Physiological Reports最新文献_第9页

Bidirectional predictors between baseline and recovery sleep measures and cardiovascular measures during sleep deprivation and psychological stress. 在睡眠剥夺和心理压力期间，基线和恢复睡眠测量和心血管测量之间的双向预测。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70374

Lauren N Pasetes, Kathleen M Rosendahl-Garcia, Namni Goel

{"title":"Bidirectional predictors between baseline and recovery sleep measures and cardiovascular measures during sleep deprivation and psychological stress.","authors":"Lauren N Pasetes, Kathleen M Rosendahl-Garcia, Namni Goel","doi":"10.14814/phy2.70374","DOIUrl":"10.14814/phy2.70374","url":null,"abstract":"For the first time, we investigated bidirectional predictors between baseline and recovery sleep and cardiovascular (CV) measures during total sleep deprivation (TSD) and psychological stress in a five-day experiment with 32 healthy adults (27-53y; 14 females). CV measures were collected in the morning after two baseline nights (B1, B2) and during TSD morning (TSD AM) and evening following psychological stress (TSD PM). Actigraphy assessed sleep during B2 before TSD and the first recovery night (R1) after TSD. Higher B2 wake after sleep onset (WASO) predicted lower TSD PM stroke volume and higher TSD PM systemic vascular resistance index (SVRI), with greater B2 percent sleep predicting inverse relationships, explaining 12.8%-15.9% of the TSD CV variance. Also, higher B2 WASO predicted higher B2 AM SVRI. Furthermore, longer TSD left ventricular ejection time predicted later R1 sleep offset, longer sleep duration, and higher WASO; by contrast, higher TSD AM and TSD PM heart rate predicted earlier R1 sleep offset. TSD CV indices explained 14.8%-24.9% of the R1 sleep variance. Notably, females showed significant predictive bidirectional relationships. Our novel results demonstrate that baseline sleep predicts CV metrics during TSD and psychological stress, and that these metrics predict recovery sleep, underscoring crucial relationships, mechanisms, and biomarkers between sleep and cardiovascular health.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70374"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12098958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Brain derived neurotrophic factor and secreted amyloid precursor protein-α response to moderate and high intensity exercise. 中高强度运动对脑源性神经营养因子和分泌性淀粉样蛋白-α的影响。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70366

Felicity S E Spencer, Richard J Elsworthy, Leigh Breen, Jon R B Bishop, Samuel J E Lucas, Sarah Aldred

{"title":"Brain derived neurotrophic factor and secreted amyloid precursor protein-α response to moderate and high intensity exercise.","authors":"Felicity S E Spencer, Richard J Elsworthy, Leigh Breen, Jon R B Bishop, Samuel J E Lucas, Sarah Aldred","doi":"10.14814/phy2.70366","DOIUrl":"10.14814/phy2.70366","url":null,"abstract":"Brain-derived neurotrophic factor (BDNF) and secreted amyloid precursor protein-alpha (sAPPα) promote neuronal growth but are lower in people with Alzheimer's Disease (AD). BDNF increases after exercise, but the response may vary with exercise intensity and across blood fractions. While sAPPα rises post-exercise in animals, its response to aerobic exercise in humans is unclear. This study examined how BDNF and sAPPα respond to moderate and high-intensity exercise in healthy young adult humans. Participants completed three exercise conditions: moderate (65% Watt maximum, 30 min), clinical-HIIT (4 × 4 min, 90% Watt maximum), and all-out-HIIT (8 × 30 s, 150% Watt maximum). Blood-based biomarkers were extracted from venous blood drawn from venepuncture at baseline, immediately after exercise, and after 30 min rest. BDNF concentration was measured in serum, plasma, platelet-poor plasma, and platelets; sAPPα in serum via ELISAs. Data were primarily analyzed using mixed effects models. BDNF increased in plasma and platelet-poor plasma across conditions but rose in serum only after clinical-HIIT and moderate intensity exercise. BDNF concentration in platelets was unaffected. sAPPα increased after moderate and clinical-HIIT sessions. Measurement of BDNF in serum alone may not fully represent the changes in BDNF post-exercise. Further research is required in adults at risk of AD.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70366"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12099066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Loss of hepatic autophagy induces α-cell proliferation through impaired glutamine-dependent gluconeogenesis. 肝自噬丧失通过谷氨酰胺依赖性糖异生损伤诱导α-细胞增殖。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70381

Jesse N Velasco-Silva, Joseph L Wilkerson, Daniela Ramos, Hayden K Low, Faith Bowman, Kimberley J Evason, Sihem Boudina, William L Holland, Gregory S Ducker

{"title":"Loss of hepatic autophagy induces α-cell proliferation through impaired glutamine-dependent gluconeogenesis.","authors":"Jesse N Velasco-Silva, Joseph L Wilkerson, Daniela Ramos, Hayden K Low, Faith Bowman, Kimberley J Evason, Sihem Boudina, William L Holland, Gregory S Ducker","doi":"10.14814/phy2.70381","DOIUrl":"10.14814/phy2.70381","url":null,"abstract":"Autophagy, the highly conserved process of protein and organelle degradation, is suppressed in the liver by obesity and metabolic dysfunction-associated fatty liver disease and associated with the development of insulin resistance. We generated adult liver-inducible ATG3 knockout mice (Atg3iLKO) to characterize pathways linking hepatic autophagy with metabolic homeostasis. Genetic loss of hepatic autophagy leads to a reduction in 16-h fasted glucose levels, a decrease in endogenous glucose production rates, and an increase in serum amino acids across the fed and fasted states. These changes collectively reflect a loss of hepatic gluconeogenic enzyme activity and not a general inability to degrade amino acids in the liver. Increased circulating glutamine levels resulting from this are associated with an induction of α-cell hyperplasia, leading to constitutively elevated glucagon levels. However, the loss of hepatic gluconeogenesis renders these animals highly glucagon resistant. Collectively, our data demonstrate that loss of hepatic autophagy is sufficient to activate the hepatic α-islet cell axis, leading to hyperglucagonemia with impaired glucose production.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70381"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modulation of stretch activation influences the stretch-shortening cycle effect in in vivo human knee extensors. 调节拉伸激活影响人体膝关节伸肌的拉伸-缩短周期效应。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70377

Iseul Jo, Wolfgang Seiberl, Hae-Dong Lee

{"title":"Modulation of stretch activation influences the stretch-shortening cycle effect in in vivo human knee extensors.","authors":"Iseul Jo, Wolfgang Seiberl, Hae-Dong Lee","doi":"10.14814/phy2.70377","DOIUrl":"10.14814/phy2.70377","url":null,"abstract":"This study investigated the effects of progressively increasing voluntary activation during the stretch phase on force and work production in the stretch-shortening cycle (SSC) of human knee extensors. Fifteen young adults performed SSCs under four stretch activation conditions: passive stretch (ST0%-SC), feedback-guided active stretch (ST40%-SC and ST80%-SC), and maximal effort stretch (ST100%-SC). All conditions involved maximal voluntary activation during shortening, followed by a fixed-end contraction at 20°. Outcome measures included joint torque and work, estimated fascicle force and work, vastus lateralis fascicle length and velocity, and quadriceps activation. Compared to passive stretch, active stretch conditions produced greater SSC effects, with no significant differences between ST80%-SC and ST100%-SC. Fascicle work did not differ significantly across conditions, suggesting a decoupling between joint-level output and fascicle-level contribution. Active stretch primarily enhanced force production during early shortening; however, the SSC effect persisted until mid-to-late shortening (80° to 38°) in ST80%-SC. ST0%-SC also showed nearly twice the fascicle shortening velocity of other conditions. Following shortening, ST100%-SC exhibited greater residual force depression during the isometric phase, despite similar activation. These findings demonstrate that voluntary activation during stretch modulates SSC effect through a complex interplay involving muscle-tendon unit decoupling and history-dependent effects, fascicle dynamics, and tendon compliance.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70377"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Heat therapy preserves myofibre size and SERCA-mediated Ca²⁺ uptake in the mouse soleus after tenotomy surgery. 热疗法保留肌腱切断术后小鼠比目鱼肌肌纤维大小和serca介导的Ca2+摄取。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70385

Michael K Barfoot, Jessica L Braun, Phillip J Wallace, Bianca M Marcella, Ryan W Baranowski, Rebecca E K MacPherson, Stephen S Cheung, Val A Fajardo

{"title":"Heat therapy preserves myofibre size and SERCA-mediated Ca2+ uptake in the mouse soleus after tenotomy surgery.","authors":"Michael K Barfoot, Jessica L Braun, Phillip J Wallace, Bianca M Marcella, Ryan W Baranowski, Rebecca E K MacPherson, Stephen S Cheung, Val A Fajardo","doi":"10.14814/phy2.70385","DOIUrl":"10.14814/phy2.70385","url":null,"abstract":"Heat therapy (HT) has been shown to induce physiological adaptations in muscle, including a reduction in the severity of muscle atrophy resulting from unloading. The muscle atrophy caused by unloading can be partially attributed to the dysregulation of Ca2+ in the muscle cell, which can activate calpain-mediated proteolysis. The sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) is a primary regulator of Ca2+ in muscle, and SERCA dysfunction has been repeatedly demonstrated in various models of muscle unloading. Heat shock protein 70 (HSP70) is a heat-inducible chaperone protein that binds to SERCA and protects against its dysfunction. While previous research has shown HT to upregulate HSP70 in rodent muscle, even in the unloaded state, the effects of HT on SERCA function in rodent skeletal muscle under these conditions remain unknown. Here, we characterized the effects of 4 weeks of HT on soleus muscle size, HSP70 expression, SERCA function, and maximal calpain activity in male C57BL/6J mice subjected to muscle unloading through tenotomy. Four weeks of HT preserved the cross-sectional area of soleus myofibres following tenotomy, while also upregulating HSP70, maintaining SERCA-mediated Ca2+ uptake, and reducing maximal calpain activity. Therefore, our research offers new insights into the advantages of HT for muscle health and physiology.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70385"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12099063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Occupational cold stress and rewarming alters skin temperature thresholds for manual dexterity decrements: An exploratory study. 职业性冷应激和复温可改变手灵巧性下降的皮肤温度阈值：一项探索性研究。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70342

Christopher L Chapman, Brandon M Roberts, Erica A Schafer, John W Castellani, Karl E Friedl, Adam W Potter, David P Looney

{"title":"Occupational cold stress and rewarming alters skin temperature thresholds for manual dexterity decrements: An exploratory study.","authors":"Christopher L Chapman, Brandon M Roberts, Erica A Schafer, John W Castellani, Karl E Friedl, Adam W Potter, David P Looney","doi":"10.14814/phy2.70342","DOIUrl":"https://doi.org/10.14814/phy2.70342","url":null,"abstract":"The skin temperature thresholds at which precipitous reductions in dexterity occur in cold environments, and whether they are altered by rewarming, are not well defined. In three environmental conditions (20°C, 10°C, and 0°C air temperatures), 14 healthy adults (three females; age: 24 ± 6 years) completed five dexterity tests (Placing Test) over ~130 min of various light-to-moderate physical activities to simulate occupational work demands while minimally dressed. Brief passive rewarming (10 min in ~22°C air temperature) and a final dexterity test upon reentry to the environment was then performed. Dexterity was evaluated as the absolute (seconds) or percent change from an individual's best baseline performance. Prior to rewarming, segmented regression revealed thresholds for greater dexterity loss during progressive cold strain occurred at skin temperatures of ~22.9°C (fingers), ~24.9°C (hand), and ~22.4°C (forearm) (all p ≤ 0.002). After rewarming, this threshold shifted upwards to ~25.7°C for the fingers (p ≤ 0.007). The hand skin temperature threshold after rewarming was ~27.1°C (for absolute changes, p < 0.001), but one was not identified with percent change (p = 0.074). A forearm skin temperature threshold was not identified following rewarming (p ≥ 0.058). These findings indicate that, in non-hypothermic conditions, skin temperature thresholds for dexterity loss during prolonged occupational cold stress may be modified with rewarming.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 9","pages":"e70342"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CIAPIN1 promotes proliferation and migration of PDGF-BB-activated airway smooth muscle cells via the PI3K/AKT and JAK2/STAT3 signaling pathways. CIAPIN1通过PI3K/AKT和JAK2/STAT3信号通路促进pdgf - bb激活的气道平滑肌细胞的增殖和迁移。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70360

Ling Zhu, Jin Zhou, Yunfan Gu, Yongtian Xu, Yanfang Guo

{"title":"CIAPIN1 promotes proliferation and migration of PDGF-BB-activated airway smooth muscle cells via the PI3K/AKT and JAK2/STAT3 signaling pathways.","authors":"Ling Zhu, Jin Zhou, Yunfan Gu, Yongtian Xu, Yanfang Guo","doi":"10.14814/phy2.70360","DOIUrl":"https://doi.org/10.14814/phy2.70360","url":null,"abstract":"Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is an essential anti-apoptotic protein; however, its role and associated molecular pathways in asthma remain largely unexplored. This study aimed to investigate the potential effects of CIAPIN1 on the proliferation and migration of platelet-derived growth factor BB (PDGF-BB)-induced ASMCs and the underlying mechanisms involved. Considering these aspects, ASMCs are activated with PDGF-BB as a cellular model for asthma. CIAPIN1 is then downregulated using small interfering ribonucleic acid (siRNA). Western blot analysis was performed to assess protein expression. Elevated levels of CIAPIN1 were observed, demonstrating a positive correlation with cytokine levels. CIAPIN1 expression is significantly increased in PDGF-BB-induced human ASMCs. In addition, CIAPIN1 knockdown inhibited proliferation, inflammatory cytokine production, and migration ability, while elevating apoptosis in PDGF-BB-induced human ASMCs. Moreover, CIAPIN1 knockdown inhibited phosphorylated phosphoinositide 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated Janus kinase 2 (p-JAK2), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) protein expression. In conclusion, the results indicate that CIAPIN1 regulates the proliferation and migration of human ASMC in response to PDGF-BB by inhibiting the PI3K/AKT and JAK2/STAT3 pathways.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 9","pages":"e70360"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12058325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The pulmonary resistance-compliance relationship: Real or mathematical artifact? 肺阻力-顺应性关系：真实的还是数学的人工产物？

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70355

Sara Hungerford, Navin Kapur, Stuart Rich, Daniel Burkhoff

{"title":"The pulmonary resistance-compliance relationship: Real or mathematical artifact?","authors":"Sara Hungerford, Navin Kapur, Stuart Rich, Daniel Burkhoff","doi":"10.14814/phy2.70355","DOIUrl":"https://doi.org/10.14814/phy2.70355","url":null,"abstract":"Pulmonary vascular resistance (PVR) and arterial compliance (PAC) have been reported to share an inverse hyperbolic relationship, with their product-the pulmonary vascular time constant (τ)-remaining more or less constant across disease states. However, PAC is often estimated as stroke volume (SV) divided by pulse pressure (PACclinical = SV/PP), introducing potential mathematical coupling with PVR, which is dependent on SV. This inherent relationship may artificially produce hyperbolic correlations. We conducted joint density analysis (JDA) and hemodynamic simulations using data from patients with pulmonary hypertension due to left-sided disease. PACclinical was calculated as SV/PAPP, and PVR as (PAM - PCWP)/CO. Log-transformed values were analyzed to assess the PVR-PACclinical relationship. JDA demonstrated a strong inverse correlation between PVR and PACclinical (Spearman's R = -0.88, CI -0.92 to -0.82), increasing to -0.92 with bootstrapping. Hemodynamic simulations confirmed a first-order hyperbolic decay (PAC = τavg/PVR; r2 = 0.86, p < 0.001). The relationship shifted downward with increasing PCWP. Our findings replicate the reported PVR-PACclinical relationship, highlighting its mathematical dependence. Further studies using more accurate PAC estimation methods are needed to determine whether this association is truly physiological or an artifact of calculation.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 9","pages":"e70355"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Low-dose ASA therapy does not alter core or skin temperature during hot-dry or warm-humid heat stress (PSU HEAT project). 在干热或湿热应激期间，低剂量ASA治疗不会改变核心或皮肤温度（PSU heat项目）。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70375

Kat G Fisher, Olivia K Leach, Rachel M Cottle, Lacy M Alexander, W Larry Kenney

{"title":"Low-dose ASA therapy does not alter core or skin temperature during hot-dry or warm-humid heat stress (PSU HEAT project).","authors":"Kat G Fisher, Olivia K Leach, Rachel M Cottle, Lacy M Alexander, W Larry Kenney","doi":"10.14814/phy2.70375","DOIUrl":"10.14814/phy2.70375","url":null,"abstract":"Nearly 40% of US adults over the age of 50 use aspirin (ASA) therapy for the primary or secondary prevention of cardiovascular disease. Systemic platelet cyclooxygenase inhibition with low-dose ASA attenuates reflex cutaneous vasodilation and accelerates the rate of rise of core temperature during passive heating in middle-aged adults. The functional effect of low-dose ASA therapy on thermoregulatory and cardiovascular responses to hot and humid environmental extremes in older (>65 years) adults has not been determined. Eleven older adults (5F; 66-80 years) were exposed to progressive heat stress in an environmental chamber at a metabolic rate comparable to activities of daily living (~80 W∙m-2) in a warm-humid (WH; 36°C, 52% rh) and hot-dry (HD; 40°C, 21% rh) environment following 7 days of low-dose ASA (81 mg/day) or placebo. Core temperature (Tc), skin temperature (Tsk), heart rate (HR), mean arterial pressure (MAP) and forearm blood flow (FBF) were measured, and rate-pressure product was subsequently calculated. Low-dose ASA attenuated FBF and forearm vascular conductance (all p ≤ 0.04) but had no effect on Tc or Tsk in either environment. In conclusion, low-dose ASA attenuates the skin blood flow response during minimal activity heat stress in both dry and humid environments but does not alter Tc.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 9","pages":"e70375"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12066818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis. 在流感相关的肺曲霉病期间，IL-6信号调节炎症反应而不影响病原体负担。

IF 2.2

Physiological Reports Pub Date : 2025-05-01 DOI: 10.14814/phy2.70372

Lokesh Sharma, Ravineel B Singh, Nathaniel J Tolman, Caden Ngeow, Alexis M Duray, Nima Naghshtabrizi, Aijaz Ahmad, William Bain, Keven M Robinson

{"title":"IL-6 signaling regulates the inflammatory response without impacting pathogen burden during influenza-associated pulmonary aspergillosis.","authors":"Lokesh Sharma, Ravineel B Singh, Nathaniel J Tolman, Caden Ngeow, Alexis M Duray, Nima Naghshtabrizi, Aijaz Ahmad, William Bain, Keven M Robinson","doi":"10.14814/phy2.70372","DOIUrl":"10.14814/phy2.70372","url":null,"abstract":"Viral infections increase host susceptibility to opportunistic pathogens like Aspergillus fumigatus (AF), exacerbating disease severity and prolonging its clinical course. Interleukin-6 (IL-6) drives pathological inflammation in viral infections such as COVID-19, but its role in influenza, particularly with secondary AF infection, remains unclear. Using a mouse model of post-influenza AF infection, including IL-6 knockout mice, we found that IL-6 signaling promotes neutrophilic lung inflammation but is not required for pathogen clearance of either influenza or AF. However, IL-6 deficiency increases epithelial cell damage, as indicated by elevated RAGE levels in bronchoalveolar lavage fluid. In contrast, lung capillary permeability (measured by IgM levels in BAL) and tissue injury (assessed histologically) remain unaffected in the absence of IL-6 signaling. These findings reveal a nuanced role for IL-6 in post-influenza AF infection, underscoring its contribution to lung inflammation and epithelial integrity.","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"13 10","pages":"e70372"},"PeriodicalIF":2.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0