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Biomedical subjects

G Macchi

Publications and source records attributed to G Macchi.

At least 91 records · Page 5Linked to original sources
PubMed1977

Anatomo-clinical correlations in normotensive hydrocephalus. Reports on three cases.

The brains of 3 adult subjects suffering from normotensive hydrocephalus have been examined pathologically. The diagnosis of normotensive hydrocephalus was based on clinical symptoms, pneumoencephalography and isotope cisternography, in 1 case integrated with the results of the constant-infusion manometric test. Part of the neuropathological findings were common to the 3 patients: leptomeningeal non-obstructive fibrosis, ventricular ependymal disruption, subependymal glial reaction, periventricular demyelination and spongiosis. Other neuropathological abnormalities were peculiar to each patient: leptomeningeal signs of previous subarachnoid haemorrhage; arteriosclerosis and multiple brain cystic infarcts; Alzheimer's plaques in the gray matter. The possible pathogenetic significance of the neuropathological findings summarized above in relation to the development of normotensive hydrocephalus is discussed.

Adult↗
PubMed1975

Quantitative data on cell loss and cellular atrophy of intralaminar nuclei following cortical and subcortical lesions.

Morphological changes in the intralaminar nuclei centralis medialis, paracentralis and centralis lateralis of the thalamus of adult cats after cortical excisions have been determined by means of a quantitative method. The number and size of the remaining neurons on the operated side have been compared with those of the normal side. The differences between the normal and the operated side have been compared to those found between the two sides in the control animals. The most important result is the demonstration that after cortical ablations the intralaminar nuclei show not only chromatolytic or atrophic changes of their cells but also a true cell loss. These reactions are qualitatively similar to those observed in the specific nuclei of the thalamus, the only difference being a quantitative one. As a consequence it can be suggested that some intralaminar nuclei project to certain areas of the cerebral cortex which also receive projections from one or other specific thalamic nucleus. A large essential connection of the intralaminar nuclei, in particular the nucleus centralis medialis, with subcortical structures is confirmed.

Animals↗
PubMedDate not supplied

Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension.

We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 +/- 1.6 (mean +/- SE) to 101 +/- 1.4 mm Hg (p less than 0.01), and mean pulmonary artery pressure from 21 +/- 0.59 to 17 +/- 1.05 mm Hg (p less than 0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 +/- 0.85 to 29 +/- 0.72 U/m2 (p less than 0.01) and from 4.3 +/- 0.17 to 3.8 +/- 0.18 U/m2 (p less than 0.01), respectively. Indapamide did not change cardiac index (CI) (3,311 +/- 61.6 vs. 3,325 +/- 72.1 ml/min/m2), heart rate (HR) (75 +/- 1.7 vs. 75 +/- 9 beats/min), mean rate of left ventricular ejection index 140 +/- 2.04 vs. 139 +/- 1.99 ml/s/m2, and stroke index (44 +/- 5.6 vs. 43 +/- 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 +/- 0.6 to 5 +/- 0.5 mm Hg (p less than 0.05). Body weight, 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.

Adult↗
PubMedDate not supplied

The nucleus basalis of Meynert in parkinsonism-dementia of Guam: a morphometric study.

The nucleus basalis of Meynert (nbM) was studied morphometrically in three Guamanians with parkinsonism-dementia (PD) and in two Guamanian and two non-Guamanian controls. Paraffin-embedded blocks of the nbM were serially sectioned (20 microns thick) at increments of 200 microns so that a total of 24 sections (eight each from the anterior, intermediate and posterior sectors of the nbM) were studied. The mean cell density was determined for each sector and the diameter of 50 neurons, randomly chosen in the region of apparent maximal density, was calculated. A decrease of the mean cell density, due to the loss of neurons with diameters larger than 20 microns, was found in the PD cases compared to the controls. Two PD patients exhibited striking neuronal loss (65-95%) with predominant involvement of the intermediate and posterior sectors, while the third case showed only minimal neuronal loss in these sectors (15-40%). In both Guamanian and non-Guamanian controls large neurons (diameters greater than or equal to 20 microns) exceeded small neurons while the reverse was true in all sectors of the nbM for the PD cases. These data, while confirming a previous study reporting neuronal loss in the nbM of PD patients, underline the importance of detailed morphometric analysis of the different sectors of the nbM to recognize those patients in whom lesions are not uniformly distributed.

Aged↗
PubMedDate not supplied

Does PRNP gene control the clinical and pathological phenotype of human spongiform transmissible encephalopathies?

BACKGROUND: Human spongiform transmissible encephalopathies (TSE) are a group of neurodegenerative diseases caused by a transmissible not yet recognized agent; their distinctive neuropathological features are astrocytosis, spongiform lesions of the neuropil, neuronal loss and occasionally amyloid plaques in the cortical and subcortical gray matter. TSE are biochemically characterized by the deposition in the nervous system of an amyloid-type protein, PrPres derived from the post-translational modification of a normal protein, PrPsen. The expression of this protein is controlled by the PRNP gene mapped on chromosome 20 in man. A number of point mutations of the PRNP gene have been described in the familial forms of these TSE. Some of these mutations have been associated with differences in the phenotypic expression of the disease. MATERIAL AND METHODS: This study was designed to verify whether it was possible to identify a selective phenotype depending upon a given PRNP modified genotye; for this purpose, a group of familial TSE cases (CJD 210ILE, CJD 201LYS, FFI 178ASN) were selected and their neuropathological profiles have been compared with those of a large series of sporadic CJD cases. RESULTS: No significant differences were found between the topography and severity of lesions in the cerebral cortex, cerebellum, hippocampus, basal ganglia and thalamus between the two groups. Two differences were found: the clinical duration of the disease which appeared significantly (p = 0.02) shorter in the 210ILE-mutated cases compared to that of non-mutated sporadic cases. The highly selective vulnerability of thalamus in FFI showing a severe pathology especially in its dorso-medial part in comparison with that of the sporadic CJD cases. CONCLUSION: The results of this study confirm that the different polymorphism at codon 129 of the PRNP gene, which could be involved in the structural "domains" of human PrP, might modulate the pathological phenotype of TSE.

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