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Biomedical subjects

R Pereira

Publications and source records attributed to R Pereira.

At least 55 records · Page 3Linked to original sources
PubMed1994

The activity of synaptosomal calcium channels is inversely correlated with working memory performance in memory impaired, aged rats.

Aged, memory-impaired rats do not learn an 8-arm radial maze task but differ in their performance along testing. The aim of this study was to determine whether any of the systems that govern calcium homeostasis in synaptosomes may be related to that difference in performance. A negative correlation between initial (5 s) K(+)-stimulated 45Ca2+ uptake and the behavioral scores from the last testing sessions was obtained K(+)-stimulated 45Ca2+ uptake showed also a negative correlation with an improvement score that evaluates the progress made by the rat along testing. The results support the notion that calcium inflow through synaptosomal voltage gated calcium channels in old rats is inversely correlated with their behavior. This may explain the beneficial effects of organic calcium channel blockers on behavioral performance in aged animals.

Aging↗
PubMed1994

Phlebotomines (Diptera: Psychodidae) collected at a Costa Rican dairy farm in a vesicular stomatitis endemic area.

This study determined the species composition of sand flies in a vesicular stomatitis endemic area, at Carrizal, Alajuela, Costa Rica. Eight species were collected as follows: Lutzomyia volcanensis (Fairchild & Hertig), L. shannoni (Dyar), Lu. pia (Fairchild & Hertig), L. sanguinaria (Fairchild & Hertig), L. youngi Feliciangeli & Murillo, L. longipalpis (Lutz & Neiva), L. serrana (Damasceno & Arouck), and L. gomezi (Nitzulescu).

Animals↗
PubMed1994

Phenotypic variability and incomplete penetrance of spontaneous fractures in an inbred strain of transgenic mice expressing a mutated collagen gene (COL1A1).

Phenotype variability and incomplete penetrance are frequently observed in human monogenic diseases such as osteogenesis imperfecta. Here an inbred strain of transgenic mice expressing an internally deleted gene for the pro alpha 1(I) chain of type I procollagen (COL1A1) was bred to wild type mice of the same strain so that the inheritance of a fracture phenotype could be examined in a homogeneous genetic background. To minimize the effects of environmental factors, the phenotype was evaluated in embryos that were removed from impregnated females 1 d before term. Examination of stained skeletons from 51 transgenic embryos from 11 separate litters demonstrated that approximately 22% had a severe phenotype with extensive fractures of both long bones and ribs, approximately 51% had a mild phenotype with fractures of ribs only, and approximately 27% had no fractures. The ratio of steady-state levels of the mRNA from the transgene to the level of mRNA from the endogenous gene was the same in all transgenic embryos. The results demonstrated that the phenotypic variability and incomplete penetrance were not explained by variations in genetic background or levels in gene expression. Instead, they suggested that phenotypic variation is an inherent feature of expression of a mutated collagen gene.

Animals↗
PubMed1994

[Identification of the corn mosaic virus, a rhabdovirus, in Costa Rica].

Maize mosaic virus (MMV), a rhabdovirus, was identified associated to maize field plants, showing stunting and continuous chlorotic stripes uniformly distributed over the leaf blade. The virus was detected in field samples by agar-gel immunodifussion. Enveloped, bacilliform virus particles were observed by electron microscopy in thin sections of naturally infected leaf tissue.

Costa Rica↗
PubMed1993

Mutations in type 1 procollagen that cause osteogenesis imperfecta: effects of the mutations on the assembly of collagen into fibrils, the basis of phenotypic variations, and potential antisense therapies.

Work by a large number of investigators over the last decade has established that over 90% of patients with osteogenesis imperfecta have mutations in one of the two genes for type I procollagen, that most unrelated probands have different mutations in the genes, and that the mutations found in most of the serious variants of the disease cause synthesis of abnormal pro alpha chains of the protein. The results have demonstrated that synthesis of structurally abnormal but partially functional pro alpha chains can interfere with folding of the central region of the protein into a triple-helical conformation, prevent processing of the N-terminal propeptides of procollagen, or produce subtle alterations in conformation that interfere with the self-assembly of the protein into collagen fibrils. One of the unsolved mysteries about the disease is why some mutations produce severe phenotypes, whereas very similar mutations produce mild phenotypes. Recent studies in transgenic mice suggest that nongenetic factors, such as stochastic events during development, may determine the severity of the disease phenotype produced by a specific mutation. Also, recent results raised the possibility that strategies of antisense gene therapy may be effective in treating the disease some time in the future. Specific inhibition of expression of a mutated collagen gene has been obtained with antisense oligonucleotides in cell culture experiments. However, there is no means of selective delivery of antisense oligonucleotides to the appropriate tissues.

Cells, Cultured↗
PubMed1993

Comparative light and electron microscopic analyses of tenuivirus major noncapsid protein (NCP) inclusion bodies in infected plants, and of the NCP in vitro.

Tenuivirus infections are associated with the formation of abundant inclusion bodies and with the accumulation of large quantities of a viral noncapsid protein (NCP) in infected plants. Examination of maize stripe virus and rice hoja blanca virus-infected plant tissues using light, immunofluorescent, and electron microscopy showed that the inclusion bodies induced by the two viruses were very similar. Light microscopy revealed that both induced arrays of ring-like, figure-eight-like, and amorphous inclusions, frequently with a substructure of needle-shaped crystals. Immunofluorescent staining showed that all types of inclusion bodies contained the viral NCP but not the viral N protein, associated to the viral RNA. Electron microscopy revealed abundant amorphous semi-electron-opaque inclusion bodies; these had a fibrillar appearance but also occurred as compact, more electron-dense structures. Filamentous electron-opaque inclusion bodies were also detected. Immunogold labeling of ultrathin sections confirmed that all inclusion bodies included NCP and that none included viral N protein. Examination of purified NCP showed that it can form similar amorphous and crystalline arrays in vitro to the inclusion bodies observed in vivo. We propose that the common presence of NCP in all inclusion bodies implies the existence of a single type of intracellular inclusion body, the different developmental stages of which have previously been considered to be distinct inclusion bodies.

Inclusion Bodies, Viral↗
PubMed1993

Transgenic mice expressing a partially deleted gene for type I procollagen (COL1A1). A breeding line with a phenotype of spontaneous fractures and decreased bone collagen and mineral.

A line of transgenic mice was prepared that expressed moderate levels of an internally deleted human gene for the pro alpha 1(I) chain of type I procollagen. The gene construct was modeled after a sporadic in-frame deletion of the human gene that produced a lethal variant of osteogenesis imperfecta by causing biosynthesis of shortened pro alpha 1(I) chains. 89 transgenic mice from the line were examined. About 6% had a lethal phenotype with extensive fractures at birth, and 33% had fractures but were viable. The remaining 61% of the transgenic mice had no apparent fractures as assessed by x ray examination on the day of birth. Brother-sister matings produced eight litters in which approximately 40% of the mice had the lethal phenotype, an observation indicating that expression of the exogenous gene was more lethal in putative homozygous mice from the line. Examination of femurs from the transgenic mice indicated that the bones were significantly shorter in length and had a decrease in wet weight, mineral content, and collagen content. However, there was no statistically significant change in the mineral to collagen ratio. Biomechanical measurements on femurs from the mice at 6 wk indicated a decrease in force and energy to failure. There was also a decrease in strain to failure and an increase in Young's modulus of elasticity, observations indicating increased brittleness of bone matrix. The results suggested that the transgenic mice may be an appropriate model for testing potential therapies for osteogenesis imperfecta. They may also be a useful model for studying osteoporosis.

Animals↗
PubMed1993

An inbred line of transgenic mice expressing an internally deleted gene for type II procollagen (COL2A1). Young mice have a variable phenotype of a chondrodysplasia and older mice have osteoarthritic changes in joints.

Studies were carried out on a line of transgenic mice that expressed an internally deleted COL2A1 gene and developed a phenotype resembling human chondrodysplasias (Vandenberg et al. 1991. Proc. Natl. Acad. Sci. USA. 88:7640-7644. Marked differences in phenotype were observed with propagation of the mutated gene in an inbred strain of mice in that approximately 15% of the transgenic mice had a cleft palate and a lethal phenotype, whereas the remaining mice were difficult to distinguish from normal littermates. 1-d- and 3-mo-old transgenic mice that were viable showed microscopic signs of chondrodysplasia with reduced amounts of collagen fibrils in the cartilage matrix, dilatation of the rough surfaced endoplasmic reticulum in the chondrocytes, and decrease of optical path difference in polarized light microscopy. The transgenic mice also showed signs of disturbed growth as evidenced by lower body weight, lower length and weight of the femur, decreased bone collagen, decreased bone mineral, and decreased resistance of bone to breakage. Comparisons of mice ranging in age from 1 d to 15 mo demonstrated that there was decreasing evidence of a chondrodysplasia as the mice grew older. Instead, the most striking feature in the 15-mo-old mice were degenerative changes of articular cartilage similar to osteoarthritis.

Aging↗
PubMed1992

In situ immunogold labeling analysis of the rice hoja blanca virus nucleoprotein and major noncapsid protein.

Ribonucleoprotein particles (RNPs) of rice hoja blanca virus (RHBV) were purified and used for electron microscopic analysis and antibody production. Antibodies made to RNPs specifically decorated purified RNPs. The RNPs typically showed characteristic tenuivirus morphologies. They were approximately 8 nm in diameter, mostly circular in nature, and exhibited branching and a high degree of superhelicity. When the RNP antibodies were used for in situ immunogold labeling analysis of RHBV-infected tissues, no specific structures were identified, but gold particles were distributed throughout the cytosol of RHBV-infected but not healthy plants. However, amorphous semi-electron opaque inclusion bodies (ASO-IBs) were abundant in cells of RHBV-infected plants. While the ASO-IBs were not labeled with the anti-RNP antiserum, they were specifically labeled with antibodies to the RHBV major noncapsid protein (NCP) and with antibodies to the NCP of another tenuivirus, maize stripe virus.

Gold↗
PubMed1992

[Prevalence of extracranial carotid occlusive disease. Non-invasive study].

Cerebrovascular disease is the most important cause of mortality and morbility in some European Countries, but the prevalence of carotid occlusive disease has not been adequately assessed. From 1985 to 1987, 1,143 patients were consecutively evaluated in the Vascular Laboratory in order to determine the presence of extracranial carotid occlusive disease. 638 (55.8%) were males and 505 (44.2%) females and mean age was 58 years (16-87). 509 had previously focal brain ischemia, ocular and/or hemispheric (Group I), 78 had assymptomatic cervical bruit (Group II), 55 non-hemispheric neurologic dysfunction (Group III) and 501 had atypical symptoms for cerebrovascular disease (Group IV). Diagnostic criteria for carotid disease: were peak frequency greater than 4.0 KHz; spectral broadening greater than 40% and late sysstolic turbulence. Global prevalence of carotid disease was 31.8% and the results in each group were: Gr. I-37.2%; Gr. II-57.7%; Gr. III-43.6%; Gr. IV-21.2%. 49% of the patients had hypertension, 22.8% dyslipidemia, 22.4% evidence of coronary disease and 13.6% had diabetes. Hypertension, diabetes, coronary disease and the coexistence of two risk factors were significantly more prevalent in the group of patients with carotid disease. These results confirm a high prevalence of carotid disease in this population, which is comparable to the one is northern european populations.

Adolescent↗
PubMed1989

[Mitral valve prolapse as a probable cause of cerebral ischemia. A case report].

A 32 year old female patient, documented clinically and echocardiographically to have a competent prolapse of the mitral valve (MVP), developed a sudden ischemic cerebrovascular accident (CVA), suggestive of embolism. There were no predisposing factors to cerebrovascular disease, except for past use of contraceptive pills. Tomographic study disclosed an ischemic right-parietal "wedge-shaped" defect. The patients's recovery, with physiotherapy and AAS, was satisfactory. The authors discuss the association of MVP and CVA, considering physiopathogenic, prophylactic and therapeutic aspects, emphasizing the need to consider MVP as a cause of CVA in young adults.

Adult↗
PubMed1987

The complete nucleotide sequence of the ilvGMEDA operon of Escherichia coli K-12.

In this report we present the complete nucleotide sequence of the ilvGMEDA operon of Escherichia coli. This operon contains five genes encoding four of the five enzymes required for the biosynthesis of isoleucine and valine. We identify and describe the coding regions for these five structural genes and the structural and functional features of the flanking and internal regulatory regions of this operon. This new information contributes to a more complete understanding of the overall control of the biosynthesis of isoleucine and valine.

Amino Acid Sequence↗
PubMed1987

Phospholipid and fatty acid changes produced by cholecalciferol on intestinal mitochondrial membranes.

Cholecalciferol administration to vitamin D-deficient chicks produces, 24 h after treatment, a specific increase of the phosphatidylcholine content in the intestinal mitochondrial inner membrane plus matrix fraction without changes in its proportion in the outer membrane. The ratio of unsaturated/saturated fatty acids in the outer membrane phosphatidylcholine was increased by that treatment. The inner membrane plus matrix presents a decrease of 16:1 in phosphatidylethanolamine and 18:0 in the phosphatidylcholine fraction. Cardiolipin shows the largest change in the ratio of unsaturated/saturated fatty acids predominantly by an increase in the linoleic acid. The present data suggest that phosphatidylcholine and fatty acids modifications in both mitochondrial subfractions caused by vitamin D3 might have some role in the intestinal mitochondrial Ca transport.

Animals↗