Ultrastructural observations of organelle accumulation in the equine recurrent laryngeal nerve

Summary The left recurrent laryngeal nerves from five horses with sub-clinical neuropathy were examined by light and electron microscopy in a study designed to examine accumulation of axonal organelles at paranodal and internodal locations. Transverse sections of the nerve showed scattered fibres with split myelin sheaths and axonal accumulation of organelles. On longitudinal sections these collections were seen to result from an axonal outpouching in which dense lamellar bodies and mitochondria had accumulated. These paranodal collections, which could be found on both sides of the node, were often associated with infoldings of the terminal loops of myelin and with occasional paranodal demyelination. The fact that many of the organelles in the outpouches were lysosomal in nature was confirmed by their positive staining for cathepsin D activity. Longitudinal sections demonstrated a number of axons which were swollen over a long distance and which contained focal accumulations of similar organelles. In places, however, there was a clear separation between these organelles and the cytoskeletal proteins. In each case these swollen axons were surrounded by Schwann cell nuclei and their processes, forming well-ordered onion bulbs. The possibility that these two types of changes, i.e. the paranodal accumulations and the axonal swellings could result from a disturbance in axonal transport in this distal axonopathy is discussed.     

Partial deletion of short arm of chromosome 8

46, XY, del(8) (p21-pter) aberration was found in a 5 year old boy with moderate craniofacial dysmorphia, mental and somatic retardation. The cytogenetic and clinical features of the patient were compared to 11 cases found in the literature. Partial 8p monosomy does not produce a unique phenotypic alteration. Postnatal growth deficiency, craniofacial dysmorphia and mental retardation are the main and common characteristics of many structural autosomal aberrations. The importance of cytogenetic analysis in such cases is stressed.     

Elaboration by mammalian mesenchymal cells infected with Trypanosoma cruzi of a fibroblast-stimulating factor that may contribute to chagasic cardiomyopathy.

Myocardial fibrosis can occur as a complication of chronic infection of the heart with Trypanosoma cruzi (Chagas' disease) and can lead to serious disability. To assess whether there might be a direct relationship between intracellular parasitization and subsequent tissue fibrosis in this disease, we tested serum-free conditioned media from cultures of fibroblasts, vascular smooth-muscle cells, and myocardial cells for fibroblast-stimulating activity. Conditioned media from all infected cultures, but not from uninfected cultures, stimulated fibroblast [3H]thymidine incorporation, DNA and protein synthesis, and cell proliferation. Fibroblast-stimulating activity was also detected in extracts of amastigotes but not of trypomastigotes or epimastigotes. We conclude that parasitization of mesenchymal cells, including myocardial cells, results in elaboration of a fibroblast-stimulating factor(s), perhaps of parasite origin. We postulate that this factor may play a role in initiation of myocardial fibrosis in Chagas' disease.     

Effects of chronic exposure to arsenate on the cardiovascular function of rats.

Cardiovascular function was studied in anaesthetised male rats which received 50 micrograms/ml of arsenic (as sodium arsenate) in deionised drinking water for 320 days. High urinary excretion of arsenic was found at the end of treatment and the metal accumulated considerably in the kidneys and liver, which both presented slight alterations. No histopathological modifications were evident in other organs. Base line blood pressure, cardiac inotropism, and chronotropism and cardiovascular reactivity to noradrenaline, acetylcholine, angiotensin II, bradykinin, histamine, and serotonin did not differ in exposed or in control animals. In the exposed group, however, there was potentiation of the effects of vascular beta-adrenoceptor stimulation and a reduction in the vascular responsiveness to angiotensin I. Chronic arsenic exposure did not affect the baroreflex sensitivity but was able to induce sympathetic hyperactivity or hypersensitivity, or both, possibly associated with an antivagal action. Our results might help to explain the cardiovascular alterations seen in people chronically exposed to high concentrations of arsenic.