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Biomedical subjects

C Morales

Publications and source records attributed to C Morales.

At least 127 records · Page 7Linked to original sources
PubMed1994

Influence of the postnatal administration of tumor necrosis factor plus interferon-alpha 2b on the development of ethyl-nitrosourea-induced brain tumors in rats.

Using the experimental model of brain tumors induced by ethyl-nitrosourea (ENU), interferon-alpha 2b and human recombinant tumor necrosis factor-alpha (TNF) have been administered to Wistar rats between 100 and 130 days of life (one injection each week, by intraperitoneal route, of 100 micrograms of TNF and 10(4) IU of interferon-alpha 2b, in a total volume of 1 ml per injection). The results obtained suggest, that at this time, this association achieves a reduction in the number of so-called 'malignant schwannomas', but it does not influence the time of appearance nor the number of so-called 'malignant schwannomas', but it does not influence the time of appearance nor the number of so-called 'oligodendroglioma-like tumors'. On the basis of previous observations about cytokine modulation of these ENU-induced neoplasms, a different course of time for obtaining a postnatal biomodulation of both type of tumors is suggested.

Aging↗
PubMed1994

Gangliosides modulate the development of ethyl-nitrosourea induced brain tumors in rats.

The possible effect of gangliosides as biological modifiers of the ethyl-nitrosourea (ENU) model of neurocarcinogenesis in rats is studied. Wistar rats that were exposed to ENU during fetal life, were treated with gangliosides at a postnatal age corresponding to a stage of pretumor or microtumor development. The results obtained suggest that postnatal administration of gangliosides can influence the development of ENU-induced brain tumors, delaying the appearance of symptomatic neoplasms and improving survival with respect to controls. This finding suggests the potential usefulness of gangliosides in the control of neuroectodermal tumors.

Animals↗
PubMed1994

Ultrastructural and immunocytochemical study of skin fibroblasts from normal and sialidosis patients.

The objectives of this study were to analyze morphologically, morphometrically and immunocytochemically the lysosomal compartment of normal fibroblasts and of fibroblasts with neuraminidase deficiency. The immunocytochemical analyses consisted of quantifying the distribution of saposins and beta-galactosidase in the lysosomes of these cells to test the hypothesis that neuraminidase deficiency is associated with an impairment in the transport of these proteins to the lysosomal compartment. To test this idea, cultured skin fibroblasts of patients with or without sialidosis were prepared for electron microscopy and probed with antibodies against lysosomal beta-galactosidase and lysosomal saposins. The lysosomes of the affected cells had an abnormal accumulation of incompletely digested membranes which was associated with a significant lowering in the density of antigenic sites per lysosome. However, due to a significant increase in the number of lysosomes per affected cell, the total number of antigenic sites in control and neuraminidase deficient cells was similar. This presumably compensatory effect indicates that although the rate of production of beta-galactosidase and saposins remains unchanged, the transport of these molecules to the lysosomes is somehow affected. Our data also indicate that in the fibroblasts, lysosomes require a normal concentration of the three enzymes to maintain neuraminidase activity and sphingolipid degradation.

Cell Compartmentation↗
PubMed1994

Effects of growth hormone and prolactin on testicular macrophages in long-term hypophysectomized rats.

Long-term hypophysectomized (LTHX) rats were treated for 1 week with growth hormone (rGH, 600 micrograms/kg body wt.), prolactin (rPRL, 600 micrograms/kg body wt.), combined rGH/rPRL or vehicle, to study the effects of these hormones on testicular macrophages. Growth hormone and, to a lesser extent, prolactin significantly increased the number and size of testicular macrophages. The in vivo phagocytic capacity of testicular macrophages was tested by their ability to clear the testicular interstitium of dead Leydig cells after treatment with the specific cytotoxic reagent ethylene dimethane sulphonate (EDS). In vehicle- or rPRL-treated rats, abundant EDS-killed Leydig cells (about 50% of the pre-existent population) remained in the testicular interstitium 72 h after EDS treatment, whereas clearance of the testicular interstitium of dead Leydig cells was largely achieved in rGH- or rGH/rPRL-treated rats. These results indicate that growth hormone and prolactin have stimulatory effects on testicular macrophages in LTHX rats.

Animals↗
PubMed1994

New pattern of hyperechogenicity in thalamus and basal ganglia studied by color Doppler flow imaging.

Thirty-seven infants whose cerebral real-time B-mode ultrasound (CUS) documented hyperechogenic areas in the thalamus and basal ganglia (HTBG) either of linear or fine punctate pattern, were studied prospectively by color Doppler imaging (CDI). This study aimed to establish a relationship between these areas and the regional vasculature, to analyze associated disorders to establish pathogenesis, and to determine clinical significance. HTBG were diagnosed in the first 4 days of life in all but 7 infants. Different patterns of HTBG were observed: punctate in 11 infants, linear in 12, and mixed in 14. The basal ganglia were affected in all patients, 9 also had involvement of the thalamus. CDI confirmed that HTBG were allocated along the gangliothalamic vessels. Blood flow velocity waves were obtained at this level in all patients. Real-time spectral analyses were performed in 35 patients and compared with a control group of 20 healthy neonates. Differences were not significant. Computed tomography and magnetic resonance imaging failed to indicate this abnormality. Necropsy revealed basophilic deposits in the walls of involved arteries. Congenital infections manifested in 5 patients, chromosomal abnormality in 1, dysmorphic syndromes in 9 (3 unidentified), isolated congenital defects in 5, and diverse congenital disorders in 3. In the remaining 14, no congenital disorders nor infections were found. This CDI study demonstrates the vascular location of these HTBG. Supported by early CUS diagnosis, it is speculated that vascular injury in that region has a prenatal origin. This abnormality does not appear to alter regional blood flow. HTBG are associated with very heterogeneous disorders and in most patients the etiology and pathogenesis remain unclear.

Arteries↗
PubMed1994

Immunohistochemical distribution pattern of intermediate filament proteins and muscle actin in feline and human mammary carcinomas.

Thirty-seven feline and 38 human spontaneous mammary gland carcinomas were studied immunohistochemically. Commercially available antibodies directed against high and low molecular weight keratins (RCK-102 and NCL-5D3), vimentin, desmin, glial fibrillary acidic protein (GFAP), neurofilament (NF) proteins and muscle actin (HHF35) were used in the avidin biotin peroxidase complex (ABC) technique on formalin-fixed paraffin wax-embedded tumour tissue samples. Healthy feline and human mammary gland tissue adjacent to the neoplasms was also examined. The distribution pattern of intermediate filament proteins and muscle actin was comparable in healthy mammary gland tissue of the two species: both RCK-102 and NCL-5D3 antibodies reacted with luminal epithelial cells of ducts and acini, but basal/myoepithelial cells were stained by RCK-102 exclusively. In addition, basal/myoepithelial cells expressed vimentin and muscle actin in both species, and GFAP was found in some feline basal/myoepithelial cells. No immunoreactivity to desmin and NF proteins was observed. Feline mammary gland carcinoma cells reacted with RCK-102 (89%), NCL-5D3 (62%), vimentin (76%) and GFAP (30%) antibodies, while human mammary gland carcinoma cells reacted with RCK-102 (95%), NCL-5D3 (100%) and vimentin (13%) antibodies. HHF35 immunoreactivity was observed in stromal cells only. These results indicate that mammary gland carcinomas of both species share a heterogeneous immunophenotype with respect to intermediate filament proteins, which adds to the list of known similarities between mammary gland carcinomas of both species.

Actins↗
PubMed1994

Primary degeneration of the granular layer of the cerebellum. A study of 14 patients and review of the literature.

Primary degeneration of the granular layer of the cerebellum is an autosomal recessive disorder exhibiting characteristic clinical features: hypotonia, strabismus, delayed motor development, nonprogressive ataxia, delayed language development with dysarthria and mental retardation. We studied fourteen children, seven of each gender. Neuroimaging tests including pneumoencephalography, computed tomography (CT) and magnetic resonance imaging (MRI) showed severe cerebellar atrophy in all. MRI best demonstrated the cerebellar lesion, revealing great uniformity amongst the cases. Vertebrobasilar angiography was performed in two cases and showed marked hypoplasia of the cerebellar arteries, predominantly the posterior inferior cerebellar artery (PICA) and its branches. Necropsy was performed in three cases; cerebellar atrophy with loss of granular cells and diverse abnormalities of the Purkinje cells was found in two. The third, the sister of one of the other two cases, had a similar but shorter clinical course and died at three months of age. Her sister, who died at 5 years of age, presented a severe cerebellar atrophy with typical changes in the granular cell layer and Purkinje cells. In the third patient, who lived three months, only focal cerebellar folial atrophy with no microscopic changes in the granular cell layers was present. Though this case cannot objectively be included in the cerebellar atrophy syndrome with granular cell loss, her family history and clinical picture suggest the same disease. The findings observed in our series and the study of cases described in the literature, suggest that there are several forms of this disease which differ mainly in severity and neurological evolution. The cerebellar lesion seems to be a progressive atrophic process with the most severe changes during the early years of life.

Adolescent↗
PubMed1994

Benign mitochondrial myopathy with decreased succinate cytochrome C reductase activity.

In most of the cases previously described, the defect on complex II was suggested by low activity of succinate cytochrome C reductase (SCCR). The clinical pattern of the previous 10 cases is heterogeneous and may be limited to one particular tissue or be of a more general nature. We report a 22-year-old-woman, daughter of consanguineous parents, with generalized muscle weakness, easy fatigability and benign course, who showed a decrease of SCCR activity in mitochondria of muscle fibers. Free carnitine (FC) concentration was decreased in muscle as well. The muscle biopsy showed a mild variation in fiber size, with fiber type I predominance, subsarcolemmal oxidative DPNH accumulations, excess of neutral lipids and abnormally large mitochondria with paracrystalline inclusions. A possible inheritance pattern is discussed. Coenzyme Q10 therapy in this patient induced a significant increase of global MRC index score and a decrease of the turns-mean amplitude ratio in the automatic analysis of the EMG.

Adult↗
PubMed1994

Aluminium allergy in patients hyposensitized with aluminium-precipitated antigen extracts.

During hyposensitization therapy with aluminium-precipitated antigen solutions, a small % of patients develop persistent subcutaneous nodules at the injection site; the existence of delayed sensitivity to aluminium has been implicated in the pathogenesis of these nodules. We studied the prevalence of aluminium sensitivity (using patch, prick and intradermal tests) and common contact allergens (TRUE Test) in 20 healthy subjects, and in 40 patients treated with aluminium-containing extracts, 20 of whom had persistent subcutaneous nodules that remained for more than 2 months, the other half having no nodular reactions or nodules that remained for less than 2 months. Aluminium sensitivity was found only in those patients of the treated group who had persistent nodular reactions, 4 cases of positivity to an aluminium chloride patch test being found. All 4 cases were women, nodules remained for more than 6 months, and intracutaneous tests were negative. 3 of them also had contact sensitivity to nickel. In 2 cases, nodules were removed for histological and histochemical examination, showing non-specific inflammatory granulomas, and aluminium crystals being found in only 1 case. It is concluded that delayed sensitivity to aluminium appears to be implicated in the pathogenesis of persistent nodular reactions, but sensitivity to aluminium was not found in patients treated with aluminium-precipitated extracts without persistent nodular reactions.

Adolescent↗
PubMed1994

Serpentine aneurysm: regrowth after a superficial temporal artery-middle cerebral artery bypass and internal carotid artery ligation: case report.

Giant serpentine aneurysms (GSAs) are infrequent. We present a 37-year-old patient with a giant serpentine aneurysm of the left middle cerebral artery that was treated with a superficial temporal artery to middle cerebral artery bypass and ligature of the left internal carotid artery. After 2 years, the patient presented new symptoms of neurological deterioration and the computed tomographic scan and arteriography showed regrowth of the aneurysm, which was excised. Enlargement of a giant serpentine aneurysm once it has been treated with ipsilateral carotid ligation and/or bypass anastomosis is rare, and only two cases have been described previously.

Adult↗
PubMed1994

Selective depletion of testicular macrophages and prevention of Leydig cell repopulation after treatment with ethylene dimethane sulfonate in rats.

Testicular macrophages were selectively eliminated with dichloromethylene diphosphonate-containing liposomes (Cl2MDP-lp) to study the role of these cells in the repopulation of Leydig cells after treatment with ethylene dimethane sulfonate (EDS). Right testes were injected with Cl2MDP-lp to deplete macrophages and left testes were injected with sodium chloride and served as controls. Injection of Cl2MDP-lp produced a 97% reduction in the number of macrophages 10 days after treatment. Twenty-one days after destruction of the existing Leydig cells with EDS, abundant differentiating Leydig cells were present in the left (macrophage-containing) testes. On the contrary, in the right (macrophage-depleted) testes, differentiating Leydig cells were scarce, and was 3% of that found in the control testes. The inhibition of Leydig cell repopulation in macrophage-depleted testes was more evident at 30 days after EDS treatment, when the number of Leydig cells in the right testes was 1% of that found in control testes. The lack of Leydig cell development was also indirectly shown by the lower mass and more atrophic seminiferous epithelium of the right testes, as well as the decreased weight of the ipsilateral epididymis compared with the left testes. These results indicate that testicular macrophages are central to the proliferation and differentiation of new Leydig cells after EDS treatment, and point out the significance of paracrine regulatory mechanisms in rat testes.

Animals↗
PubMed1994

Decreased number and size and the defective function of testicular macrophages in long-term hypophysectomized rats are reversed by treatment with human gonadotrophins.

Macrophages are a common cell type in the testicular interstitium of the rat and are morphologically and functionally related to Leydig cells. We investigated the number of macrophages and Leydig cells in long-term (24 weeks) hypophysectomized (LTHX) or sham-operated rats. LTHX rats showed a 76% decrease in the number of macrophages, whereas the number of Leydig cells was only slightly decreased (by 18%). The profile areas of both macrophages and Leydig cells were very much decreased (46% and 66% respectively). Sham-operated and LTHX rats were treated with vehicle or human FSH and LH (hFSH/hLH; 75 IU/kg body weight per day) for 1 week. This treatment induced a 286% increase in the number of macrophages and a 32% increase in the number of Leydig cells in LTHX rats. The profile areas of macrophages and Leydig cells were also increased (212% and 184% respectively). About 80% of macrophages showed vacuolization of the cytoplasm. Gonadotrophin treatment did not induce changes in cell numbers in sham-operated animals but about 30% of macrophages showed large cytoplasmic vacuoles. Vehicle- or hormone-treated LTHX rats were given a single injection of ethylene dimethane sulphonate (EDS) and killed 72 h later. Leydig cells were absent from the testicular interstitium of sham-operated rats but there were large numbers of dead Leydig cells (about 40% of the pre-existing population) in the testicular interstitium of LTHX rats 3 days after EDS treatment. Complete clearance of the testicular interstitium from EDS-killed Leydig cells was found in LTHX rats treated with hFSH/hLH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Clinical and investigative approaches in mitochondrial diseases. A review of 15 cases].

The results of laboratory investigations in concerning 15 patients suspected of mitochondrial disease (MD) are presented. Our purpose is to provide an outline of the investigative modalities that support the clinical suspicion and have been found to be useful in the diagnosis. Five clinical groups were studied including 5 exercise intolerances (2 with inflammatory myopathy), 3 with myopathies (1 with dilated cardiomyopathy), 2 with progressive external oftalmoplegia (1 associated with cerebellar ataxia+epilepsy+hypertrophic cardiomyopathy+pes cavus), 4 with encephalopathies (3 with myoclonic encephalopathies with ataxia and dementia and 1 with epilepsy and tremor), and 1 with metabolic acidosis and cardiomyopathy. We used the following categories of investigative procedures: clinical phenotype analysis including pedigree study, neurophysiological tests, bicycle ergometric evaluation, neuroimaging, microscopic study of skeletal muscle biopsy, post-mortem examination, biochemical assays and molecular genetic studies. EMG showed myopathic changes in 5 cases, features of neuropathy in 2, mixed myopathic and neuropathic pattern in 1 and nonspecific changes in 3. EMG was normal in 3 patients. The most common skeletal muscle abnormalities were variation in fiber size (60%), lipid inclusions (33.3%), oxidative subsarcolemmal aggregates (26.7%) and ragged-red fibers (26.7%). Electron microscopy revealed mitochondrial abnormalities in 8 out of 14 patients' muscle biopsies, and in myocardiac and hepatic tissues of another. Site of biochemical defect was located in 12 patients. Complex I defect in 6, complexes I+IV deficiencies in 3, complex II defect in 1, complex IV deficiency in 1, complexes II+IV deficiencies in 1, and complex III defect in 1. In 2 patients the biochemical defect was not located. Mitochondrial DNA alterations were not found in 7 investigated patients. The clinical spectrum of MD has become increasingly wider. After the clinica suspicion, the diagnosis depends up on the appropriate use of skeletal muscle biopsy, biochemical investigations and molecular genetic techniques. Conventional EMG and automatic measurement of the electromyogram are particularly helpful in confirming the clinical suspicion in patients with predominantly central nervous system disease or in cases in which clinical signs are few.

Adolescent↗
PubMed1994

[Idiopathic granulomatous angiitis of the central nervous system].

We diagnosed idiopathic granulomatous angiitis of the central nervous system in a 51-year-old man by leptomeningeal and cortical biopsy. The patient's disease was prolonged, with symptoms recurring over a period of 15 years. Treatment with prednisone and cyclophosphamide produced total remission after a follow-up of 22 months. Computerized tomography was less sensitive and revealed fewer lesions than did magnetic resonance imaging. Angiography was not sensitive and leptomeningeal and cortical biopsy were essential for diagnosis in this patient.

Age of Onset↗
PubMed1993

Type I familial amyloid polyneuropathy and pontine haemorrhage.

A Portuguese female, aged 47 years, who had emigrated to Spain, was admitted to the hospital in 1991 for pontine haematoma. The patient, four siblings and her father were affected by a peripheral neuropathy, indicating autosomal dominant inheritance. The patient presented in the 2nd decade with sensory and motor neuropathy beginning in the lower extremities. Alternating constipation and diarrhoea, and urinary incontinence became uncontrollable. She had to be colostomised, and, eventually, confined to a wheelchair from the age of 43. Neurological examination showed bilateral facial involvement, and severe signs of sensory and motor peripheral neuropathy, and later right hemiplegia. There were abnormalities of atrial rhythm and left bundle branch block. Computerised axial tomography and magnetic resonance images demonstrated left-sided pontine haemorrhage. Nerve conduction studies revealed severe diminution of motor conduction velocity and absence or reduction of amplitude of sensory and motor action potentials. Inanition and a respiratory infection led to her death. Clinical diagnosis was type I familial amyloid polyneuropathy (FAP). Postmortem examination demonstrated amyloid deposits in peripheral nerves, including spinal roots and cranial nerves, leptomeninges, thyroid, breasts, heart, adrenal glands, kidneys, intestines, pancreas, and meningeal and some pontine vascular structures. Advanced pontine haematoma was verified. Cerebral haemorrhage usually occurs with cerebrovascular amyloidosis, but exceptionally with FAP. A minority of patients presenting with CNS haemorrhage showed arteriovenous malformation or embolism [Da Silva Horta and Dias Coelho (1960) Arch 'de Vecchi' Anal Patol Med Clin 31 = 163-172].(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed1993

Hyaline globules in uterine malignant mixed müllerian tumours. A diagnostic aid?

In order to evaluate the presence of hyaline globules (HGs) in uterine malignant mixed müllerian tumours (MMMT), and its possible diagnostic value in haematoxylin & eosin stained sections, a retrospective microscopic study of 38 cases (13 homologous and 25 heterologous) was carried out. Intra- and extracellular HGs were found in 31 MMMT (81.6%), 8 homologous (61.5%) and 23 heterologous (92%). In addition, strong alpha-1-antitrypsin immunoreactivity was also noted in the HGs of 10 cases out of 13 investigated. In initial diagnostic curettage material, HGs were observed in 18 of 22 cases (81.8%), 6 of 9 homologous (66.7%) and 12 of 13 heterologous (92.3%). In view of the high incidence of HGs in curettage specimens, their finding in haematoxylin & eosin stained sections could orientate a histopathologic preoperative diagnosis of MMMT, specially of heterologous type, and may be considered a diagnostic tool in order to indicate an early, planned therapy and staging in these neoplasms of poor prognosis.

Female↗