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Search Results (1,696)

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10 pages, 713 KiB  
Article
Pulse Steroid Therapy for Severe Acute Respiratory Distress Syndrome: A Propensity Score-Matched Analysis
by Yasumasa Kawano, Junichi Maruyama, Mitsuaki Nishikimi, Hisatomi Arima, Yuhei Irie, Shinichi Morimoto, Kentaro Muranishi, Maiko Nakashio and Yoshihiko Nakamura
J. Clin. Med. 2025, 14(15), 5547; https://doi.org/10.3390/jcm14155547 - 6 Aug 2025
Abstract
Background/Objectives: Low-dose corticosteroids have gained popularity in the treatment of acute respiratory distress syndrome (ARDS); however, the efficacy of high-dose corticosteroids as pulse steroid therapy remains controversial. This study aimed to evaluate the efficacy of pulse steroid therapy in patients with severe ARDS [...] Read more.
Background/Objectives: Low-dose corticosteroids have gained popularity in the treatment of acute respiratory distress syndrome (ARDS); however, the efficacy of high-dose corticosteroids as pulse steroid therapy remains controversial. This study aimed to evaluate the efficacy of pulse steroid therapy in patients with severe ARDS requiring venovenous (V-V) extracorporeal membrane oxygenation (ECMO), where enhanced anti-inflammatory effects may be beneficial. Methods: Using data from the J-CARVE registry, which included patients with severe ARDS managed with V-V ECMO across 24 Japanese hospitals between January 2012 and December 2022, we identified 373 patients treated with corticosteroids. The patients were divided into two groups: pulse steroid therapy and non-pulse steroid therapy. Propensity score matching was performed, and all-cause hospital mortality and ECMO-free days within 28 days were compared between groups. Pulse steroid therapy was defined as methylprednisolone at a dose of 1000 mg/day. Results: After matching, 48 patients were included in each group. The all-cause hospital mortality rates were 41.7% (20/48) in the pulse steroid group and 47.9% (23/48) in the non-pulse steroid group, with no significant difference (odds ratio, 1.28; 95% confidence interval: 0.53–3.12, p = 0.68). The median ECMO-free days were 9.5 (interquartile range [IQR]: 0–17.3) in the pulse steroid group and 3 (IQR: 0–17) in the non-pulse steroid group, showing no significant difference (p = 0.69). Conclusions: Pulse steroid therapy did not improve all-cause hospital mortality or ECMO-free days in patients with severe ARDS who required V-V ECMO. Full article
(This article belongs to the Section Emergency Medicine)
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12 pages, 2363 KiB  
Article
MCC950 Alleviates Fat Embolism-Induced Acute Respiratory Distress Syndrome Through Dual Modulation of NLRP3 Inflammasome and ERK Pathways
by Chin-Kuo Lin, Zheng-Wei Chen, Yu-Hao Lin, Cheng-Ta Yang, Chung-Sheng Shi, Chieh-Mo Lin, Tzu Hsiung Huang, Justin Ching Hsien Lu, Kwok-Tung Lu and Yi-Ling Yang
Int. J. Mol. Sci. 2025, 26(15), 7571; https://doi.org/10.3390/ijms26157571 - 5 Aug 2025
Abstract
Fat embolism is a critical medical emergency often resulting from long bone fractures or amputations, leading to acute respiratory distress syndrome (ARDS). The NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome, a key regulator of innate immunity, is activated by reactive oxygen species and [...] Read more.
Fat embolism is a critical medical emergency often resulting from long bone fractures or amputations, leading to acute respiratory distress syndrome (ARDS). The NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome, a key regulator of innate immunity, is activated by reactive oxygen species and tissue damage, contributing to inflammatory responses. This study examines the role of NLRP3 in fat embolism-induced ARDS and evaluates the therapeutic potential of MCC950, a selective NLRP3 antagonist. Fat embolism was induced by fatty micelle injection into the tail vein of Sprague Dawley rats. Pulmonary injury was assessed through lung weight gain as an edema indicator, NLRP3 expression via Western blot, and IL-1β levels using ELISA. Histological damage and macrophage infiltration were evaluated with hematoxylin and eosin staining. Fat embolism significantly increased pulmonary NLRP3 expression, lipid peroxidation, IL-1β release, and macrophage infiltration within four hours, accompanied by severe pulmonary edema. NLRP3 was localized in type I alveolar cells, co-localizing with aquaporin 5. Administration of MCC950 significantly reduced inflammatory responses, lipid peroxidation, pulmonary edema, and histological damage, while attenuating MAPK cascade phosphorylation of ERK and Raf. These findings suggest that NLRP3 plays a critical role in fat embolism-induced acute respiratory distress syndrome, and its inhibition by MCC950 may offer a promising therapeutic approach. Full article
(This article belongs to the Section Molecular Biology)
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14 pages, 1588 KiB  
Case Report
Fatal Cytokine Collision: HLH–AIHA in Advanced AIDS—Case Report and Literature Review
by Xiaoyi Zhang, Maria Felix Torres Nolasco, Wing Fai Li, Toru Yoshino and Manasa Anipindi
Reports 2025, 8(3), 137; https://doi.org/10.3390/reports8030137 - 4 Aug 2025
Viewed by 62
Abstract
Background and Clinical Significance: Hemophagocytic lymphohistiocytosis (HLH) and autoimmune hemolytic anemia (AIHA) are both life-threatening hematologic syndromes that rarely present together outside of malignancy. Advanced acquired immunodeficiency syndrome (AIDS) creates a milieu of profound immune dysregulation and hyperinflammation, predisposing patients to atypical [...] Read more.
Background and Clinical Significance: Hemophagocytic lymphohistiocytosis (HLH) and autoimmune hemolytic anemia (AIHA) are both life-threatening hematologic syndromes that rarely present together outside of malignancy. Advanced acquired immunodeficiency syndrome (AIDS) creates a milieu of profound immune dysregulation and hyperinflammation, predisposing patients to atypical overlaps of these disorders. Case Presentation: A 30-year-old woman with poorly controlled AIDS presented with three weeks of jaundice, fever, and fatigue. Initial labs revealed pancytopenia, hyperbilirubinemia, and elevated ferritin level. Direct anti-globulin testing confirmed warm AIHA (IgG+/C3d+) with transient cold agglutinins. Despite intravenous immunoglobulin (IVIG), rituximab, and transfusions, she developed hepatosplenomegaly, extreme hyperferritinemia, and sIL-2R > 10,000 pg/mL, meeting HLH-2004 criteria. Bone marrow biopsy excluded malignancy; further work-up revealed Epstein–Barr virus (EBV) viremia and cytomegalovirus (CMV) reactivation. Dexamethasone plus reduced-dose etoposide transiently reduced soluble interleukin-2 receptor (sIL-2R) but precipitated profound pancytopenia, Acute respiratory distress syndrome (ARDS) from CMV/parainfluenza pneumonia, bilateral deep vein thrombosis (DVT), and an ST-elevation myocardial infarction (STEMI). She ultimately died of hemorrhagic shock after anticoagulation despite maximal supportive measures. Conclusions: This case underscores the diagnostic challenges of HLH-AIHA overlap in AIDS, where cytopenias and hyperferritinemia mask the underlying cytokine storm. Pathogenesis likely involved IL-6/IFN-γ overproduction, impaired cytotoxic T-cell function, and molecular mimicry. While etoposide remains a cornerstone of HLH therapy, its myelotoxicity proved catastrophic in this immunocompromised host, highlighting the urgent need for cytokine-targeted agents to mitigate treatment-related mortality. Full article
(This article belongs to the Section Allergy/Immunology)
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13 pages, 1001 KiB  
Review
Old and New Definitions of Acute Respiratory Distress Syndrome (ARDS): An Overview of Practical Considerations and Clinical Implications
by Cesare Biuzzi, Elena Modica, Noemi De Filippis, Daria Pizzirani, Benedetta Galgani, Agnese Di Chiaro, Daniele Marianello, Federico Franchi, Fabio Silvio Taccone and Sabino Scolletta
Diagnostics 2025, 15(15), 1930; https://doi.org/10.3390/diagnostics15151930 - 31 Jul 2025
Viewed by 303
Abstract
Lower respiratory tract infections remain a leading cause of morbidity and mortality among Intensive Care Unit patients, with severe cases often progressing to acute respiratory distress syndrome (ARDS). This life-threatening syndrome results from alveolar–capillary membrane injury, causing refractory hypoxemia and respiratory failure. Early [...] Read more.
Lower respiratory tract infections remain a leading cause of morbidity and mortality among Intensive Care Unit patients, with severe cases often progressing to acute respiratory distress syndrome (ARDS). This life-threatening syndrome results from alveolar–capillary membrane injury, causing refractory hypoxemia and respiratory failure. Early detection and management are critical to treat the underlying cause, provide protective lung ventilation, and, eventually, improve patient outcomes. The 2012 Berlin definition standardized ARDS diagnosis but excluded patients on non-invasive ventilation (NIV) or high-flow nasal cannula (HFNC) modalities, which are increasingly used, especially after the COVID-19 pandemic. By excluding these patients, diagnostic delays can occur, risking the progression of lung injury despite ongoing support. Indeed, sustained, vigorous respiratory efforts under non-invasive modalities carry significant potential for patient self-inflicted lung injury (P-SILI), underscoring the need to broaden diagnostic criteria to encompass these increasingly common therapies. Recent proposals expand ARDS criteria to include NIV and HFNCs, lung ultrasound, and the SpO2/FiO2 ratio adaptations designed to improve diagnosis in resource-limited settings lacking arterial blood gases or advanced imaging. However, broader criteria risk overdiagnosis and create challenges in distinguishing ARDS from other causes of acute hypoxemic failure. Furthermore, inter-observer variability in imaging interpretation and inconsistencies in oxygenation assessment, particularly when relying on non-invasive measurements, may compromise diagnostic reliability. To overcome these limitations, a more nuanced diagnostic framework is needed—one that incorporates individualized therapeutic strategies, emphasizes lung-protective ventilation, and integrates advanced physiological or biomarker-based indicators like IL-6, IL-8, and IFN-γ, which are associated with worse outcomes. Such an approach has the potential to improve patient stratification, enable more targeted interventions, and ultimately support the design and conduct of more effective interventional studies. Full article
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36 pages, 1583 KiB  
Review
SARS-CoV-2 Pneumonia: Advances in Diagnosis and Treatment
by Olga Adriana Caliman-Sturdza, Iuliana Soldanescu and Roxana Elena Gheorghita
Microorganisms 2025, 13(8), 1791; https://doi.org/10.3390/microorganisms13081791 - 31 Jul 2025
Viewed by 288
Abstract
The development of severe SARS-CoV-2 pneumonia is characterized by extensive lung inflammation, which, in turn, leads to respiratory distress and a decline in blood oxygen levels. Hospital admission, along with intensive care or ventilator usage, becomes necessary because this condition leads to serious [...] Read more.
The development of severe SARS-CoV-2 pneumonia is characterized by extensive lung inflammation, which, in turn, leads to respiratory distress and a decline in blood oxygen levels. Hospital admission, along with intensive care or ventilator usage, becomes necessary because this condition leads to serious respiratory problems. This review aims to provide a comprehensive overview of the pathophysiological mechanisms, diagnostic methods, and current therapeutic options for pneumonia caused by the SARS-CoV-2 virus. The pathophysiological process of severe pneumonia due to SARS-CoV-2 infection is characterized by direct lung damage from viral replication, an excessive immune system response, inflammation, impaired gas exchange, and multi-organ failure. The coexistence of various medical conditions leads to substantial lung impairment, resulting in hypoxia and respiratory failure, which can ultimately lead to fatal outcomes. The diagnosis of severe SARS-CoV-2 pneumonia is made through a combination of clinical, radiologic, and laboratory findings. A multifaceted approach integrating antiviral therapy, corticosteroids, oxygen supplementation, ventilatory management, and immunomodulation is imperative to control inflammation and enhance clinical outcomes. Early intervention, meticulous monitoring, and personalized care are paramount for enhancing survival and mitigating complications in critically ill patients with COVID-19 pneumonia. Full article
(This article belongs to the Special Issue Editorial Board Members’ Collection Series: SARS-CoV-2 and COVID-19)
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17 pages, 307 KiB  
Article
The Use of Heart Rate Variability-Biofeedback (HRV-BF) as an Adjunctive Intervention in Chronic Fatigue Syndrome (CSF/ME) in Long COVID: Results of a Phase II Controlled Feasibility Trial
by Giulia Cossu, Goce Kalcev, Diego Primavera, Stefano Lorrai, Alessandra Perra, Alessia Galetti, Roberto Demontis, Enzo Tramontano, Fabrizio Bert, Roberta Montisci, Alberto Maleci, Pedro José Fragoso Castilla, Shellsyn Giraldo Jaramillo, Peter K. Kurotschka, Nuno Barbosa Rocha and Mauro Giovanni Carta
J. Clin. Med. 2025, 14(15), 5363; https://doi.org/10.3390/jcm14155363 - 29 Jul 2025
Viewed by 653
Abstract
Background: Emerging evidence indicates that some individuals recovering from COVID-19 develop persistent symptoms, including fatigue, pain, cognitive difficulties, and psychological distress, commonly known as Long COVID. These symptoms often overlap with those seen in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME), underscoring the need for [...] Read more.
Background: Emerging evidence indicates that some individuals recovering from COVID-19 develop persistent symptoms, including fatigue, pain, cognitive difficulties, and psychological distress, commonly known as Long COVID. These symptoms often overlap with those seen in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME), underscoring the need for integrative, non-pharmacological interventions. This Phase II controlled trial aimed to evaluate the feasibility and preliminary efficacy of Heart Rate Variability Biofeedback (HRV-BF) in individuals with Long COVID who meet the diagnostic criteria for CFS/ME. Specific objectives included assessing feasibility indicators (drop-out rates, side effects, participant satisfaction) and changes in fatigue, depression, anxiety, pain, and health-related quality of life. Methods: Participants were assigned alternately and consecutively to the HRV-BF intervention or Treatment-as-usual (TAU), in a predefined 1:1 sequence (quasirandom assignment). The intervention consisted of 10 HRV-BF sessions, held twice weekly over 5 weeks, with each session including a 10 min respiratory preparation and 40 min of active training. Results: The overall drop-out rate was low (5.56%), and participants reported a generally high level of satisfaction. Regarding side effects, the mean total Simulator Sickness Questionnaire score was 24.31 (SD = 35.42), decreasing to 12.82 (SD = 15.24) after excluding an outlier. A significantly greater improvement in severe fatigue was observed in the experimental group (H = 4.083, p = 0.043). When considering all outcomes collectively, a tendency toward improvement was detected in the experimental group (binomial test, p < 0.0001). Conclusions: HRV-BF appears feasible and well tolerated. Findings support the need for Phase III trials to confirm its potential in mitigating fatigue in Long COVID. Full article
19 pages, 750 KiB  
Article
Parents as First Responders: Experiences of Emergency Care in Children with Nemaline Myopathy: A Qualitative Study
by Raúl Merchán Arjona, Juan Francisco Velarde-García, Enrique Pacheco del Cerro and Alfonso Meneses Monroy
Nurs. Rep. 2025, 15(8), 271; https://doi.org/10.3390/nursrep15080271 - 29 Jul 2025
Viewed by 270
Abstract
Background: Nemaline myopathy is a rare congenital neuromuscular disease associated with progressive weakness and frequent respiratory complications. In emergency situations, families often serve as the first and only responders. The aim of this study is to explore how parents in Spain care [...] Read more.
Background: Nemaline myopathy is a rare congenital neuromuscular disease associated with progressive weakness and frequent respiratory complications. In emergency situations, families often serve as the first and only responders. The aim of this study is to explore how parents in Spain care for children with nemaline myopathy during emergency situations, focusing on the clinical responses performed at home and the organizational challenges encountered when interacting with healthcare systems. Methods: A qualitative phenomenological study was conducted with 17 parents from 10 families belonging to the Asociación Yo Nemalínica. Semi-structured interviews were performed via video calls, transcribed verbatim, and analyzed using Giorgi’s descriptive method and ATLAS.ti software (version 24). Methodological rigor was ensured through triangulation, reflexivity, and member validation. Results: Four themes were identified. First, families were described as acting under extreme pressure and in isolation during acute home emergencies, often providing cardiopulmonary resuscitation and respiratory support without professional backup. Second, families managed ambiguous signs of deterioration using clinical judgment and home monitoring tools, often preventing fatal outcomes. Third, parents frequently assumed guiding roles in emergency departments due to a lack of clinician familiarity with the disease, leading to delays or errors. Finally, the transition to the Pediatric Intensive Care Unit was marked by emotional distress and rapid decision-making, with families often participating in critical choices about invasive procedures. These findings underscore the complex, multidisciplinary nature of caregiving. Conclusions: Parents play an active clinical role during emergencies and episodes of deterioration. Their lived experience should be formally integrated into emergency protocols and the continuity of care strategies to improve safety and outcomes. Full article
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8 pages, 855 KiB  
Case Report
Severe Malaria Due to Plasmodium falciparum in an Immunocompetent Young Adult: Rapid Progression to Multiorgan Failure
by Valeria Sanclemente-Cardoza, Harold Andrés Payán-Salcedo and Jose Luis Estela-Zape
Life 2025, 15(8), 1201; https://doi.org/10.3390/life15081201 - 28 Jul 2025
Viewed by 273
Abstract
Plasmodium falciparum malaria remains a major cause of morbidity and mortality, particularly in endemic regions. We report the case of a 21-year-old male with recent travel to an endemic area (Guapi, Colombia), who presented with febrile symptoms, severe respiratory distress, and oxygen saturation [...] Read more.
Plasmodium falciparum malaria remains a major cause of morbidity and mortality, particularly in endemic regions. We report the case of a 21-year-old male with recent travel to an endemic area (Guapi, Colombia), who presented with febrile symptoms, severe respiratory distress, and oxygen saturation below 75%, necessitating orotracheal intubation. During the procedure, he developed pulseless electrical activity cardiac arrest, achieving return of spontaneous circulation after advanced resuscitation. Diagnosis was confirmed by thick blood smear, demonstrating P. falciparum infection. The patient progressed to multiorgan failure, including acute respiratory distress syndrome with capillary leak pulmonary edema, refractory distributive shock, acute kidney injury with severe hyperkalemia, and consumptive thrombocytopenia. Management included invasive mechanical ventilation, vasopressor support, sedation-analgesia, neuromuscular blockade, methylene blue, unsuccessful hemodialysis due to hemorrhagic complications, and platelet transfusions. Despite these interventions, the patient experienced a second cardiac arrest and died. This case highlights the severity and rapid progression of severe malaria with multisystem involvement, underscoring the critical importance of early diagnosis and intensive multidisciplinary management. It also emphasizes the need for preventive strategies for travelers to endemic areas and the development of clinical protocols to improve outcomes in complicated malaria. Full article
(This article belongs to the Section Medical Research)
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24 pages, 3590 KiB  
Article
Mesocricetus auratus (Golden Syrian Hamster) Experimental Model of SARS-CoV-2 Infection Reveals That Lung Injury Is Associated with Phenotypic Differences Between SARS-CoV-2 Variants
by Daniela del Rosario Flores Rodrigues, Alexandre dos Santos da Silva, Arthur Daniel Rocha Alves, Bárbara Araujo Rossi, Richard de Almeida Lima, Sarah Beatriz Salvador Castro Faria, Oswaldo Gonçalves Cruz, Rodrigo Muller, Julio Scharfstein, Amanda Roberta Revoredo Vicentino, Aline da Rocha Matos, João Paulo Rodrigues dos Santos, Pedro Paulo Abreu Manso, Milla Bezerra Paiva, Debora Ferreira Barreto-Vieira, Gabriela Cardoso Caldas, Marcelo Pelajo Machado and Marcelo Alves Pinto
Viruses 2025, 17(8), 1048; https://doi.org/10.3390/v17081048 - 28 Jul 2025
Viewed by 457
Abstract
Despite the current level of public immunity to SARS-CoV-2, the early inflammatory events associated with respiratory distress in COVID-19 patients are not fully elucidated. Syrian golden hamsters, facultative hibernators, recapitulate the phenotype of SARS-CoV-2-induced severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)—induced severe acute [...] Read more.
Despite the current level of public immunity to SARS-CoV-2, the early inflammatory events associated with respiratory distress in COVID-19 patients are not fully elucidated. Syrian golden hamsters, facultative hibernators, recapitulate the phenotype of SARS-CoV-2-induced severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)—induced severe acute lung injury seen in patients. In this study, we describe the predominance of the innate immune response in hamsters inoculated with four different SARS-CoV-2 variants, underscoring phenotypic differences among them. Severe inflammatory lung injury was chronologically associated with acute and significant weight loss, mainly in animals inoculated with A.2 and Delta variants. Omicron-infected animals had lower overall histopathology scores compared to other variants. We highlight the central role of endothelial injury and activation in the pathogenesis of experimental SARS-CoV-2 infection in hamsters, characterised by the presence of proliferative type I and type II pneumocytes with abundant surfactant expression, thereby maintaining hyperinflated alveolar fields. Additionally, there was evidence of intrapulmonary lymphatic vessel proliferation, which was accompanied by a lack of detectable microthrombosis in the lung parenchyma. However, white microthrombi were observed in lymphatic vessels. Our findings suggest that the physiological compensatory mechanisms that maintain respiratory homeostasis in Golden Syrian hamsters prevent severe respiratory distress and death after SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Emerging Concepts in SARS-CoV-2 Biology and Pathology, 3rd Edition)
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12 pages, 1276 KiB  
Article
Influence of Diabetes Mellitus on Perioperative Outcomes Following Surgical Stabilization of Rib Fractures: A National Health Insurance Research Database Analysis
by Yang-Fan Liu, Te-Li Chen, Jian-Wei Guo, Shih-Ching Liu and Wen-Ching Wang
Medicina 2025, 61(8), 1358; https://doi.org/10.3390/medicina61081358 - 26 Jul 2025
Viewed by 163
Abstract
Background and Objectives: Diabetes mellitus (DM) significantly impacts post-surgical recovery and fracture healing; however, few studies have specifically investigated the impact of DM on outcomes in patients undergoing surgical stabilization of rib fractures (SSRF). This study investigated the potential influence of DM on [...] Read more.
Background and Objectives: Diabetes mellitus (DM) significantly impacts post-surgical recovery and fracture healing; however, few studies have specifically investigated the impact of DM on outcomes in patients undergoing surgical stabilization of rib fractures (SSRF). This study investigated the potential influence of DM on perioperative outcomes following SSRF, using data from Taiwan’s National Health Insurance Research Database (NHIRD). Materials and Methods: Data of 1603 patients with multiple rib fractures who underwent SSRF between 2001 and 2019 were retrospectively analyzed. Patients were categorized into three groups: no DM, DM without chronic complications, and DM with chronic complications. The associations between DM status and perioperative outcomes, including hospital length of stay (LOS), in-hospital mortality, readmission rates, and complications such as pneumonia, surgical site infection (SSI), acute myocardial infarction (AMI), and total hospital costs were determined using univariate and multivariable regression analyses. Results: The mean age of the 1603 patients was 52.0 years, and 71% were male. Patients with DM and chronic complications had higher risks of 14-day readmission (adjusted odds ratio [aOR] = 2.99; 95% confidence interval [CI]: 1.18–7.62), 15–30 day readmission (aOR = 3.28; 95% CI: 1.25–8.60), SSI (aOR = 2.90; 95% CI: 1.37–6.14), AMI (aOR = 3.44; 95% CI: 1.28–9.24), and acute respiratory distress syndrome (ARDS) (aOR = 1.96; 95% CI: 1.03–3.74). In conclusion, DM, particularly DM with chronic complications, significantly increases the risk of adverse short-term outcomes following SSRF. Conclusions: These findings emphasize the need for enhanced care for patients with DM to optimize the outcomes of SSRF. Full article
(This article belongs to the Section Epidemiology & Public Health)
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16 pages, 3032 KiB  
Article
Severe Scrub Typhus with Acute Kidney Injury: Urine PCR Evidence from an East Coast Malaysian Cluster
by Siti Roszilawati Ramli, Nuridayu Arifin, Mohd Fahmi Ismail, Shirley Yi Fen Hii, Nur Suffia Sulaiman, Ernieenor Faraliana Che Lah and Nik Abdul Hadi Nik Abdul Aziz
Trop. Med. Infect. Dis. 2025, 10(8), 208; https://doi.org/10.3390/tropicalmed10080208 - 25 Jul 2025
Viewed by 487
Abstract
Background: Scrub typhus (ST) is caused by Orientia tsutsugamushi (OT) infection, which is transmitted to humans through the bites of infected chiggers. The clinical presentations range from mild to life-threatening multi-organ dysfunction. This report describes a cluster of ST cases involving five oil [...] Read more.
Background: Scrub typhus (ST) is caused by Orientia tsutsugamushi (OT) infection, which is transmitted to humans through the bites of infected chiggers. The clinical presentations range from mild to life-threatening multi-organ dysfunction. This report describes a cluster of ST cases involving five oil palm estate workers in Pekan district, Pahang, Malaysia. Methods: The clinical history, laboratory, and entomological investigation were conducted on the patients, including the index case and four suspected cases in the cluster. Polymerase chain reaction (PCR) tests for OT and genotyping were performed on the patients’ blood and urine samples. Serological testing by indirect immunoperoxidase (IIP) test against Rickettsial diseases was also conducted. Principal Findings: Patients presented with fever, myalgia, headache, rash, cough, and eschar. The index case developed severe ST complicated by acute kidney injury (AKI) and respiratory distress, requiring intubation and ventilation at the intensive care unit of a tertiary hospital. ST was confirmed through PCR analysis of a urine sample, showcasing a novel diagnostic approach. The other four cases were confirmed by a four-fold rise in immunoglobulin G (IgG) antibody titers. Conclusions: oil palm estate workers are at high risk for chigger exposure in Malaysia. Awareness among clinicians and the public of ST is crucial for effective prevention, accurate diagnosis, and optimal management. Full article
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15 pages, 1211 KiB  
Review
Epigenetic Regulation of Neutrophils in ARDS
by Jordan E. Williams, Zannatul Mauya, Virginia Walkup, Shaquria Adderley, Colin Evans and Kiesha Wilson
Cells 2025, 14(15), 1151; https://doi.org/10.3390/cells14151151 - 25 Jul 2025
Viewed by 333
Abstract
Acute respiratory distress syndrome (ARDS) is an inflammatory pulmonary condition that remains at alarming rates of fatality, with neutrophils playing a vital role in its pathogenesis. Beyond their classical antimicrobial functions, neutrophils contribute to pulmonary injury via the release of reactive oxygen species, [...] Read more.
Acute respiratory distress syndrome (ARDS) is an inflammatory pulmonary condition that remains at alarming rates of fatality, with neutrophils playing a vital role in its pathogenesis. Beyond their classical antimicrobial functions, neutrophils contribute to pulmonary injury via the release of reactive oxygen species, proteolytic enzymes, and neutrophil extracellular traps (NETs). To identify targets for treatment, it was found that epigenetic mechanisms, including histone modifications, hypomethylation, hypermethylation, and non-coding RNAs, regulate neutrophil phenotypic plasticity, survival, and inflammatory potential. It has been identified that neutrophils in ARDS patients exhibit abnormal methylation patterns and are associated with altered gene expression and prolonged neutrophil activation, thereby contributing to sustained inflammation. Histone citrullination, particularly via PAD4, facilitates NETosis, while histone acetylation status modulates chromatin accessibility and inflammatory gene expression. MicroRNAs have also been shown to regulate neutrophil activity, with miR-223 and miR-146a potentially being biomarkers and therapeutic targets. Neutrophil heterogeneity, as evidenced by distinct subsets such as low-density neutrophils (LDNs), varies across ARDS etiologies, including COVID-19. Single-cell RNA sequencing analyses, including the use of trajectory analysis, have revealed transcriptionally distinct neutrophil clusters with differential activation states. These studies support the use of epigenetic inhibitors, including PAD4, HDAC, and DNMT modulators, in therapeutic intervention. While the field has been enlightened with new findings, challenges in translational application remain an issue due to species differences, lack of stratification tools, and heterogeneity in ARDS presentation. This review describes how targeting neutrophil epigenetic regulators could help regulate hyperinflammation, making epigenetic modulation a promising area for precision therapeutics in ARDS. Full article
(This article belongs to the Section Cell Microenvironment)
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11 pages, 796 KiB  
Review
Prenatal Rare 16q24.1 Deletion Between Genomics and Epigenetics: A Review
by Valentina Fumini, Romina Bonora, Anna Busciglio, Francesca Cartisano, Paola Celli, Ilaria Gabbiato, Nicola Guercini, Barbara Mancini, Donatella Saccilotto, Anna Zilio and Daniela Zuccarello
Genes 2025, 16(8), 873; https://doi.org/10.3390/genes16080873 - 24 Jul 2025
Viewed by 231
Abstract
Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, often fatal congenital disorder characterized by severe neonatal respiratory distress and associated with complex multisystem malformations. In approximately 90% of cases, the condition is linked to deletions or mutations affecting the [...] Read more.
Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, often fatal congenital disorder characterized by severe neonatal respiratory distress and associated with complex multisystem malformations. In approximately 90% of cases, the condition is linked to deletions or mutations affecting the FOXF1 gene or its upstream enhancer region on chromosome 16q24.1. This review analyzes reported prenatal cases with 16q24.1 deletion involving FOXF1, aiming to identify recurrent sonographic features and elucidate the underlying genomic and epigenetic mechanisms. We reviewed prenatal cases reported in the literature involving deletions of the 16q24.1 region, including the FOXF1 gene. Here, we expand the case series by reporting a fetus with increased nuchal translucency measuring 8 mm and a de novo 16q24.1 deletion. We identified nine prenatal cases with a 16q24.1 deletion, all involving the FOXF1 gene or its enhancer region. The main ultrasound findings included increased nuchal translucency and cystic hygroma during the first trimester, and cardiac, renal, and intestinal malformations from 20 weeks of gestation onward. Prenatal diagnosis of ACDMPV based solely on ultrasound findings is challenging. In most reported cases, the pregnancy was carried to term, with the diagnosis being confirmed by post-mortem histopathological examination. In the only case in which the pregnancy was terminated at 14 weeks’ gestation, histological examination of the fetal lungs, despite them being in the early stages of development, revealed misaligned pulmonary veins in close proximity to the pulmonary arteries and bronchioles. Evidence highlights the significance of non-coding regulatory regions in the regulation of FOXF1 expression. Differential methylation patterns, and possible contributions of parental imprinting, highlight the complexity of FOXF1 regulation. Early detection through array comparative genomic hybridization (array CGH) or next-generation sequencing to identify point mutations in the FOXF1 gene, combined with increased awareness of ultrasound markers suggestive of the condition, could improve the accuracy of prenatal diagnosis and genetic counseling. Further research into the epigenetic regulation of FOXF1 is crucial for refining recurrence risk estimates and improving genetic counseling practices. Full article
(This article belongs to the Section Human Genomics and Genetic Diseases)
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20 pages, 2796 KiB  
Systematic Review
Comparative Efficacy and Safety Profile of the Combination of Pulmonary Surfactant and Budesonide vs. Surfactant Alone in the Management of Neonatal Respiratory Distress Syndrome: An Updated Meta-Analysis
by Urooj Fatima, Naveera Naveed, Zahra Riaz, Emaan Khalid, Aemon Qamer, Shehmeen Baig, Roshaan Fatima, Asawir Hussain, Zoya Mustunsar, Ayesha Khan, Sadia Mangan, Mehak Kumari, Soban Ali Qasim, Ali Hasan and Raheel Ahmed
Medicina 2025, 61(8), 1329; https://doi.org/10.3390/medicina61081329 - 23 Jul 2025
Viewed by 295
Abstract
Background and Objectives: Neonatal respiratory distress syndrome (NRDS), resulting from a deficiency of pulmonary surfactant (PS), can cause alveoli to collapse. Glucocorticoids reduce inflammation and are effective in reducing pulmonary swelling. This study aims to assess the effectiveness of the combination of PS [...] Read more.
Background and Objectives: Neonatal respiratory distress syndrome (NRDS), resulting from a deficiency of pulmonary surfactant (PS), can cause alveoli to collapse. Glucocorticoids reduce inflammation and are effective in reducing pulmonary swelling. This study aims to assess the effectiveness of the combination of PS and budesonide in the management of NRDS. Materials and Methods: Publications between 21 May and 24 November were screened through PubMed, Cochrane and Embase. Data analysis was performed on RevMan 5.3 software. Subgroup analysis was performed to evaluate the routes of administrations. Results: The use of budesonide along with pulmonary surfactant for treating NRDS revealed the following results: (1) a reduced duration of invasive mechanical ventilation (standardized mean difference (SMD) = −1.06, 95% confidence interval (CI) = −1.55 to −0.56, p < 0.0001); (2) reduced rate of bronchopulmonary dysplasia (BPD) occurrence (relative risk (RR) = 0.72, 95% CI = 0.60 to 0.86, p = 0.0003); (3) reduced duration for hospital admittance (SMD = −0.38, 95% CI = −0.64 to −0.11, p = 0.005). The occurrence of complications, i.e., sepsis, pneumothorax, retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), rate of mortality, hyperglycemia and intraventricular hemorrhage (IVH), was not significantly different among the intervention and comparison group except for patent ductus arteriosus (PDA) and pulmonary hemorrhage, with their incidence being higher in the control group (p = 0.002 and p = 0.05, respectively). Conclusions: The combination of pulmonary surfactant and budesonide decreases the occurrence of BPD, duration of mechanical ventilation, length of hospital stay and risk of pulmonary hemorrhage and PDA. It does not increase the risk of complications and death and is clinically safe. Full article
(This article belongs to the Section Obstetrics and Gynecology)
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27 pages, 1201 KiB  
Review
Non-Viral Therapy in COVID-19: Where Are We Standing? How Our Experience with COVID May Help Us Develop Cell Therapies for Long COVID Patients
by Aitor Gonzaga, Gema Martinez-Navarrete, Loreto Macia, Marga Anton-Bonete, Gladys Cahuana, Juan R. Tejedo, Vanessa Zorrilla-Muñoz, Eduardo Fernandez-Jover, Etelvina Andreu, Cristina Eguizabal, Antonio Pérez-Martínez, Carlos Solano, Luis Manuel Hernández-Blasco and Bernat Soria
Biomedicines 2025, 13(8), 1801; https://doi.org/10.3390/biomedicines13081801 - 23 Jul 2025
Viewed by 457
Abstract
Objectives: COVID-19, caused by the SARS-CoV-2 virus, has infected over 777 million individuals and led to approximately 7 million deaths worldwide. Despite significant efforts to develop effective therapies, treatment remains largely supportive, especially for severe complications like acute respiratory distress syndrome (ARDS). [...] Read more.
Objectives: COVID-19, caused by the SARS-CoV-2 virus, has infected over 777 million individuals and led to approximately 7 million deaths worldwide. Despite significant efforts to develop effective therapies, treatment remains largely supportive, especially for severe complications like acute respiratory distress syndrome (ARDS). Numerous compounds from diverse pharmacological classes are currently undergoing preclinical and clinical evaluation, targeting both the virus and the host immune response. Methods: Despite the large number of articles published and after a preliminary attempt was published, we discarded the option of a systematic review. Instead, we have done a description of therapies with these results and a tentative mechanism of action. Results: Preliminary studies and early-phase clinical trials have demonstrated the potential of Mesenchymal Stem Cells (MSCs) in mitigating severe lung damage in COVID-19 patients. Previous research has shown MSCs to be effective in treating various pulmonary conditions, including acute lung injury, idiopathic pulmonary fibrosis, ARDS, asthma, chronic obstructive pulmonary disease, and lung cancer. Their ability to reduce inflammation and promote tissue repair supports their potential role in managing COVID-19-related complications. This review demonstrates the utility of MSCs in the acute phase of COVID-19 and postulates the etiopathogenic role of mitochondria in Long-COVID. Even more, their combination with other therapies is also analyzed. Conclusions: While the therapeutic application of MSCs in COVID-19 is still in early stages, emerging evidence suggests promising outcomes. As research advances, MSCs may become an integral part of treatment strategies for severe COVID-19, particularly in addressing immune-related lung injury and promoting recovery. However, a full pathogenic mechanism may explain or unify the complexity of signs and symptoms of Long COVID and Post-Acute Sequelae (PASC). Full article
(This article belongs to the Section Gene and Cell Therapy)
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