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A Rivera

Publications and source records attributed to A Rivera.

At least 19 recordsLinked to original sources
PubMed2002

Cation mass dependence of the nearly constant dielectric loss in alkali triborate glasses.

Electrical ac conductivity measurements on alkali triborate glasses ( M2O x 3B2O3, M = Li, Na, K, and Rb) were performed at temperatures down to 8 K and frequencies up to 1 GHz. All samples show a nearly constant dielectric loss (NCL), at the limit of high frequencies and/or low temperatures. The magnitude of the NCL is found to decrease as m(-1/3) with increasing alkali ion mass m. This quantitative result for the NCL, closely related to the mean-square displacement of ions, indicates that the origin of the NCL might be related to vibrational relaxation of the ions in the anharmonic potentials that cage them, and the cage is decaying very slowly with time.

Journal Article↗
PubMed2002

Nystagmus surgery.

Explore the source record for details and available documents.

Head Movements↗
PubMed2001

The consequences of chromosomal aneuploidy on gene expression profiles in a cell line model for prostate carcinogenesis.

Here we report the genetic characterization of immortalized prostate epithelial cells before and after conversion to tumorigenicity using molecular cytogenetics and microarray technology. We were particularly interested to analyze the consequences of acquired chromosomal aneuploidies with respect to modifications of gene expression profiles. Compared with nontumorigenic but immortalized prostate epithelium, prostate tumor cell lines showed high levels of chromosomal rearrangements that led to gains of 1p, 5, 11q, 12p, 16q, and 20q and losses of 1pter, 11p, 17, 20p, 21, 22, and Y. Of 5700 unique targets on a 6.5K cDNA microarray, approximately 3% were subject to modification in expression levels; these included GRO-1, -2, IAP-1,- 2, MMP-9, and cyclin D1, which showed increased expression, and TRAIL, BRCA1, and CTNNA, which showed decreased expression. Thirty % of expression changes occurred in regions the genomic copy number of which remained balanced. Of the remainder, 42% of down-regulated and 51% of up-regulated genes mapped to regions present in decreased or increased genomic copy numbers, respectively. A relative gain or loss of a chromosome or chromosomal arm usually resulted in a statistically significant increase or decrease, respectively, in the average expression level of all of the genes on the chromosome. However, of these genes, very few (e.g., 5 of 101 genes on chromosome 11q), and in some instances only two genes (MMP-9 and PROCR on chromosome 20q), were overexpressed by > or =1.7-fold when scored individually. Cluster analysis by gene function suggests that prostate tumorigenesis in these cell line models involves alterations in gene expression that may favor invasion, prevent apoptosis, and promote growth.

Aneuploidy↗
PubMed2001

A1 adenosine receptor activation inhibits neurite process formation by Rho kinase-mediated pathways.

A1 adenosine receptors (A1ARs) are expressed in the brain during critical periods of neurogenesis and neuronal differentiation. To examine influences of A1AR activation on neuronal development we studied the effects of A1AR activation on process growth in PC12 cells expressing A1ARs and in primary cultures of cortical and hippocampal neurons. In PC12 cells, we found that A1AR activation potently inhibited nerve growth factor (NGF)-induced neurite growth and induced stress fiber formation. A1ARs action was not mediated by inhibition of p44/42 MAP kinase activity, as inhibition of MEK/MAP kinase had no effects on A1AR action. When Rho kinase activity was blocked, A1AR agonists no longer inhibited neurite growth and stress fiber formation was blocked. In neurons, A1AR activation also inhibited process growth, and A1AR action was also mediated by Rho kinase. These data show that A1AR activation inhibits neurite growth and that the inhibitory effects of A1AR are dependent on Rho kinase.

Animals↗
PubMed2001

A gene therapy approach for treating T-cell-mediated autoimmune diseases.

Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease of the central nervous system (CNS) that serves as a model for multiple sclerosis (MS) in humans. In mice, EAE is mediated by Th1 type CD4(+) T cells specific for various myelin proteins which migrate from the periphery to the CNS. Removal or blocking of CD4(+) cells before or shortly after disease induction was shown to prevent disease onset and/or disease progression but also results in general immune suppression. Most treatment regimens for autoimmune diseases currently rely on general suppression of the T-cell compartment most commonly by steroids. In this paper, an experimental, gene therapy-based model is presented in which susceptible mice are made resistant to EAE induction by specifically down-regulating an autoreactive T-cell population. By using a retroviral gene transfer protocol, normal B cells were genetically modified to constitutively express the SJL-specific proteolipid (PLP) encephalitogenic determinant and then adoptively transferred into syngeneic hosts. To ensure appropriate presentation of the exogenous encephalitogenic peptide in association with MHC class II, the encephalitogenic sequence was fused to a lysosomal targeting sequence. Adoptive transfer of syngeneic B cells expressing the PLP encephalitogenic determinant into normal, naive, genetically susceptible mice induced PLP-specific unresponsiveness and completely protected the majority (62% and 83% using an intermediate and a high titer retroviral vector, respectively) of the animals from EAE induction. The remaining animals had a delayed disease onset and/or lower disease severity. All protected mice expressed the exogenous gene in the spleen as detected by reverse transcriptase-polymerase chain reaction.

Adoptive Transfer↗
PubMed2001

Origin of constant loss in ionic conductors.

We have analyzed the constant loss contribution to the ac conductivity in the frequency range 10 Hz-1 MHz and temperatures down to 8 K, for two Li ionic conductors, one crystalline (Li(0.18)La(0.61)TiO(3)) and the other glassy (61SiO(2);35Li(2)O.3Al(2)O3.P(2)O(5)). As temperature is increased a crossover is observed from a nearly constant loss to a fractional power law frequency dependence of the ac conductivity. At any fixed frequency omega, this crossover occurs at a temperature T such that omega approximately nu(0)exp(-E(m)/k(B)T), where nu(0) is the attempt frequency and E(m) is identified with the barrier for Li+ ions to leave their wells.

Journal Article↗
PubMed2001

[Prevalence of antiphospholipid syndrome in patients under 65 years of age with acute myocardial infarction].

BACKGROUND: The antiphospholipid antibody syndrome (AAS), which is characterized by thromboembolic events and/or fetal loss and/or low platelet count associated with antiphospholipid antibodies, may evolve with acute myocardial infarction (AMI). The presence of AAS among young patients with AMI ranges from 14% to 21%, and this condition implies specific therapeutic attitudes as new thrombotic events may occur, according to some authors. MATERIALS AND METHODS: A prospective study was undertaken with 25 patients aged > or = 65 years with AMI that were admitted to our institution during one year who were compared with control patients with similar risk factors. IgG and IgM anticardiolipin antibodies (ACA) were measured in the first 24 hours since the onset of AMI symptoms and three months later. RESULTS: The follow-up ranged from three months to one year. Among patients, ACA positivity in the two measurements was higher (12%) than that observed in the control group (5%) (p = 0.36). ACA positivity on two occasions was not a risk factor for new thrombotic events. CONCLUSION: ACA positivity is higher among AMI patients (measured early and at three months) than among the general population although the presence of such antibodies does not increase the risk for new post-infarction thrombotic events.

Adult↗
PubMed2001

Cacalolides from Senecio madagascariensis.

14-Isovaleryloxy-O-methyl-1,2-dehydrocacalol (1) and cycloart-23-ene-3,25-diol, beta-sitosterol, and stigmasterol, along with five new cacalolides, 1-hydroxy-2-methoxy-1,2,3,4-dehydro-6-dehydroxycacalone (2), 1-hydroxy-2-methoxy-1,2,3,4-dehydrocacalone (3), 1,2-dimethoxy-1,2,3,4-dehydro-6-dehydroxycacalone (4), 1,2-dimethoxy-1,2,3,4-dehydrocacalone (5), and 2-methoxy-O-methyl-1-oxo-2,3-dehydrocacalol (6), were isolated from Senecio madagascariensis collected from Colombia. The structures of the new compounds were determined using one- and two-dimensional NMR techniques. In addition, the structure of 2 was corroborated by derivatizations and single-crystal X-ray diffraction studies.

Asteraceae↗
PubMed2001

Role of B cells as antigen-presenting cells in vivo revisited: antigen-specific B cells are essential for T cell expansion in lymph nodes and for systemic T cell responses to low antigen concentrations.

Studies in B cell-deficient mice generated by continuous injection of anti-mu antibodies (muSM) showed that T cell priming in lymph nodes was dependent on antigen presentation by B cells. This concept has recently become controversial since a wide range, from complete deficiency to near normal T cell responses, was reported in studies carried out with B cell-deficient mice generated by gene disruption (muMT). In this study we show that in the absence of B cells, T cell responses are greatly reduced in all the available muMT mouse strains although responses in muMT of the C57BL/6 background (which were used for most studies with muMT) were much more variable and could reach up to 42% of control. In contrast, T cell responses in muMT --> F(1) bone marrow chimeras which have the same phenotype as muMT were totally impaired, suggesting a principle difference between mice developing without B cells (muMT mice) and muSM which are made B cell deficient only after birth. Normal T cell priming was completely restored by reconstitution of muMT and muMT --> F(1) mice with syngeneic B cells. Interestingly, only B cell populations containing antigen-specific B cells were capable of reconstituting T cell responses. Monoclonal B cells taken from Ig transgenic mice could not reconstitute responses to an irrelevant antigen. We also found that B cells were also required for systemic T cell priming when antigen concentrations were limiting but were not required for priming (for T cell help) when mice were immunized with a high antigen dose.

Adoptive Transfer↗
PubMed2000

A comprehensive survey of sequence variation in the ABCA4 (ABCR) gene in Stargardt disease and age-related macular degeneration.

Stargardt disease (STGD) is a common autosomal recessive maculopathy of early and young-adult onset and is caused by alterations in the gene encoding the photoreceptor-specific ATP-binding cassette (ABC) transporter (ABCA4). We have studied 144 patients with STGD and 220 unaffected individuals ascertained from the German population, to complete a comprehensive, population-specific survey of the sequence variation in the ABCA4 gene. In addition, we have assessed the proposed role for ABCA4 in age-related macular degeneration (AMD), a common cause of late-onset blindness, by studying 200 affected individuals with late-stage disease. Using a screening strategy based primarily on denaturing gradient gel electrophoresis, we have identified in the three study groups a total of 127 unique alterations, of which 90 have not been previously reported, and have classified 72 as probable pathogenic mutations. Of the 288 STGD chromosomes studied, mutations were identified in 166, resulting in a detection rate of approximately 58%. Eight different alleles account for 61% of the identified disease alleles, and at least one of these, the L541P-A1038V complex allele, appears to be a founder mutation in the German population. When the group with AMD and the control group were analyzed with the same methodology, 18 patients with AMD and 12 controls were found to harbor possible disease-associated alterations. This represents no significant difference between the two groups; however, for detection of modest effects of rare alleles in complex diseases, the analysis of larger cohorts of patients may be required.

ATP-Binding Cassette Transporters↗
PubMed2000

Pancreatic homeodomain transcription factor IDX1/IPF1 expressed in developing brain regulates somatostatin gene transcription in embryonic neural cells.

Hox-like homeodomain proteins play a critical role during embryonic development by regulating the transcription of genes that are important for the generation of specific organs or cell types. The homeodomain transcription factor IDX1/IPF1, the expression of which was thought until recently to be restricted to the pancreas and foregut, is required for pancreas development and for the expression of genes controlling glucose homeostasis. We report that IDX1/IPF1 is also expressed in embryonic rat brain at a time coincident with active neurogenesis. Electrophoretic mobility shift assays with nuclear extracts of embryonic brains indicated that IDX1/IPF1 binds to two somatostatin promoter elements, SMS-UE-B and the recently discovered SMS-TAAT3. The requirement of these elements for IDX1/IPF1 transactivation of the somatostatin gene in neural cells was confirmed in transfection studies using embryonic cerebral cortex-derived RC2.E10 cells. Immunohistochemical staining of rat embryos showed IDX1/IPF1-positive cells located near the ventricular surface in germinative areas of the developing central nervous system. Cellular colocalization of IDX1/IPF1 and somatostatin was found in several areas of the developing brain, including cortex, ganglionic eminence, hypothalamus, and inferior colliculus. These results support the notion that IDX1/IPF1 regulates gene expression during development of the central nervous system independent of its role on pancreas development and function.

Animals↗
PubMed2000

Fine-needle aspiration of cytomegalovirus sialadenitis in a patient with acquired immunodeficiency syndrome: pitfalls of diff-quik staining.

A case of cytomegalovirus (CMV) sialadenitis in a patient with acquired immunodeficiency syndrome (AIDS) diagnosed by fine-needle aspiration biopsy (FNAB) is reported. Although a diagnosis of CMV sialadenitis can be established on Diff-Quik-stained slides, the characteristic viral changes are the best appreciated on slides stained by the Papanicolaou (Pap) technique. Differential pitfalls are discussed. It needs to be stressed that clinically unsuspected diagnosis of CMV infection may uncover congenital or acquired defects of cellular immunity, and particularly AIDS. Diagn. Cytopathol. 2000;22:101-103.

AIDS-Related Opportunistic Infections↗
PubMed2000

Phase I clinical trial of a recombinant canarypoxvirus (ALVAC) vaccine expressing human carcinoembryonic antigen and the B7.1 co-stimulatory molecule.

The generation of cytotoxic effector T cells requires delivery of two signals, one derived from a specific antigenic epitope and one from a costimulatory molecule. A phase I clinical trial was conducted with a non-replicating canarypoxvirus (ALVAC) constructed to express both human carcinoembryonic antigen (CEA) and the B7.1 costimulatory molecule. This was the first study in cancer patients to determine if the delivery of costimulation with a tumor vaccine was feasible and improved immune responses. Three cohorts of six patients, each with advanced CEA-expressing adenocarcinomas, were treated with increasing doses of an ALVAC-CEA-B7.1 vaccine (4.5 x 10(6), 4.5 x 10(7), and 4.5 x 10(8) plaque-forming units, PFU). Patients were vaccinated by intramuscular injection every 4 weeks for 3 months and monitored for side-effects, tumor growth and anti-CEA immune responses. ALVAC-CEA-B7.1 at doses up to 4.5 x 10(8) PFU was given without evidence of significant toxicity or autoimmune reactions. Three patients experienced clinically stable disease that correlated with increasing CEA-specific precursor T cells, as shown by in vitro interferon-gamma enzyme-linked immunoassay spot tests (ELISPOT). These three patients underwent repeated vaccination resulting in augmented CEA-specific T cell responses. This study represents the first use of costimulation to enhance antitumor vaccines in cancer patients. This approach resulted in CEA-specific immunity associated with stable diseases in three patients. This study also demonstrated that CEA-specific T cell responses could be sustained by repeated vaccinations. Although the number of patients was small, the addition of B7.1 to virus-based vaccines may improve immunological and stable diseases to vaccination against tumor-associated antigens with tolerable toxicity.

Adenocarcinoma↗
PubMed2000

Dopamine D5 receptors of rat and human brain.

In contrast to dopamine D1 receptors, the anatomical distribution of D5 receptors in the CNS is poorly described. Therefore, we have studied the localization of dopamine D5 receptors in the brain of rat and human using our newly prepared subtype-specific antibody. Western blot analysis of brain tissues and membranes of cDNA transfected cells, and immunoprecipitation of brain dopamine receptors suggest that this antibody is highly selective for native dopamine D5 receptors. The D5 antibody labeled dopaminergic neurons of mesencephalon, and cortical and subcortical structures. In neostriatum, the D5 receptors were localized in the medium spiny neurons and large cholinergic interneurons. The D5 labeling in caudate nucleus was predominantly in spines of the projection neurons that were frequently making asymmetric synapses. Occasionally, the D5 receptors were also found at the symmetric synapses. Within the cerebral cortex and hippocampus, D5 antibody labeling was prominent in the pyramidal cells and their dendrites. Dopamine D5 receptors were also prominent in the cerebellum, where dopamine innervation is known to be very modest. Differences in the localization of D5 receptors between both species were generally indistinguishable except in hippocampus. In rat, the hippocampal D5 receptor was concentrated in the cell body, whereas in human it was also associated with dendrites. These results show that D5 receptors are localized in the substantia nigra-pars compacta, hypothalamus, striatum, cerebral cortex, nucleus accumbens and olfactory tubercle. Furthermore, the presence of D5 receptors in the areas of dopamine pathways suggests that this receptor may participate actively in dopaminergic neurotransmission.

Animals↗
PubMed2000

Mutations in the VMD2 gene are associated with juvenile-onset vitelliform macular dystrophy (Best disease) and adult vitelliform macular dystrophy but not age-related macular degeneration.

Recently, the VMD2 gene has been identified as the causative gene in juvenile-onset vitelliform macular dystrophy (Best disease), a central retinopathy primarily characterised by an impaired function of the retinal pigment epithelium. In this study we have further characterised the spectrum of VMD2 mutations in a series of 41 unrelated Best disease patients. Furthermore we expanded our analysis to include 32 unrelated patients with adult vitelliform macular dystrophy (AVMD) and 200 patients with age-related macular degeneration (AMD). Both AVMD and AMD share some phenotypic features with Best disease such as abnormal subretinal accumulation of lipofuscin material, progressive geographic atrophy and choroidal neovascularisation, and may be the consequence of a common pathogenic mechanism. In total, we have identified 23 distinct disease-associated mutations in Best disease and four different mutations in AVMD. Two of the mutations found in the AVMD patients were also seen in Best disease suggesting a considerable overlap in the aetiology of these two disorders. There were no mutations found in the AMD group. In addition, four frequent intragenic polymorphisms did not reveal allelic association of the VMD2 locus with AMD. These data exclude a direct role of VMD2 in the predisposition to AMD.

Adolescent↗
PubMed2000

SB-253514 and analogues: novel inhibitors of lipoprotein associated phospholipase A2 produced by Pseudomonas fluorescens DSM 11579. II. Physico-chemical properties and structure elucidation.

A series of novel inhibitors of lipoprotein associated phospholipase A2 were isolated from the culture broths of Pseudomonas fluorescens strain DSM11579. The inhibitors fall into two structurally isomeric classes each of which comprise compounds incorporating glycosylated hydrocarbon chains. The structure elucidation for the major member of each structural class is reported. The crystal structure of a non-glycosylated analogue of the 5,5-series, produced through biotransformation, is also reported.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗