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Biomedical subjects

L Moita

Publications and source records attributed to L Moita.

2 recordsLinked to original sources

[Diffuse tracheo-bronchial amyloidosis].

The case of a 52 year old man, whose initial clinical manifestations were dyspnea, bloodstained sputum and malaise is reported. After the initial cancer hypothesis, a diagnosis of diffuse primary tracheo-bronchial amyloidosis was made. The amyloid substance present was not of A A type and the plasma cells next to the deposits were polyclonal. The piece-meal removal of the masses by bronchoscopy led to profuse bleeding. The patient died with sepsis. The clinical, pathological and therapeutical aspects of lower respiratory tract amyloidosis are reviewed.

Amyloidosis↗

Reinnervation of post-arthritic joints in the rat.

OBJECTIVE: To clarify the role of articular innervation during the acute and post-arthritic phases, we investigated the changes taking place over time in the nerve fibers from joint tissues of adjuvant arthritic rats. METHODS: Nerve densities (i.e., the number of nerve fibers observed per unit area of tissue section) were estimated in periarticular tissues, synovium and epiphysis from ankle joints. Nerves were identified by immunofluorescence microscopy using antibodies against general neuronal markers (Protein Gene Product 9.5, synaptophysin, neurofilaments and Schwann cells), and markers specific for either sensory or sympathetic nerves (Substance P, calcitonin gene related peptide, neuropeptide tyrosine and its C-terminal flanking peptide, and the catecholamine synthesising enzyme tyrosine hydroxilase). RESULTS: In arthritic rats, the density of nerve fibers in the periarticular tissues, epiphysis and synovium was significantly reduced when compared to control animals. This decrease was observed using antibodies for both non releasable neuronal products (Protein Gene Product 9.5, synaptophysin, neurofilaments and Schwann cells) and neuropeptides (Substance P, calcitonin gene related peptide, neuropeptide tyrosine and its C-terminal flanking peptide), thus suggesting the existence of a structural nervous lesion with the parallel depletion of peptides. As the clinical arthritis subsided, there was a progressive reinnervation of all the articular structures analysed, which often exceeded the density of nerves in the control animals. CONCLUSION: This work supports a close relationship between the nervous system and arthritis. We propose that cycles of nerve destruction and regeneration may be related to the characteristic periods of remission and activity of some forms of chronic arthritis.

Acute Disease↗