Chronic expanding hematoma is defined as a progressively enlarging soft tissue mass persisting beyond 1 month, typically resulting from prior trauma or surgical procedures. Although the condition is rare, its occurrence within deep musculature—particularly with bilateral involvement of the gluteus maximus—is exceedingly uncommon. No previously published English-language reports were identified describing bilateral gluteus maximus hematomas associated with gluteal muscle contracture (GMC).
Case Report
This report describes a 29-year-old male presenting with bilateral chronic expanding hematomas involving the gluteus maximus muscles, accompanied by clinical features consistent with GMC.
Conclusion
Chronic expanding hematoma should be considered a potential underlying etiology in individuals presenting with GMC, particularly when involving deep gluteal musculature.
{"title":"Bilateral Chronic Expanding Hematomas of the Gluteus Maximus Presenting With Gluteal Muscle Contracture: A Case Report","authors":"Xi-Qing Pan, Jin-Hui Liu, Jiang-Li Zhang, Ya-Ya Zhang, Jian-Yong Zhang, Lei Shu, Wei Zhao","doi":"10.1002/iid3.70336","DOIUrl":"10.1002/iid3.70336","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Chronic expanding hematoma is defined as a progressively enlarging soft tissue mass persisting beyond 1 month, typically resulting from prior trauma or surgical procedures. Although the condition is rare, its occurrence within deep musculature—particularly with bilateral involvement of the gluteus maximus—is exceedingly uncommon. No previously published English-language reports were identified describing bilateral gluteus maximus hematomas associated with gluteal muscle contracture (GMC).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Report</h3>\u0000 \u0000 <p>This report describes a 29-year-old male presenting with bilateral chronic expanding hematomas involving the gluteus maximus muscles, accompanied by clinical features consistent with GMC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Chronic expanding hematoma should be considered a potential underlying etiology in individuals presenting with GMC, particularly when involving deep gluteal musculature.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12805526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984678","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}
Yuewen Qi, Xinchen Wang, Yan Liu, Ying Zhang, Qiyu Sun, Chen Wei, Ge Song, Jingyi Liu, Fei Shi, Lixian Sun
Background and Aims
The geriatric nutritional risk index (GNRI) has shown good predictive value for some diseases. However, its association with major adverse cardiovascular events (MACEs) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) remains uncertain. This study investigated the correlation between the GNRI and MACEs.
Patients and Methods
This was a prospective cohort study. We consecutively enrolled 1515 ACS patients who underwent PCI. The median duration of follow-up was 1000 days. The primary endpoints were MACEs, including all-cause mortality, severe heart failure rehospitalization, revascularization, acute myocardial infarction (AMI) recurrence, and restenosis/intrastent thrombosis.
Results
ROC curve analysis revealed an area under the curve of 0.603, with a GNRI cutoff value of 110.78. Cox regression analysis indicated that lower GNRI levels were independently associated with an increased risk of MACEs, a finding supported by risk score assessments. Kaplan–Meier survival curves and log-rank tests indicated significantly lower cumulative survival rates in patients with lower GNRI value. Lower GNRI levels were also correlated with a higher risk of rehospitalization and cardiovascular death, as confirmed by the competing risk model. These associations remained significant after adjustments (all p for interaction > 0.05). RCS analysis and trend tests (all p < 0.05) further supported these findings.
Conclusion
GNRI, as an indicator of nutritional status, was correlated with the risk of MACEs in ACS patients undergoing PCI, particularly in predicting cardiac death and rehospitalization, suggesting that the GNRI level may serve as a valid indicator for predicting poor prognosis in patients with ACS undergoing PCI.
{"title":"Association of the Geriatric Nutritional Risk Index With Prognosis in Patients With Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention","authors":"Yuewen Qi, Xinchen Wang, Yan Liu, Ying Zhang, Qiyu Sun, Chen Wei, Ge Song, Jingyi Liu, Fei Shi, Lixian Sun","doi":"10.1002/iid3.70321","DOIUrl":"10.1002/iid3.70321","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>The geriatric nutritional risk index (GNRI) has shown good predictive value for some diseases. However, its association with major adverse cardiovascular events (MACEs) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) remains uncertain. This study investigated the correlation between the GNRI and MACEs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Patients and Methods</h3>\u0000 \u0000 <p>This was a prospective cohort study. We consecutively enrolled 1515 ACS patients who underwent PCI. The median duration of follow-up was 1000 days. The primary endpoints were MACEs, including all-cause mortality, severe heart failure rehospitalization, revascularization, acute myocardial infarction (AMI) recurrence, and restenosis/intrastent thrombosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ROC curve analysis revealed an area under the curve of 0.603, with a GNRI cutoff value of 110.78. Cox regression analysis indicated that lower GNRI levels were independently associated with an increased risk of MACEs, a finding supported by risk score assessments. Kaplan–Meier survival curves and log-rank tests indicated significantly lower cumulative survival rates in patients with lower GNRI value. Lower GNRI levels were also correlated with a higher risk of rehospitalization and cardiovascular death, as confirmed by the competing risk model. These associations remained significant after adjustments (all <i>p</i> for interaction > 0.05). RCS analysis and trend tests (all <i>p</i> < 0.05) further supported these findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>GNRI, as an indicator of nutritional status, was correlated with the risk of MACEs in ACS patients undergoing PCI, particularly in predicting cardiac death and rehospitalization, suggesting that the GNRI level may serve as a valid indicator for predicting poor prognosis in patients with ACS undergoing PCI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12805523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984642","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}
César A. Galván, Rafael Durán, José Ignacio Larco, Juan Carlos Gomez de la Torre
Background
Accurate identification of respiratory allergen sensitization is essential for managing asthma and allergic rhinitis (AR). While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools, exploratory comparative data for the novel Allergy Explorer 2 (ALEX-2) test in Latin American populations remain scarce. While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools with limited allergen panels per test, the novel Allergy Explorer 2 (ALEX-2) multiplex platform can simultaneously assess multiple allergens. However, exploratory comparative data for ALEX-2 in Latin American populations remain scarce.
Methods
This prospective cross-sectional study evaluated the concordance between SPT, ImmunoCAP, and ALEX-2 in detecting respiratory allergen sensitization among 57 patients with asthma or AR recruited consecutively from a private allergy clinic in Lima, Peru. Concordance was assessed using Cohen's κ coefficient.
Results
The highest overall agreement was observed between ALEX-2 and SPT (κ = 0.5649, p < 0.0001), followed by ALEX-2 and ImmunoCAP (κ = 0.4911, p < 0.0001), and ImmunoCAP and SPT (κ = 0.4688, p < 0.0001). ALEX-2 and ImmunoCAP aligned on 7 of 10 allergens, while both ImmunoCAP and SPT, as well as ALEX-2 and SPT, agreed on 5 of 9 allergens. The strongest concordance was found for dust mites, particularly Dermatophagoides farinae (κ = 0.6323, p < 0.0001) between ALEX-2 and SPT.
Conclusions
ALEX-2 demonstrates moderate agreement with SPT and ImmunoCAP, with the highest concordance for dust mites, suggesting potential as a complementary diagnostic tool pending validation in diverse populations.
{"title":"Concordance Analysis of ALEX-2, ImmunoCAP, and Prick Test for Respiratory Allergies in Lima, Peru","authors":"César A. Galván, Rafael Durán, José Ignacio Larco, Juan Carlos Gomez de la Torre","doi":"10.1002/iid3.70325","DOIUrl":"10.1002/iid3.70325","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Accurate identification of respiratory allergen sensitization is essential for managing asthma and allergic rhinitis (AR). While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools, exploratory comparative data for the novel Allergy Explorer 2 (ALEX-2) test in Latin American populations remain scarce. While Skin Prick Test (SPT) and ImmunoCAP are standard diagnostic tools with limited allergen panels per test, the novel Allergy Explorer 2 (ALEX-2) multiplex platform can simultaneously assess multiple allergens. However, exploratory comparative data for ALEX-2 in Latin American populations remain scarce.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This prospective cross-sectional study evaluated the concordance between SPT, ImmunoCAP, and ALEX-2 in detecting respiratory allergen sensitization among 57 patients with asthma or AR recruited consecutively from a private allergy clinic in Lima, Peru. Concordance was assessed using Cohen's <i>κ</i> coefficient.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The highest overall agreement was observed between ALEX-2 and SPT (<i>κ</i> = 0.5649, <i>p</i> < 0.0001), followed by ALEX-2 and ImmunoCAP (<i>κ</i> = 0.4911, <i>p</i> < 0.0001), and ImmunoCAP and SPT (<i>κ</i> = 0.4688, <i>p</i> < 0.0001). ALEX-2 and ImmunoCAP aligned on 7 of 10 allergens, while both ImmunoCAP and SPT, as well as ALEX-2 and SPT, agreed on 5 of 9 allergens. The strongest concordance was found for dust mites, particularly <i>Dermatophagoides farinae</i> (<i>κ</i> = 0.6323, <i>p</i> < 0.0001) between ALEX-2 and SPT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>ALEX-2 demonstrates moderate agreement with SPT and ImmunoCAP, with the highest concordance for dust mites, suggesting potential as a complementary diagnostic tool pending validation in diverse populations.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145959305","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}
Charles Nkansah, Felix Osei-Boakye, Samuel K. Appiah
Background
Alterations in hematological parameters in SARS-CoV-2 infection may contribute to disease severity and poor outcomes. This study reports the hematological profile of COVID-19 patients.
Methods
This was a cross-sectional study involving 169 confirmed COVID-19 patients conducted at Sunyani Teaching Hospital between January and August, 2022. Sociodemographic, clinical, and laboratory data were obtained. Full blood count was performed using an automated hematology analyzer, and systemic inflammatory indices were calculated.
Results
Participants were mostly young adults (51.5%), females (53.8%), resided in urban settings (41.4%), and aged 20-81 years with a median age of 35.0 (29.0–47.0) years. Overall, anemia was present in 60.4% of the COVID-19 patients (56.4% in males and 63.7% in females), with 23.7%, 23.7%, and 13.0% experiencing mild, moderate, and severe anemia, respectively. The COVID-19 patients mostly had normocytic normochromic anemia (50.3%), and 37.9% had macrocytic normochromic anemia. Older adults (6.600 times, p = 0.004), middle-aged adults (4.435 times, p = 0.034), and rural dwellers (3.759 times, p = 0.012) were associated with anemia among the COVID-19 patients. Thrombocytopenia was detected in 56.2% of the patients, and 36.7%, 16.0%, and 2.4% had mild, moderate and severe thrombocytopenia respectively. Leucocyte alterations among the patients included leucopenia (22.5%), leucocytosis (17.2%), neutropenia (40.8%), and lymphocytosis (39.6%). Total leucocyte count (AUC: 0.818, p < 0.001), absolute neutrophil count (AUC: 0.816, p < 0.001), and absolute lymphocyte count (AUC: 0.804, p < 0.001) predicted severe COVID-19 among the participants. Bicytopenia and pancytopenia were observed in 37.3% and 17.8%, respectively.
Conclusion
COVID-19 is associated with diverse and clinically relevant hematological abnormalities, remarkably anemia, thrombocytopenia, and leucocyte alterations, and usually relate with disease severity. Routine blood cell analysis is essential in the management of COVID-19, particularly in resource-limited settings.
{"title":"COVID-19-Related Hematological Abnormalities Among Adults; A Cross-Sectional Study in a Resource-Limited Setting","authors":"Charles Nkansah, Felix Osei-Boakye, Samuel K. Appiah","doi":"10.1002/iid3.70322","DOIUrl":"10.1002/iid3.70322","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Alterations in hematological parameters in SARS-CoV-2 infection may contribute to disease severity and poor outcomes. This study reports the hematological profile of COVID-19 patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This was a cross-sectional study involving 169 confirmed COVID-19 patients conducted at Sunyani Teaching Hospital between January and August, 2022. Sociodemographic, clinical, and laboratory data were obtained. Full blood count was performed using an automated hematology analyzer, and systemic inflammatory indices were calculated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Participants were mostly young adults (51.5%), females (53.8%), resided in urban settings (41.4%), and aged 20-81 years with a median age of 35.0 (29.0–47.0) years. Overall, anemia was present in 60.4% of the COVID-19 patients (56.4% in males and 63.7% in females), with 23.7%, 23.7%, and 13.0% experiencing mild, moderate, and severe anemia, respectively. The COVID-19 patients mostly had normocytic normochromic anemia (50.3%), and 37.9% had macrocytic normochromic anemia. Older adults (6.600 times, <i>p</i> = 0.004), middle-aged adults (4.435 times, <i>p</i> = 0.034), and rural dwellers (3.759 times, <i>p</i> = 0.012) were associated with anemia among the COVID-19 patients. Thrombocytopenia was detected in 56.2% of the patients, and 36.7%, 16.0%, and 2.4% had mild, moderate and severe thrombocytopenia respectively. Leucocyte alterations among the patients included leucopenia (22.5%), leucocytosis (17.2%), neutropenia (40.8%), and lymphocytosis (39.6%). Total leucocyte count (AUC: 0.818, <i>p</i> < 0.001), absolute neutrophil count (AUC: 0.816, <i>p</i> < 0.001), and absolute lymphocyte count (AUC: 0.804, <i>p</i> < 0.001) predicted severe COVID-19 among the participants. Bicytopenia and pancytopenia were observed in 37.3% and 17.8%, respectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>COVID-19 is associated with diverse and clinically relevant hematological abnormalities, remarkably anemia, thrombocytopenia, and leucocyte alterations, and usually relate with disease severity. Routine blood cell analysis is essential in the management of COVID-19, particularly in resource-limited settings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12796507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145959332","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}
Ameen Jubber, Maumer Durrani, Abdullah Almayahi, Kehinde Sunmboye
Background
Anti-signal recognition particle (anti-SRP) antibodies are myositis-specific autoantibodies associated with immune-mediated necrotizing myopathy. This study was undertaken to better understand how patients with anti-SRP antibodies have been managed at our tertiary centre and to assess the spectrum of clinical features and outcomes in routine clinical practice.
Methods
We conducted a retrospective evaluation of 25 patients with anti-SRP antibodies identified via line-blot immunoassay at a tertiary care centre (2019–2024). Demographic, clinical, serological, and imaging data were reviewed.
Results
The group of patients had a mean age of 60.1 years, with a female-to-male ratio of 10:15. Eight patients (32%) were diagnosed with myositis, primarily presenting with proximal muscle weakness. Interstitial lung disease was observed in 53% of the group of patients, and 50% of the subset of patients with myositis. Coexisting myositis-specific autoantibodies were present in 32%, and 48% had positive antinuclear antibody titres (≥ 1:400). Cardiac involvement was reported in two myositis patients. Corticosteroids, often combined with mycophenolate mofetil or other immunosuppressants, formed the basis of treatment.
Conclusion
Anti-SRP antibodies are associated with a heterogeneous clinical spectrum, with many patients lacking myositis features. There was a high prevalence of coexisting autoantibodies. Further studies are needed to elucidate the pathogenic role of anti-SRP and optimise management strategies.
{"title":"Clinical Characteristics of Patients With Anti-Signal Recognition Particle Antibody: A Cohort Study","authors":"Ameen Jubber, Maumer Durrani, Abdullah Almayahi, Kehinde Sunmboye","doi":"10.1002/iid3.70297","DOIUrl":"10.1002/iid3.70297","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Anti-signal recognition particle (anti-SRP) antibodies are myositis-specific autoantibodies associated with immune-mediated necrotizing myopathy. This study was undertaken to better understand how patients with anti-SRP antibodies have been managed at our tertiary centre and to assess the spectrum of clinical features and outcomes in routine clinical practice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a retrospective evaluation of 25 patients with anti-SRP antibodies identified via line-blot immunoassay at a tertiary care centre (2019–2024). Demographic, clinical, serological, and imaging data were reviewed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The group of patients had a mean age of 60.1 years, with a female-to-male ratio of 10:15. Eight patients (32%) were diagnosed with myositis, primarily presenting with proximal muscle weakness. Interstitial lung disease was observed in 53% of the group of patients, and 50% of the subset of patients with myositis. Coexisting myositis-specific autoantibodies were present in 32%, and 48% had positive antinuclear antibody titres (≥ 1:400). Cardiac involvement was reported in two myositis patients. Corticosteroids, often combined with mycophenolate mofetil or other immunosuppressants, formed the basis of treatment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Anti-SRP antibodies are associated with a heterogeneous clinical spectrum, with many patients lacking myositis features. There was a high prevalence of coexisting autoantibodies. Further studies are needed to elucidate the pathogenic role of anti-SRP and optimise management strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12790825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951164","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}
Macrophages are a key component of innate immunity and regulate cardiac phenotypes by their polarization state. The classical M1 macrophages are activated by pro-inflammatory stimuli, whereas M2 macrophages are activated by anti-inflammatory stimuli. The balance between M1 and M2 polarization is important and tightly controlled to maintain tissue homeostasis.
Objective
This review aims to explain the diversity of the ability to regenerate among humans and zebrafish, the role of the immune system in heart regeneration, and macrophage function in normal conditions and disease. It also investigates age-related effects on macrophage function and therapeutic strategies to manipulate macrophage polarization in the treatment of heart injury.
Methods
Systematic review of the literature was conducted focusing on macrophage polarization, cardiac regeneration mechanisms, and immunomodulatory therapy.
Results
Macrophage polarization imbalances of M1-M2 are involved in inflammatory and cardiac disease. Mechanisms of macrophage function under various states and in various species are useful for insightful comprehension of novel therapy strategies. Macrophage polarization modulation is a future potential strategy for cardiac repair and the treatment of cardiac disease.
Conclusion
Targeting macrophage polarization to restore balance and homeostasis is a promising strategy for supporting cardiac regeneration and the treatment of inflammatory cardiac disease.
{"title":"Role of Macrophages in Cardiac Remodeling: Cues From Zebrafish Heart","authors":"Himanshu Gaur, Maram Hasan, Huseyin C. Yalcin","doi":"10.1002/iid3.70282","DOIUrl":"10.1002/iid3.70282","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Macrophages are a key component of innate immunity and regulate cardiac phenotypes by their polarization state. The classical M1 macrophages are activated by pro-inflammatory stimuli, whereas M2 macrophages are activated by anti-inflammatory stimuli. The balance between M1 and M2 polarization is important and tightly controlled to maintain tissue homeostasis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This review aims to explain the diversity of the ability to regenerate among humans and zebrafish, the role of the immune system in heart regeneration, and macrophage function in normal conditions and disease. It also investigates age-related effects on macrophage function and therapeutic strategies to manipulate macrophage polarization in the treatment of heart injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Systematic review of the literature was conducted focusing on macrophage polarization, cardiac regeneration mechanisms, and immunomodulatory therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Macrophage polarization imbalances of M1-M2 are involved in inflammatory and cardiac disease. Mechanisms of macrophage function under various states and in various species are useful for insightful comprehension of novel therapy strategies. Macrophage polarization modulation is a future potential strategy for cardiac repair and the treatment of cardiac disease.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Targeting macrophage polarization to restore balance and homeostasis is a promising strategy for supporting cardiac regeneration and the treatment of inflammatory cardiac disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12790826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951135","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}
Liduo Yue, Kai Wang, Rongyuan Wang, Linbei Lu, Lihong Fan
<div> <section> <h3> Background</h3> <p>Sustained pulmonary inflammation contributes significantly to lung carcinogenesis. Macrophages play a pivotal role in perpetuating inflammatory responses, undergoing a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis upon activation. The interplay between metabolic reprogramming and macrophage polarization remains poorly defined. The objective of this study is to examines the anti-inflammatory mechanism of lipoic acid (LA), focusing on its ability to modulate immunometabolism in activated macrophages.</p> </section> <section> <h3> Methods</h3> <p>We utilized lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and a murine acute lung injury (ALI) model to evaluate the anti-inflammatory effects of LA. Inflammatory cytokine expression was assessed by qPCR, ELISA, and Western blot. Metabolic profiling was performed using Seahorse XF technology to measure oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), evaluating glycolytic and oxidative metabolic functions.</p> </section> <section> <h3> Results</h3> <p>This study systematically elucidates the molecular mechanism by which LA modulates macrophage inflammatory responses through targeting the HIF1α/glycolysis axis. The main findings are as follows: (1) In LPS-induced RAW264.7 macrophages, LA treatment significantly inhibited the expression of M1 macrophage markers (iNOS, CD86) and the secretion of proinflammatory cytokines (IL-1β, IL-6, etc.). (2) LA effectively reduced the expression of GSDMD, the key executor of pyroptosis, demonstrating its inhibitory effect on macrophage pyroptosis. (3) Metabolic analysis revealed that LA reversed LPS-induced metabolic reprogramming by decreasing the ECAR and increasing the OCR, thereby suppressing glycolysis. (4) Mechanistic studies showed that siRNA-mediated knockdown of HIF1α replicated both the anti-inflammatory and metabolic regulatory effects of LA, confirming HIF1α as the key target in this pathway. (5) In an ALI mouse model, LA treatment significantly reduced HIF1α expression in lung tissues and effectively alleviated inflammatory responses, further validating the proposed mechanism.</p> </section> <section> <h3> Conclusion</h3> <p>LA exerts potent anti-inflammatory effects by targeting HIF1α-mediated metabolic reprogramming in macrophages. Our results highlight the therapeutic potential of targeting immunometabolic pathways in inflammatory lung diseases, providing new insights into the mechanism by which LA ameliorates pulmonary inflammation.</p> </secti
{"title":"Lipoic Acid Ameliorates Lipopolysaccharide-Induced Inflammation via Inhibition of Glycolysis in RAW264.7 Macrophages","authors":"Liduo Yue, Kai Wang, Rongyuan Wang, Linbei Lu, Lihong Fan","doi":"10.1002/iid3.70313","DOIUrl":"10.1002/iid3.70313","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Sustained pulmonary inflammation contributes significantly to lung carcinogenesis. Macrophages play a pivotal role in perpetuating inflammatory responses, undergoing a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis upon activation. The interplay between metabolic reprogramming and macrophage polarization remains poorly defined. The objective of this study is to examines the anti-inflammatory mechanism of lipoic acid (LA), focusing on its ability to modulate immunometabolism in activated macrophages.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We utilized lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and a murine acute lung injury (ALI) model to evaluate the anti-inflammatory effects of LA. Inflammatory cytokine expression was assessed by qPCR, ELISA, and Western blot. Metabolic profiling was performed using Seahorse XF technology to measure oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), evaluating glycolytic and oxidative metabolic functions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>This study systematically elucidates the molecular mechanism by which LA modulates macrophage inflammatory responses through targeting the HIF1α/glycolysis axis. The main findings are as follows: (1) In LPS-induced RAW264.7 macrophages, LA treatment significantly inhibited the expression of M1 macrophage markers (iNOS, CD86) and the secretion of proinflammatory cytokines (IL-1β, IL-6, etc.). (2) LA effectively reduced the expression of GSDMD, the key executor of pyroptosis, demonstrating its inhibitory effect on macrophage pyroptosis. (3) Metabolic analysis revealed that LA reversed LPS-induced metabolic reprogramming by decreasing the ECAR and increasing the OCR, thereby suppressing glycolysis. (4) Mechanistic studies showed that siRNA-mediated knockdown of HIF1α replicated both the anti-inflammatory and metabolic regulatory effects of LA, confirming HIF1α as the key target in this pathway. (5) In an ALI mouse model, LA treatment significantly reduced HIF1α expression in lung tissues and effectively alleviated inflammatory responses, further validating the proposed mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>LA exerts potent anti-inflammatory effects by targeting HIF1α-mediated metabolic reprogramming in macrophages. Our results highlight the therapeutic potential of targeting immunometabolic pathways in inflammatory lung diseases, providing new insights into the mechanism by which LA ameliorates pulmonary inflammation.</p>\u0000 </secti","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70313","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145916498","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}
Md. Haydar Ali, Joydeep Paul, Romana Parvin, Md. Shahadat Hossain, Sharmin Shahid Labony, Nusrat Nowrin Shohana, Md. Mahmudul Alam, Umme Razia Islam, Anita Rani Dey, Md. Abu Hadi Noor Ali Khan, Md. Abdul Alim, Anisuzzaman
Background
Fasciolosis is a food-borne parasitic zoonotic disease caused by widespread liver flukes that affect ruminants and humans, and is responsible for non-resolving hepatic damage. Although fasciolosis occurs in both acute and chronic forms, chronic fasciolosis is more common.
Objectives
This study investigates the pathological changes and immunological cascade in the livers of Fasciola gigantica infected cattle, both at the transcriptional and translational levels.
Methods
Normal and suspected liver samples from cattle were collected and examined. Affected tissues were subjected to routine histological and immunohistochemical analysis. Transcription factors and interleukins (IL) were measured by sqRT-PCR and ELISA.
Results
In chronic fasciolosis, liver became atrophied, marked with whitish fibrotic patches, calcification and bile duct hyperplasia filled with blackish-brown sandy contents. Histopathological examinations showed massive loss of hepatocytes, fibrous proliferation, and infiltration of mononuclear cells and eosinophils. In addition, a huge deposition of amyloid was noticed in severely affected livers. T-bet (T-box expressed in T cells protein) remained at the basal level, whereas expression of GATA-3 (GATA-binding protein 3) was dramatically increased in severe fasciolosis. Also, there was a noticeable increase in the GATA-3 positive cells, while T-bet positive cells were largely absent, displaying a drift towards Th2 type immune response. In severe infection, mRNAs of IL-4, IL-5, IL-6, IL-10 and IL-13 highly expressed compared to the non-infected control, but the interferon- (INF)-γ expression remained unaltered. Similarly, we detected significant (p < 0.01) elevation of IL-4, IL-5, IL-6 and IL-13 in severely affected liver lysate. To further validate the notion, bovine peripheral blood mononuclear cells (bPBMCs) were treated with F. gigantica-culture milieu (FCM). FCM treatment elevated IL-4, IL-5, IL-6 and IL-13 in a time dependent manner, confirming liver fluke-induced Th2-biased immune response.
Conclusion
This study reveals distinct pathology and dysregulation of transcription factors and cytokines profiles in F. gigantica infected cattle.
{"title":"Liver Cirrhosis Caused by Food-Borne Zoonotic Fasciola gigantica in Cattle in Bangladesh: Pathology and Immunological Orchestra","authors":"Md. Haydar Ali, Joydeep Paul, Romana Parvin, Md. Shahadat Hossain, Sharmin Shahid Labony, Nusrat Nowrin Shohana, Md. Mahmudul Alam, Umme Razia Islam, Anita Rani Dey, Md. Abu Hadi Noor Ali Khan, Md. Abdul Alim, Anisuzzaman","doi":"10.1002/iid3.70320","DOIUrl":"https://doi.org/10.1002/iid3.70320","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Fasciolosis is a food-borne parasitic zoonotic disease caused by widespread liver flukes that affect ruminants and humans, and is responsible for non-resolving hepatic damage. Although fasciolosis occurs in both acute and chronic forms, chronic fasciolosis is more common.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This study investigates the pathological changes and immunological cascade in the livers of <i>Fasciola gigantica</i> infected cattle, both at the transcriptional and translational levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Normal and suspected liver samples from cattle were collected and examined. Affected tissues were subjected to routine histological and immunohistochemical analysis. Transcription factors and interleukins (IL) were measured by sqRT-PCR and ELISA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In chronic fasciolosis, liver became atrophied, marked with whitish fibrotic patches, calcification and bile duct hyperplasia filled with blackish-brown sandy contents. Histopathological examinations showed massive loss of hepatocytes, fibrous proliferation, and infiltration of mononuclear cells and eosinophils. In addition, a huge deposition of amyloid was noticed in severely affected livers. T-bet (T-box expressed in T cells protein) remained at the basal level, whereas expression of GATA-3 (GATA-binding protein 3) was dramatically increased in severe fasciolosis. Also, there was a noticeable increase in the GATA-3 positive cells, while T-bet positive cells were largely absent, displaying a drift towards Th2 type immune response. In severe infection, mRNAs of IL-4, IL-5, IL-6, IL-10 and IL-13 highly expressed compared to the non-infected control, but the interferon- (INF)-γ expression remained unaltered. Similarly, we detected significant (<i>p</i> < 0.01) elevation of IL-4, IL-5, IL-6 and IL-13 in severely affected liver lysate. To further validate the notion, bovine peripheral blood mononuclear cells (bPBMCs) were treated with <i>F. gigantica-</i>culture milieu (FCM). FCM treatment elevated IL-4, IL-5, IL-6 and IL-13 in a time dependent manner, confirming liver fluke-induced Th2-biased immune response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study reveals distinct pathology and dysregulation of transcription factors and cytokines profiles in <i>F. gigantica</i> infected cattle.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"14 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145915827","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}
Nanlin Cao, Yuan Li, Zhijie Chen, Zuliang Deng, Yangzhi Hu
Background
Colorectal cancer (CRC) is a leading cause of cancer-related mortality, which necessitates the exploration of novel therapeutic targets.
Objective
This study aims to investigate the effects of Prolyl 4-hydroxylase subunit alpha-1 (P4HA1) inhibition on CRC tumor growth, metastasis, and tumor-associated macrophage (TAM) infiltration.
Methods
The association between P4HA1 expression and CRC progression as well as tumor immune infiltration was analyzed. In vitro experiments were performed to evaluate the effect of targeting P4HA1 on CRC cell proliferation and migration. The secretion of CCL2, CCL4, and CCL7 and recruitment of TAMs were detected after P4HA1 knockdown. Mechanistic studies were conducted to explore the interaction between P4HA1 and P4HA2 and its regulation on the PI3K-AKT signaling pathway. In vivo experiments were also carried out to verify the effect of P4HA1 knockdown on CRC tumor growth, metastasis, and TAM infiltration polarization.
Results
P4HA1 expression was found to be associated with CRC progression and tumor immune infiltration. Targeting P4HA1 significantly suppressed CRC cell proliferation and migration in vitro. Moreover, P4HA1 knockdown reduced the secretion of CCL2, CCL4, CCL7 and the recruitment of TAMs. Mechanistically, P4HA1 interacted with P4HA2, thereby disrupting the PI3K-AKT signaling pathway which is crucial for CRC progression and TAMs recruitment. In vivo experiments confirmed that P4HA1 knockdown inhibited CRC tumor growth, metastasis, and TAM infiltration polarization.
Conclusion
Our findings elucidate the importance of the P4HA1-P4HA2-PI3K-AKT axis in CRC and identify P4HA1 as a promising therapeutic target to impede CRC growth and metastasis while altering the tumor immune landscape. This research provides a foundation for further investigations into P4HA1-targeted therapies, which may improve clinical outcomes for patients with CRC.
{"title":"Targeting P4HA1 Inhibits Colorectal Cancer Growth, Metastasis, and Tumor-Associated Macrophage Infiltration via P4HA2-PI3K-AKT Pathway","authors":"Nanlin Cao, Yuan Li, Zhijie Chen, Zuliang Deng, Yangzhi Hu","doi":"10.1002/iid3.70315","DOIUrl":"10.1002/iid3.70315","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Colorectal cancer (CRC) is a leading cause of cancer-related mortality, which necessitates the exploration of novel therapeutic targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aims to investigate the effects of Prolyl 4-hydroxylase subunit alpha-1 (P4HA1) inhibition on CRC tumor growth, metastasis, and tumor-associated macrophage (TAM) infiltration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The association between P4HA1 expression and CRC progression as well as tumor immune infiltration was analyzed. In vitro experiments were performed to evaluate the effect of targeting P4HA1 on CRC cell proliferation and migration. The secretion of CCL2, CCL4, and CCL7 and recruitment of TAMs were detected after P4HA1 knockdown. Mechanistic studies were conducted to explore the interaction between P4HA1 and P4HA2 and its regulation on the PI3K-AKT signaling pathway. In vivo experiments were also carried out to verify the effect of P4HA1 knockdown on CRC tumor growth, metastasis, and TAM infiltration polarization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>P4HA1 expression was found to be associated with CRC progression and tumor immune infiltration. Targeting P4HA1 significantly suppressed CRC cell proliferation and migration in vitro. Moreover, P4HA1 knockdown reduced the secretion of CCL2, CCL4, CCL7 and the recruitment of TAMs. Mechanistically, P4HA1 interacted with P4HA2, thereby disrupting the PI3K-AKT signaling pathway which is crucial for CRC progression and TAMs recruitment. In vivo experiments confirmed that P4HA1 knockdown inhibited CRC tumor growth, metastasis, and TAM infiltration polarization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings elucidate the importance of the P4HA1-P4HA2-PI3K-AKT axis in CRC and identify P4HA1 as a promising therapeutic target to impede CRC growth and metastasis while altering the tumor immune landscape. This research provides a foundation for further investigations into P4HA1-targeted therapies, which may improve clinical outcomes for patients with CRC.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12753198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862924","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}
EXPRESSION OF CONCERN: X. Zheng, X. Zhang, L. Dong, J. Zhao, C. Zhang and R. Chen, “Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β,” Immunity, Inflammation and Disease 11, no. 10 (2023): e1030, https://doi.org/10.1002/iid3.1030.
This Expression of Concern is for the above article, published online on 04 October 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley & Sons Ltd. The Expression of Concern has been agreed upon due to inconsistencies and discrepancies identified in Figure 2. Although the authors provided some raw data corresponding to the study, the data supplied was incomplete. Additionally, the authors were unable to provide documentation of ethics approval granted prior to the commencement of the study, as required. Instead, retrospective approval was obtained. The journal is issuing this expression of concern to alert readers.
{"title":"EXPRESSION OF CONCERN: Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β","authors":"","doi":"10.1002/iid3.70314","DOIUrl":"10.1002/iid3.70314","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: X. Zheng, X. Zhang, L. Dong, J. Zhao, C. Zhang and R. Chen, “Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β,” <i>Immunity, Inflammation and Disease</i> 11, no. 10 (2023): e1030, https://doi.org/10.1002/iid3.1030.</p><p>This Expression of Concern is for the above article, published online on 04 October 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley & Sons Ltd. The Expression of Concern has been agreed upon due to inconsistencies and discrepancies identified in Figure 2. Although the authors provided some raw data corresponding to the study, the data supplied was incomplete. Additionally, the authors were unable to provide documentation of ethics approval granted prior to the commencement of the study, as required. Instead, retrospective approval was obtained. The journal is issuing this expression of concern to alert readers.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12753327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862976","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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