PubMed Health⌕ Search

Biomedical subjects

J A Del Rio

Publications and source records attributed to J A Del Rio.

15 recordsLinked to original sources

Duplicate publication and 'paper inflation' in the Fractals literature.

The similarity of documents in a large database of published Fractals articles was examined for redundancy. Three different text matching techniques were used on published Abstracts to identify redundancy candidates, and predictions were verified by reading full text versions of the redundancy candidate articles. A small fraction of the total articles in the database was judged to be redundant. This was viewed as a lower limit, because it excluded cases where the concepts remained the same, but the text was altered substantially. Far more pervasive than redundant publications were publications that did not violate the letter of redundancy but rather violated the spirit of redundancy. There appeared to be widespread publication maximization strategies. Studies that resulted in one comprehensive paper decades ago now result in multiple papers that focus on one major problem, but are differentiated by parameter ranges, or other stratifying variables. This 'paper inflation' is due in large part to the increasing use of metrics (publications, patents, citations, etc) to evaluate research performance, and the researchers' motivation to maximize the metrics.

Algorithms↗

Chipping away at complex behavior: transcriptome/phenotype correlations in the mouse brain.

Highly parallel gene expression profiling has the potential to provide new insight into the molecular mechanisms of complex brain diseases and behavioral traits. We review how gene expression profiling in various brain regions of inbred mouse strains has been used to identify genes that may contribute to strain-specific phenotypes. New data, which demonstrate the use of gene expression profiling in combination with behavioral testing to identify candidate genes involved in mediating variation in running wheel activity, are also presented. These and other studies suggest that a combination of gene expression profiling and more traditional genetic approaches, such as quantitative trait locus analysis, can be used to identify genes responsible for specific neurobehavioral phenotypes.

Animals↗

Regional and strain-specific gene expression mapping in the adult mouse brain.

To determine the genetic causes and molecular mechanisms responsible for neurobehavioral differences in mice, we used highly parallel gene expression profiling to detect genes that are differentially expressed between the 129SvEv and C57BL/6 mouse strains at baseline and in response to seizure. In addition, we identified genes that are differentially expressed in specific brain regions. We found that approximately 1% of expressed genes are differentially expressed between strains in at least one region of the brain and that the gene expression response to seizure is significantly different between the two inbred strains. The results lead to the identification of differences in gene expression that may account for distinct phenotypes in inbred strains and the unique functions of specific brain regions.

Animals↗

Antioxidant activity and radioprotective effects against chromosomal damage induced in vivo by X-rays of flavan-3-ols (Procyanidins) from grape seeds (Vitis vinifera): comparative study versus other phenolic and organic compounds.

The quantitative distribution of several flavan-3-ols was determined using HPLC in a grape (Vitis vinifera) seed extract (GSE) of four cultivars grown in the region of Murcia. Polymer >/= C(4) units made up the largest group of procyanidins in the GSE (90.92%, expressed as HPLC % area). The antioxidant activity of GSE and other reference compounds was investigated by measuring their ability to scavenge the ABTS(*)(+) radical cation (TEAC). The most effective compounds were, in order: GSE > rutin > (+)-catechin > diosmin >/= ascorbic acid. The radioprotective effects of GSE and other reference compounds were determined by using the micronucleus test for anticlastogenic activity, any reduction of the frequency of micronucleated polychromatic erythrocytes (MnPCEs) being evaluated in the bone marrow of mouse exposed to X-rays. The most effective compounds were, in order: GSE > rutin > dimethyl sulfoxide (DMSO) > ascorbic acid > 6-n-propyl-2-thiouracil-6c (PTU) > diosmin. The higher ABTS(*)(+) scavenging capacity and anticlastogenic activity of GSE can be explained, structurally, by the high number of conjugated structures between the catechol groups in the B-rings and the 3-OH free groups of the polymeric polyphenolic skeleton and, in addition, by the stability of the aroxyl flavonoid radical generated in the above processes.

Animals↗

Semaphorins III and IV repel hippocampal axons via two distinct receptors.

The semaphorins are the largest family of repulsive axon guidance molecules. Secreted semaphorins bind neuropilin receptors and repel sensory, sympathetic and motor axons. Here we show that CA1, CA3 and dentate gyrus axons from E15-E17 mouse embryo explants are selectively repelled by entorhinal cortex and neocortex. The secreted semaphorins Sema III and Sema IV and their receptors Neuropilin-1 and -2 are expressed in the hippocampal formation during appropriate stages. Sema III and Sema IV strongly repel CA1, CA3 and dentate gyrus axons; entorhinal axons are only repelled by Sema III. An antibody against Neuropilin-1 blocks the repulsive action of Sema III and the entorhinal cortex, but has no effect on Sema IV-induced repulsion. Thus, chemorepulsion plays a role in axon guidance in the hippocampus, secreted semaphorins are likely to be responsible for this action, and the same axons can be repelled by two distinct semaphorins via two different receptors.

Animals↗

Ethanol in utero induces epithelial cell damage and altered kinetics in the developing rat intestine.

The effect of prenatal ethanol exposure on the intestinal maturation of rat fetuses was investigated to understand the nutritional alterations found in the offspring of alcoholic mothers. Female Wistar rats were maintained on solid diet and 25% ethanol solution as drinking fluid during pregnancy, and non-alcoholic isocaloric pregnant mothers were used as controls. At birth, intestines from unsuckled pups were removed for study. The weight and length of the intestine decreased significantly when ethanol was present in utero. Ultrastructural evaluation of the epithelium revealed loss of contact between neighboring enterocytes and abnormal dilation of the cisternae of the Golgi apparatus in ethanol-exposed pups. Further, increased lysosome-like vesiculation and enhanced lysosomal beta-galactosidase activity was observed in these neonates. The total number of absorptive enterocytes in the epithelium was reduced by 30% in ethanol-exposed neonates as compared to controls, due to altered cell growth and death during fetal life. Ethanol in utero stimulated epithelial cell migration which compensated cell loss, as demonstrated by 5'-Bromodeoxyuridine labeling. These findings could have important implications for the assimilation of nutrients and failure to thrive in infants with fetal alcohol syndrome.

Animals↗

Transient colocalization of parvalbumin and calbindin D28k in the postnatal cerebral cortex: evidence for a phenotypic shift in developing nonpyramidal neurons.

In the adult rat cerebral cortex the calcium-binding proteins parvalbumin and calbindin D28k are present in essentially non-overlapping populations of GABAergic interneurons. These proteins follow different developmental patterns in the cortex: calbindin D28k-immunoreactive nonpyramidal neurons are abundant until the second postnatal week and decrease markedly thereafter; it is at this time that parvalbumin immunoreactivity develops in cortical nonpyramidal neurons. To determine whether parvalbumin-immunoreactive neurons derive from calbindin D38k positive cells we used double-immunofluorescence studies for both calcium-binding proteins, together with combined immunocytochemistry for calbindin D28k and in situ hybridization for parvalbumin mRNA during postnatal development. Double-labelled cells were found in all cortical layers between P9 and P21, coinciding with the onset of parvalbumin expression. The percentage of colocalization of the two calcium-binding proteins depended on the age and layer examined. Colocalization reached a peak (80-100%) during the second postnatal week. Double-labelled neurons were rare in layer V at all ages studied. The present results indicate a phenotypic shift during the development of some cortical interneurons that halts the expression of calbindin D28k while parvalbumin expression starts. These findings agree with lineage analyses reporting that different types of nonpyramidal neuron arise from a common progenitor.

Animals↗

Effects of short term exposure to 60 Hz electromagnetic fields on interleukin 1 and interleukin 6 production by peritoneal exudate cells.

The relationship between exposure to electromagnetic fields (EMF) and human health is of increasing interest. Exposure to EMF has been linked to leukemia and brain tumors in some but not all epidemiological studies. The effects of separate and combined alternating electric and magnetic fields on interleukin 1 (IL-1) and interleukin 6 (IL-6) production were measured in this study. Helmholtz coils and parallel plate electrodes were used to create uniform field characteristics (300 V/in., 0.3 mT). Effects were studied at a combined field frequency of 60 Hz. This frequency did not elevate culture temperatures above ambient room temperature. Murine thioglycollate-elicited peritoneal exudate cells (PEC) were exposed to an electric field (E), magnetic field (M), combined electric and magnetic field (EM), or no field (control). Three samples of PEC from each mouse were cultured with lipopolysaccharide in each field. Using commercial ELISA kits, supernatants of cell cultures were tested in duplicate after 24 hours of exposure for IL-1 alpha levels and after 48 hours of exposure for IL-6 levels. Results were evaluated using one-way analysis of variance (ANOVA). As a group, IL-1 production by the PEC from five mice and IL-6 production by the PEC from nine mice were unaffected by electric, magnetic, or combined electric and magnetic fields. Results from these experiments indicate that the 24-hour exposure to 60 Hz electric, magnetic, or combined electromagnetic fields had no effect on IL-1 production. Forty-eight hours of exposure to the same fields did not affect IL-6 production.

Analysis of Variance↗

Gonadal hormones down-regulate reactive gliosis and astrocyte proliferation after a penetrating brain injury.

Astrocytes are a target for gonadal steroids in the normal brain. The putative modulation by gonadal hormones of the astrocytic reaction to brain injury was assessed in this study. Male and female adult Wistar albino rats were gonadectomized and, one month later, their brains were lesioned by a longitudinal incision crossing the parietal cerebral cortex, the CA1 field of the dorsal hippocampus and the dentate gyrus. Males were injected either with testosterone (20 micrograms/rat) or vehicle immediately after surgery. Females were injected either with 17 beta estradiol (250 micrograms/rat), progesterone (500 micrograms/rat) or vehicle. Hormonal injections were repeated 24 and 48 h after brain injury. All animals received injections of 5'-bromodeoxyuridine (BrdU) to label proliferating cells. Histological sections from the brain of animals killed 72 h after surgery were used for the double immunohistochemical localization of BrdU and glial fibrillary acidic protein (GFAP). The number of GFAP-immunoreactive astrocytes and the number of double labelled astrocytes (GFAP + BrdU) were recorded as a function of the distance to the lesion site in the parietal cerebral cortex, the CA1 field of the hippocampus and the dentate gyrus. Testosterone, estradiol and progesterone treatments resulted in a significant decrease in the number of GFAP-immunolabeled reactive astrocytes in the vicinity of the wound. The number of double labelled cells and the labelling index (proportion of GFAP-immunoreactive astrocytes labelled with BrdU) varied according to the cerebral area, the distance to the wound and the sex of the animals, and were significantly decreased by gonadal steroids in all the areas examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Development of GABA-immunoreactivity in the neocortex of the mouse.

The prenatal and postnatal development of GABAergic elements in the neocortex of the mouse was analyzed by GABA-immunocytochemistry. Radial distribution of cells and laminar numerical densities were calculated at each developmental stage to substantiate qualitative observations. The first immunoreactive neurons were observed in the cortical anlage at embryonic day 12-embryonic day 13 (E12-E13) in the primitive plexiform layer. At following prenatal stages (E14-E19), most GABA-positive neurons were present in the marginal zone, subplate, and subventricular zone. GABA-immunoreactivity in the cortical plate appeared early (E14), although the complete maturation of its derivatives was achieved postnatally. At prenatal stages we noted a well-developed system of immunopositive fibers in the subplate. As indicated by the direction of growth cones, most of these fibers had an extracortical origin and invaded the cortex laterally through the internal capsule and striatum. In rostral and middle telencephalic levels, fibers originating in the septal region contributed to the cingulate bundle. Presumably corticofugal fibers and callosal axons were also noticed. At postnatal stages the maturation of GABA-immunoreactivity appeared to be a complex, long-lasting process, in which the adult pattern was produced at the same time as the appearance of certain regressive phenomena. Thus, between postnatal day 0 and postnatal day 8 (P0-P8), GABA-positive populations disappeared from the subventricular zone, marginal zone and to a lesser extent from the subplate. At the same ages we noticed the presence of morphologically abnormal, GABA-immunoreactive neurons in the subventricular zone and subplate which are interpreted as correlates of neuronal degeneration. Most GABA-positive subplate fibers also disappeared whereas GABA-immunoreactive axons were seen in the cingulate bundle until the adult stage. In the derivatives of the cortical plate, the maturation of GABA-immunoreactive elements progressed according to the "inside-out" gradient of cortical development, with the important exception of layer IV, which was the last layer to exhibit an adult-like appearance. Within each layer deriving from the cortical plate (layers VIa to II-III), GABA-immunoreactivity showed a protracted maturation in which the first GABA-positive cells were detected a few days after cell birth but substantial numbers of neurons began to express GABA considerably later. The later phase occurred concurrently with the maturation of GABA-positive axonal plexuses. These results suggest that different GABA-positive populations show different developmental regulation of GABA expression during cortical ontogenesis.

Aging↗

Late appearance of parvalbumin-immunoreactive neurons in the rodent cerebral cortex does not follow an 'inside-out' sequence.

Parvalbumin (PARV), a Ca(2+)-binding protein believed to play a role in neuronal excitability, is contained in certain GABAergic inhibitory neurons of the cerebral cortex. Here we report that expression of PARV in the developing neocortex of rats and mice occurs with a sequence which does not follow the usual 'inside-out' gradient of cortical development. Thus, PARV-immunoreactive neurons appear first in layer V and only thereafter in the remaining cortical layers. An adult-like pattern of immunoreactivity is reached simultaneously in layers II-III and VIb. These observations indicate that the mechanisms regulating the functional maturation of PARV-containing inhibitory neurons are different from those that generally govern developmental processes in the cortex.

Animals↗

A transitory population of substance P-like immunoreactive neurones in the developing cerebral cortex of the mouse.

Immunocytochemical methods were used to investigate the developmental expression of substance P (SP) in mouse cerebral cortex. SP-like-immunoreactive cells were first detected at postnatal day 0 (P0), their numbers being notably increased by P2. Immunopositive cells were especially abundant in layer VIb and in the subjacent future white matter, although they were also present in layer V. Between P5 and P8 the number of SP-like-immunoreactive cells gradually decreased, being almost completely absent by P12. At these stages cells were only observed in the deepest cortical layers. From P16 onwards, the adult pattern of SP-like immunoreactivity emerged with a few immunopositive cells scattered throughout the cortical layers. The present data show a transitory population of SP-like-immunoreactive cells present in the mouse cerebral cortex during the first postnatal week. On the basis of close correlations of SP-like expression with the distribution or transitory populations and the timing of cell death in rodents, we propose that most of the SP-like-immunoreactive cells reported here would probably disappear by cell death.

Aging↗

Zinc-positive boutons in the cerebral cortex of lizards show glutamate immunoreactivity.

Zinc-positive boutons, originating in the medial cortex of lizards, exhibit glutamate immunoreactivity. This finding supports the presumed homology between lizard zinc-positive boutons and the hippocampal mossy fibres of mammals, which are also glutamate-immunoreactive and zinc-positive. Zinc-positive boutons of lizards contain a chelatable pool of zinc located in the hippocampal mossy fibres of mammals. These synaptic systems also contain glutamate, which indicates a possible simultaneous action of zinc and glutamate during synaptic transmission.

Animals↗

Simultaneous immunocytochemical visualization of bromodeoxyuridine and neural tissue antigens.

5'-Bromodeoxyuridine (BrdU) is a thymidine analogue which can be detected by monoclonal antibodies (MAb). We have developed a method for the simultaneous visualization of BrdU and a wide range of neural antigens in paraformaldehyde-fixed brain sections. Pregnant mice were injected intraperitoneally with a single pulse of BrdU. Young adult offspring were processed for immunocytochemistry following a double immunoperoxidase sequence. BrdU was detected using diaminobenzidine (DAB) intensified with nickel ammonium sulfate and neural antigen-containing elements were visualized with DAB alone. BrdU-positive nuclei and tissue antigen-immunoreactive cells were easily differentiated. Furthermore, double-labeled cells characterized by the presence of a black immunoreactive nucleus surrounded by a brown immunopositive cytoplasm were unambiguously recognized. Satisfactory results were obtained using either MAb or polyclonal antibodies against a variety of cell antigens, including neuropeptides, CA++ binding proteins, and cytoskeletal components of the glial cells. The method reported here permits analysis of the neurogenesis and proliferation of subsets of neurons and glial cells, identified by immunocytochemical markers.

Animals↗

Rats choose cocaine over dopamine agonists in a two-lever self-administration preference test.

Rats will self-administer dopamine D(1) and D(2) agonists, alone or in combination. Response rates and patterns for the D(1):D(2) combinations are nearly identical to those induced by cocaine. Here we examine whether rats prefer cocaine over D(1) or D(2) agonists presented alone or in D(1):D(2) combinations. During daily 3-h tests in a two-lever box, cocaine was available at either the right or left lever and the active side was alternated daily. After response rates had stabilized (+/-10% for 2 days), different groups were offered cocaine (800 microg/kg/injection) at one lever and either another dose (267, 1600, or 2400 microg/kg/injection) of cocaine or a dopamine agonist at the other lever. Animals consistently chose the higher of the presented cocaine doses over the low cocaine dose (267 microg). In choices between cocaine and dopamine agonists, the preferred cocaine dose (800 microg) was chosen over doses of the D(1) (SKF 82958) or D(2) ((+)-PHNO) agonist. However, no preference was shown between 800 microg cocaine and D(1):D(2) agonist mixtures, and the high-dose agonist mixture was preferred to the low cocaine dose. These results suggest that neither D(1) nor D(2) agonists alone fully duplicate the reinforcing actions of cocaine, but agonist combinations may approximate cocaine's reinforcement strength.

Animals↗