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Biomedical subjects

M L Rossi

Publications and source records attributed to M L Rossi.

124 records · Page 7Linked to original sources
PubMed1977

Post-synaptic potentials recorded from afferent nerve fibres of the posterior semicircular canal in the frog.

Glass microelectrode recordings were made from single fibres of the posterior ampullary nerve in the isolated labyrinth of the frog (Rana esculenta). Potentials were recorded both at rest and during rotatory stimulation of the canal. At rest, the tracings revealed an intense background of small, largely summated potentials (0.5-10 mV amplitude, 3-6 msec duration), which underlay the discharge of spikes in all the impaled units. The frequency of the subthreshold events was related to the frequency of the propagated spikes, the latter ranging from 0 to 40/sec. Stimulation modulated the frequency of both spikes and subthreshold potentials, whose summation during excitation led to a positive shift of the fibre membrane potential. The small potentials proved to be dependent on Ca2+ and Mg2+ levels in the bath. Antidromic-stimulation of the posterior ampullary nerve indicated that the observed events do not represent an artifact due to extracellular field interference related to spike activity in the neighbouring fibres. Tetrodotoxin (10(-7)-10(-6) g/ml) applied externally to the preparation or previously perfused through the frog vessels abolishes the propagated spikes but left unaffected the small potentials which, even under drug treatment, were normally modulated by the stimulus. The subthreshold potentials thus appear to be EPSPs generated at the cyto-neural junction between the hair cells and the endings of the ampullary nerve fibres.

Action Potentials↗
PubMed1977

Adaptive distortions in the generator potential of semicircular canal sensory afferents.

The generator potential in sensory afferents of frog crista ampullaris was extracellularly recorded from the cut end of the posterior ampullary nerve by means of suction electrodes. A servocontrolled turntable allowed suitable rotatary stimulations. The analysis of the recorded generator potential revealed a different time course from that predicted on the basis of the pendulum model. Adaptation and undershoots in the responses to velocity ramps, steps and sinusoids, were mainly responsible for the deviations, which became very evident only when fairly high acceleration rates were applied. Both adaptation and undershoots were produced presumably by the activation of an electrogenic pump, probably located in nerv terminals contacting the hair cells. In fact, the time course of the generator potential became much more consistent with the predictions from the pendulum model under treatments capable of hindering the ion pump activity.

Acceleration↗
PubMedDate not supplied

Epithelial membrane antigen expression in ependymomas.

Twenty-seven ependymomas were studied (18 'benign' or low grade and nine 'malignant' or high grade) by means of a monoclonal antibody to epithelial membrane antigen (E29) and an antiserum to glial fibrillary acidic protein (GFAP). The E29 antibody reacted with 'benign' ependymomas but not with 'malignant' ones. Staining was located on the cell surface and especially that facing rosette lumina. Cells forming papillary structures and ependymal epithelium showed a similar distribution of staining. Glial fibrillary acidic protein (GFAP) reactivity was seen in all tumours, with a perivascular accentuation in 'malignant' ones. Staining occurred in the cytoplasm of scattered cells and in those forming papillary structures, ependymal epithelium and rosettes. Our results may have implications in relation to the cytogenesis of these tumours and may also be useful in the histological assessment of 'benign' versus 'malignant' ependymomas.

Brain Neoplasms↗
PubMedDate not supplied

Phenotype commitment in vascular smooth muscle cells derived from coronary atherosclerotic plaques: differential gene expression of endothelial nitric oxide synthase.

Unstable angina and myocardial infarction are the clinical manifestations of the abrupt thrombotic occlusion of an epicardial coronary artery as a result of spontaneous atherosclerotic plaque rupture or fissuring, and the exposure of highly thrombogenic material to blood. It has been demonstrated that the proliferation of vascular smooth muscle cells (VSMCs) and impaired bioavailabilty of nitric oxide (NO) are among the most important mechanisms involved in the progression of atherosclerosis. It has also been suggested that a NO imbalance in coronary arteries may be involved in myocardial ischemia as a result of vasomotor dysfunction triggering plaque rupture and the thrombotic response. We used 5' nuclease assays (TaqMan PCRs) to study gene expression in coronary plaques collected by means of therapeutic directional coronary atherectomy from 15 patients with stable angina (SA) and 15 with acute coronary syndromes (ACS) without ST elevation. Total RNA was extracted from the 30 plaques and the cDNA was amplified in order to determine endothelial nitric oxide synthase (eNOS) gene expression. Analysis of the results showed that the expression of eNOS was significantly higher (p<0.001) in the plaques from the ACS patients. Furthermore, isolated VSMCs from ACS and SA plaques confirmed the above pattern even after 25 plating passages. In situ RT-PCR was also carried out to co-localize the eNOS messengers and the VSMC phenotype. The eNOS gene was more expressed in ACS plaques and VSMCs cultured from them, thus indicating that: a) the expression of the most important differentiation markers is retained under in vitro conditions; and b) NO may play a pivotal role in coronary artery disease. Our findings suggest a new cell system model for studying the pathophysiology of unstable angina and myocardial infarction.

Angina Pectoris↗
PubMedDate not supplied

Infantile cerebellar thrombosis: a case of lupus anticoagulants?

Lupus Anticoagulants (LA) pathology is a disease frequently associated with venous and/or arterial thrombosis. The authors describe a 6 year-old boy complaining cephalea and emesis, followed by lethargy, in whom antiphospholipids antibodies were detected. Brain magnetic resonance scans showed lesions of the cerebellum. The characteristics of LA disease are discussed.

Antibodies, Antiphospholipid↗
PubMedDate not supplied

Muscle phosphoglycerate mutase deficiency: a study of a family with metabolic myopathy.

Muscle phosphoglycerate mutase deficiency results in a myopathic condition characterised by repeated cramps, possible myoglobinuria and muscle pain. We present a family with muscle phosphoglycerate mutase (PGaM) deficiency, mild glycogen storage and some exertional myalgia. Investigations of muscle biopsy tissue showed a residual PGaM activity in muscle due to a small amount of brain isoenzyme. The enzyme was also measured in blood cells and a full investigation of muscle metabolism was also carried out. Electron microscopy revealed mitochondria with similar morphological features in two patients investigated.

Adolescent↗
PubMedDate not supplied

Peripheral nerve protein glycation and muscle fructolysis: evidence of abnormal carbohydrate metabolism in ALS.

Conversion of glucose to fructose via sorbitol depends upon the enzymes aldose reductase and sorbitol dehydrogenase and is called the polyol pathway. It is particularly active in muscle from patients with X-linked muscular dystrophies (15). This investigation shows enhanced metabolism of glucose to fructose in muscle from patients with ALS. Evidence is also presented showing increased activities of ketohexokinase and F-1-P splitting aldolase, which suggests that further metabolism of fructose may occur via a fructolytic pathway. Investigation of protein glycation, by an adapted fructosamine assay, in post mortem muscle, sural nerve and blood indicates that there is an increased concentration of glucose in muscle and nerve in the period prior to sampling, but blood glucose concentrations were within normal limits. The implications of fructolysis and the relationship of altered glucose metabolism in ALS are discussed.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

Interaction of motor neurone disease plasma with glucose transport.

Abnormal glucose metabolism has been implicated in motor neurone disease (MND) and this was studied by measuring the transport of non-metabolisable glucose analogue, 3-O-methyl-D-glucose in normal erythrocyte at 20 degrees C, pH 7.4, in the presence of plasma from normal controls and patients with MND. The glucose uptake was elevated by 34% in the presence of plasma from MND patients (n = 21) when compared with age matched controls (n = 28; p < 0.001). The uptake of glucose was not influenced by gender or any age dependent variations. The relationship of this effect to glucose under-utilisation in the CNS needs to be explored.

Adult↗
PubMedDate not supplied

Immunocytochemistry on paraffin wax Golgi-Cox impregnated central nervous tissue.

We present a new application of an immunocytochemical technique on central nervous tissue which utilizes Golgi-Cox impregnated paraffin embedded material. Sections of normal and pathological brain and spinal cord, from both Golgi-Cox impregnated tissue and for comparison formol saline fixed tissue, were studied with the following antibodies: glial fibrillary acidic protein, myelin basic protein, neurofilament, neurone specific enolase, protein gene product 9.5, ubiquitin and vimentin. Optimal results were obtained with most of the antibodies after adapting the technique by using different pretreatments including enzymes and de-impregnation methods. In addition to the Golgi-Cox impregnated structures, neuronal, glial and mesenchymal antigens were well demonstrated and the relationships between these structures clearly visible. The antigenic retention of the tissue after Golgi-Cox impregnation allowed successful immunostaining to be performed either alone or as a combined procedure. It is therefore possible to study a variety of antigens and neuronal processes in the same section with maximum results. Immunocytochemical methodology in combination with this fixative opens a new avenue for the immunocytochemical and cytomorphological study of central nervous tissue with the added advantage of making the best use of the versatility and durability of paraffin embedded material.

Astrocytes↗
PubMedDate not supplied

Muscle pyruvate kinase deficiency: glycogen storage disease or mitochondrial myopathy?

Defects of muscle glycogen metabolism are well documented causes of metabolic myopathy, presenting with a spectrum of symptoms which show some relationship to the position of defective enzyme within the glycolytic pathway. We present three women with metabolic myopathic conditions which show some features associated with a glycogen storage disease and some features of a mitochondrial defect. Muscle histochemistry and electron microscopy showed only minor and non-specific changes. However biochemical analysis of muscle biopsies in these three cases revealed a defect in glycolysis at the level of pyruvate kinase (PK), a defect as yet undescribed. Further investigation of the enzyme's properties, revealed that the residual muscle PK activity was due to the muscle (M1) isoform.

Adolescent↗