21 CHARACTERIZATION OF THE micro-RNA TRANSCRIPTOME IN LUNG TISSUES OF CLONED CALVES SUFFERING FROM RESPIRATORY DISTRESS SYNDROME

2015 ◽  
Vol 27 (1) ◽  
pp. 103
Author(s):  
Y. Liu ◽  
Y. Zhang ◽  
H.-S. Hao ◽  
W.-H. Du ◽  
H.-B. Zhu ◽  
...  
Keyword(s):  
Respiratory Distress Syndrome ◽  
Western Blot ◽  
Respiratory Distress ◽  
Small Rna ◽  
Distress Syndrome ◽  
Normal Lung ◽  
Regulation Of Transcription ◽  
Primary Role ◽  
Healthy Individuals ◽  
Micro Rnas

Developmental deficiency leads to low survival rates of newborns, especially in cloned animals. Alveoli collapse leading to respiratory failure is one of the major causes of death in newborn cloned calves. The present study provides an insight into the expression pattern of micro-RNAs (miRNAs) in lung tissues and their role in the respiratory distress syndrome (RDS) in the cloned calves. Short RNA high-throughput sequencing and bioinformatic analysis from small RNA libraries created from collapsed lung tissues from 4 newborn cloned calves with RDS and normal lung tissues from 4 age-matched healthy individuals were implemented. Lung tissues were collected by dissection from newborns that died due to RDS and from healthy individuals on the first day after birth. RNA samples from the lung tissues were processed to generate small RNA libraries that were further used for deep sequencing. Expression profiles of surfactant-associated protein B (SPB), surfactant-associate protein C (SPC), and their key transcription regulator thyroid transcription factor-1 (TTF-1), which are responsible for stabilising alveolar surface, reducing surface tension, and thus preventing alveoli collapse, were verified through real-time RT-PCR, Western blot, and immunohistochemistry (IHC). Differentially expressed (DE) miRNAs were quantified by edgeR (empirical analysis of digital gene expression data in R), and their target genes were predicted by both TargetScan and miRanda software. Only miRNAs with P values <0.05 were considered statistically significant (Fisher exact test). Sequence analysis revealed the presence of 1592 and 1777 miRNAs in the RDS and healthy groups, respectively. A total of 326 miRNAs were DE between the two groups according to our criteria, of which 179 miRNAs were up-regulated and 147 were down-regulated in the RDS group. Gene ontological analysis showed that the DE miRNAs had a primary role in DNA-dependent regulation of transcription, cytoplasm biosynthesis, and nucleotide binding. Eleven miRNAs (bta-miR-186, bta-miR-2284x_R+1, bta-miR-24–3p_R-2, bta-miR-424–3p, bta-miR-592_L-1, bta-miR-660, bta-miR-150_R-1, bta-miR-2478_L-2, bta-miR-450b_R-1, bta-miR-134_L+2R-2 and bta-miR-326_R+1) were DE between the 2 groups and were predicted to target SPB, SPC, and TTF-1, respectively. Among these DE miRNAs, 5 miRNAs (bta-miR-134_L+2R-2, bta-miR-424–3p, bta-miR-660, bta-miR-2478_L-2, bta-miR-450b_R-1) were up-regulated in the RDS group. Western blot and IHC confirmed the down-regulation of SPB, SPC, and TTF-1 at the protein level in RDS group. This increase in abundance of miRNAs targeting key regulatory genes in lung of newborn cloned calves may take part in the dysregulation of alveolus development leading to alveoli collapse and RDS. The assay for target gene verification and analysis of gene transcription profile are under study.Y. Liu and Y. Zhang contributed equally to this work. This project was supported by the National Natural Science Foundation of China (No. 31301977) and the National Nonprofit Institute Research Grant (No. 2011cj-11).

PHYSIOLOGY OF RESPIRATION IN NEWBORN INFANTS AND IN THE RESPIRATORY DISTRESS SYNDROME

PEDIATRICS ◽  
1959 ◽  
Vol 24 (6) ◽  
pp. 1069-1101
Author(s):  
L. Stanley James
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Newborn Infants ◽  
Clinical Signs ◽  
Birth Asphyxia ◽  
The Body ◽  
Normal Lung ◽  
Term Infants ◽  
Lung Expansion

To improve our understanding of the respiratory distress syndrome, the importance of early examination of the infant, preferably at delivery, cannot be overemphasized. An attempt should be made to estimate clinically the degree of birth asphyxiation by a method such as the Apgar Score. The nature of respirations as well as the rate should be noted, particularly retractions and grunting. Decreased response to stimuli or poor tone, and a low blood pressure are significant signs. In this review, a number of comparisons have been drawn, including evidence from adult medicine or animal experiments. While these may appear unrelated, irrelevant or unduly speculative, they have been introduced for several purposes: to draw attention to aspects of the syndrome other than respiratory distress; to acquaint the general reader with more recent physiology which is deemed pertinent; and to emphasize the importance of relating one system to another, especially respiration to circulation. Many of the studies of respiratory function point to cardiac as well as pulmonary failure, notably the need for oxygen in the presence of a normal tidal and increased minute volume. Other circumstantial evidence of cardiac failure is abundant. Asphyxia appears to play a central role, affecting almost every system in the body and every phase of metabolism. It is probably responsible for the normal or low venous pressures occurring with a failing myocardium. It also accounts for the higher incidence of respiratory distress in the smaller prematures who are unable to achieve and maintain normal lung expansion. The syndrome is uncommon in larger full-term infants and in these instances is associated with obstetrical complications causing more severe degrees of birth asphyxia. The clinical picture includes a number of variations depending upon whether respiratory depression or symptoms relating to the central nervous or gastrointestinal systems predominate. Nevertheless, diagnosis of the respiratory distress syndrome should rely not on the presence or absence of membranes at necropsy, but rather on the history, symptoms and clinical signs. Inasmuch as asphyxia is not a disease, it would seem more logical to regard the syndrome as a failure in adaptation to extrauterine life. Failure to comprehend the many adaptations which newborn infants must make, both cardiopulmonary and biochemical, together with a narrow view centering only around the hyaline membranes, have for so many years cloaked this syndrome with mystery. Physiologic measurements in sick infants are difficult, and many of the determinations and calculations arduous. Some of the studies require confirmation, and others remain to be done, employing new or improved technics which are free from disadvantages of older methods. Because of many variables, caution should be exercised in drawing conclusions from a small number of cases. Early pioneering work has contributed greatly and has paved the way for future investigations. The value of serial studies correlated with careful clinical observations in order that the precise nature of a dynamic process may be more fully revealed has been clearly shown.

scholarly journals Lung Microbiome in Critically Ill Patients

Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 7
Author(s):  
Mélanie Fromentin ◽  
Jean-Damien Ricard ◽  
Damien Roux
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Bacterial Pathogen ◽  
Normal Lung ◽  
Ventilator Associated Pneumonia ◽  
Bacterial Populations ◽  
Chronic Respiratory Diseases

The historical hypothesis of sterility of the lungs was invalidated over a decade ago when studies demonstrated the existence of sparse but very diverse bacterial populations in the normal lung and the association between pulmonary dysbiosis and chronic respiratory diseases. Under mechanical ventilation, dysbiosis occurs rapidly with a gradual decline in diversity over time and the progressive predominance of a bacterial pathogen (mainly Proteobacteria) when lung infection occurs. During acute respiratory distress syndrome, an enrichment in bacteria of intestinal origin, mainly Enterobacteriaceae, is observed. However, the role of this dysbiosis in the pathogenesis of ventilator-associated pneumonia and acute respiratory distress syndrome is not yet fully understood. The lack of exploration of other microbial populations, viruses (eukaryotes and prokaryotes) and fungi is a key issue. Further analysis of the interaction between these microbial kingdoms and a better understanding of the host-microbiome interaction are necessary to fully elucidate the role of the microbiome in the pathogenicity of acute diseases. The validation of a consensual and robust methodology in order to make the comparison of the different studies relevant is also required. Filling these different gaps should help develop preventive and therapeutic strategies for both acute respiratory distress syndrome and ventilator-associated pneumonia.

Increased Levels of Nuclear Factor κB and Fos-Related Antigen 1 in Lung Tissues From Patients With Acute Respiratory Distress Syndrome

2011 ◽  
Vol 135 (5) ◽  
pp. 647-654
Author(s):  
Rafal Fudala ◽  
Timothy Craig Allen ◽  
Agnieszka Krupa ◽  
Philip T. Cagle ◽  
Sandra Nash ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Nuclear Factor Κb ◽  
Surfactant Protein ◽  
Normal Lung ◽  
Confocal Laser ◽  
Nuclear Factor ◽  
Epithelial Cell Marker

Abstract Context.—Both nuclear factor κB and Fos-related antigen 1 have been implicated in the pathogenesis of inflammatory lung diseases, including acute lung injury/acute respiratory distress syndrome. Objective.—To evaluate lung tissues from patients with acute respiratory distress syndrome for presence of nuclear factor κB and Fos-related antigen 1. Design.—Lung tissue sections from 5 patients with acute respiratory distress syndrome and sections of normal lung tissues of 4 patients were stained with antibodies against epithelial cell marker (surfactant protein B) and nuclear factor κB or Fos-related antigen 1. Samples were analyzed using confocal laser microscopy. Results.—We have detected significantly increased levels of activated nuclear factor κB and Fos-related antigen 1 in lung tissues from patients with acute respiratory distress syndrome compared with control tissues, suggesting that these transcription factors undergo activation in lungs of patients suffering from acute respiratory distress syndrome. Conclusions.—Our data demonstrate that activated nuclear factor κB and Fos-related antigen 1 are elevated in epithelial cells in lung tissues of patients with acute respiratory distress syndrome.

scholarly journals Dinucleotide repeats in the human surfactant protein-B gene and respiratory-distress syndrome

1995 ◽  
Vol 305 (2) ◽  
pp. 583-590 ◽  
Author(s):  
J Floros ◽  
S V Veletza ◽  
P Kotikalapudi ◽  
L Krizkova ◽  
A M Karinch ◽  
...  
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Surfactant Protein ◽  
Normal Lung ◽  
Dinucleotide Repeats ◽  
Conserved Sequence ◽  
Surfactant Protein B ◽  
Genomic Dnas ◽  
Protein B

Pulmonary surfactant, a lipoprotein complex, is essential for normal lung function, and deficiency of surfactant can result in respiratory-distress syndrome (RDS) in the prematurely born infant. Some studies have pointed towards a genetic contribution to the aetiology of RDS. Because the surfactant protein B (SP-B) is important for optimal surfactant function and because it is involved in the pathogenesis of pulmonary disease, we investigated the genetic variability of the SP-B gene in individuals with and without RDS. We identified a 2.5 kb BamHI polymorphism and studied its location, nature and frequency. We localized this polymorphism in the first half of intron 4 and found that it is derived by gain or loss in the number of copies of a motif that consists of two elements, a 20 bp conserved sequence and a variable number of CA dinucleotides. Variability in the number of motifs resulting from either deletion (in 55.3% of the cases with the variation) or insertion (44.7%) of motifs was observed in genomic DNAs from unrelated individuals. Analysis of 219 genomic DNAs from infants with (n = 82) and without (n = 137) RDS showed that this insertion/deletion appears with significantly higher frequency in the RDS population (29.3 as against 16.8%, P < 0.05).

scholarly journals Does Prone Positioning Improve Oxygenation and Reduce Mortality in Patients with Acute Respiratory Distress Syndrome?

2014 ◽  
Vol 21 (4) ◽  
pp. 213-215 ◽  
Author(s):  
William R Henderson ◽  
Donald EG Griesdale ◽  
Paolo Dominelli ◽  
Juan J Ronco
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Clinical Evidence ◽  
Distress Syndrome ◽  
Lung Parenchyma ◽  
Normal Lung ◽  
Prone Positioning ◽  
Computed Tomography Imaging

The emergence of computed tomography imaging more than 25 years ago led to characterization of acute respiratory distress syndrome (ARDS) as areas of relatively normal lung parenchyma juxtaposed with areas of dense consolidation and atelectasis. Given that this heterogeneity is often dorsally distributed, investigators questioned whether care for ARDS patients in the prone position would lead to improved mortality outcomes. This clinical review discusses the physiological rationale and clinical evidence supporting prone positioning in treating ARDS, in addition to its complications and contraindications.

scholarly journals Quantitative image analysis in COVID-19 acute respiratory distress syndrome: a cohort observational study.

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1266
Author(s):  
Tamas Dolinay ◽  
Dale Jun ◽  
Abigail Maller ◽  
Augustine Chung ◽  
Brandon Grimes ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Lung Damage ◽  
Normal Lung ◽  
Care Hospital ◽  
Supplementary Oxygen

Background Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury commonly associated with pneumonia, including coronavirus disease-19 (COVID-19). The resultant effect can be persistent lung damage, but its extent is not known. We used quantitative high resolution computed tomography (QHR-CT) lung scans to radiographically characterize the lung damage in COVID-19 ARDS (CARDS) survivors. Methods Patients with CARDS (N=20) underwent QHR-CT lung scans 60 to 90 days after initial diagnosis, while hospitalized at a long-term acute care hospital (LTACH). QHR-CT assessed for mixed disease (QMD), ground glass opacities (QGGO), consolidation (QCON) and normal lung tissue (QNL). QMD was correlated with respiratory support on admission, tracheostomy decannulation and supplementary oxygen need on discharge. Results Sixteen patients arrived with tracheostomy requiring invasive mechanical ventilation. Four patients arrived on nasal oxygen support. Of the patients included in this study 10 had the tracheostomy cannula removed, four remained on invasive ventilation, and two died. QHR-CT showed 45% QMD, 28.1% QGGO, 3.0% QCON and QNL=23.9%. Patients with mandatory mechanical ventilation had the highest proportion of QMD when compared to no mechanical ventilation. There was no correlation between QMD and tracheostomy decannulation or need for supplementary oxygen at discharge. Conclusions Our data shows severe ongoing lung injury in patients with CARDS, beyond what is usually expected in ARDS. In this severely ill population, the extent of mixed disease correlates with mechanical ventilation, signaling formation of interstitial lung disease. QHR-CT analysis can be useful in the post-acute setting to evaluate for interstitial changes in ARDS.

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