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Biomedical subjects

J Cano

Publications and source records attributed to J Cano.

At least 55 records · Page 3Linked to original sources
PubMed2000

Synthesis, structural characterisation, and Monte Carlo simulation of the magnetic properties of the 3D-stacked honeycomb Cs(n)

Two new polymeric manganese-azido systems with formula Cs(n)-[[Mn(N3)3]n] (1) and [[N(C2H5)4]n][[Mn2-(N3)5(H2O)]n] (2) were synthesised and structurally characterised. Compound 1 crystallises in the P2(1)/n group and consists of a three-dimensional system with end-to-end and end-on azido bridges with the caesium atoms in the holes of the net. Magnetically, compound 1 is a rare case of a three-dimensional network with alternate ferro-antiferromagnetic interactions. Compound 2 crystallises in the P1 group and consists of double chains of manganese atoms bridged by end-on and, the exceptional, (mu-1,1,1)-azido bridges. Magnetically, compound 2 shows net ferromagnetic behaviour. Exact fit of the magnetic data was performed for the two compounds by means of Monte Carlo simulations based on the Metropolis algorithm on sets of 10 x 10 x 10 (1) and 1 x 1 x 320 (2) S = 5/2 classical spin centres.

Journal Article↗
PubMed2000

Asymmetry and magnetism in bis(oximato)-bridged heterobimetallic compounds: a computational approach.

A density functional study of exchange coupling was carried out for a series of heterobinuclear oximato-bridged transition metal complexes. Model calculations were used to examine the influence of the electronic configuration of the metal atoms on the coupling constants. This analysis was complemented by a study of the variation of the coupling constant with the most usual structural distortions within this family of compounds. The influence of the nature of the terminal ligands as well as that of the symmetry on the bridge were also investigated.

Journal Article↗
PubMed2000

Upregulation of BDNF mRNA and trkB mRNA in the nigrostriatal system and in the lesion site following unilateral transection of the medial forebrain bundle.

We have performed unilateral transection of the medial forebrain bundle (MFB) and studied BDNF mRNA and trkB mRNA levels at different postlesion times in the nigrostriatal system by means of in situ hybridization. BDNF mRNA levels were transiently induced in the substantia nigra pars compacta at 1 day postaxotomy. The disposition of BDNF mRNA expressing cells at this postlesion time in substantia nigra mimicked that of the dopaminergic neurons expressing the mRNA for the dopamine transporter. TrkB mRNA levels remained unaltered in the ventral mesencephalon at the different postlesion times examined-1 to 14 days. In contrast, trkB mRNA levels were significantly induced in the striatum at the longer postlesion time examined-14 days-when all neurodegenerative events are completed. It is becoming apparent that nigral BDNF mRNA levels are anterogradely transported to its target tissue in striatum. However, following axotomy, the lesion site represents a second potential target for BDNF action. Consequently, we also analyzed the pattern of mRNA expression for BDNF and trkB at the lesion site where dopaminergic axons are disconnected. There, we found notable inductions of both BDNF mRNA and trkB mRNA levels at 4 days postaxotomy. BDNF mRNA expressing cells were confined at the site of axotomy, which coincided precisely to that showing induction of trkB mRNA. Altogether, our results anticipate promising trophic roles of BNDF in the injured nigrostriatal system.

Animals↗
PubMed2000

The single intranigral injection of LPS as a new model for studying the selective effects of inflammatory reactions on dopaminergic system.

We have injected lipopolysaccharide (LPS) into the nigrostriatal pathway of rats in order to address the role of inflammation in Parkinson's disease (PD). LPS induced a strong macrophage/microglial reaction in Substantia nigra (SN), with a characteristic clustering of macrophage cells around blood-vessels. The SN was far more sensitive than the striatum to the inflammatory stimulus. Moreover, only the dopaminergic neurons of the SN were affected, with no detectable damage to either the GABAergic or the serotoninergic neurons. The damage to the DA neurons in the SN was permanent, as observed 1 year postinjection. Unlike the direct death of dopaminergic neurons caused by agents as MPP(+) or 6-OHDA, LPS seems to cause indirect death due to inflammatory reaction. Therefore, we suggest that the injection of a single dose of LPS within the SN is an interesting model for studying the selective effects of inflammatory reaction on dopaminergic system and also potentially useful for studying PD.

Animals↗
PubMed2000

[Reversible dementia in hypothyroidism].

Hypothyroidism is one of the most important causes of potentially reversible dementia. The present case demonstrates a relatively rapid remission of cognitive and noncognitive symptoms within a period of a few months. For separating dementia in hypothyroidism from dementia with hypothyroidism, cross-sectional and longitudinal assessment of the clinical features is crucial. Various case studies in the literature have shown the reversibility of dementia in hypothyroidism and therefore indicate that the evaluation of thyroid laboratory parameters is indispensable in the differential diagnosis of dementia and observation of its course.

Aged↗
PubMed2000

Decreased messenger RNA expression of key markers of the nigrostriatal dopaminergic system following vitamin E deficiency in the rat.

We have evaluated the effect of a vitamin E-deficient diet on the rat nigrostriatal dopaminergic system. After 15 days of deficient diet, the amount and activity of striatal and nigral tyrosine hydroxylase increased, which contrasted with a decreased messenger RNA expression for tyrosine hydroxylase and the dopamine transporter in the ventral mesencephalon. When we prolonged the deficiency of vitamin E for 30 days, dopamine levels did not differ in both areas. In contrast, messenger RNA levels for tyrosine hydroxylase and the dopamine transporter were markedly reduced in 30-day deficient rats. In addition, the number of oxidatively modified proteins significantly increased in the striatal and nigral areas studied. Overall, we propose that these changes suggest an important role of vitamin E in maintaining the normal equilibrium of the dopaminergic nigrostriatal system.

Animals↗
PubMed2000

The endogenous amine 1-methyl-1,2,3,4- tetrahydroisoquinoline prevents the inhibition of complex I of the respiratory chain produced by MPP(+).

The endogenous monoamine 1-methyl-1,2,3,4-tetrahydroisoquinoline has been shown to prevent the neurotoxic effect of MPP(+) and other endogenous neurotoxins, which produce a parkinsonian-like syndrome in humans. We have tested its potential protective effect in vivo by measuring the protection of 1-methyl-1,2,3,4-tetrahydroisoquinoline in the neurotoxicity elicited by MPP(+) in rat striatum by tyrosine hydroxylase immunocytochemistry. Because we know that cellular damage caused by MPP(+) is primarily the result of mitochondrial respiratory inhibition at the complex I level, we have extended the study further to understand this protective mechanism. We found that the inhibitory effect on the mitochondrial respiration rate induced by MPP(+) in isolated rat liver mitochondria and striatal synaptosomes was prevented by addition of 1-methyl-1,2,3,4-tetrahydroisoquinoline. This compound has no antioxidant capacity; therefore, this property is not involved in its protective effect. Thus, we postulate that the preventive effect that 1-methyl-1,2,3,4-tetrahydroisoquinoline has on mitochondrial inhibition for MPP(+) could be due to a "shielding effect," protecting the energetic machinery, thus preventing energetic failure. These results suggest that this endogenous amine may protect against the effect of several parkinsonism-inducing compounds that are associated with progressive impairment of the mitochondrial function.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2000

Histamine infusion induces a selective dopaminergic neuronal death along with an inflammatory reaction in rat substantia nigra.

We have evaluated the effects of a direct infusion of histamine, as mediator of inflammatory response, in substantia nigra, striatum, medial septum, and medial lemniscus. Injection of 100 and 250 nmol of histamine in substantia nigra produced a selective damage in dopaminergic neurons evidenced by the loss of tyrosine hydroxylase mRNA-expressing cells, tyrosine hydroxylase-immunolabeled-positive cell bodies, and dopamine and 3,4-dihydroxyphenylacetic acid levels. In parallel we found an acute inflammatory response manifested by a loss of glial fibrillary acidic protein-immunolabeled astrocytes and, at precisely the same area, an activation of microglia. In the striatum, only high doses (500 nmol) produced an evident terminal degeneration. The selective neurotoxicity of histamine for dopaminergic cells was demonstrated by the unaltered transcription of glutamic acid decarboxylase mRNA in substantia nigra. Moreover, intraseptal injection of 100 nmol of histamine failed to alter the pattern of choline acetyltransferase mRNA-expressing cells, and intraparenchymal injection of histamine in medial lemniscus failed to alter the pattern of serotonin-immunolabeled cells. We conclude that the substantia nigra is highly sensitive to histamine-derived neurotoxicity, where inflammatory processes mediated by histamine could be important in the pathological changes that lead to dopaminergic neuronal damage after histamine infusion.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Emerging pathogens.

The ever increasing numbers of immunosuppressed individuals has led to a significant increase in the incidence of opportunistic infections, particularly those caused by fungi. The epidemiology of infections caused by the common fungal pathogens such as Candida albicans, Cryptococcus neoformans and Aspergillus fumigatus has been well documented. However, in addition to these, a number of species which have previously been unrecognized (e.g., C. dubliniensis) or have previously been assumed to be non-pathogenic (e.g., Saccharomyces cerevisiae, Scedosporium spp. and Fusarium spp.) have emerged as agents of human disease. Since these species have only been identified recently as human pathogens, their role in disease is poorly understood. In most cases, identification of these species is problematic and therefore their epidemiology has yet to be elucidated adequately. In addition, several of these species fail to respond to conventional antifungal therapies. In this article, we describe the emergence of two separate yeast species (C. dubliniensis and S. cerevisiae) and two separate groups of moulds (Scedosporium prolificans and Fusarium spp.), as human pathogens. It is apparent from what we already know, that much work has yet to be performed before we have a clear understanding of how these species cause disease and most importantly how they can be controlled.

Candida↗
PubMed2000

[Molecular epidemiology for the detection of outbreaks of nosocomial aspergillosis].

The most important molecular techniques used in the diagnosis of Aspergillus spp. and typing of the most pathogen species of this genus are described and discussed. The former, are mainly based in PCR amplification of a concrete DNA fragment and posterior confirmation with Southern-blot; RAPD techniques and less frequently microsatellite markers analysis and DNA-DNA hybridization to a moderately repeated, inactive, retrotransposon-like DNA Afut1 are used in typing clinical isolates.

English Abstract↗
PubMed1999

New PCR method to differentiate species in the Aspergillus niger aggregate.

The DNA that encodes the 5.8S gene of the ribosomal RNA and the two intergenic spacers ITS1 and ITS2 of the two proposed type strains of the Aspergillus niger aggregate (A. niger and Aspergillus tubingensis) have been sequenced. By comparison of sequences we have found that both species could be differentiated by RsaI digestion of the PCR products of the mentioned regions. This method could be a useful tool in the identification of strains of the A. niger aggregate, especially in studies that involve a large number of isolates.

Aspergillus niger↗
PubMed1999

Differential upregulation of aquaporin-4 mRNA expression in reactive astrocytes after brain injury: potential role in brain edema.

Astrocytes and aquaporin-4 (AQP4) play a significant role in brain ion homeostasis. Consequently the regulation of AQP4 mRNA in the CNS after different neurological insults was of interest. A single intrastriatal injection of ringer or quinolinic acid strongly induced AQP4 mRNA in the striatum, specially at the core of the lesion. Colocalization studies demonstrated that AQP4 mRNA induction was restricted to hypertrophic astrocytes. The extent of striatal AQP4 mRNA induction did not correlate with neuronal degeneration, but it did with extravasation of Evans blue dye as a marker of BBB disruption. Distant lesions were additionally induced by either 6-OHDA or a knife cut in the medial forebrain bundle (MFB). The former, but not the latter, induced a high AQP4 mRNA expression in the lesioned substantia nigra. However, axotomy of the MFB induced a high AQP4 mRNA expression at the lesion site. We conclude that the induction of AQP4 mRNA expression is related to disruption of the blood-brain barrier and under brain edema conditions this water channel plays a key role in the reestablishment of the brain osmotic equilibrium.

Animals↗
PubMed1999

Localization of aquaporin-3 mRNA and protein along the gastrointestinal tract of Wistar rats.

Since specific proteins responsible for water transport (aquaporins, AQPs) have been identified in a great variety of tissues, we decided to study the presence of AQP3 in the gastrointestinal tract (GIT) of Wistar rats. Poly(A+) RNA was purified from the mucosa of the stomach, jejunum, ileum and colon, and gross detection of AQP3 mRNA was done by Northern blot analysis. In situ hybridization studies were carried out to precisely localize the distribution of this transcript. Sections of the different tissues were hybridized with @400-bp [35S]riboprobes. The results presented here demonstrate that AQP3 is expressed throughout the GIT, with its expression in the colon and ileum greater than that in the stomach. Immunohistochemistry experiments, using a polyclonal antibody against AQP3, revealed that AQP3 protein is present at the basolateral membrane of the epithelial cells lining the villus tip of the small intestine and colon. The finding of AQP3 in the intestinal epithelia strongly suggests that this protein functions as a pathway for water transport in this epithelium.

Animals↗
PubMed1999

Serotonin hyperinnervation in the adult rat ventral mesencephalon following unilateral transection of the medial forebrain bundle. Correlation with reactive microglial and astroglial populations.

We have previously studied changes in the serotoninergic and dopaminergic nigrostriatal systems following transection of the medial forebrain bundle and found a long-term axotomy-induced increase in the levels of serotonin and its main metabolite, 5-hydroxyindolacetic acid in substantia nigra [Venero et al. (1997) J. Neurochem. 68, 2458-2468]. In an attempt to find a rationale for this effect, we have performed an immunohistochemical study. Transection of the medial forebrain bundle of the rat interrupted most of the ascending serotoninergic pathways from the raphe nuclei as revealed by serotonin immunoreactivity. While serotonin immunostaining was almost absent in striatum, it doubled in the ventral mesencephalon at 21 days postlesion. This axotomy-induced increase was accompanied by an increased density of the serotonin nerve terminal network in the ipsilateral substantia nigra and ventral tegmental area. The increase in serotonin immunoreactivity was in line with the measured levels of serotonin and 5-hydroxyindolacetic acid in substantia nigra. In addition, the distribution pattern of glial fibrillary acidic protein-immunoreactive astrocytes and OX42-immunoreactive microglia correlated highly with the location of increased serotonin fibre density in the ventral mesencephalon, especially in ventral tegmental area and in the most medial part of substantia nigra. We suggest that a pruning effect may underly the axotomy-induced increase in serotonin immunoreactivity in the ventral mesencephalon, and further, that activated astroglia and microglia may play a role in directing serotoninergic axonal regeneration following axotomy.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Detailed localization of aquaporin-4 messenger RNA in the CNS: preferential expression in periventricular organs.

We have performed a detailed in situ hybridization study of the distribution of aquaporin-4 messenger RNA in the CNS. Contrary to expectation, we demonstrate that aquaporin-4 is ubiquitously expressed in the CNS. Strong hybridization labeling was detected in multiple olfactory areas, cortical cells, medial habenular nucleus, bed nucleus of the stria terminalis, tenia tecta, pial surface, pontine nucleus, hippocampal formation and multiple thalamic and hypothalamic areas. A low but significant hybridization signal was found, among others, in the choroid plexus of the lateral ventricles, ependymal cells, dorsal raphe and cerebellum. Overall, a preferential distribution of aquaporin-4 messenger RNA-expressing cells was evident in numerous periventricular organs. From the distribution study, the presence of aquaporin-4 messenger RNA-expressing cells in neuronal layers was evident in neuronal layers including the CA1 -CA3 hippocampal pyramidal cells, granular dentate cells and cortical cells. Further evidence of neuronal expression comes from the semicircular arrangement of aquaporin-4 messenger RNA-expressing cells in the bed nucleus of the stria terminalis and medial habenular nucleus exhibiting Nissl-stained morphological features typical of neurons. Combined glial fibrillary acidic protein immunohistochemistry and aquaporin-4 messenger RNA in situ hybridization demonstrated that aquaporin-4 messenger RNA is expressed by glial fibrillary acidic protein-lacking cells. We conclude that aquaporin-4 messenger RNA is present in a collection of structures typically involved in the regulation of water and sodium intake and that aquaporin-4 water channels could be the osmosensor mechanism responsible for detecting changes in cell volume by these cells.

Animals↗
PubMed1999

Delayed apoptotic pyramidal cell death in CA4 and CA1 hippocampal subfields after a single intraseptal injection of kainate.

We have performed a detailed time-course analysis of cell death in the hippocampal formation, basal forebrain and amygdala following a single intraseptal injection of kainate in adult rats. Acetylcholinesterase histochemistry revealed a profound loss of staining in the medial septum but not in the diagonal band, and cholinergic fiber density was highly reduced in the hippocampus and amygdala at 10 days postinjection. Terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphatebiotin nick end labeling (TUNEL) histochemistry was performed for precise location of apoptotic cells. Both the medial septum and amygdala exhibited numerous TUNEL-positive nuclei after the intraseptal injection of kainate, while the lateral septum exhibited a lower but significant incidence in terms of apoptotic cells. In the medial septum, the presence of apoptotic cells was at a location displaying acetylcholinesterase staining. TUNEL histochemistry revealed a time-dependent sequential apoptotic cell death in hippocampal pyramidal cells. During the first two days postinjection, apoptosis in the hippocampus was only evident in the CA3 region. At five days postinjection, the entire CA4 region became apoptotic. At 10 days postinjection, the whole extent of the CA1 pyramidal cell layer exhibited numerous TUNEL-positive nuclei. The time-course of kainate-induced apoptosis in Ammons's horn correlated with the disappearance of hippocampal pyramidal neurons as detected by Nissl staining, which is suggestive of a prominent apoptotic death for these cells. The temporal delayed distant damage to CA4 and CA1 hippocampal subfields after a single intraseptal kainate injection is not seen in other models employing kainate and may be a valuable tool for exploring the cellular mechanisms leading to cell death in conditions of status epilepticus.

Acetylcholinesterase↗
PubMed1999

The non-NMDA glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline, but not NMDA antagonists, block the intrastriatal neurotoxic effect of MPP+.

Altered glutamatergic neurotransmission appears to be central to the pathophysiology of Parkinson's disease; consequently, considerable effort has been made to elucidate neuroprotective mechanisms against such toxicity. In the present study, the possible neuroprotective effect of glutamate receptor antagonists against MPP+ neurotoxicity on dopaminergic terminals of rat striatum was investigated. Different doses of glutamate receptor antagonists were coinfused with 1.5 microg of MPP+ into the striatum; kynurenic acid, a nonselective antagonist of glutamate receptors (30 and 60 nmol), partially protected dopaminergic terminal degeneration in terms of rescue of dopamine levels and tyrosine hydroxylase immunohistochemistry. Dizocilpine, a channel blocker of the NMDA receptor (1, 4, and 8 nmol), and 7-chlorokynurenic acid, a selective antagonist at the glycine site of the NMDA receptor (1 and 10 nmol), failed to protect dopaminergic terminals from MPP+ toxicity. However, 6-cyano-7-nitroquinoxaline-2,3-dione (0.5 and 1 nmol) and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (1 nmol), two AMPA-kainate receptor antagonists, protected against MPP toxicity. Our findings suggest that the toxic effects of MPP+ on dopaminergic terminals are not mediated through a direct interaction with the NMDA subtype of glutamate receptor, but with the AMPA-kainate subtype.

1-Methyl-4-phenylpyridinium↗