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At least 397 records · Page 22Linked to original sources
PubMed2003

Embryological origins and development of the rat diaphragm.

Textbooks of embryology provide a standard set of drawings and text reflecting the traditional interpretation of phrenic nerve and diaphragm development based on anatomical dissections of embryonic tissue. Here, we revisit this issue, taking advantage of immunohistochemical markers for muscle precursors in conjunction with mouse mutants to perform a systematic examination of phrenic-diaphragm embryogenesis. This includes examining the spatiotemporal relationship of phrenic axon outgrowth and muscle precursors during different stages of myogenesis. Additionally, mutant mice lacking c-met receptors were used to visualize the mesenchymal substratum of the developing diaphragm in the absence of myogenic cells. We found no evidence for contributions to the diaphragm musculature from the lateral body wall, septum transversum, or esophageal mesenchyme, as standard dogma would state. Nor did the data support the hypothesis that the crural diaphragm is of distinct embryological origins. Rather, we found that myogenic cells and axons destined to form the neuromuscular component of the diaphragm coalesce within the pleuroperitoneal fold (PPF). It is the expansion of these components of the PPF that leads to the formation of the diaphragm. Furthermore, we extended these studies to examine the developing diaphragm in an animal model of congenital diaphragmatic hernia (CDH). We find that malformation of the PPF mesenchymal substratum leads to the defect characteristic of CDH. In summary, the data demonstrates that a significant revision of narratives describing normal and pathological development of the diaphragm is warranted.

Animals↗
PubMed1997

Early postnatal lethality in Hoxa-5 mutant mice is attributable to respiratory tract defects.

To uncover roles for the Hoxa-5 gene during embryogenesis, we have focused on identifying structural and functional defects in organ systems underlying the perinatal lethality in Hoxa-5 homozygous mutants. Analysis of the mutant phenotype shows that Hoxa-5 is essential for normal organogenesis and function of the respiratory tract. In homozygous newborn mutants, improper tracheal and lung morphogenesis can lead to tracheal occlusion, and to respiratory distress associated with a marked decrease in the production of surfactant proteins. Collectively, these defects likely underlie the pronounced mortality of homozygous mutant pups. Furthermore, the loss of Hoxa-5 function results in altered TTF-1, HNF-3 beta, and N-myc gene expression in the pulmonary epithelium. Since expression of Hoxa-5 is confined to the mesenchymal component of the developing trachea and lung, the effects observed in epithelial cells may result from a disruption of normal epithelial-mesenchymal interactions.

Animals↗
PubMed2005

Adult case of accessory cardiac bronchus presenting with bloody sputum.

We report an adult case of accessory cardiac bronchus (ACB) which extended from the carina to the diaphragm. A 32-year-old woman, with a history of frequent respiratory infections since childhood, recently presented with bloody sputum, and was admitted to our hospital. The ACB was detected as a supernumerary bronchus diverging from tracheal bifurcation. Complete resection of the ACB was performed by video-assisted thoracic surgery via minithoracotomy, approaching from the 5th intercostal space. The bloody sputum was caused by chronic inflammation of the ACB. She has been asymptomatic since surgery.

Adult↗
PubMed2000

Diagnostic yield of the lactate stress test in 160 patients with suspected respiratory chain disorder.

Aim of the present study was to investigate the diagnostic yield of the lactate-stress-test in unselected patients with suspected respiratory-chain disorder (RCD). Serum lactate was determined before, during and after a 15-minute, constant 30W workload on a bicycle in 48 controls and 160 patients with suspected RCD. 122 had definite RCD, 38 neurological disorders other than RCD. The sensitivity, specificity, positive predictive value, negative predictive value and pre-test likelihood of the test was 69, 74, 89, 42 and 76% respectively. In conclusion, the lactate-stress-test proved a powerful tool to assess impaired oxidative metabolism in RCDs.

Adolescent↗
PubMed2005

Prenatal diagnosis of horseshoe lung: contribution of MRI.

Horseshoe lung is a very rare pulmonary anomaly that is characterized by an isthmus of lung parenchyma bridging the right and left lungs and extending through the mediastinum. We report on the prenatal diagnosis of such a malformation in a 33-week-gestation fetus. The diagnosis was initially suspected on antenatal ultrasonography performed at 33 weeks and confirmed by fetal MRI and subsequent pathological examination after termination of pregnancy. To our knowledge, this is the first reported case of antenatal diagnosis of horseshoe lung.

Adult↗
PubMed2006

CT of tracheal agenesis.

BACKGROUND: Tracheal agenesis is a rare and usually lethal anomaly. In the past, opaque contrast medium was injected via the esophagus to demonstrate the anatomy. OBJECTIVE: To demonstrate the utility of helical and multidetector CT in delineating the aberrant anatomy in newborns with tracheal agenesis. MATERIALS AND METHODS: Four newborns with tracheal agenesis were identified from three institutions. Imaging studies and medical records were reviewed. Each child was imaged with chest radiography. One child was imaged on a single-detector helical CT scanner and the other three on multidetector scanners. RESULTS: Helical and multidetector CT with 2D and 3D reconstructions clearly delineated the aberrant tracheobronchial and esophageal anatomy in each infant. Minimum intensity projection reformatted CT images were particularly helpful. One infant each had type I and type II tracheal agenesis. Two infants had type III tracheal agenesis. All four infants died. CONCLUSION: CT is a useful tool for delineating the aberrant anatomy of newborns with tracheal agenesis and thus helps in making rational clinical decisions.

Artifacts↗
PubMed2003

Prenatal vitamin E improves lung and heart hypoplasia in experimental diaphragmatic [correction of diaphragamatic] hernia.

Nitrofen induces in rats diaphragmatic hernia (CDH) with heart and lung hypoplasia by a mechanism involving oxidation. The aim of this study was to examine if prenatal administration of the anti-oxidant agent vitamin E (VitE) prevents to some extent heart and lung hypoplasia. Pregnant rats received on E9.5 either 100 mg of nitrofen alone or followed by 150 IU of VitE on E16.5-E20.5. Control animals received either vehicle or VitE alone. The fetuses were recovered on E21. The hearts and lungs were weighed and DNA and proteins were measured. Sections of the heart and lung were immunohistochemically stained for ki-67, Tunel and TTF-1, and the proportions of proliferating, apoptotic and TTF-1-expressing cells were determined. Cultured human pneumocytes were exposed to the same agents and similarly processed. TTF-1 expression and the proportion of proliferating cells were quantitated. The ANOVA or Kruskall-Wallis tests were used for comparison with p<0.05 as threshold of significance. Nitrofen-exposed rats had decreased lung and heart weight/body weight ratios, lung and heart DNA and protein, lung TTF-1 expression and proportion of proliferating cells in lung and heart. Additional treatment with VitE ameliorated these decreases except for lung TTF-1 and heart weight. In cultured pneumocytes, TTF-1 expression was decreased by nitrofen and rescued by VitE. Cell proliferation followed the same pattern. Antioxidant VitE partially reverses the effects of nitrofen on the heart and lungs of exposed rats. The same effects are observed in cultured human pneumocytes. These results further substantiate the oxidative nature of the effects of nitrofen and suggest that anti-oxidant agents could have a potential clinical application.

Animals↗
PubMed2003

Increased expression of ICAM-1 and VCAM-1 in the lung of nitrofen-induced congenital diaphragmatic hernia in rats.

Recently, increased expression of inflammatory cytokine, tumor necrosis factor (TNF)-alpha, has been reported in both humans and animal models with CDH and the decreased TNF-alpha expression in CDH lung after antenatal dexamethasone (Dex) treatment. Intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 are induced by several inflammatory cytokines such as TNF-alpha. The aim of this study was to investigate pulmonary ICAM-1 and VCAM-1 expression in CDH lung in rats and to determine the effect of antenatal glucocorticoid. CDH model was induced in pregnant rats following administration of nitrofen on day 9.5 of gestation. In control animals, the same dose of olive oil was given without nitrofen. Dex (0.25 mg/kg) was given on day 18.5 and 19.5 of gestation. RT-PCR was performed to evaluate the relative amount of ICAM-1 and VCAM-1 mRNA expression. Fluorescein immunohistochemistry using anti-ICAM-1 and anti-VCAM-1 antibody was performed using light and confocal microscopy. ICAM-1 and VCAM-1 mRNA expression and ICAM-1 and VCAM-1 immunoreactivity were markedly increased in CDH lung compared to controls. Dex downregulated the expression of both adhesion molecules in the hypoplastic lung. Increased ICAM-1 and VCAM-1 mRNA expression in hypoplastic lungs would suggest that the increased local synthesis of pulmonary adhesion molecules may induce respiratory distress in CDH. Decreased expression of adhesion molecules in CDH lungs after Dex treatment suggests that antenatal glucocorticoids therapy may improve pulmonary immaturity and associated respiratory distress in nitrofen-induced CDH lung.

Animals↗
PubMed1976

Diagnosis of obstruction of the upper and central airways.

Patients with obstruction of the upper airways are often treated for long periods of time for other disorders. Correct diagnosis is important since treatment is quite specific. Such patients may present with a characteristic history and findings on physical examination. Certain physiologic tests such as flow-volume loops with and without helium help to prove the diagnosis. Patients with upper airway obstruction may also have sleep apneas and the sleep deprivation syndrome. Methods of diagnosis of upper airway obstruction are presented and three instructive cases are reviewed.

Airway Obstruction↗
PubMed1988

Cilia-lacking respiratory cells in ciliary aplasia.

This report describes the ultrastructural alterations observed in the nasal and bronchial mucosa of an 11-yr-old male suffering from immotile cilia syndrome (ICS). The morphological features observed in this patient are consistent with a ciliary aplasia. In fact, ciliated cells appeared to be replaced by columnar cells lacking cilia and basal bodies, and bearing on their surface cilium-like projections without any internal axonemal structure. In spite of the absence of basal bodies, centrioles, and kinocilia, these cells unexpectedly showed mature striated roots and centriolar precursor material scattered throughout the apical cytoplasm. These data suggest that control over basal body assembly is distinct from control over striated root formation. The presence of the above-reported structures in cells otherwise presenting many morphological features of normal ciliated cells is discussed on the basis of current knowledge of respiratory cilia biogenesis.

Bronchi↗
PubMed1995

A system for rapid identification of respiratory abnormalities using a neural network.

Potential victims of Sudden Infant Death Syndrome (SIDS) can usefully be monitored in the home environment. Conventional respiration movement monitors can be helpful but may not detect potentially dangerous hypoxaemic episodes. Thus oxygen monitoring is to be preferred but can be difficult to use in the home. In an attempt to overcome these difficulties this paper presents the results of an exploratory experiment into the use of a neural network to link the output of a respiration pressure monitor to the classification of breathing patterns as effective or otherwise. It has been shown that it is possible to predict changes in oxygen saturation, which could signify potentially dangerous episodes earlier than when other methods are employed.

Humans↗
PubMed2005

Congenital diaphragmatic hernia: searching for answers.

BACKGROUND: Pulmonary hypoplasia and hypertension are the primary causes of morbidity and mortality in infants with congenital diaphragmatic hernia (CDH). At present, the origin of CDH and the causes of pulmonary hypoplasia and hypertension are unknown. DATA SOURCES: This article reviews the available published data regarding the origin of CDH and the pathogenesis of the associated pulmonary hypertension and hypoplasia. These investigations have employed human tissues as well as two types of CDH animal models. CONCLUSIONS: Investigations performed to date have not yet provided definitive answers regarding the pathogenesis of CDH. However, they have yielded many new and exciting discoveries and several opportunities for intervention. Ongoing research should open new possibilities to improve the outcome for these unfortunate babies with CDH.

Animals↗