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At least 109 records · Page 6Linked to original sources
PubMed1996

[Respiratory system involvement in pseudotuberculosis].

Clinical, microbiological, x-ray and immunological examinations of 1376 patients with pseudotuberculosis and 465 patients with acute respiratory diseases of viral or coccal origin, the trends in annual morbidity for the above diseases followed up within 7 years in the populations where the patients were registered and experimental investigations on rabbits provided evidence for primarily generalized pattern of pseudotuberculosis infection and a direct relationship between pulmonary lesions in the animals and effective dose of the infectant, route of the infection. The patients had nonspecific (non-yersiniosis) lesions of the respiratory system. Frequency of the infection was greater in cold seasons, especially in those who did not complete social and biological adaptation to new conditions, and depended on seasonal fluctuations of respiratory infection morbidity in nonrandom populations.

Acute Disease↗
PubMed1999

Proton translocation in the respiratory chain involving ubiquinone--a hypothetical semiquinone switch mechanism for complex I.

The protonmotive Q-cycle is the generally accepted reaction scheme of the cytochrome bc1 complex of the respiratory chain. It employs the redox-dependent protonation and deprotonation of ubiquinone (coenzyme Q10) to translocate protons across the inner mitochondrial or bacterial plasma membrane. The requirements for the operation of a similar mechanism in proton translocating NADH:ubiquinone oxidoreductase (complex I) and the specific roles of the 'Rieske' iron-sulfur center in the cytochrome bc1 complex and iron-sulfur center N-2 in complex I are discussed. Recent results suggest that there is only one ubiquinone-reactive site in complex I which seems to exclude a classical Q-cycle type mechanism. Therefore, a "semiquinone switch" mechanism is proposed involving one tightly bound and one substrate quinone. It is based on the same principles as a Q-cycle, but is a localized rather than a ligand conduction type mechanism.

Animals↗
PubMed1983

Mitochondrial myopathy with respiratory muscle involvement: a case report.

A case of a 10-year-old patient with a benign congenital myopathy, suddenly aggravated because of an accentuated deficit in respiratory muscles is reported. The institution of assisted respiration at night allowed the patient to return to her daily activities. Examination of muscular biopsy with ultra-microscope permitted the diagnosis of mitochondrial myopathy.

Child↗
PubMed1991

Structural similarities between a mitochondrially encoded polypeptide and a family of prokaryotic respiratory toxins involved in plasmid maintenance suggest a novel mechanism for the evolutionary maintenance of mitochondrial DNA.

Subunit 8 of mitochondrial ATP synthase (A8), a mitochondrially encoded polypeptide, has no known homologue in any prokaryotic or plastid ATP synthase, suggesting that it has been recruited to its present role in the enzyme from an extraneous source. The polypeptide is poorly conserved at the primary sequence level, but shows a well-conserved hydropathy profile. The hydropathy profiles of A8 from diverse taxa were compared with those of the hok family of prokaryotic respiratory toxins, some of whose members are involved in plasmid maintenance, through postsegregational killing of cells that lose the plasmid at cell division. Such comparisons revealed a highly significant degree of similarity, suggesting a functional relationship. Based on these findings, it is proposed that A8 evolved from a hok-like protein, whose original role was the maintenance of an extrachromosomal replicon in the endosymbiont ancestor of mitochondria. An aggressive mechanism for the evolutionary maintenance of mitochondrial DNA overcomes many of the failings of traditional explanations for its retention as a separate genome.

Biological Evolution↗
PubMed2000

Brainstem and hypothalamic areas involved in respiratory chemoreflexes: a Fos study in adult rats.

The adaptation to hypoxia and hypercapnia requires the activation of several anatomical structures along the neuraxis. In this study, using Fos immunoreactivity, we sought to map neuronal populations involved in chemoreflex networks activated during the responses to moderate hypoxia (O(2) 11%), and hypercapnia (CO(2) 5%) in the brainstem and the hypothalamus of the rat. In the medulla, hypoxia elicited marked and significant staining in the nucleus of the solitary tract (NTS), and in parapyramidal neurons located near the ventral surface, whereas hypercapnia evoked significantly c-fos only near the ventral surface in paraolivar neurons. In contrast, within pontine and suprapontine structures, both hypoxia and hypercapnia evoked similarly Fos immunoreactivity in the lateral parabrachialis area, the central grey, the caudal hypothalamus (dorsomedial and posterior hypothalamic nuclei), and in a ventro-lateral hypothalamic area, extending from the rostral limit of the mammillary nuclei to the retrochiasmatic area. More rostrally, labelling was observed in the paraventricular nucleus of the hypothalamus in response to hypercapnia, and in the supraoptic nucleus in response to hypoxia. These results support the hypothesis that chemoreflexes pathways are not only restricted to medulla and pons but also involved mesencephalic and hypothalamic regions. The parabrachialis area and the central grey may be key relays between caudal and ventral hypothalamic neurons, and medullary neurons involved in the response to hypoxia and hypercapnia.

Animals↗
PubMed1993

The lung in inflammatory bowel disease.

Respiratory involvement in patients with inflammatory bowel disease (IBD) has been reported mainly since 1976. This form of involvement should clearly be separated from interstitial lung disease due to sulfasalazine or mesalamine, although the distinction may be difficult in some cases. We report the data of an ongoing Registry containing 33 cases (23 cases receiving no drug therapy) with ulcerative colitis or, less often, Crohn's disease, who developed varied bronchopulmonary problems. In several cases, the exact diagnosis and the relation of the bronchopulmonary disease to IBD had not been established for many years, thus delaying effective treatment with steroids. In most cases (28/33), respiratory involvement followed the onset of IBD (8 of these 28 cases were postcolectomy), and in the remainder, respiratory manifestations predated the IBD. Patterns of involvement included: 1) Airway inflammation, in the form of subglottic stenosis, chronic bronchitis, severe chronic bronchial suppuration, bronchiectasis, and chronic bronchiolitis. In cases with large airway involvement, endoscopy showed exuberant inflammatory tissue in the airways and narrowing of tracheal and/or bronchial lumen. Histologically, airways were heavily infiltrated by a dense aggregate of inflammatory cells, and there were mucosal ulcerations. 2) Varied patterns of interstitial lung disease, mainly bronchiolitis obliterans with organizing pneumonia, and pulmonary infiltrates and eosinophilia. (3) Miscellaneous other forms of involvement including striking neutrophilic necrotic parenchymal nodules (corresponding histologically to sterile aggregates of neutrophils), and serositis. Steroids were very effective in the majority of cases. Inhaled steroids were of durable benefit in patients with chronic bronchitis, but less often so in those with chronic bronchial suppuration, bronchiectasis, or chronic bronchiolitis. Steroids administered orally led to marked improvement in patients with interstitial lung disease and necrotic nodules, but lacked effectiveness in several patients with severe airway inflammation or chronic bronchiolitis. Intravenous steroids were required in the initial management of life-threatening complications such as asphyxiating subglottic stenosis or extensive interstitial lung disease. Bronchial lavages with methylprednisolone were effective in some patients with severe airway inflammation. Patients with IBD can develop varied inflammatory complications in the lung, and a sizable fraction of these complications is steroid-sensitive.

Adolescent↗
PubMedDate not supplied

Respiratory muscle involvement in nemaline myopathy.

A boy who had experienced generalized muscle weakness and hypotonia since early infancy was diagnosed as having nemaline myopathy on the basis of muscle biopsy at 3 years of age. At 8 years of age, he developed severe respiratory failure and required respiratory support during sleep. Because of recurrent pneumothorax, he underwent thoracic surgery, at which time biopsy specimens were obtained from the respiratory and truncal muscles. The histologic findings of the respiratory muscles included marked variation in fiber size with a notable increase in fibrous tissue, type 2 fiber deficiency, elevated acid phosphatase activity, and a disorganized intermyofibrillar network. The findings from the truncal muscles were similar to those of the biceps brachii muscle: little variation in fiber size, numerous nemaline bodies in all fibers, and type 1 fiber predominance. The preferential damage to the respiratory muscles was probably responsible for the sudden onset of severe respiratory failure.

Biopsy↗
PubMed2004

Respiratory tract infections in Greenland: results of an audit project.

OBJECTIVES: To elucidate and improve quality of diagnosis and treatment of respiratory tract infections in Greenland. STUDY DESIGN: All district medical officers and nursing staff in the Greenlandic coastal health services were invited to participate in the study. Twenty-five district medical officers and the nursing staff from nine districts completed the project and registered in a 3-week period 1,163 contacts involving respiratory tract infections. METHODS: Self-registration according to the Audit Project Odense (APO) method on a simple APO registration chart. All contacts involving respiratory tract infections were registered with regard to sex, type of contact, contact form, infection focus, diagnosis and treatment, origin of infection, antibiotic treatment, choice of antibiotics and possible sick-leave. RESULTS: Of the 1,163 registered contacts lung infections represented 26%, throat infections 22% and otitis media 16%. Paraclinical tests were performed in 32% of the cases, 47% of the cases were treated with antibiotics, in 2/3 of the cases with penicillin V. The use of paraclinical tests was somewhat lower and the use of antibiotics was higher than in Denmark. CONCLUSION: The study showed that it is possible to carry out an APO audit in Greenland, and that there was a moderate difference in the diagnosis and treatment between Greenland and Denmark. An increased use of paraclinical tests may result in quality improvement.

Anti-Bacterial Agents↗
PubMed1994

Hantavirus pulmonary syndrome: recognition and emergency department management.

Hantavirus infection with respiratory involvement is a new clinical entity. The respiratory and cardiovascular abnormalities associated with hantavirus infection define the hantavirus pulmonary syndrome (HPS). We present two cases of HPS and discuss the presentation, epidemiology, emergency department management, and differential diagnosis. Treatment of HPS involves intensive care monitoring, airway management, and cardiovascular support. Because human hantavirus infection with respiratory involvement has been recognized recently in all geographic regions of the United States, it is important for emergency physicians to recognize this syndrome's characteristic symptoms and laboratory abnormalities. The fulminant clinical course of HPS and its 65% mortality rate underscore the importance of early recognition if potentially life-saving interventions are to be initiated.

Acute Disease↗