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P Cervera

Publications and source records attributed to P Cervera.

At least 19 recordsLinked to original sources

Comparison of somatostatin receptor expression in human gliomas and medulloblastomas.

The expression of the five somatostatin receptor subtypes, sst1-5 was compared on tissue containing glial tumours (glioblastomas or oligodendrogliomas), medulloblastomas, and on normal human cortex. By semiquantitative reverse transcription coupled to polymerase chain reaction, the receptor expression profiles were high in cortex and in tissue containing oligodendrogliomas. It was moderate in medulloblastomas. Tissue containing glioblastomas displayed lower expression of somatostatin receptor subtypes, sst1 and sst3 being mostly expressed. By 125I-Tyr0DTrp8 somatostatin-14 or 125I-Leu8DTrp22 Tyr25 somatostatin-28 autoradiography combined with synaptophysin immunohistochemistry, it was possible to differentiate between isolated tumoral cell component infiltrating the cerebral parenchyma (cortex or white matter) and tumoral tissue (without residual parenchyma) in glioblastomas or oligodendrogliomas. Glial tumoral tissue per se presented few somatostatin receptors. By contrast, medulloblastoma tumoral cells exhibited numerous octreotide sensitive somatostatin receptors. sst2 immunocytochemistry demonstrated immunostaining of neuronal cells and neuropile; sst2 and sst3 immunostaining was identified on glioblastoma proliferating vessels endothelial cells and on medulloblastomas tumoral cells. Faint sst2 immunostaining among glial tumoral cells was due to microglia, while glioma cells did not significantly stain. In summary, medulloblastoma tumoral cells express sst2/sst3 receptors at a high level while glioma cells do not. In gliomas, sst expression is restricted to endothelial cells on proliferating vessels (displaying both sst2 and sst3 receptors), including parenchyma and reactive microglia (only sst2). The differential expression of sst2/sst3 receptors on gliomas and medulloblastomas has implications for the therapy of these tumours.

Adolescent↗

Assessment of dietary adequacy for an elderly population based on a Mediterranean model.

This study analysed whether at different energy levels, a varied diet based on Mediterranean Diet patterns would meet the RDIs for specific nutrients in a population > 65 y. Based on RDIs for elderly persons > 65 y for PRO, FAT CHO, phosphorus, calcium, magnesium, iron, zinc, vitamin C, B6, folate and fibre, menu models based on Mediterranean diet food patterns were calculated for the following calorie levels: 1400, 1500, 1600, 1700 and 1800 kcals. 15 menu variations for each calorie level were then created based on the previously calculated models. Utilising the Program for Alimentation and Nutrition (PAN) database, nutritional analysis was carried out for all menus and the mean nutrient values for a 2 week period were calculated for each calorie level. Intakes at all calorie levels provided adequate amounts of folate, phosphorus, iron and Vitamin B6. Intakes were low in all groups for Calcium, Zinc, Magnesium and Vitamin E, with the exception of the 1800 kcal level for Vitamin E. Results show that at low energy levels, meeting nutrient needs was difficult and that even at higher calorie intakes, contrary to what was expected, certain nutrients were found to be inadequate.

Aged↗

Dietary guidelines for the breast-feeding woman.

Sociodemographic and economic changes in Spain have played a role in the choice of infant feeding as more and more women enter the workforce. Nevertheless, the prevalence of breast-fed-only infants at 6 weeks remains fairly high, at 65.5% in 1999, although there is a sharp decline by 3 and 6 months postpartum. Achieving adequate nutritional status for lactation principally begins during pregnancy, as this constitutes the biological stage for accumulating nutrient stores. The benefits of breast-feeding for the mother and infant are presented, along with nutrition and dietary guidelines for the nursing woman. Apart from dietary considerations, special attention should be paid to encouraging a positive attitude and environment for breast-feeding success.

Adult↗

[Obstetric trauma. A current problem?].

Advances in obstetric practice have decreased birth traumas in the last years, although they are still an important chapter in neonatal age. Between 1993-1998 a total of 21,375 stillborns were registered with a total of 309 birth injuries in 303 neonates (1.44%). The diagnoses were: 2 liver subcapsular hematomas, 105 cephalohematomas, 16 parietal fractures, 11 subdural hemorrhages, 107 clavicular fractures, 10 miscellaneous fractures, 8 soft tissue injuries, 25 facial nerve injuries and 25 braquial palsy. About relation between type of labor and birth trauma was found that clavicular fracture and cephalic vaginal delivery were associated in 50% of the cases, cephalohematoma and forceps in 51%, braquial palsy and vaginal delivery in 44% and forceps in 36%. High weight at birth was another risk factor for entities such as clavicular fracture and braquial palsy. We conclude that birth trauma is a pathology with a relevant incidence and their epidemiology factor had to be known.

Birth Injuries↗

Characterization and distribution of Hxt1, a Na(+)/Cl(-)-dependent orphan transporter, in the human brain.

Rxt1, a transporter-like protein structurally related to the large family of Na(+)/Cl(-)-dependent carriers, was isolated from the rat brain. In the present study, Hxt1, the homologue of Rxt1, was isolated from human cortex cDNA. Comparison of their respective nucleotidic sequences revealed a 96% conservation between Hxt1 and Rxt1. Genetic mapping with human genome radiation hybrids allowed the location of the gene coding for Hxt1 between 323ya5 and 084xb3 AFM markers, on a portion of chromosome 1p which spans over 7 cM or 118 cRay. Northern blot analyses demonstrated that Hxt1 mRNA ( approximately 7.5 Kb) is expressed in the human brain but not in peripheral tissues. The immunodistribution of Hxt1 was determined with antibodies raised against the C-terminus of Rxt1. Hxt1 is concentrated in the cerebral cortex, caudate-putamen, substantia nigra, hippocampus, and cerebellum, appearing as a diffuse or a punctate labeling at the light microscope level. This regional and cellular distribution suggests that Hxt1, as its rat homologue, could be present in axon terminals of glutamatergic neurons. The high pressure of selection exerted upon this protein, its strategic anatomical and subcellular distributions suggest that this orphan transporter could be involved in critical functions in the central nervous system.

Amino Acid Sequence↗

Edg-2 in myelin-forming cells: isoforms, genomic mapping, and exclusion in Charcot-Marie-Tooth disease.

Edg-2 is an heptahelical receptor whose spatio-temporal distribution during rat brain development is consistent with a role in the control of myelination. We have now identified two splice variants of Edg-2 mRNA in rat brain that encode two receptor isoforms differing by a stretch of 18 amino acids in the NH2-terminal extracellular tail of the receptor. Prenatally (i.e., before oligodendrocyte myelination), the two variants detected by selective in situ hybridization are equally abundant, vary in parallel, and remain restricted to proliferative zones in the brain. Postnatally, the long isoform becomes predominant in myelinating structures, where its abundance increases sharply during the period of myelination. In the adult human brain, only the long variant was detected, while in situ hybridization showed it selectively expressed in the white matter and in clusters of cells showing features of oligodendrocytes of the temporal cerebral cortex. Consequently, the human Edg-2 gene was studied to assess its possible contribution in inherited neuropathies. The coding sequence was found to be contained in three exons and to map to chromosome 9q31.3-32 by using radiation hybrid panel and Yeast-Artificial Chromosomes. Two intragenic bi-allelic polymorphisms and a rare mutation were identified. As a first application to molecular genetic studies, they were used to exclude the Edg-2 gene in six families with phenotype of demyelinating Charcot-Marie-Tooth disease of unknown origin.

Adult↗

Oligodendrogliomas. Part I: Patterns of growth, histological diagnosis, clinical and imaging correlations: a study of 153 cases.

The present study has attempted to demonstrate that the morphological spectrum of oligodendrogliomas includes tumors which are traditionally misinterpreted as 'diffuse fibrillary astrocytoma'. We have shown that these tumors are in fact made of isolated neoplastic oligodendrocytes which are entrapped in a fibrillary background composed of axons and fibrillary reactive gliosis. Analysis in a series of 153 'pure' supratentorial oligodendrogliomas composed of 'classical' or pseudo 'diffuse fibrillary oligodendrogliomas' diagnosed by imaging-based serial stereotactic biopsies showed that 2/3 of the tumors were exclusively made of isolated tumor cells (ITCs) (structure type III) and that only 1/3 of them exhibited both ITCs and solid tumor tissue components (structure type II). The tumor tissue destroys the brain parenchyma and contains new formed microblood vessels whereas ITCs do not destroy the parenchyma and are not associated with microangiogenesis. These fundamentally opposite morphological characteristics were reflected by the following findings: 1) contrast enhancement was observed in 64% of structure type II but was never seen in structure type III oligodendrogliomas. 2) a neurological deficit occurred in 57% of structure type II but in only 8% of structure type III oligodendrogliomas. 3) using the new grading system described in the companion paper to this study, we found that the biological behavior of oligodendrogliomas was also closely related to the patterns of tumor growth. From a synthesis of data gathered in this study it is suggested that emergence of microangiogenesis within a tumor which at first grows slowly with a structure type III pattern is a crucial event toward more aggressive behavior.

Astrocytoma↗

Oligodendrogliomas. Part II: A new grading system based on morphological and imaging criteria.

This second part of our study of 'pure' oligodendrogliomas focuses on survival data analysis. In order to identify potentially useful prognostic factors and to assess the effectiveness of a new grading system, the 79 patients in the previously analyzed series for whom adequate follow-up could be obtained (52%) were entered in the present analysis. Statistical analysis demonstrated that contrast enhancement and endothelial hyperplasia had powerful and similar influence on survival. Median survival with and without contrast enhancement were: 3 versus 11 years, and with or without endothelial hyperplasia were: 3.5 versus 11 years. Conversely, the degree of nuclear atypia and presence or absence of mitosis or necrosis were not correlated with survival. These findings allowed us to devise a simple grading system which discriminates two malignancy grades as follows: absence of endothelial hyperplasia and of contrast enhancement = Grade A, presence of endothelial hyperplasia and/or of contrast enhancement = Grade B. Of the 79 oligodendrogliomas in this study, 59 tumors were categorized as grade A and 20 as grade B. Median survival were: 11 years in grade A and 3.5 years in grade B. Five-year and 8-year survival rates were: 89% and 60% in grade A and: 33% and 15% in grade B. Double blind grading between two independent observers was concordant in 96% of the cases. Application of this simple efficient and reproducible grading scheme should permit reliable comparison of retrospective or prospective therapeutic data emanating from various institutions.

Brain Neoplasms↗

Mechanisms of lysis by activated cytotoxic cells expressing perforin and granzyme-B genes and the protein TIA-1 in muscle biopsies of myositis.

OBJECTIVE: Polymyositis (PM) and cermatomyositis (DM) are inflammatory muscle diseases of autoimmune origin. A chronic mononuclear cell infiltrate is always present around PM and DM muscle damage. In PM, the predominant cells are activated cytotoxic cells, natural killer, and CD8+ T lymphocytes. Cytotoxic cells can kill the target cells via 2 mechanisms. Both pathways induce target cell death by releasing the molecules (granule exocytosis) perforin (PF), which attacks the target cell membrane and causes cell death by necrosis, and TIA-1 protein and granzyme-B (GZB), possibly responsible for apoptosis. We studied the mechanisms of lysis in muscle biopsies of myositis. METHODS: We used a panel of monoclonal antibodies to determine the phenotypes of reactive lymphocyte subsets, in situ hybridization to study the expression of PF and GZB genes, and immunohistochemistry to evaluate TIA-1 protein production in muscle biopsies from 14 patients with myositis (11 PM/3 DM). Results were compared to those obtained from muscle biopsies of 12 control patients with muscle weakness, including patients with muscle dystrophy and vasculitis, but without myositis. RESULTS: Abundant CD8+ cells, especially in endomysial sites in PM, formed the predominant phenotype. The predominant mononuclear cells observed in DM were CD4+ T cells and CD22+ B lymphocytes, in perivascular sites. The GZB and PF genes and the TIA-1 protein were expressed simultaneously in muscle samples from patients with myositis. GZB, PF, and TIA-1 positive cells were predominantly located in endomysial sites of PM, in the nonnecrotic muscle fibers. In DM, these positive cells were rare. CONCLUSION: In myositis, especially PM, cytotoxic cells may cause muscle damage and muscle cell necrosis and/or apoptosis by releasing several proteins (PF, GZB, and TIA-1 proteins) responsible for the lysis of these stimulating target cells. Some drugs (prednisone and cyclosporine) inhibit the release of GZB and PF. Their efficacy may be due in part to this inhibitory effect.

Adult↗

[Low-grade papillary adenocarcinoma of the endolymphatic sac. Report of three cases with immunohistochemical study].

Glandular tumors involving the mastoid and the middle ear are rare, and distinguishing between adenoma and adenocarcinoma remains difficult. Among these latter lesions, two distinct patterns are accepted. One of them, the papillary form takes a more aggressive course with wider regional spread and must be separated from the other type, the middle ear carcinoma. Its microscopic appearance and clinical course have been extensively described by Heffner who considered it as "low-grade adenocarcinoma of probable endolymphatic sac origin". A few cases have been associated with von Hippel-Lindau disease. Three cases of papillary adenocarcinoma of endolymphatic sac origin are reported. One concerned an isolated tumor, the two others were associated with von Hippel-Lindau disease. Their clinical, pathological and immunohistochemical data are presented.

Adenocarcinoma, Papillary↗

Short- and long-term effects of calcitonin and calcium administration on blood calcium, magnesium and inorganic phosphorus in post menopausal osteoporosis.

This paper studies the effects of the administration of calcitonin (CT) and Ca on post menopausal osteoporosis, immediately (short-term) and after three months (long-term) of treatment, on total and ionic calcium (Ca), magnesium (Mg), inorganic phosphorus (Pi), calcitonin (CT) and parathyroid hormone (PTH) in plasma. The short-term results show a decrease in total and ionic Ca and Pi four hours after the beginning of the treatment; at seven hours, only Pi varies. A decrease in the total and ionic Ca was observed after three months of CT treatment (long-term effects). No hormonal (PTH and CT) variations were found either in the short or the long-term. However, the PTH/CT ratio decreased significantly during the experiment and this may be an important factor in explaining the long-term Ca variations.

Aged↗

Role of pontine nuclei damage in smooth pursuit impairment of progressive supranuclear palsy: a clinical-pathologic study.

We performed a quantitative study of the pontine nuclei in the basis pontis and a semiquantitative study of extrapontine structures involved in smooth pursuit in four patients with severe impairment of horizontal smooth pursuit and histopathologically confirmed diagnosis of progressive supranuclear palsy (PSP). There were only slight changes in the extrapontine structures involved in smooth pursuit, but there was a significant neuronal loss--massive in three patients and mild in one patient--in all nuclei of the basis pontis. Our results suggest that degenerative lesions affecting the pontine nuclei are largely responsible for the horizontal smooth pursuit impairment in PSP.

Aged↗

Alzheimer's disease: is the decrease of the cholinergic innervation of the hippocampus related to intrinsic hippocampal pathology?

Consistent findings in the hippocampi of patients with Alzheimer's disease are the presence of neurofibrillary tangles in pyramidal neurons and the loss of choline acetyltransferase activity due to degeneration of hippocampal cholinergic terminals. The present study sought to clarify, in the brains of five patients with Alzheimer's disease and four controls, whether the loss of cholinergic terminals in the hippocampal stratum pyramidale in Alzheimer's disease is related to degenerative changes in hippocampal pyramidal cells. A polyclonal antibody to human choline acetyltransferase was employed to visualize immunohistochemically cholinergic terminals. Hippocampal neurons were stained with Cresyl Violet, neurofibrillary tangles with thioflavin S and a monoclonal antibody against phosphorylated neurofilament (RT97). Quantification of the stained structures was performed in CA4, CA1 and the subiculum, on five sections selected from the entire anteroposterior extent of each hippocampus. In the group of Alzheimer patients, the densities of cholinergic terminals were homogeneously diminished in the three hippocampal subregions in comparison with the controls (32-33%). In contrast, a significant loss of pyramidal neurons was found only in CA1, and the density of neurofibrillary tangles was markedly increased only in CA1 and the subiculum in Alzheimer's disease. These findings suggest that there is no relationship between the loss of cholinergic terminals and the degeneration of pyramidal cells in the hippocampus of patients with Alzheimer's disease.

Aged↗