ACS Materials Letters最新文献

{"title":"Elevated Suicide Risk in Idiopathic Pulmonary Fibrosis Patients.","authors":"Jui-Ting Yu, Chen-Pi Li, Hui-Chin Chang, Shuo-Yan Gau","doi":"10.1164/rccm.202407-1359LE","DOIUrl":"10.1164/rccm.202407-1359LE","url":null,"abstract":"","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1276-1277"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"One for All and All for One: Multikingdom Interplay in Severe Viral Pneumonia.","authors":"Matthias Egger, Martin Hoenigl","doi":"10.1164/rccm.202406-1237ED","DOIUrl":"10.1164/rccm.202406-1237ED","url":null,"abstract":"","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1176-1178"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucosal Petechiae and Hemorrhage in Pulmonary Barotrauma in Breath-Hold Diving: Direct Observation of a Suspected Pathophysiologic Mechanism.","authors":"Fernando Silva, Emmanuel Gouin, Peter Lindholm","doi":"10.1164/rccm.202308-1505IM","DOIUrl":"10.1164/rccm.202308-1505IM","url":null,"abstract":"","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"e14-e15"},"PeriodicalIF":19.3,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141625718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity-related Asthma: A Pathobiology-based Overview of Existing and Emerging Treatment Approaches.","authors":"Meghan D Althoff, Kristina Gaietto, Fernando Holguin, Erick Forno","doi":"10.1164/rccm.202406-1166SO","DOIUrl":"10.1164/rccm.202406-1166SO","url":null,"abstract":"<p><p>Although obesity-related asthma is associated with worse asthma outcomes, optimal treatment approaches for this complex phenotype are still largely unavailable. This state-of-the-art review article synthesizes evidence for existing and emerging treatment approaches for obesity-related asthma and highlights pathways that offer potential targets for novel therapeutics. Existing treatments targeting insulin resistance and obesity, including metformin and GLP-1 (glucagon-like-peptide 1) receptor agonists, have been associated with improved asthma outcomes, although GLP-1R agonist data in asthma are limited to individuals with comorbid obesity. Monoclonal antibodies approved for treatment of moderate to severe asthma generally appear to be effective in individuals with obesity, although this is based on retrospective or secondary analysis of clinical trials; moreover, although most of these asthma biologics are approved for use in the pediatric population, the impact of obesity on their efficacy has not been well studied in youth. Potential therapeutic targets being investigated include IL-6, arginine metabolites, nitro-fatty acids, and mitochondrial antioxidants, with clinical trials for each currently underway. Potential therapeutic targets include adipose tissue eosinophils and the GLP-1-arginine-advanced glycation end products axis, although data in humans are still needed. Finally, transcriptomic and epigenetic studies of \"obese asthma\" demonstrate enrichment of IFN-related signaling pathways, Rho-GTPase pathways, and integrins, suggesting that these too could represent future treatment targets. We advocate for further study of these potential therapeutic mechanisms and continued investigation of the distinct inflammatory pathways characteristic of obesity-related asthma, to facilitate effective treatment development for this unique asthma phenotype.</p>","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1186-1200"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Legacy of Redlining: Increasing Childhood Asthma Disparities through Neighborhood Poverty.","authors":"Patrick H Ryan, Antonella Zanobetti, Brent A Coull, Howard Andrews, Leonard B Bacharier, Dakota Bailey, Paloma I Beamer, Jeff Blossom, Cole Brokamp, Soma Datta, Tina Hartert, Gurjit K Khurana Hershey, Daniel J Jackson, Christine C Johnson, Christine Joseph, Jorja Kahn, Nathan Lothrop, Margee Louisias, Heike Luttmann-Gibson, Fernando D Martinez, Eneida A Mendonça, Rachel L Miller, Dennis Ownby, Sima Ramratnam, Christine M Seroogy, Cynthia M Visness, Anne L Wright, Edward M Zoratti, James E Gern, Diane R Gold","doi":"10.1164/rccm.202309-1702OC","DOIUrl":"10.1164/rccm.202309-1702OC","url":null,"abstract":"<p><p><b>Rationale:</b> Identifying the root causes of racial disparities in childhood asthma is critical for health equity. <b>Objectives:</b> To determine whether the racist policy of redlining in the 1930s led to present-day disparities in childhood asthma by increasing community-level poverty and decreasing neighborhood socioeconomic position (SEP). <b>Methods:</b> We categorized census tracts at the birth address of participants from the Children's Respiratory and Environmental Workgroup birth cohort consortium into categories A, B, C, and D as defined by the Home Owners Loan Corporation, with D being the highest perceived risk. Surrogates of present-day neighborhood-level SEP were determined for each tract, including the percentage of low-income households, the CDC's Social Vulnerability Index, and other tract-level variables. We performed causal mediation analysis, which, under the assumption of no unmeasured confounding, estimates the direct and mediated pathways by which redlining may cause asthma disparities through tract-level mediators adjusting for individual-level covariates. <b>Measurements and Main Results:</b> Of 4,849 children, the cumulative incidence of asthma through age 11 was 26.6%, and 13.2% resided in census tracts with a Home Owners Loan Corporation grade of D. In mediation analyses, residing in Grade-D tracts (adjusted odds ratio = 1.03 [95% confidence interval = 1.01, 1.05]) was significantly associated with childhood asthma, with 79% of this increased risk mediated by percentage of low-income households; results were similar for the Social Vulnerability Index and other tract-level variables. <b>Conclusions:</b> The historical structural racist policy of redlining led to present-day asthma disparities in part through decreased neighborhood SEP. Policies aimed at reversing the effects of structural racism should be considered to create more just, equitable, and healthy communities.</p>","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1201-1209"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141309352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell Analysis Reveals Novel Immune Perturbations in Fibrotic Hypersensitivity Pneumonitis.","authors":"Amy Y Zhao, Avraham Unterman, Nebal S Abu Hussein, Prapti Sharma, Fadi Nikola, Jasper Flint, Xiting Yan, Taylor S Adams, Aurelien Justet, Tomokazu S Sumida, Jiayi Zhao, Jonas C Schupp, Micha Sam B Raredon, Farida Ahangari, Giuseppe Deluliis, Yingze Zhang, Ivette Buendia-Roldan, Ayodeji Adegunsoye, Anne I Sperling, Antje Prasse, Changwan Ryu, Erica Herzog, Moises Selman, Annie Pardo, Naftali Kaminski","doi":"10.1164/rccm.202401-0078OC","DOIUrl":"10.1164/rccm.202401-0078OC","url":null,"abstract":"<p><p><b>Rationale:</b> Fibrotic hypersensitivity pneumonitis (FHP) is a debilitating interstitial lung disease driven by incompletely understood immune mechanisms. <b>Objectives:</b> To elucidate immune aberrations in FHP in single-cell resolution. <b>Methods:</b> Single-cell 5' RNA sequencing was conducted on peripheral blood mononuclear cells and BAL cells obtained from 45 patients with FHP, 63 patients with idiopathic pulmonary fibrosis (IPF), 4 patients with nonfibrotic hypersensitivity pneumonitis, and 36 healthy control subjects in the United States and Mexico. Analyses included differential gene expression (Seurat), TF (transcription factor) activity imputation (DoRothEA-VIPER), and trajectory analyses (Monocle3 and Velocyto-scVelo-CellRank). <b>Measurements and Main Results:</b> Overall, 501,534 peripheral blood mononuclear cells from 110 patients and control subjects and 88,336 BAL cells from 19 patients were profiled. Compared with control samples, FHP has elevated classical monocytes (adjusted-<i>P</i> = 2.5 × 10^-3) and is enriched in CCL3^hi/CCL4^hi and S100A^hi classical monocytes (adjusted-<i>P</i> < 2.2 × 10^-16). Trajectory analyses demonstrate that S100A^hi classical monocytes differentiate into SPP1^hi lung macrophages associated with fibrosis. Compared with both control subjects and IPF, cells from patients with FHP are significantly enriched in GZM^hi cytotoxic T cells. These cells exhibit TF activities indicative of TGFβ and TNFα and NFκB pathways. These results are publicly available at http://ildimmunecellatlas.com. <b>Conclusions:</b> Single-cell transcriptomics of patients with FHP uncovered novel immune perturbations, including previously undescribed increases in GZM^hi cytotoxic CD4⁺ and CD8⁺ T cells-reflecting this disease's unique inflammatory T cell-driven nature-as well as increased S100A^hi and CCL3^hi/CCL4^hi classical monocytes also observed in IPF. Both cell populations may guide the development of new biomarkers and therapeutic interventions.</p>","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1252-1266"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141454667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Domestic Mixed-Dust Pneumoconiosis.","authors":"Thomas Villeneuve, Simon Foulquier, Alexandre N'Guyen, Anna Vigier, Grégoire Prévot","doi":"10.1164/rccm.202312-2356IM","DOIUrl":"10.1164/rccm.202312-2356IM","url":null,"abstract":"","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1267-1268"},"PeriodicalIF":19.3,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reply to Yu <i>et al</i>.: Elevated Suicide Risk in Idiopathic Pulmonary Fibrosis Patients.","authors":"Bo-Guen Kim, Kyungdo Han, Hyun Lee","doi":"10.1164/rccm.202407-1417LE","DOIUrl":"10.1164/rccm.202407-1417LE","url":null,"abstract":"","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1277"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141981500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Etomidate Use and Association with Mortality Compared with Ketamine among Critically Ill Patients.","authors":"Hannah Wunsch, Nicholas A Bosch, Anica C Law, Emily A Vail, May Hua, Burton H Shen, Peter K Lindenauer, David N Juurlink, Allan J Walkey, Hayley B Gershengorn","doi":"10.1164/rccm.202404-0813OC","DOIUrl":"10.1164/rccm.202404-0813OC","url":null,"abstract":"<p><p><b>Rationale:</b> Uncertainty remains regarding the risks associated with single-dose use of etomidate. <b>Objectives:</b> To assess the use of etomidate in critically ill patients and compare outcomes for patients who received etomidate versus ketamine. <b>Methods:</b> We assessed patients who received invasive mechanical ventilation (IMV) and were admitted to an ICU in the Premier Healthcare Database between 2008 and 2021. The exposure was receipt of etomidate on the day of IMV initiation, and the main outcome was hospital mortality. Using multivariable regression, we compared patients who received IMV within the first 2 days of hospitalization who received etomidate with propensity score-matched patients who received ketamine. We also assessed whether receipt of corticosteroids in the days after intubation modified the association between etomidate and mortality. <b>Measurements and Main Results:</b> Of 1,689,945 patients who received IMV, nearly half (738,855; 43.7%) received etomidate. Among those who received IMV in the first 2 days of hospitalization, we established 22,273 matched pairs administered either etomidate or ketamine. In the primary analysis, receipt of etomidate was associated with greater hospital mortality relative to ketamine (21.6% vs. 18.7%; absolute risk difference, 2.8%; 95% confidence interval, 2.1%, 3.6%; adjusted odds ratio, 1.28, 95% confidence interval, 1.21,1.34). This was consistent across subgroups and sensitivity analyses. We found no attenuation of the association with mortality with receipt of corticosteroids in the days after etomidate use. <b>Conclusions:</b> Use of etomidate on the day of IMV initiation is common and associated with a higher odds of hospital mortality than use of ketamine. This finding is independent of subsequent treatment with corticosteroids.</p>","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1243-1251"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142034894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Chronic Altitude Exposure on Chronic Obstructive Pulmonary Disease Outcomes in the SPIROMICS Cohort: An Observational Cohort Study.","authors":"Rajat Suri, Daniela Markovic, Han Woo, Mehrdad Arjomandi, R Graham Barr, Russell P Bowler, Gerard Criner, Jeffrey L Curtis, Mark T Dransfield, M Bradley Drummond, Spyridon Fortis, MeiLan K Han, Eric A Hoffman, Robert J Kaner, Joel D Kaufman, Jerry A Krishnan, Fernando J Martinez, Jill Ohar, Victor E Ortega, Robert Paine, Xavier Soler, Prescott G Woodruff, Nadia N Hansel, Christopher B Cooper, Donald P Tashkin, Russell G Buhr, Igor Z Barjaktarevic","doi":"10.1164/rccm.202310-1965OC","DOIUrl":"10.1164/rccm.202310-1965OC","url":null,"abstract":"<p><p><b>Rationale:</b> Individuals with chronic obstructive pulmonary disease (COPD) have airflow obstruction and maldistribution of ventilation. For those living at high altitude, any gas exchange abnormality is compounded by reduced partial pressures of inspired oxygen. <b>Objectives:</b> Does residence at higher altitude exposure affect COPD outcomes, including lung function, imaging characteristics, symptoms, health status, functional exercise capacity, exacerbations, and mortality? <b>Methods:</b> From the SPIROMICS (Subpopulation and Intermediate Outcome Measures in COPD Study) cohort, we identified individuals with COPD living below 1,000 ft (305 m) elevation (<i>n</i> = 1,367) versus above 4,000 ft (1,219 m) elevation (<i>n</i> = 288). Multivariable regression models were used to evaluate associations of exposure to high altitude with COPD-related outcomes. <b>Measurements and Main Results:</b> Living at higher altitude was associated with reduced functional exercise capacity as defined by 6-minute-walk distance (-32.3 m [95% confidence interval, -49.8 to -14.8 m]). There were no differences in patient-reported outcomes as defined by symptoms (COPD Assessment Test and modified Medical Research Council dyspnea scale), or health status (St. George's Respiratory Questionnaire). Higher altitude was not associated with a different rate of FEV₁ decline. Higher altitude was associated with lower odds of severe exacerbations (incidence rate ratio, 0.65 [95% confidence interval, 0.46 to 0.90]). There were no differences in small airway disease, air trapping, or emphysema. In longitudinal analyses, higher altitude was associated with increased mortality (hazard ratio, 1.25 [95% confidence interval, 1.0 to 1.55]); however, this association was no longer significant when accounting for air pollution. <b>Conclusions:</b> Long-term altitude exposure is associated with reduced functional exercise capacity in individuals with COPD, but this did not translate into differences in symptoms or health status. In addition, long-term high-altitude exposure did not affect progression of disease as defined by longitudinal changes in spirometry. Clinical trial registered with www.clinicaltrials.gov (NCT01969344).</p>","PeriodicalId":19,"journal":{"name":"ACS Materials Letters","volume":" ","pages":"1210-1218"},"PeriodicalIF":9.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140179143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}