proteins, has been shown to promote tumor growth and inhibit the antitumor response of the tumor microenvironment (TME) in various ways. However, the complex mechanism of this modification in gastric cancer, particularly nonhistone lactylation and its interplay with tumor metabolism and immune escape, remains enigmatic.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using single-cell RNA sequencing data and the AddModuleScore algorithm, we screened for lactylation-related genes at the single-cell level. We then integrated 10 machine learning algorithms and 101 combinations of these to construct a lactylation-related gene signature (LRS) model. The results were validated in the GEO dataset. Ultimately, we identified genes with prognostic predictive value, forming three gene feature profiles. We further analyzed the associations between lactylation-related gene risk scores and clinical features, mutation profiles, biological functions, immune cell infiltration, and immunotherapy response. For the core genes, we explored in-depth biological mechanisms through bioinformatics analysis and in vitro experiments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We identified 119 lactylation-related genes at the single-cell level. Utilizing a computational framework with 101 combinations of machine learning algorithms, we successfully constructed a risk prediction model that includes three lactylation-associated genes. This model showed excellent performance in prognosis prediction and clinical translation. The study also found significant differences in clinical features, biological functions, immune cell infiltration, immune checkpoint expression, and immunotherapy response among patients in different risk groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The LRS model demonstrates significant potential for improving the management of gastric cancer patients and enhancing treatment outcomes, particularly in the areas of immunotherapy and immune escape. This discovery highlights the clinical importance of overall lactic acidification in gastric cancer and provides a foundation for mechanistic studies and targeted therapeutic strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/1954934","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145845977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Boqian Yu, Shiyuan Zhang, Hao Yu, Rongjie Ye, Danping Wu, Xiaotian Yang, Kun Qiao, Chunlei Tan, Shuqiang Liu, Quan Yuan, Yuanxi Huang
Background
The global cancer survivor population is growing rapidly. Heavy metals like lead (Pb), cadmium (Cd), and mercury (Hg) can affect cancer progression and mortality, but systematic studies on their impact are limited.
Method
We analyzed data from the National Health and Nutrition Examination Survey (NHANES) (2005–2018) on 2,369 cancer survivors. Serum levels of Pb, Cd, and Hg were measured using mass spectrometry. We used Kaplan–Meier (KM) curves and Cox regression models to study the effects of these metals on mortality.
Results
Higher serum levels of Pb and Cd were associated with increased all-cause, cancer-specific, and noncancer mortalities, as shown by KM curves. Cox regression showed that cancer survivors with higher levels of Pb and Cd had significantly higher risks of all-cause (hazard ratios [HRs]: 2.37 and 3.17), cancer-specific (HRs: 2.45 and 3.37), and noncancer mortalities (HRs: 2.73 and 3.80). Combined high levels of Pb and Cd were linked to the highest risks of all-cause and noncancer mortalities compared with low exposure levels. Hg exposure was not significantly linked to mortality outcomes. Survivors with high levels of both Pb and Cd had greater risks of all-cause, cancer-specific, and noncancer mortalities than those exposed to just one metal.
Conclusion
Cancer survivors with higher serum levels of Pb and Cd face increased mortality risks. The lack of a significant association between Hg exposure and mortality is notable. The synergistic effect of Pb and Cd on mortality risk highlights the importance of considering multiple heavy metal exposures when assessing health risks in this population.
{"title":"Joint Association of Heavy Metals Exposure With Mortality Among Cancer Survivors","authors":"Boqian Yu, Shiyuan Zhang, Hao Yu, Rongjie Ye, Danping Wu, Xiaotian Yang, Kun Qiao, Chunlei Tan, Shuqiang Liu, Quan Yuan, Yuanxi Huang","doi":"10.1155/ijcp/2944889","DOIUrl":"https://doi.org/10.1155/ijcp/2944889","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The global cancer survivor population is growing rapidly. Heavy metals like lead (Pb), cadmium (Cd), and mercury (Hg) can affect cancer progression and mortality, but systematic studies on their impact are limited.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>We analyzed data from the National Health and Nutrition Examination Survey (NHANES) (2005–2018) on 2,369 cancer survivors. Serum levels of Pb, Cd, and Hg were measured using mass spectrometry. We used Kaplan–Meier (KM) curves and Cox regression models to study the effects of these metals on mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Higher serum levels of Pb and Cd were associated with increased all-cause, cancer-specific, and noncancer mortalities, as shown by KM curves. Cox regression showed that cancer survivors with higher levels of Pb and Cd had significantly higher risks of all-cause (hazard ratios [HRs]: 2.37 and 3.17), cancer-specific (HRs: 2.45 and 3.37), and noncancer mortalities (HRs: 2.73 and 3.80). Combined high levels of Pb and Cd were linked to the highest risks of all-cause and noncancer mortalities compared with low exposure levels. Hg exposure was not significantly linked to mortality outcomes. Survivors with high levels of both Pb and Cd had greater risks of all-cause, cancer-specific, and noncancer mortalities than those exposed to just one metal.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Cancer survivors with higher serum levels of Pb and Cd face increased mortality risks. The lack of a significant association between Hg exposure and mortality is notable. The synergistic effect of Pb and Cd on mortality risk highlights the importance of considering multiple heavy metal exposures when assessing health risks in this population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/2944889","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145845983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vagal modulation is achieved directly by transcutaneous auricular vagus nerve stimulation, whereas breathing exercises stimulate arterial baroreceptors. In this study, we aimed to compare these two methods, which have similar effects.
Methods
88 healthy participants aged 18–35 were randomly divided into breathing exercises (Group BE) and vagus stimulation (Group VNS). Thoracic expansion exercise was performed in the BE group. In the VNS group, biphasic electrical stimulation was applied to both ears with a pulse width of 300 ms, a frequency of 10 Hz, and 20 min. Pulmonary function tests were measured on the first and last days. Heart rate, systolic and diastolic blood pressure, RMSSD, PNN50, LF/HF, LF Power, and HF Power values were measured before and after each of the 10 sessions for both groups.
Results
Heart rate decreased significantly in both groups, with significant superiority in the BE group compared to that in the VNS group. In both groups, blood pressure values decreased significantly. RMSSD, PNN50, and HF values increased significantly in the VNS group, while LF and LF/HF values decreased significantly in the BE group. In pulmonary function test results, the FEV1 value increased significantly in both groups. A significant increase in the FVC value was observed in both groups, but the BE group was superior. The two groups had no significant superiority in the FEV1/FVC value.
Conclusion
As a result, auricular vagus stimulation seems superior to breathing exercises in increasing the parasympathetic system activity, reducing sympathetic activity, and partially increasing respiratory functions.
{"title":"Comparison of Breathing Exercises and Auricular Vagus Nerve Stimulation Effects on Autonomic Nervous System Activity and Respiratory Functions in Healthy Adults: An Active Comparative Controlled Study","authors":"Gulay Yalcin, Ali Veysel Özden","doi":"10.1155/ijcp/5131519","DOIUrl":"https://doi.org/10.1155/ijcp/5131519","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Vagal modulation is achieved directly by transcutaneous auricular vagus nerve stimulation, whereas breathing exercises stimulate arterial baroreceptors. In this study, we aimed to compare these two methods, which have similar effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>88 healthy participants aged 18–35 were randomly divided into breathing exercises (Group BE) and vagus stimulation (Group VNS). Thoracic expansion exercise was performed in the BE group. In the VNS group, biphasic electrical stimulation was applied to both ears with a pulse width of 300 ms, a frequency of 10 Hz, and 20 min. Pulmonary function tests were measured on the first and last days. Heart rate, systolic and diastolic blood pressure, RMSSD, PNN50, LF/HF, LF Power, and HF Power values were measured before and after each of the 10 sessions for both groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Heart rate decreased significantly in both groups, with significant superiority in the BE group compared to that in the VNS group. In both groups, blood pressure values decreased significantly. RMSSD, PNN50, and HF values increased significantly in the VNS group, while LF and LF/HF values decreased significantly in the BE group. In pulmonary function test results, the FEV1 value increased significantly in both groups. A significant increase in the FVC value was observed in both groups, but the BE group was superior. The two groups had no significant superiority in the FEV1/FVC value.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>As a result, auricular vagus stimulation seems superior to breathing exercises in increasing the parasympathetic system activity, reducing sympathetic activity, and partially increasing respiratory functions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Clinical Trial Registration</h3>\u0000 \u0000 <p>NCT06531954</p>\u0000 </section>\u0000 </div>","PeriodicalId":13782,"journal":{"name":"International Journal of Clinical Practice","volume":"2025 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ijcp/5131519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145845791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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