Gas Exchange Function Research Articles

Effect of HIV on Lung Function and Structure: A Systematic Review and Meta-analysis.

Obstructive lung disease (OLD) pathogenesis includes inhalational (e.g., smoking) and non-inhalational mechanisms (e.g., infections). HIV has been suggested as a novel OLD risk factor. Substantial data have recently emerged about its effects on lung function and structure, especially in low-to-middle-income countries and regarding longitudinal lung function. To assess the association of HIV infection with OLD, impaired gas exchange, and emphysema. In this systematic review and meta-analysis, we searched PubMed, EMBASE, CENTRAL, CDSR, WoS, Scopus, CINAHL, and GIM through April 2023 for controlled and observational studies of people living with and without HIV reporting pulmonary function and/or emphysema. Primary outcomes were OLD by spirometry, gas exchange impairment by diffusing capacity for carbon monoxide, and visual emphysema by computed tomography. We performed random-effects meta-analyses using odds ratios (OR) with 95% confidence intervals (CIs). This study was registered in PROSPERO (CRD42021268498). We included 95 publications pertaining to 43 unique studies. HIV was associated with OLD (OR 1.29; 95% CI 1.02-1.63), impaired gas exchange (OR 2.63; 95% CI 0.96-7.24), emphysema (OR 1.46; 95% CI 1.02-2.09), and faster lung function decline. OLD risk was greatest in Africans with HIV. There were no gas exchange or emphysema data from Africa. Certainty of evidence was low to very low, primarily due to studies' observational design. People living with HIV have increased risk for OLD, gas exchange impairment, faster lung function decline, and emphysema. OLD risk in HIV varies regionally. We recommend both spirometry and DLCO be measured in people living with HIV and respiratory symptoms. Future studies should develop and validate HIV-specific screening and case-finding strategies for chronic lung disease.

Pulmonary epithelial wound healing and the immune system. Mathematical modelling and bifurcation analysis of a bistable system

Respiratory diseases such as asthma, acute respiratory distress syndrome (ARDS), influenza or COVID-19 often directly target the epithelium. Elevated immune levels and a ‘cytokine storm’ are directly associated with defective healing dynamics of lung diseases such as COVID-19 or ARDS. The infected cells leave wounded regions in the epithelium which must be healed for the lung to return to a healthy state and carry out its main function of gas-exchange. Due to the complexity of the various interactions between cells of the lung epithelium and surrounding tissue, it is necessary to develop models that can complement experiments to fully understand the healing dynamics. In this mathematical study we model the mechanism of epithelial regeneration. We assume that healing is exclusively driven by progenitor cell proliferation, induced by a chemical activator such as epithelial growth factor (EGF) and cytokines such as interleukin-22 (IL22). Contrary to previous studies of wound healing, we consider the immune system, specifically the T effector cells TH1, TH17, TH22 and Treg to strongly contribute to the healing process, by producing IL22 or regulating the immune response. We therefore obtain a coupled system of two ordinary differential equations for the epithelial and immune cell densities and two functions for the levels of chemicals that either induce epithelial proliferation or recruit immune cells. These functions link the two cell equations. We find that to allow the epithelium to regenerate to a healthy state, the immune system must not exceed a threshold value at the onset of the healing phase. This immune threshold is supported experimentally but was not explicitly built into our equations. Our assumptions are therefore sufficient to reproduce experimental results concerning the ratio TH17/Treg cells as a threshold to predict higher mortality rates in patients. This immune threshold can be controlled by parameters of the model, specifically the base-level growth factor concentration. This conclusion is based on a mathematical bifurcation analysis and linearization of the model equations. Our results suggest treatment of severe cases of lung injury by reducing or suppressing the immune response, in an individual patient, assessed by their disease parameters such as course of lung injury and immune response levels.

USE OF PULMONARY METABOLIC FUNCTION INDICATORS AS MARKERS OF ASPHYXIAL DEATH BY HANGING

During forensic examinations to establish the cause of death by asphyxiation in various types of mechanical asphyxiation, especially hanging, the greatest attention is paid to changes in the lungs. Despite the complexity of the genesis of death in mechanical asphyxia, the most common cause of death is asphyxia. Therefore, an important link in the progression of the asphyxia process is its effect on a vital organ such as the lungs. In order to address issues related to the development of pathological changes in the lungs, histochemical studies aimed at detecting markers of mechanical asphyxia are becoming increasingly important, in addition to the generally accepted macro- and micromorphological studies. The aim of the study is to analyse the current research on changes in the lungs during death by mechanical asphyxia due to hanging. Results. When establishing the cause of death with signs of mechanical asphyxia due to hanging, attention is drawn to the macromorphological manifestations of asphyxia genesis in the form of general signs of asphyxia that are not specific to this type of death. However, it has been found that their appearance is associated with the release of a number of biologically active substances into the body, since the process of dying by hanging is a strong stress factor. This is also indicated by micromorphological changes in various organs. The lungs receive the most attention in the study, as they are a crucial link in the asphyxiation process. The lungs are known to perform a number of important non-respiratory functions in addition to their primary function of gas exchange. The lung is an organ of biosynthesis and metabolism of many biologically active substances, regulating their levels in the blood. Some of these substances are released into the bloodstream in pathological conditions and significantly affect metabolic processes both in the lungs and throughout the body. Therefore, such substances can be used as biomarkers to prove the asphyxial genesis of death. Conclusions. Since the course of the asphyxiation process significantly affects the function of the lungs, which are the organ of biosynthesis and metabolism of many biologically active substances, the possibility of using these substances as markers of the asphyxial genesis of death in mechanical asphyxia, especially in hanging, has been demonstrated.

Repair and regeneration of the alveolar epithelium in lung injury.

Considerable progress has been made in understanding the function of alveolar epithelial cells in a quiescent state and regeneration mechanism after lung injury. Lung injury occurs commonly from severe viral and bacterial infections, inhalation lung injury, and indirect injury sepsis. A series of pathological mechanisms caused by excessive injury, such as apoptosis, autophagy, senescence, and ferroptosis, have been studied. Recovery from lung injury requires the integrity of the alveolar epithelial cell barrier and the realization of gas exchange function. Regeneration mechanisms include the participation of epithelial progenitor cells and various niche cells involving several signaling pathways and proteins. While alveoli are damaged, alveolar type II (AT2) cells proliferate and differentiate into alveolar type I (AT1) cells to repair the damaged alveolar epithelial layer. Alveolar epithelial cells are surrounded by various cells, such as fibroblasts, endothelial cells, and various immune cells, which affect the proliferation and differentiation of AT2 cells through paracrine during alveolar regeneration. Besides, airway epithelial cells also contribute to the repair and regeneration process of alveolar epithelium. In this review, we mainly discuss the participation of epithelial progenitor cells and various niche cells involving several signaling pathways and transcription factors.

Erythroid anion transport, nitric oxide, and blood pressure.

Glycophorin A and glycophorin B are structural membrane glycoproteins bound in the band 3 multiprotein complexes on human red blood cells (RBCs). Band 3 is an erythroid-specific anion exchanger (AE1). AE1-mediated HCO3 - transport provides the substrate for the enzyme-catalyzed conversion HCO3 - (aq) ⇌ CO2(g), which takes place inside the RBCs. Bicarbonate transport via AE1 supports intravascular acid-base homeostasis and respiratory excretion of CO2. In the past decade, we conducted several comparative physiology studies on Taiwanese people having the glycophorin variant GPMur RBC type (which accompanies greater AE1 expression). We found that increased anion transport across the erythrocyte membrane not only enhances gas exchange and lung functions but also elevates blood pressure (BP) and reduces nitric oxide (NO)-dependent vasodilation and exhaled NO fraction (FeNO) in healthy individuals with GP.Mur. Notably, in people carrying the GPMur blood type, the BP and NO-dependent, flow-mediated vasodilation (FMD) are both more strongly correlated with individual hemoglobin (Hb) levels. As blood NO and nitrite (NO2 -) are predominantly scavenged by intraerythrocytic Hb, and NO2 - primarily enters RBCs via AE1, could a more monoanion-permeable RBC membrane (i.e., GPMur/increased AE1) enhance NO2 -/NO3 - permeability and Hb scavenging of NO2 - and NO to affect blood pressure? In this perspective, a working model is proposed for the potential role of AE1 in intravascular NO availability, blood pressure, and clinical relevance.

EFEKTIVITAS KOMBINASI FISIOTERAPI DADA DAN SUCTION TERHADAP PENURUNAN PRODUKSI SPUTUM PADA PASIEN GAGAL NAFAS DI RUANG ICU RUMAH SAKIT SWASTA 2024: CASE REPORT

Respiratory failure is a failure in the gas exchange function between oxygen and carbon dioxide which can cause decreased consciousness. One of the complications of decreased consciousness that is often encountered is sputum retention. The intervention carried out was chest physiotherapy combined with suction. Based on a preliminary study, it was found that 24 (80%) experienced respiratory failure. To reduce sputum production in patients with respiratory failure with chest physiotherapy intervention combined with suction in the ICU of a private hospital. The research method used in this research is a case report by conducting intervention observations and also airway clearance research with 1 respondent. After chest physiotherapy combined with suction, the results showed an increase in oxygen saturation from 88% to 99% and sputum production decreased from ± 10 cc to ± 7 cc. After chest physiotherapy combined with suction for 3 days, significant results were obtained, namely an increase in oxygen saturation and also a decrease in sputum production. ICU nurses are expected to be able to apply chest physiotherapy combined with suction to reduce sputum production in patients with respiratory failure in the ICU by paying attention to vital signs. Intervention is carried out once a day.

The origins of gas exchange and ion regulation in fish gills: evidence from structure and function.

Gill function in gas exchange and ion regulation has played key roles in the evolution of fishes. In this review, we summarize data from the fields of palaeontology, developmental biology and comparative physiology for when and how the gills first acquired these functions. Data from across disciplines strongly supports a stem vertebrate origin for gas exchange structures and function at the gills with the emergence of larger, more active fishes. However, the recent discovery of putative ionocytes in extant cephalochordates and hemichordates suggests that ion regulation at gills might have originated much earlier than gas exchange, perhaps in the ciliated pharyngeal arches in the last common ancestor of deuterostomes. We hypothesize that the ancestral form of ion regulation served a filter-feeding function in the ciliated pharyngeal arches, and was later coopted in vertebrates to regulate extracellular ion and acid-base balance. We propose that future research should explore ionocyte homology and function across extant deuterostomes to test this hypothesis and others in order to determine the ancestral origins of ion regulation in fish gills.

Иммунометаболический статус крыс при моно-КВЧ-терапии отека легких

In pulmonary oedema, the accumulation of tissue fluid in the interstitial spaces of the lungs as well as in the cavities of the alveoli prevents the respiratory system from performing the gas exchange function. The ineffectiveness of various therapeutic approaches proposed to combat SARS-CoV-2 justifies the search for new therapeutic agents. Extremely high frequency (EHF) therapy could be one of the alternative treatment methods. The purpose of this article was to evaluate the immunometabolic status of rats in mono-EHF therapy of pulmonary oedema. Materials and methods. The paper evaluated the concentration of circulating immune complexes in the blood serum and the activity of lactate dehydrogenase in the lung tissue at experimental pulmonary oedema and a course of EHF therapy. The study involved 60 rats divided into 3 groups (intact, control and experimental). In the control and experimental groups, pulmonary oedema was simulated by intraperitoneal administration of adrenaline hydrochloride. A 10-day EHF therapy course was given to the experimental group using the CEMTECH device (40−43 GHz, Russia) by targeting three acupuncture points. Results. Pulmonary oedema was shown to increase the level of circulating immune complexes in the blood and the activity of lactate dehydrogenase in the lung tissue. Exposure to EHF radiation restored the normal values of these parameters. EHF therapy proved to be a promising treatment and rehabilitation method for pulmonary oedema. The selected markers for assessing the immunometabolic status could serve as an addition to the traditional methods of diagnosing this pathology, including in experimental conditions.

Pulmonary AVM Embolization

Pulmonary arteriovenous malformations (PAVMs) are rare fistulous connections between pulmonary arteries and veins that, as in our case, are commonly associated with hereditary hemorrhagic telangiectasia (HHT). Embolotherapy, the mainstay of treatment for PAVMs, is a procedure in which the feeding arteries of a malformation are endovascularly occluded under fluoroscopic guidance. Effective and well-tolerated, embolotherapy has been shown to decrease right-to-left shunting following treatment and decrease risks of paradoxical embolization and lung hemorrhage and to improve pulmonary gas exchange and lung function. Patients are selected for treatment according to clinical suspicion for the presence of a PAVM and feeding artery diameter. The occlusion of PAVMs with arteries that exceed 2-3 mm in diameter is recommended. Diagnostic contrast-enhanced pulmonary angiography is performed via injection of contrast through a percutaneous catheter to characterize and confirm PAVMs suitable for embolization. Lesions are then treated by catheter-directed placement of embolic material— vascular plugs in our case—into the feeding artery, terminating blood flow to the area of the lesion. Although multiple PAVMs may be embolized during a single session, in patients with HHT, who may present with large numbers of PAVMs, treatment is limited by maximum contrast dosage, and additional sessions may be performed if PAVMs remain perfused.

The use of protective mechanical ventilation during extracorporeal membrane oxygenation for the treatment of acute respiratory failure.

Acute respiratory failure (ARF) strikes an estimated two million people in the United States each year, with care exceeding US$50 billion. The hallmark of ARF is a heterogeneous injury, with normal tissue intermingled with a large volume of low compliance and collapsed tissue. Mechanical ventilation is necessary to oxygenate and ventilate patients with ARF, but if set inappropriately, it can cause an unintended ventilator-induced lung injury (VILI). The mechanism of VILI is believed to be overdistension of the remaining normal tissue known as the 'baby' lung, causing volutrauma, repetitive collapse and reopening of lung tissue with each breath, causing atelectrauma, and inflammation secondary to this mechanical damage, causing biotrauma. To avoid VILI, extracorporeal membrane oxygenation (ECMO) can temporally replace the pulmonary function of gas exchange without requiring high tidal volumes (VT) or airway pressures. In theory, the lower VT and airway pressure will minimize all three VILI mechanisms, allowing the lung to 'rest' and heal in the collapsed state. The optimal method of mechanical ventilation for the patient on ECMO is unknown. The ARDSNetwork Acute Respiratory Management Approach (ARMA) is a Rest Lung Approach (RLA) that attempts to reduce the excessive stress and strain on the remaining normal lung tissue and buys time for the lung to heal in the collapsed state. Theoretically, excessive tissue stress and strain can also be avoided if the lung is fully open, as long as the alveolar re-collapse is prevented during expiration, an approach known as the Open Lung Approach (OLA). A third lung-protective strategy is the Stabilize Lung Approach (SLA), in which the lung is initially stabilized and gradually reopened over time. This review will analyze the physiologic efficacy and pathophysiologic potential of the above lung-protective approaches.

Ab. No. 63 Immediate Effect of Intercostal Stretch Versus Anterior Stretch Basal Lift on Lung Compliance, Tidal Volume, Respiratory Rate, Heart Rate and SPO2 in Mechanically Ventilated Patients: An Experimental Study

Introduction: Mechanical ventilation is a useful modality for patients who are unable to sustain the level of ventilation necessary to maintain gas exchange function. Proprioceptive Neuromuscular Facilitation (PNF) of respiration is the use of selective external proprioceptive and tactile stimuli that alter depth and rate of breathing to assist respiration. Several PNF techniques are reported to increase the depth of breathing, decrease respiratory rate and increase arousal in patient with a decreased level of consciousness. Intercostal stretch and basal lift are commonly used techniques, having beneficial effects among ventilatory patients. The purpose is to compare the effect of the Intercostal stretch versus Anterior Stretch Basal Lift on Tidal Volume, Lung Compliance, SpO2, Heart Rate and Respiratory Rate Methods: After screening for inclusion and exclusion criteria, a total of 30 subjects were randomized into 2 groups of n=15 each: 1) Intercostal Stretch 2) Basal Lift. After randomization, along with chest physiotherapy, both groups received respective PNF techniques (3 sets of 10 repetition). Pre and post outcomes were analyzed. Result: Significant changes (p<0.05) seen in all the outcomes in Intercostal group. In Basal lift group, Tidal volume, compliance and SpO2 has shown significant improvement (p<0.05). Inter group analysis didn’t show significant improvement (p>0.05). Conclusion: Both these PNF techniques aids chest physiotherapy in enhancing the results for patients on mechanical ventilation. But Intercostal Stretch showed more significant results than Basal Lift, and is more feasible to perform in day to day practice. Implications: It is safe to apply these techniques in mechanically ventilated patients for better outcomes.

Relationship between Pulmonary Gas Exchange Function and Brain Uptake Dynamics Investigated with Hyperpolarized 129Xe MR Imaging and Spectroscopy in a Murine Model of Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a complex multisystem disease associated with comorbidities outside the lungs. The aim of this study was to measure changes in metrics of pulmonary gas exchange function and brain tissue metabolism in a mouse model of COPD using hyperpolarized 129Xe (HP 129Xe) MRI/MR spectroscopy (MRS) and investigate the relationship between the metrics of lung and brain. COPD phenotypes were induced in 15 mice by 6-week administration of cigarette smoke extract (CSE) and lipopolysaccharide (LPS). A separate negative control (NC) group was formed of 6 mice administered with saline for 6 weeks. After these 6-week administrations, the pulmonary gas exchange function parameter fD (%) and the rate constant, α (s-1), which are composed of the cerebral blood flow Fi and the longitudinal relaxation rate 1/T1i in brain tissue, were evaluated by HP 129Xe MRI/MRS. The fD of CSE-LPS mice was significantly lower than that of NC mice, which was in parallel with an increase in bronchial wall thickness. The α in the CSE-LPS mice decreased with the decrease of fD in contrast to the trend in the NC mice. To further elucidate the opposed trend, the contribution of T1i was separately determined by measuring Fi. The T1i in the CSE-LPS mice was found to correlate negatively with fD as opposed to the positive trend in the NC mice. The opposite trend in T1i between CSE-LPS and NC mice suggests hypoxia in the brain, which is induced by the impaired oxygen uptake as indicated by the reduced fD. This study demonstrates the feasibility of using HP 129Xe MRI/MRS to study pathological mechanisms of brain dysfunction in comorbidities with COPD.

Cellular therapies for idiopathic pulmonary fibrosis: current progress and future prospects.

Idiopathic pulmonary fibrosis (IPF) is an interstitial, fibrotic lung disease characterized by progressive damage. Lung tissues with IPF are replaced by fibrotic tissues with increased collagen deposition, modified extracellular matrix, all which overall damages the alveoli. These changes eventually impede the gas exchange function of the alveoli, and eventually leads to fatal respiratory failure of the lung. Investigations have been conducted to further understand IPF's pathogenesis, and significant progress in understanding its development has been made. Additionally, two therapeutic treatments, Nintedanib and Pirfenidone, have been approved and are currently used in medical applications. Moreover, cell-based treatments have recently come to the forefront of developing disease therapeutics and are the focus of many current studies. Furthermore, a sizable body of research encompassing basic, pre-clinical, and even clinical trials have all been amassed in recent years and hold a great potential for more widespread applications in patient care. Herein, this article reviews the progress in understanding the pathogenesis and pathophysiology of IPF. Additionally, different cell types used in IPF therapy were reviewed, including alveolar epithelial cells (AECs), circulating endothelial progenitors (EPCs), mixed lung epithelial cells, different types of stem cells, and endogenous lung tissue-specific stem cells. Finally, we discussed the contemporary trials that employ or explore cell-based therapy for IPF.

Childhood interstitial lung disease: When to suspect and what to do

Childhood Interstitial lung Disease (chILD) is a heterogeneous group of more than 200 respiratory disorders characterized by the impairement of alveolar-capillary gas exchange and lung function. These disorders usually have a chronic course. Morbidity and mortality greatly vary depending on the disorder considered. Interstitial lung disease are associated with respiratory distress. During infancy the most common symptom to pay attention to is tachypnea, whilst in older children clinical presentation may be more insidious. When chILD is suspected, it is advisable to send the patient to a pediatric pulmonology center in order to set up a diagnostic work-up and an adequate treatment. A European protocol called the “Delphi method” has been standardizing empirical treatment since 2015.

Effect of tocilizumab on pulmonary gas exchange function in patients with severe COVID-19

Introduction. COVID-19 causes cytokine storm and acute respiratory distress syndrome, which can lead to severe lung damage and multiple organ dysfunction. Early use of monoclonal antibodies has shown promising results in cytokine storm therapy, but the effects on lung gas exchange function have not yet been studied.Aim. To evaluate the effect of tocilizumab on the dynamics of gas exchange parameters in patients with severe COVID-19. Material and methods. The study included 26 patients in whom gas exchange parameters (PaO2, PaCO2, P/f ratio), blood oxygen saturation (saturation), respiration rate, duration and parameters of high-flow oxygen therapy and noninvasive mechanical ventilation, length of stay in intensive care unit and total hospital length of stay were assessed.Results. Tocilizumab significantly improved oxygenation on the third day (p=0.001) from the time of drug administration.Conclusion. In the presented and analyzed cohort of patients with severe COVID-19 and cytokine storm, the normalization and significant increase of oxygenation parameters (PaO2, p=0.001; P/f ratio, p=0.001) were observed within three days after a single-dose tocilizumab administration in a complex intensive therapy. No significant dynamics in the respiratory support parameters was revealed, nor an effect of this therapy on the duration of the respiratory support or the reduction in the aggressiveness of its parameters was observed within three days after tocilizumab administration (p>0.05).

The Use of Extracorporeal Membrane Oxygenation (ECMO) and Protective Mechanical Ventilation in the Treatment of Acute Respiratory Failure

Acute respiratory failure (ARF) affects 2 million people in the United States each year. The ARF's hallmark is a heterogeneous injury, with normal tissue intermingled with a large volume of low compliance and collapsed tissue. Mechanical ventilation is necessary to oxygenate and ventilate those patients but if set inappropriately can cause ventilator-induced lung injury (VILI). To avoid VILI, extracorporeal membrane oxygenation (ECMO) can replace the pulmonary function of gas exchange . The optimal method of mechanical ventilation for the patient on ECMO is unknown. Rest the Lung Approach (RLA) buys time for the lung to heal in the collapsed state. Open Lung Approach (OLA) attempts to open the entire lung very quickly. ARDS-related mortality has not been further reduced using the RLA and even it increases with OLA. Thus, the Mechanical Breath Profile (MBP) component of time would play a critical role in both lung opening and collapses. The Time-Controlled Adaptive Ventilation (TCAV) method of setting and adjusting the Airway Pressure Release Ventilation (APRV) mode uses an extended time at inspiration to open viscoelastic lung tissue and a very brief expiratory time to prevent re-collapse during exhalation. The expiratory time is personalized and adaptive as it is set by changes in respiratory system compliance (CRS). The TCAV method is a novel Stabilize the Lung Approach (SLA). We postulate that the SLA TCAV method would be a highly lung-protective ventilation strategy that would protect from VILI and gradually reopen the lung allowing the patient to be liberated from ECMO.

Insuficiencia respiratoria aguda

Acute respiratory failure (ARF) is the inability of the respiratory system to perform its function of oxygen and carbon dioxide gas exchange; its onset occurs in a short period of time. It is a potentially fatal disease that requires rapid identification and intervention by emergency department physicians. The most important symptom is dyspnea. There are many causes that can trigger it. Treatment of ARF is based on correcting oxygenation and ventilation and treating the triggering cause.

Genome-wide identification of transcriptional enhancers during human placental development and association with function, differentiation, and disease†.

The placenta is a dynamic organ that must perform a remarkable variety of functions during its relatively short existence in order to support a developing fetus. These functions include nutrient delivery, gas exchange, waste removal, hormone production, and immune barrier protection. Proper placenta development and function are critical for healthy pregnancy outcomes, but the underlying genomic regulatory events that control this process remain largely unknown. We hypothesized that mapping sites of transcriptional enhancer activity and associated changes in gene expression across gestation in human placenta tissue would identify genomic loci and predicted transcription factor activity related to critical placenta functions. We used a suite of genomic assays [i.e., RNA-sequencing (RNA-seq), Precision run-on-sequencing (PRO-seq), and Chromatin immunoprecipitation-sequencing (ChIP-seq)] and computational pipelines to identify a set of >20000 enhancers that are active at various time points in gestation. Changes in the activity of these enhancers correlate with changes in gene expression. In addition, some of these enhancers encode risk for adverse pregnancy outcomes. We further show that integrating enhancer activity, transcription factor motif analysis, and transcription factor expression can identify distinct sets of transcription factors predicted to be more active either in early pregnancy or at term. Knockdown of selected identified transcription factors in a trophoblast stem cell culture model altered the expression of key placental marker genes. These observations provide a framework for future mechanistic studies of individual enhancer-transcription factor-target gene interactions and have the potential to inform genetic risk prediction for adverse pregnancy outcomes.

Dynamics of functional changes in the respiratory system after COVID-19-associated lung injury at one year after hospital discharge

Morphological examination reveals microcirculation disorders in combination with small areas of lung damage in the long term after COVID-19. Therefore, the function of the respiratory system should be assessed after COVID-19. Aim of this study was to evaluate the dynamics of respiratory dysfunction in patients with COVID-19-associated lung injury using a complex examination of lung function (spirometry, body plethysmography, and lung diffusion testing) one year after hospital discharge. Methods. 60 patients (38 men/22 women, aged 39 to 80 years) with a diagnosis of “COVID-19-associated interstitial process in the lungs” were examined. Lung function (spirometry, body plethysmography, and lung diffusion capacity testing) was examined in all patients twice, at 1 – 6 months (visit 1) and at 12 – 24 months (visit 2) after hospital discharge. Results. At visit 1, 60% of patients had restrictive pulmonary ventilation disorders. Obstructive ventilation disorders were detected in only 1 patient. Decreased lung diffusion capacity (D CO corr.) was found in 78% of patients. At visit 2, obstructive disorders were detected in 1 patient, and the frequency of restrictive ventilation disorders was 29%. Decreased DLCO corr. was noted in 57% of cases. The parameters of pulmonary ventilation and pulmonary gas exchange function differed significantly between visits. Significant correlations were found between changes in the functional parameters of the respiratory system and disorders identified at visit 1 after hospital discharge. Conclusion. Thus, there is a decrease in the lung diffusion capacity and the rate of restrictive ventilation disorders even one year after severe COVID-19-associated lung injury. However, our results suggest a marked improvement in respiratory system function over time.

Interesting effects of interleukins and immune cells on acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a medical condition characterized by widespread inflammation in the lungs with consequent proportional loss of gas exchange function. ARDS is linked with severe pulmonary or systemic infection. Several factors, including secretory cytokines, immune cells, and lung epithelial and endothelial cells, play a role in the development and progression of this disease. The present study is based on Pubmed database information (1987-2022) using the words "Acute respiratory distress syndrome", "Interleukin", "Cytokines" and "Immune cells". Cytokines and immune cells play an important role in this disease, with particular emphasis on the balance between pro-inflammatory and anti-inflammatory factors. Neutrophils are one of several important mediators of Inflammation, lung tissue destruction, and malfunction during ARDS. Some immune cells, such as macrophages and eosinophils, play a dual role in releasing inflammatory mediators, recruitment inflammatory cells and the progression of ARDS, or releasing anti-inflammatory mediators, clearing the lung of inflammatory cells, and helping to improve the disease. Different interleukins play a role in the development or inhibition of ARDS by helping to activate various signaling pathways, helping to secrete other inflammatory or anti-inflammatory interleukins, and playing a role in the production and balance between immune cells involved in ARDS. As a result, immune cells and, inflammatory cytokines, especially interleukins play an important role in the pathogenesis of this disease Therefore, understanding the relevant mechanisms will help in the proper diagnosis and treatment of this disease.