Publications by authors named "Nuno Castelo Branco"

Context: Only a few studies evaluated the digestive alterations caused by low frequency noise (LFN) and most focused only on mucosal alterations.

Objectives: To investigate the morphological injury of LFN-exposed gastric wall, beyond the epithelial layer.

Methods: Wistar rats were exposed to low frequency noise (LFN), during increasing periods, 1 to 13 weeks.

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Background: In 1987, the autopsy of a vibroacoustic disease (VAD) patient disclosed two tumours: a renal cell carcinoma and a malignant glioma in the brain. Since 1987, malignancy in VAD patients has been under close surveillance. To date, in a universe of 945 individuals, there are 46 cases of malignancies, of which 11 are multiple.

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At present, infrasound (0-20 Hz) and low-frequency noise (20-500 Hz) (ILFN, 0-500 Hz) are agents of disease that go unchecked. Vibroacoustic disease (VAD) is a whole-body pathology that develops in individuals excessively exposed to ILFN. VAD has been diagnosed within several professional groups employed within the aeronautical industry, and in other heavy industries.

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Background: Long-term low frequency noise exposure (LFN) (< or = 500 Hz, including infrasound) may lead to the development of vibroacoustic disease (VAD), a systemic pathology characterized by the abnormal growth of extra-cellular matrices. The respiratory system is a target for LFN. Fibrosis of the respiratory tract epithelia was observed in VAD patients through biopsy, and confirmed in animal models exposed to LFN.

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Article Synopsis
  • * A study used the P0.1 value to assess the respiratory drive in VAD patients and found that while pulmonary function tests were normal, the P0.1 (CO2) index in VAD patients was significantly lower than in controls, indicating potential respiratory control impairment.
  • * The results suggest that the dysfunction in breathing response to CO2 in VAD patients may be rooted in brainstem control mechanisms, highlighting the need for further investigation into neurological impacts related to LFN exposure.
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Introduction: Exposure to low frequency noise (LFN) can lead to vibroacoustic disease (VAD), recognized as a systemic disease with lesions in a broad spectrum of organs. Although gastrointestinal complaints are common among individuals exposed to noise, only few studies tried to evaluate the digestive lesions. The authors performed this study in order to investigate gastric lesions in an animal model of VAD.

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Earlier studies of Wistar rat respiratory epithelia exposed to low frequency noise (LFN) (< or =500 Hz, including infrasound) showed that LFN effects trauma on the respiratory tract. In rats gestated and born in LFN environments, trauma was still treated in accordance with 86/609/EC. Respiratory epithelial fragments were prepared for light and scanning/transmission electron microscopy.

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Previous studies show that exposure to low frequency noise (LFN) (< or =500 Hz, including infrasound) produces irreversible lesions in Wistar rat respiratory epithelia. Recovery periods for LFN-induced lesions have thus become an object of interest. Changes in the respiratory epithelia of Wistar rats after continuous short-term exposure to LFN are described.

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Morphofunctional changes of respiratory epithelia became the object of intense study in Wistar rats after previous research showed that occupationally-simulated exposure to low frequency noise (500 Hz, including infrasound) induced irreversible lesions in these tissues. Aspects of normal respiratory epithelia in rats are lacking in the literature, and are the object of this report. Ten Wistar rats were kept in silence, fed standard rat food, and had unrestrained access to water (treated in accordance with 86/609/CE).

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Noise-induced pulmonary pathology is still an issue that is regarded with much suspicion despite the significant body of evidence demonstrating that acoustic phenomena target the respiratory tract. The goal of this review paper is threefold: a) to describe acoustic phenomena as an agent of disease, and the inadequacies of current legislation regarding noise-induced, non-auditory pathology; b) to trace how the interest in noise-induced pulmonary pathology emerged within the scope of studies on vibroacoustic disease; and c) to bring to light other studies denouncing noise as an agent of disease that impinges on the respiratory tract. As concluding remarks, future perspectives in LFN-related research will be discussed.

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