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Biomedical subjects

I Ferrer

Publications and source records attributed to I Ferrer.

At least 37 records · Page 2Linked to original sources
PubMed1991

Adult type of leukodystrophy. Krabbe's disease?

A 24-year-old man developed progressive dementia in seven years. The patient suffered a severe bronchopneumonia and eventually died few days later. Brain coronal sections showed a soft gray-brownish discoloration of white matter of centrum ovale but the subcortical arcuate fibers and the interne capsule were preserved. Microscopically, the white matter showed marked loss of myelin and oligodendrocytes, abundant hypertrophic astrocytes and numerous "globoid cells". The latter showed strong positivity in immunostains for a mouse monoclonal antigalactocerebroside antibody. The presence of these cells in the brain white matter might be the morphological basis to classify the present case as one of Krabbe's Leukodystrophy.

Adult↗
PubMed1991

Blood lymphocytes are sensitized to branchial plexus nerves in patients with neuralgic amyotrophy.

The percentage of lymphocytic subsets in the blood of cases with neuralgic amyotrophy (NA), and the proliferative response of blood lymphocytes cultured with different nerve extracts, obtained from normal subjects at postmortem, were examined in 6 patients with NA and in 18 age-matched controls with shoulder pain not related to NA. Most (5/6) NA patients had decreased CD3 values and increased CD4/CD8 ratios due to a decreased of the CD8 subset. Lymphocytes of NA patients increased their blastogenic activity in cultures with nerve extracts from different brachial plexus nerves and its branches, but not in cultures with extracts of sacral plexus nerves. Cultures did not respond to nerve extracts in any of the control cases, although mitogenic activity was similarly elicited in cultured lymphocytes stimulated with phytohemagglutinin in both control cases and NA patients. These results suggest that NA is probably an immune mediated disease.

Adolescent↗
PubMed1991

Quantitative and morphometric analysis of Langerhans cells in non-exposed skin in renal transplant patients.

Renal transplant recipients have a high incidence of cutaneous complications such as neoplasia and viral or fungal infections. Morphologic alterations of epidermal Langerhans cells (LC) have furthermore been described in these patients. Since these changes have been mainly found in sun-exposed skin, a direct effect of immunosuppressive therapy remains a matter of discussion. A quantitative and morphometric study of epidermal LC in non-exposed skin was performed in 28 renal transplant patients (RTP). RTP were divided in two groups according to immunosuppressive treatment: group A; azathioprine + prednisone (14 cases) and group B; cyclosporine + prednisone (14 cases). Twenty sex-age matched non-immunosuppressed patients acted as controls (group C). Epidermal sheets were obtained by incubation in EDTA and stained for ATPase activity and with the monoclonal antibody T6 (CD1) using the avidin-biotin peroxidase method. Langerhans cells were counted using a calibrated graticule (400x) and expressed as the mean number of LC/mm2. The mean area of the LC and the number of primary dendrites (pd) and secondary dendrites (sd) were determined with a morphometer adapted to an Apple II computer. The mean number of positive cells in controls was: ATPase, 677 +/- 157; T6, 695 +/- 164. Patients in group A had the maximum reduction in both ATPase and T6 LC density (ATPase, 339 +/- 142; T6, 402 +/- 194). Patients in group B had an intermediate reduction in the number of LC (ATPase, 494 +/- 121; T6, 529 +/- 112).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1991

Dementia of frontal lobe type and motor neuron disease. A Golgi study of the frontal cortex.

Neuropathological findings in a 38 year old patient with dementia of frontal lobe type and motor neuron disease included pyramidal tracts, myelin pallor and neuron loss, gliosis and chromatolysis in the hypoglossal nucleus, together with frontal atrophy, neuron loss, gliosis and spongiosis in the upper cortical layers of the frontal (and temporal) lobes. Most remaining pyramidal and non-pyramidal neurons (multipolar, bitufted and bipolar cells) in the upper layers (layers II and III) of the frontal cortex (area B) had reduced dendritic arbors, proximal dendritic varicosities and amputation of dendrites as revealed in optimally stained rapid Golgi sections. Pyramidal cells in these layers also showed depletion of dendritic spines. Neurons in the inner layers were preserved. Loss of receptive surfaces in neurons of the upper cortical layers in the frontal cortex are indicative of neuronal disconnection, and are "hidden" contributory morphological substrates for the development of dementia.

Adult↗
PubMed1991

Immunocytochemical detection of 5'-bromodeoxyuridine in fluoro-gold-labeled neurons: a simple technique to combine retrograde axonal tracing and neurogenetic characterization of neurons.

To characterize the axonal projections of 5'-bromodeoxyuridine (BrdU)-labeled neurons, we have combined retrograde tracer injection of Fluoro-Gold with the immunocytochemical detection of BrdU. Pregnant mice were labeled with pulses of BrdU at embryonic days E12, E13, E14, or E16. Young adult offspring were perfused with 4% paraformaldehyde 2 days after receiving a Fluoro-Gold injection into the cerebral cortex, thalamus, or hippocampus. Brain sections were processed for immunocytochemical visualization of BrdU using the peroxidase-anti-peroxidase method and a diaminobenzidine-nickel ammonium sulfate (DAB-Ni) reaction, and finally observed on a microscope equipped with brightfield and fluorescence optics. Both BrdU-immunoreactive nuclei and retrogradely labeled Fluoro-Gold-positive cells were detected. Double-labeled neurons were recognized by the presence of fluorescent particles in the cytoplasm and a black immunoreactive nucleus. Since both labelings occurred in different cell compartments, Fluoro-Gold granules were not obscured by the DAB-Ni precipitate. The method shown here permits a correlation of the neurogenesis of subsets of neurons identified by their BrdU content with the specific target into which such cells project.

Animals↗
PubMed1991

[Spongiform encephalopathy and multisystemic degeneration].

Onset of a neurological disease was coincidental in two members of a family. The mother died at the age of 57 and her daughter at the age of 27 years. Clinically the disease was manifested by cerebellar ataxia, visual disturbances, dystonic movements and intellectual impairment which appeared very later in the course of the disease in the younger patient. Myoclonus was only observed in the mother. The EEG examination revealed non-specific abnormalities. CT scans disclosed severe cerebellar atrophy and reduced size of the pons in the daughter. The duration of the disease was 7 months in the mother and 3 years in her daughter. The neuropathological examination showed degeneration of the thalamus, substantia nigra and inferior olives, together with loss of Purkinje cells and axonal torpedos in the granular layer of the mother. Olivopontocerebellar atrophy, atrophy of the thalamus and substantia nigra, associated to typical spongiform encephalopathy of the cerebral cortex, amygdaloid complex and striatum occurred in the daughter. These observations let us to comment whether multisystemic atrophies may be fortuitously associated to different prion-induced encephalopathies, or may be found in the context of spongiform encephalopathies.

Adult↗
PubMed1990

Neuronal alterations in patients with dementia: a Golgi study on biopsy samples.

Golgi-impregnated neurons in biopsy samples of the cerebral cortex (area 8) of patients with Alzheimer's disease (AD), Pick's disease (PD) and Creutzfeldt-Jakob disease (CJD), but not in control samples, have swellings in the proximal and mid regions of dendrites of pyramidal and non-pyramidal cells that differ from normal dendritic varicosities. Dendritic outgrowths, isolated or in clusters, and covered with spines occur only in neurons with reduced dendritic arbors mainly located in the vicinity of senile plaques. Degenerating pyramidal and non-pyramidal neurons, although distributed throughout the cerebral cortex in CJD and PD, predominate in layers II, III and VIb in patients with AD.

Adult↗
PubMed1990

Analysis of a neuronal antigen (Hu) expression in the developing rat brain detected by autoantibodies from patients with paraneoplastic encephalomyelitis.

Anti-Hu is an autoantibody that recognizes an antigen (Hu) highly restricted to neuronal nuclei. In the developing rat brain all neurons and the germinal cell layer were anti-Hu positive. Ependyma and choroid plexus were positive only in the early stages of development. The strongest expression of Hu was seen in the most mature neurons. The transitory nature of Cajal-Retzius and subplate neurons was confirmed with the anti-Hu staining. Although the Hu is also expressed by neural cells other than neurons, the strongest staining of mature neurons could indicate that Hu plays a role in the process of neuronal differentiation.

Aging↗
PubMed1990

Down's syndrome and Alzheimer's disease: dendritic spine counts in the hippocampus.

Samples of the hippocampus of four patients with Down's syndrome [two men aged 35 and 36 years with no evidence of Alzheimer's disease (AD) and two patients aged 47 and 55 years with associated AD] were obtained at post mortem and processed according to the rapid Golgi method. A significant reduction in the number of dendritic spines (DS) was found in the apical (middle, distal and oblique segments) and basilar (thick and thin segments) dendritic arbors of CA1 and CA2-3 pyramidal neurons in patients with Down's syndrome and no AD when compared to age-matched controls. An additional decrease of DS in every segment occurred in Down's patients with associated AD when compared to age-matched controls and Down's patients with no AD. In Down's syndrome (either associated or not to AD) thin basilar dendrites were the most severely involved; in AD patients CA1 pyramids were more severely affected than pyramidal neurons of the CA2-3 subfield.

Adult↗
PubMed1990

Arteriolosclerotic leucoencephalopathy in the elderly and its relation to white matter lesions in Binswanger's disease, multi-infarct encephalopathy and Alzheimer's disease.

Arteriolosclerotic leucoencephalopathy in the elderly (ALE) is characterized by white matter lesions associated with atherosclerosis and arteriolosclerosis. Mild lesions are focal and probably represent early status cribosus or incomplete lacunar infarcts. Moderate and severe lesions are diffuse areas of demyelination in the centrum semiovale in which lacunar infarcts are seldom observed. The incidence of ALE in a consecutive necropsy series of 50 cases (mean age 62.6 +/- 13.1 years) was 52%, it was rare in the fourth and fifth decades but increased thereafter to reach a prevalence of 100% at the age of 80 years. Mild lesions occurred in 19 patients and lesions were moderate or severe in 7 (14%). The mean age was higher in this group (74.7 +/- 7.6 years) than in patients with white matter changes as a whole. Dementia occurred only in 3 patients with moderate or severe ALE. These data suggest that (a) ALE is common in old age and is probably the cause of leuko-araiosis in most CT scans in the elderly; (b) ALE may be asymptomatic; (c) the severity of white matter changes may be not related to the severity of neurological deficits; and (d) multiple lacunar infarcts or associated degenerative diseases (i.e., Alzheimer's disease) may be the main cause of dementia in patients with ALE. White matter lesions in ALE, Binswanger's disease, transition areas in multi-infarct encephalopathy (MIE) and Alzheimer's disease (AD) are similar in morphology and are probably the result of a subacute hypoperfusion/hypoxic process. Increased arterial blood pressure is a frequent risk factor in ALE, Binswanger's disease and MIE, whereas congophilic angiopathy of the meningeal and cortical vessels, in addition to mild or moderate arteriolar hyalinosis in the white matter, may play a role in the pathogenesis of incomplete infarctation of the white matter in patients with AD.

Aged↗
PubMed1990

Naturally occurring cell death in the subicular complex and hippocampus in the rat during development.

Cell death in the subicular complex and hippocampus occurs from P0 to P7 in the rat. Dead cells first appear in the subcortical and subammonic plates, and predominate in the border region between the main regional subfields. Cell death in the cellular layers predominates in the subicular complex. CA1 and intermediate region between CA1 and CA3. Dead cells are almost absent in the upper plexiform layers and dentate gyrus.

Aging↗
PubMed1990

Naturally occurring cell death in the cerebral cortex of the rat and removal of dead cells by transitory phagocytes.

Regressive phenomena are common during the development of the nervous tissue. Among them, naturally occurring cell death has been observed in several regions of the nervous system. Cell death in the somatosensory cortex and medial cortical regions (hind limb, frontal cortex 1, frontal cortex 2, retrosplenial agranular, retrosplenial granular [Zilles K. et al. (1980) Anat. Embryol. 159, 335-360]) as well as in the cortical subplate (future subcortical white matter) in the rat mainly occurs during the first 10 days of postnatal life with peak values of 3.1 dead cells per 1000 live neurons at the end of the first week. Cell death progresses from birth to day 7 with a predominance of dead cells in the subplate and in layers II-III. Later, dead cells are more dispersed in the cerebral cortex, but a significant amount is still present in the subcortical white matter. This pattern correlates with the arrival and settlement of cortical afferents at the different cortical levels, as described in other studies, and points to the likelihood that transitory cellular populations are important clues in the modelling of the cerebral cortex during normal development. Transitory populations of macrophages (amoeboid or nascent microglial cells) that appear in great numbers during the same period and in the same regions are involved in the removal of dead cells.

Aging↗
PubMed1990

Progressing cerebral infarction in relation to plasma glucose in gerbils.

We studied neurologic morbidity and its evolution during hyperglycemia induced immediately after permanent unilateral common carotid artery ligation in Mongolian gerbils. A total of 60 animals were divided into five groups: one experiencing severe hyperglycemia for 1 hour after the onset of ischemia (brief hyperglycemia group, n = 13), a normoglycemic control group for the brief hyperglycemia group (n = 12), a group with severe hyperglycemia for 4 hours after the onset of ischemia (prolonged hyperglycemia group, n = 11), a normoglycemic control group for the prolonged hyperglycemia group (n = 13), and a hyperosmolar normoglycemic control group for the prolonged hyperglycemia group (n = 11). Neurologic morbidity and mortality were higher in the two hyperglycemic groups than in the three normoglycemic control groups. The neurologic deficit progressed according to the duration of severe hyperglycemia. In the three normoglycemic control groups neurologic status stabilized 120 minutes after the onset of ischemia, in the brief hyperglycemia group stabilization occurred at 210 minutes, and in the prolonged hyperglycemia group neurologic deficit progressed for approximately 360 minutes, coinciding with the death of all but one gerbil, in which the neurologic deficit remained stable until death 23 hours after ischemia. We suggest that hyperglycemia is another cause of progressing cerebral infarction.

Animals↗
PubMed1990

Cavernous angiomas of the cranial nerves. Report of two cases.

Two cavernous hemangiomas arising in the third and eighth cranial nerves, respectively, and presenting as space-occupying lesions are reported. The tumors posed problems in the preoperative differential diagnosis. The main clinicopathological features of these tumors are discussed.

Adult↗
PubMed1990

Studies with the Golgi method in central gangliogliomas and dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos disease).

The rapid Golgi method, combined with current optical and electronmicroscopical techniques, was used in three central gangliogliomas and in one dysplastic gangliocytoma of the cerebellum to study the morphology of ganglionic cells. Gangliogliomas were composed of bipolar, fusiform and radiate cells with dense core and clear vesicles in the perikaryon and cellular processes, the number of each cellular type varying from one case to another. These features, together with the fact that isodendritic neurons are considered to be phylogenetically old neurons, suggest that these tumours are composed of "primitive" neurons that are not homogeneous with regard to their morphology. In contrast, ganglionic cells in dysplastic gangliocytoma are huge cells with long, stereotyped neurites that establish unique asymmetric contacts with neighbouring perikarya and neurites by means of claw-shaped processes covered with synaptic buttons. These morphological characteristics are different from those of any other neuron of the CNS.

Adolescent↗
PubMed1989

Postnatal neurogenesis in the olfactory bulbs of a lizard. A tritiated thymidine autoradiographic study.

Autoradiographically labelled cells were observed in the olfactory bulbs of perinatal, young and adult specimens of the lizard Podarcis hispanica following intraperitoneal injection of tritiated thymidine (5 muCi/g b.wt). After survival times of 7, 18 and 28 days labelled cells were found in the granular layer of both main and accessory bulbs. A few labelled cells were observed in the ependyma, mitral and glomerular layer. In the main olfactory bulb, one week of survival time resulted in labelling of cells in the innermost part of the granular layer. Longer survival times (up to 4 weeks), resulted in labelling of cells mainly in the outermost part of the granular layer. This spatio-temporal gradient was not observed in the accessory bulb. Nevertheless, longer survival times resulted in greater number of labelled cells located in the dorsal and ventral parts of the granular layer of the accessory bulb.

Animals↗
PubMed1989

[Hairy leukoplakia: a new disease of the oral mucosa associated with infection by the human immunodeficiency virus].

In 23 out of 227 patients with positive serological tests for the human immunodeficiency virus (10%), seen between June 1987 and May 1988, lingual lesions of hairy leukoplakia (HL) were found. HL was present in 16/188 drug abusers (9%) and in 7/19 homosexuals (32%). In 3 cases HL was the only clinical manifestation of disease, in 11 it was associated with other symptoms of acquired immunodeficiency syndrome related complex (ARC), and in 9 it was found in patients with a previous or concomitant diagnosis of acquired immunodeficiency syndrome. The mean count of CD4 lymphocytes in the 23 patients was 0.22 X 10(9)/l. The diagnosis was made on the basis of the characteristic clinical features. In 3 cases biopsy was carried out, and parakeratosis and vacuolization of the spinous layer cells were found. Remarkably, particles of the herpesvirus group were also found. The lesions oscillated in size or even spontaneously disappeared, at least transiently; however, in the patients treated with zidovudine the improvement appeared to be more significant. The detection of HL discloses a likely infection by the HIV; it is usually associated with other features of ARC and/or severe immune depression, and it requires the institution of antiretroviral treatment.

AIDS-Related Complex↗