Electrical impedance tomography (EIT) is a new non-invasive functional imaging technology, which has the advantages of non-invasion, non-radiation, low cost, fast response, portability and visualization. In recent years, more and more studies have shown that EIT has great potential in the detection of lung diseases and has been applied to early diagnosis and treatment of some diseases. This paper introduced the basic principle of EIT, discussed the research and clinical application of EIT in the detection of acute respiratory distress syndrome, chronic obstructive pulmonary disease, pneumothorax and pulmonary embolism, and focused on the summary and introduction of indicators and functional images of EIT related to the detection of lung diseases. This review will help medical workers understand and use EIT, and promote the further development of EIT in lung diseases as well as other fields.
Humans ; Electric Impedance ; Tomography/methods* ; Lung Diseases/diagnosis* ; Pulmonary Disease, Chronic Obstructive/diagnosis* ; Pulmonary Embolism/diagnosis* ; Respiratory Distress Syndrome/diagnosis*

OBJECTIVES: To investigate the efficacy of volume-guaranteed high-frequency oscillatory ventilation (HFOV-VG) in preterm infants with respiratory distress syndrome (RDS) and its impact on blood flow in the middle cerebral artery (MCA). METHODS: A prospective study was conducted on 120 preterm infants with RDS who were admitted to the Department of Neonatology at Qinhuangdao Maternal and Child Health Hospital from March 2020 to December 2023. According to the mode of ventilation, the infants were divided into two groups: a conventional mechanical ventilation (CMV) group (60 infants) and an HFOV-VG group (60 infants). The two groups were compared in terms of baseline data, MCA hemodynamic parameters, complications, and outcomes. RESULTS: Compared with the CMV group, the HFOV-VG group had significantly shorter durations of mechanical ventilation and hospital stay and a significantly higher overall response rate (P<0.05). The HFOV-VG group demonstrated significantly better peak systolic velocity, end-diastolic velocity, and mean flow velocity (P<0.05). The HFOV-VG group also exhibited significantly lower 28-day mortality rates and lower incidence rates of bronchopulmonary dysplasia and intraventricular hemorrhage than the CMV group (P<0.05). CONCLUSIONS HFOV-VG can effectively improve cerebral blood perfusion, reduce cerebrovascular resistance, shorten the durations of mechanical ventilation and hospital stay, and enhance overall treatment efficacy. It has significant advantages in reducing the risk of 28-day mortality, bronchopulmonary dysplasia, and intraventricular hemorrhage in preterm infants with RDS.
Humans ; High-Frequency Ventilation/adverse effects* ; Infant, Newborn ; Respiratory Distress Syndrome, Newborn/physiopathology* ; Female ; Middle Cerebral Artery/physiology* ; Male ; Prospective Studies ; Cerebrovascular Circulation ; Infant, Premature

The patient, a 20-day-old male, was admitted due to respiratory distress that had persisted for 20 days after birth. The main clinical manifestations included gradually worsening respiratory distress and edema. The patient received treatment including mechanical ventilation and diuretics. Echocardiography indicated cardiomegaly, pulmonary hypertension, and heart failure. A comprehensive systemic examination revealed a significant blowing vascular murmur upon auscultation over the anterior fontanelle and bilateral temporal regions. Further imaging studies including cranial magnetic resonance imaging, magnetic resonance angiography, and magnetic resonance venography showed marked dilation of the superior sagittal sinus, transverse sinus, and sigmoid sinus, leading to a definitive diagnosis of dural arteriovenous fistula. After a multidisciplinary consultation, the patient underwent cerebral angiography and partial embolization of the left parietal arteriovenous fistula. Postoperatively, the patient was treated with positive inotropes, diuretics, and fluid restriction. Ultimately, the patient was weaned off the ventilator and discharged in improved condition. This article reports a case of neonatal dural arteriovenous fistula presenting with respiratory distress and discusses the multidisciplinary approach to managing this condition, which aids in early disease recognition and guides clinical decision-making.
Humans ; Male ; Infant, Newborn ; Central Nervous System Vascular Malformations/diagnosis* ; Respiratory Distress Syndrome, Newborn/etiology* ; Embolization, Therapeutic

OBJECTIVES: To investigate the application value of targeted next-generation sequencing (tNGS) in the etiological diagnosis of moderate to severe respiratory distress syndrome (RDS) in neonates. METHODS: A prospective randomized controlled trial was conducted, enrolling 81 term and late-preterm neonates with moderate to severe RDS admitted to Fujian Children's Hospital between December 2023 and December 2024. Patients were randomly assigned to the conventional microbiological test (CMT) group (n=42) or the tNGS group (n=39). For routine pathogen detection, bronchoalveolar lavage fluid was obtained via bronchoscopy, and lower respiratory tract specimens were collected via the endotracheal tube; all specimens underwent culture, and some specimens additionally underwent polymerase chain reaction or antigen testing. In the tNGS group, tNGS was performed in addition to routine pathogen detection on the same specimen types. The detection rate of pathogens, the detection rate of co-infections, and the duration of antibiotic use were compared between the two groups. RESULTS: The pathogen detection rate in the tNGS group (18/39, 46%) was significantly higher than that in the CMT group (8/42, 19%) (P=0.009). The co-infection detection rate was 13% (5/39) in the tNGS group, while no co-infections were identified in the CMT group (P=0.024). Regarding treatment, the duration of antibiotic use in the tNGS group was shorter than that in the CMT group [(12±4) days vs (15±5) days, P=0.003]. CONCLUSIONS tNGS significantly improves the pathogen detection rate in neonates with moderate to severe RDS and offers advantages in the rapid identification of co-infections and reduction of antibiotic treatment duration, suggesting it has clinical utility and potential for wider adoption.
Humans ; Prospective Studies ; Infant, Newborn ; Female ; Respiratory Distress Syndrome, Newborn/etiology* ; Male ; High-Throughput Nucleotide Sequencing/methods*

OBJECTIVE: To explore the potential effects and mechanisms of Liang-Ge-San (LGS) for the treatment of acute respiratory distress syndrome (ARDS) through network pharmacology analysis and to verify LGS activity through biological experiments. METHODS: The key ingredients of LGS and related targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. ARDS-related targets were selected from GeneCards and DisGeNET databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the Metascape Database. Molecular docking analysis was used to confirm the binding affinity of the core compounds with key therapeutic targets. Finally, the effects of LGS on key signaling pathways and biological processes were determined by in vitro and in vivo experiments. RESULTS: A total of LGS-related targets and 496 ARDS-related targets were obtained from the databases. Network pharmacological analysis suggested that LGS could treat ARDS based on the following information: LGS ingredients luteolin, wogonin, and baicalein may be potential candidate agents. Mitogen-activated protein kinase 14 (MAPK14), recombinant V-Rel reticuloendotheliosis viral oncogene homolog A (RELA), and tumor necrosis factor alpha (TNF-α) may be potential therapeutic targets. Reactive oxygen species metabolic process and the apoptotic signaling pathway were the main biological processes. The p38MAPK/NF-κ B signaling pathway might be the key signaling pathway activated by LGS against ARDS. Moreover, molecular docking demonstrated that luteolin, wogonin, and baicalein had a good binding affinity with MAPK14, RELA, and TNF α. In vitro experiments, LGS inhibited the expression and entry of p38 and p65 into the nucleation in human bronchial epithelial cells (HBE) cells induced by LPS, inhibited the inflammatory response and oxidative stress response, and inhibited HBE cell apoptosis (P<0.05 or P<0.01). In vivo experiments, LGS improved lung injury caused by ligation and puncture, reduced inflammatory responses, and inhibited the activation of p38MAPK and p65 (P<0.05 or P<0.01). CONCLUSION LGS could reduce reactive oxygen species and inflammatory cytokine production by inhibiting p38MAPK/NF-κ B signaling pathway, thus reducing apoptosis and attenuating ARDS.
Drugs, Chinese Herbal/pharmacology* ; Respiratory Distress Syndrome/enzymology* ; p38 Mitogen-Activated Protein Kinases/metabolism* ; NF-kappa B/metabolism* ; Animals ; Signal Transduction/drug effects* ; Molecular Docking Simulation ; Humans ; Male ; Network Pharmacology ; Apoptosis/drug effects* ; Mice

OBJECTIVE: To identify the underlying mechanism by which quercetin (Que) alleviates sepsis-related acute respiratory distress syndrome (ARDS). METHODS: In vivo, C57BL/6 mice were assigned to sham, cecal ligation and puncture (CLP), and CLP+Que (50 mg/kg) groups (n=15 per group) by using a random number table. The sepsisrelated ARDS mouse model was established using the CLP method. In vitro, the murine alveolar macrophages (MH-S) cells were classified into control, lipopolysaccharide (LPS), LPS+Que (10 μmol/L), and LPS+Que+acetylcysteine (NAC, 5 mmol/L) groups. The effect of Que on oxidative stress, inflammation, and apoptosis in mice lungs and MH-S cells was determined, and the mechanism with reactive oxygen species (ROS)/p38 mitogen-activated protein kinase (MAPK) pathway was also explored both in vivo and in vitro. RESULTS: Que alleviated lung injury in mice, as reflected by a reversal of pulmonary histopathologic changes as well as a reduction in lung wet/dry weight ratio and neutrophil infiltration (P<0.05 or P<0.01). Additionally, Que improved the survival rate and relieved gas exchange impairment in mice (P<0.01). Que treatment also remarkedly reduced malondialdehyde formation, superoxide dismutase and catalase depletion, and cell apoptosis both in vivo and in vitro (P<0.05 or P<0.01). Moreover, Que treatment diminished the release of inflammatory factors interleukin (IL)-1β, tumor necrosis factor-α, and IL-6 both in vivo and in vitro (P<0.05 or P<0.01). Mechanistic investigation clarifified that Que administration led to a decline in the phosphorylation of p38 MAPK in addition to the suppression of ROS expression (P<0.01). Furthermore, in LPS-induced MH-S cells, ROS inhibitor NAC further inhibited ROS/p38 MAPK pathway, as well as oxidative stress, inflammation, and cell apoptosis on the basis of Que treatment (P<0.05 or P<0.01). CONCLUSION Que was found to exert anti-oxidative, anti-inflammatory, and anti-apoptotic effects by suppressing the ROS/p38 MAPK pathway, thereby conferring protection for mice against sepsis-related ARDS.
Animals ; Sepsis/drug therapy* ; Quercetin/therapeutic use* ; Respiratory Distress Syndrome/enzymology* ; p38 Mitogen-Activated Protein Kinases/metabolism* ; Mice, Inbred C57BL ; Reactive Oxygen Species/metabolism* ; Apoptosis/drug effects* ; Male ; Oxidative Stress/drug effects* ; MAP Kinase Signaling System/drug effects* ; Lung/drug effects* ; Mice ; Lipopolysaccharides ; Macrophages, Alveolar/pathology* ; Inflammation/pathology* ; Protective Agents/therapeutic use*

INTRODUCTION

Administration of antenatal corticosteroids (ACS) between 24 and 36 weeks of gestation is recommended to pregnant women at risk of preterm delivery to decrease the risk of respiratory distress syndrome, intra-ventricular hemorrhage and neonatal death. However, it may worsen glycemic profile primarily in those with gestational diabetes mellitus (GDM).

To determine the effects of ACS on maternal glycemia in Filipino women with GDM and to analyze the factors associated with insulin use or increased insulin requirement.

A retrospective study of the medical records of Filipino women with GDM who were admitted and received ACS treatment (betamethasone) between 24- and 36-weeks age of gestation (AOG) for fetal lung maturity from 2017-2019. Clinical characteristics (age, parity, completed ACS dose, AOG at ACS administration and mode of delivery) and glycemic control were retrieved and compared before and after ACS treatment. Data collection began the day or on the day before steroids were given and continued until discharge or delivery.

Included were 42 pregnant women with GDM. Of these, 28 women with GDM were treated by diet alone (Group A) while 14 women with GDM were started on insulin in addition to diet (Group B). After betamethasone therapy was initiated, only three (Group A1; n=3/28) patients had good glycemic control with diet alone and the rest were given insulin treatment (Group A2; n=25/28). In this subpopulation of Group A2, insulin requirement within 24 hours after ACS was at 0.3 units per kg of body weight. There was a steady increase with maximum requirement observed on day 4 and decreased thereafter to 0.33 units per kg of body weight on day 5. For GDM women in Group B, only three maintained their insulin dose (Group B1; n=3/14) while 11 (Group B2; n=11/14) women with GDM previously on insulin, required further increase in insulin from day 1-2 reaching 140% increase in insulin dose on day 2. Thereafter, there was a gradual decrease of insulin dose almost returning to initial dose on day 5.

Insulin initiation was observed among GDM diet-controlled mothers (Group A) who were given ACS therapy at ≥31 weeks age of gestation. Age, parity, family history of diabetes and mode of delivery did not have significant effects on insulin use nor increased insulin requirement. Fasting capillary glucose (FCG) and one-hour post-prandial capillary glucose (PPCG) were elevated within 24 hours after administration of corticosteroid (betamethasone) in 60%-70% of our population. The FCG values remained elevated on day 2-3 in about 70% of patients. While the first hour PPCG was elevated in 85% of patients on day 2 and remained elevated in 70% of women on day 3-4, it reached 53% on day 5. Insulin requirement among Group B2 reached to 140% increase in insulin dose on day 2 followed by a gradual decrease of insulin dose almost returning to initial dose on day 5.

ACS administration caused maternal hyperglycemia in Filipino women with GDM during the first 24 hours and lasting up to five days. Both fasting glucose and post-prandial glucose were elevated, hence intensified monitoring of maternal glucose levels and temporary addition or increase of insulin doses may be necessary. The timing (≥31 weeks AOG) of administration of ACS on GDM women was associated with subsequent insulin initiation but only on patients initially controlled on diet alone.

OBJECTIVE: To analyze the risk factors of hypophosphatemia in patients with acute respiratory distress syndrome (ARDS). METHODS: A retrospective case-control study was conducted. The clinical data of the patients with ARDS admitted to Yanbian University Affiliated Hospital from January 2018 to October 2022 were collected. According to the 1-day serum phosphorus level after intensive care unit (ICU) admission, the patients with normal (0.80-1.45 mmol/L) or elevated (> 1.45 mmol/L) serum phosphorus levels were included in the non-hypophosphatemia group, while those with phosphorus levels lower than 0.80 mmol/L were included in the hypophosphatemia group. The differences in the inflammatory indicators [neutrophils percentage (NEU%), neutrophil count (NEU), lymphocyte count (LYM), high-sensitivity C-reactive protein (hs-CRP)], proteins [total protein (TP), albumin (Alb), prealbumin (PA)], blood lactic acid (Lac), neutrophil/lymphocyte ratio (NLR), neutrophil/albumin ratio (NAR), and blood lactic acid/albumin ratio (L/A) at 1, 2, 4, 6 and 8 days after ICU admission were compared between the two groups. The partial correlation method was used to analyze the correlation between the 1-day serum phosphorus level after ICU admission and the above indicators. Multivariate Logistic regression analysis was adopted to explore the risk factors of hypophosphatemia in patients with ARDS. RESULTS: All 110 patients were enrolled in the final analysis, among which there were 56 cases in the hypophosphatemia group and 54 cases in the non-hypophosphatemia group. At 1 day and 2 days after ICU admission, NEU% in the hypophosphatemia group were significantly higher than those in the non-hypophosphatemia group (1 day: 0.87±0.08 vs. 0.82±0.12, 2 days: 0.87±0.05 vs. 0.83±0.11, both P < 0.05). As the ICU admission time prolonged, LYM in the hypophosphatemia group was basically on the rise, and NEU%, hs-CRP, and NLR were first decreased and then increased. At 1 day after ICU admission, TP, Alb and PA in the hypophosphatemia group were significantly lower than those in the non-hypophosphatemia group [TP (g/L): 52.96±8.42 vs. 56.47±8.36, Alb (g/L): 29.73±5.83 vs. 33.08±7.35, PA (g/L): 69.95±50.72 vs. 121.50±82.42, all P < 0.05]. As the ICU admission time prolonged, TP and Alb in the hypophosphatemia group were basically showed a trend of first decreasing and then increasing, but at 8 days, Alb was still lower than that at 1 day, and PA basically showed an upward trend. In the non-hypophosphatemia group, the change trends of TP and Alb were consistent with those in the hypophosphatemia group. Lac and L/A both showed a downward trend in the two groups. Partial correlation analysis showed that 1-day serum phosphorus level after ICU admission was significantly negatively correlated with NEU% and hs-CRP (r value was -0.229 and -0.286, respectively, both P < 0.05), and significantly positively correlated with LYM and PA (r value was 0.231 and 0.311, respectively, both P < 0.05). Multivariate Logistic regression analysis showed that 1-day NEU% [odds ratio (OR) = 0.932, 95% confidence interval (95%CI) was 0.873-0.996, P = 0.038] and Alb (OR = 1.167, 95%CI was 1.040-1.308, P = 0.008) were the independent risk factors for hypophosphatemia in ARDS patients. CONCLUSION NEU% and Alb at 1 day after ICU admission are independent risk factors for hypophosphatemia in patients with ARDS.
Humans ; Hypophosphatemia/etiology* ; Respiratory Distress Syndrome/blood* ; Risk Factors ; Retrospective Studies ; Case-Control Studies ; Intensive Care Units ; Male ; Female ; Phosphorus/blood* ; Middle Aged ; Neutrophils ; Aged ; C-Reactive Protein

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by diffuse alveolar and interstitial edema caused by damage to alveolar-capillary and epithelial cells, often induced by infection, sepsis, trauma, and other factors. It is marked by progressive hypoxemia and respiratory distress. Due to the diverse causes of ARDS, the unclear pathogenesis, and the absence of effective predictive markers or biomarkers, there are no effective treatment measures available, resulting in a high mortality rate. ARDS is increasingly recognized for its heterogeneity, biomarkers, and the emergence of new opportunities for the development of diagnostic tools and personalized treatment strategies provided by omics technologies. A single omics analysis cannot fully reveal the heterogeneity and complexity of ARDS, while multi-omics analysis can provide a more systematic and comprehensive understanding of ARDS. Using clinical samples is closer to the actual disease situation compared to animal models. Multi-omics studies based on clinical samples have achieved significant progress in elucidating the pathophysiology of ARDS, identifying ARDS subtypes, and identifying biomarkers related to ARDS. This review focuses on the current applications of genomics, transcriptomics, metabolomics, and proteomics analyses based on clinical samples in the ARDS field, with a focus on the application of these omics methods in ARDS heterogeneity, potential biomarkers, and pathogenesis. It also introduces the differences in the application of different clinical samples in ARDS omics research, in order to gain a deeper and more comprehensive understanding of the pathogenesis of ARDS and explore new strategies for its prevention and treatment.
Respiratory Distress Syndrome/diagnosis* ; Humans ; Metabolomics ; Proteomics ; Genomics ; Biomarkers ; Multiomics

Mechanical ventilation is commonly employed for respiratory support in patients with respiratory failure. Despite the optimization of ventilator parameters and treatment methods, mechanical ventilation can still lead to both acute and chronic lung injury in patients with acute respiratory distress syndrome (ARDS) as well as in those without ARDS, a phenomenon referred to as ventilator-induced lung injury (VILI). VILI can be categorized into four types: barotrauma, volumetric injury, atelectasis injury, and biotic injury. Among these, biotic injury, characterized by inflammation, plays a significant role in the pathogenesis of VILI. Numerous studies have investigated the inflammatory mechanisms underlying VILI; however, these mechanisms remain complex and not entirely understood. At present, clinical practice lacks specific prevention and treatment strategies for VILI, aside from the implementation of protective ventilation strategies. Long non-coding RNAs (lncRNA) are a category of non-coding RNA longer than 200 nucleotides. LncRNAs regulate physiological and pathological processes such as cell proliferation, apoptosis, inflammatory response, and immune regulation, this regulation occurs through mechanisms such as modulating gene activity, inhibiting specific states, assisting in transcription initiation, affecting pre-mRNA splicing modifications, influencing translation processes, and expressing biofunctional peptides. They play an important role in the course of multiple diseases. Studies have shown that compared with control animals and cell models, lncRNAs are differentially expressed in VILI animal models and cell stretch models. Experiments have verified that certain lncRNAs play a crucial role in the pathogenesis of VILI by regulating the expression of inflammatory factors, the transformation of macrophage types, neutrophil activation, and cell apoptosis. Given the adverse effects of VILI on mechanical ventilation in critically ill patients, the important role of lncRNAs in biological regulation, and the urgent need to explore more effective strategies for the prevention and treatment of VILI, this paper summarizes the mechanisms through which lncRNA contributes to the VILI process, and discusses its possibility as a diagnostic and therapeutic target of VILI, in order to provide a reference for the clinical treatment of VILI.
RNA, Long Noncoding ; Ventilator-Induced Lung Injury ; Humans ; Respiration, Artificial/adverse effects* ; Animals ; Respiratory Distress Syndrome ; Apoptosis