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J Cano

Publications and source records attributed to J Cano.

At least 19 recordsLinked to original sources
PubMed2003

Synthesis, structure, and magnetic properties of [MnIII(salpn)NCS]n, a helical polymer, and the dimer [MnIII(salpn)NCS]2. Weak ferromagnetism in [MnIII(salpn)NCS]n related to the strong magnetic anisotropy in Jahn-Teller MnIII (salpnH2 = N,N'-bis(salicylidene)-1,3-diaminopropane).

Dimeric [Mn(salpn)NCS](2)(1) and polymeric [Mn(salpn)NCS](n)(2) are formed by the reaction of Mn(CH(3)CO(2))(2).4H(2)O, the schiff base, and thiocyanate. The formation of the two polymorphic forms is solvent and temperature dependent. 1: orthorhombic, space group Pbca, with a = 12.573(2) A, b = 13.970(7) A, c = 18.891(9) A, and Z = 8. 2: orthorhombic, space group Pna2(1), with a = 12.5277(14) A, b = 11.576(2) A, c = 11.513(2) A, and Z = 4. The dimers in 1 are held together by weak noncovalent S...pi (phenyl) interactions leading to a chain along the a-axis. Each monomeric unit of the polymer in 2 is related to its adjacent ones by a 2-fold screw axis leading to a helix along the c-axis. The exchange coupling is nondetectable in the dimer. The magnetic susceptibility of the helical chain fits a classical chain law with J = -3.2 cm(-1) and shows a weak ferromagnetic ordering below 7 K due to spin canting effects.

Journal Article↗
PubMed2003

Molecular typing of clinical and environmental isolates of Scedosporium prolificans by inter-simple-sequence-repeat polymerase chain reaction.

Invasive infections by Scedosporium prolificans have increased alarmingly in recent years, mainly in immunosuppressed patients. The epidemiology, pathogenesis and the natural habitat of this pathogen are practically unknown. Isolates of S. prolificans were distinguished from one another by inter-simple-sequence-repeat (ISSR) fingerprinting, a technique based on the high degree of polymorphism of the multisatellite genetic markers used. This technique was found useful for typing 84 isolates of S. prolificans from different countries and sources. The assemblage of S. prolificans isolates tested was extremely diverse, with 35 genotypes present. Several patients were found to have been infected or colonized by more than one strain. Overall, this technique facilitates the epidemiological study of S. prolificans infection.

Australia↗
PubMed2002

Comparative study of the neuroprotective effect of dehydroepiandrosterone and 17beta-estradiol against 1-methyl-4-phenylpyridium toxicity on rat striatum.

The effects of dehydroepiandrosterone, estradiol and testosterone on 1-methyl-4-phenylpyridium (MPP+)-induced neurotoxicity of the nigrostriatal dopaminergic system were examined in rat. They were subjected to a unilateral intrastriatal infusion of the following treatment conditions: MPP+ alone or co-injection of MPP+ plus each hormone. Four days after injection, concentrations of dopamine and their metabolites were determined from the corpus striatum. To corroborate the neurochemical data an immunohistochemical analysis of tyrosine hydroxylase-immunoreactive fibers and acetylcholinesterase histochemistry in the striatum was performed. Moreover, we performed a dose-response study of the three hormones on the high-affinity dopamine transport system in rat striatal synaptosomes. Rats co-injected within the striatum with MPP+ and either dehydroepiandrosterone or estradiol had significantly greater concentrations of dopamine and less tyrosine hydroxylase-immunoreactive fibers and acetylcholinesterase fiber density loss compared with their respective controls. In addition, 4 days after injection, the brain was fixed and cut into coronal sections, and was immunostained with major histocompatibility complex class II antigens for activated microglia, and glial fibrillary acidic protein for activated astrocytes. Dehydroepiandrosterone also attenuated microglial cell activation. In contrast, testosterone showed reductions in dopamine concentrations similar to those obtained by MPP+. The protective effect of dehydroepiandrosterone against the MPP+ neurotoxic dopaminergic system may be produced by its partial prevention of MPP+ inhibition of NADH oxidase activity, whereas the estradiol may function as a neuroprotectant by reducing the uptake of MPP+ into dopaminergic neurons. Our findings we suggest indicate that dehydroepiandrosterone and estradiol by a non-genomic effect may have an important modulatory action, capable of attenuating degeneration within the striatum, and in this way serve as neuroprotectants of the nigrostriatal dopaminergic system.

Acetylcholinesterase↗
PubMed2002

DCG-IV but not other group-II metabotropic receptor agonists induces microglial BDNF mRNA expression in the rat striatum. Correlation with neuronal injury.

We have previously described a neuroprotective action of (2S,2'R,3'R)-2-(2'3'-dicarboxycyclopropyl)glycine (DCG-IV), an agonist for group-II metabotropic receptors, on dopaminergic nerve terminals against the degeneration induced by 1-methyl-4-phenylpyridinium (MPP+). This effect was accompanied by an up-regulation of brain-derived neurotrophic factor (BDNF) mRNA expression in the rat striatum. We have now analyzed the phenotypic nature of the BDNF mRNA-expressing cells in response to intrastriatal injection of DCG-IV. Dual in situ hybridization and immunohistochemistry revealed that microglial cells but not astrocytes were responsible for this induction. Subsequent analysis demonstrated that this effect was accompanied by striking loss of striatal glutamic acid decarboxylase (GAD) mRNA and massive appearance of internucleosomal DNA fragmentation, a hallmark of apoptosis. A dose-response study demonstrated that doses of DCG-IV as low as 5 nmol was very toxic in terms GAD mRNA and apoptosis. 0.5 nmol of DCG-IV did not induce toxicity at all in terms of GAD mRNA and apoptosis. Activation of group-II metabotropic receptors in striatum with N-Acetyl-Asp-Glu (NAAG; a mGlu3 agonist) and (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (a mGlu2 and mGlu3 agonist) did not induce neither loss of GAD mRNA nor appearance of apoptosis (doses up to 20 nmol). In additional experiments, NAAG, in contrast to DCG-IV, failed to protect the striatal dopaminergic system against the degeneration induced by MPP+ as studied by microdialysis. Finally, we studied the mechanism by which DCG-IV is highly toxic. For that, selective antagonists of either metabotropic--(R,S)-alpha-methyl-4-carboxyphenylglycine and LY 341495--or ionotropic (N-methyl-D-aspartate, NMDA)--DL-2-amino-5-phosphonovaleric acid (AP-5) glutamate receptors --were co-administered with DCG-IV. Only AP-5 highly protected the striatum against the degeneration induced by DCG-IV. Since DCG-IV also activates the NMDA receptor at concentrations higher than 3 microM, it is conceivable that a intrastriatal concentration equal or higher than 3 microM after a single striatal injection of 5-20 nmol of DCG-IV. Our findings suggest that much caution must be exerted when testing the numerous neuroprotective effects ascribed to group-II metabotropic receptor activation, in particular when using DCG-IV. We conclude that the neuroprotectant capability of a given compound on a specific system does not exclude the possibility of inducing toxicity on a different one.

Animals↗
PubMed2002

The degenerative effect of a single intranigral injection of LPS on the dopaminergic system is prevented by dexamethasone, and not mimicked by rh-TNF-alpha, IL-1beta and IFN-gamma.

It is becoming widely accepted that the inflammatory response is involved in neurodegenerative disease. In this context, we have developed an animal model of dopaminergic system degeneration by the intranigral injection of lipopolysaccharide (LPS), a potent inductor of inflammation. To address the importance of the inflammatory response in the LPS-induced degeneration of nigral dopaminergic neurones, we carried out two different kinds of studies: (i) the possible protective effect of an anti-inflammatory compound, and (ii) the effect of the intranigral injection of inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) on dopaminergic neurones viability. Present results show that dexamethasone, a potent anti-inflammatory drug that interferes with many of the features characterizing pro-inflammatory glial activation, prevented the loss of catecholamine content, Tyrosine hydroxylase (TH) activity and TH immunostaining induced by LPS-injection and also the bulk activation of microglia/macrophages. Surprisingly, injection of the pro-inflammatory cytokines failed to reproduce the LPS effect. Taken together, our results suggest that inflammatory response is implicated in LPS-induced neurodegeneration. This damage may be due, at least in part, to a cascade of events independent of that described for TNF-alpha/IL-1 beta/IFN-gamma.

Animals↗
PubMed2002

Malaria vectors in Bioko Island (Equatorial Guinea): PCR determination of the members of Anopheles gambiae Giles complex (Diptera: Culicidae) and pyrethroid knockdown resistance (kdr) in An. gambiae sensu stricto.

Anopheles gambiae sensu lato Giles, 1902 and Anophelesfunestus Giles, 1900 are the main malaria vectors on the island of Bioko (Equatorial Guinea). This study was carried out to determine: a) members of the An. gambiae complex that may be present on the island of Bioko and, b) the sensitivity of An. gambiae sensu stricto to pyrethroids. The analysis by PCR detected the presence of An. gambiae s.s. as the major vector of the complex and the "forest chromosomal form" was demonstrated by cytogenetic analysis. The presence of Anopheles melas in the southwest, north and southeast of the island justifies its study as a vector. The molecular characterization of pyrethroid knockdown resistance (kdr) showed that the populations of An. gambiae s.s. were sensitive and no mutations were found. This fact justifies the implementation on a large scale of pyrethroid-impregnated bednets within the framework of the Malaria Control Program of Equatorial Guinea.

Animals↗
PubMed2002

[Susceptibility of Staphylococcus aureus isolated from blood to 11 antimicrobial agents and a review of the literature].

From November 1998 to February 2000, a total of 91 strains of Staphylococcus aureus isolated from blood were analyzed for their susceptibility to 11 antimicrobial agents using the E-test method. Fifty-two isolates were methicillin-susceptible (MSSA) and 39 were oxacillin-resistant (MRSA). All the MSSA were susceptible to gentamicin, ciprofloxacin, vancomycin, teicoplanin, rifampicin, fusidic acid, quinupristin-dalfopristin and linezolid; 90% were susceptible to erythromycin and 83% to mupirocin. All the MRSA were susceptible to vancomycin, teicoplanin, rifampicin and linezolid; 95% were susceptible to quinupristin-dalfopristin; and 92% to gentamicin, mupirocin, fusidic acid. None of the MRSA were susceptible to erythromycin or ciprofloxacin. The susceptibility of SARM to erythromycin and ciprofloxacin was low, while the susceptibility to the rest of the antimicrobial agents remained active.

Anti-Bacterial Agents↗
PubMed2001

Heterobimetallic oxalato-bridged Cu(II)Re(IV) complexes. Synthesis, crystal structure and magnetic properties.

Three copper(II)-rhenium(IV) bimetallic complexes of formula [ReCl(4)(mu-ox)Cu(phen)(2)] (1), [ReCl(4)(mu-ox)Cu(phen)(2)].CH(3)CN (2), and [ReCl(4)(mu-ox)Cu(terpy) (H(2)O)][ReCl(4)(mu-ox)Cu(terpy)(CH(3)CN)] (3) (ox = oxalate anion, phen = 1,10-phenanthroline, and terpy = 2,2':6,2"- terpyridine) have been synthesized and their crystal structures determined by single-crystal X-ray diffraction. Complex 1 crystallizes in the triclinic system, space group P(-1), with a = 9.776(2), b = 11.744(3), c = 14.183(3) A, alpha =102.09(2) degrees, beta = 109.42(2) degrees, gamma = 107.11(2) degrees, and Z = 2, whereas 2 and 3 crystallize in the monoclinic system, space groups P2(1)/n and P2(1)/c, respectively, with a = 12.837(3), b = 17.761(4), c = 12.914(3) A, beta = 91.32(2) degrees, and Z = 4 for 2, and a = 8.930(2), b = 18.543(4), c = 27.503(6) A, beta = 94.67(2) degrees, and Z = 4 for 3. The structures of 1 and 2 are made up of neutral [ReCl(4)(mu-ox)Cu(phen)(2)] bimetallic units. Re(IV) and Cu(II) metal ions exhibit distorted octahedral coordination geometries, being bridged by a bis(bidentate) oxalato ligand. The presence of acetonitrile molecules of crystallization in 2 causes a somewhat greater separation between the bimetallic complexes and a different packing of these units in the crystal structure with respect to 1. The copper-rhenium separation across oxalato is 5.628(2) in 1 and 5.649(3) A in 2. The structure of 3 is made up of two different and neutral bimetallic units, [ReCl(4)(mu-ox)Cu(terpy)(H(2)O)] and [ReCl(4)(mu-ox)Cu(terpy)(CH(3)CN)]. In the first one, the oxalate group behaves as a bis(bidentate) ligand occupying one equatorial and one axial position in the elongated octahedral environment of Cu(II). The water molecule is axially coordinated. In the second one, the oxalate group behaves as a bidentate/monodentate ligand occupying the axial position in the square pyramidal environment of Cu(II). The acetonitrile molecule occupies a basal coordination position around the copper atom. These units are arranged in such a way that a chlorine atom of the first unit (Cl(1)) points toward the copper atom (Cu(2))of the second one (3.077(2) A for Cl(1)(.)Cu(2)), forming a tetranuclear species. The copper-rhenium separation across bis(didentate) oxalato is 5.504(3) A, whereas that through bidentate/monodentate oxalato is 5.436(2) A. The magnetic behavior of 2 and 3 has been investigated over the temperature range 1.8-300 K. A very weak and nearly identical antiferromagnetic coupling between Re(IV) and Cu(II) through bis(bidentate) oxalato occurs in 2 (J = -0.90 cm(-1)) and 3 (J = -0.83 cm(-1)); it is ferromagnetic in 3 through both the bidentate-monodentate oxalato (J = +5.60 cm(-1)) and the chloro (J = +0.70 cm(-1)) bridges.

Journal Article↗
PubMed2001

Determination of residues of enrofloxacin and its metabolite ciprofloxacin in biological materials by capillary electrophoresis.

A method for the analysis of enrofloxacin and ciprofloxacin in chicken muscle using marbofloxacin as internal standard is proposed. Clean-up and pre-concentration of the samples are effected by solid-phase extraction and determination is carried out by capillary electrophoresis using a photodiode array detector. The calibration graphs are linear for enrofloxacin and ciprofloxacin from 10 to 300 microg/kg. The method recoveries for enrofloxacin and ciprofloxacin are 74 and 54%, respectively. The limit of detection for the two compounds is lower than 25 microg/kg, which allows the detection of positive muscle samples at the required maximum residue limits.

Animals↗
PubMed2001

Validity of a quantitative technique to study striatal dopaminergic neurodegeneration by in vivo microdialysis.

The development of a technique that allows the direct quantitative study of the damage produced by a toxin on a specific neurotransmitter system is very important. For that, we have used the microdialysis technique to validate a method to study the specific drug's toxicity on dopaminergic (DAergic) striatal terminals. We perfused different MPP(+) and 6-hydroxydopamine (6-OHDA) concentrations, with different toxicity for DAergic terminals, 24 h after the implantation of the microdialysis probe (day 1). One day later (day 2), MPP(+) was perfused through the microdialysis probe and DA extracellular output measured. We hypothesize that the amount of extracellular dopamine (DA) obtained on day 2 is directly proportional to the neurotoxic damage produced on day 1. To corroborate this hypothesis tyrosine hydroxylase (TH) immunohistochemistry was also carried out on day 2. There was a clear correlation index between the amount of DA measured after MPP(+) perfusion and the lack of TH immunoreactivity measured as the radius of the area showing decrease in TH immunoreactivity around the cannula. These results show the possibility to measure DAergic remaining terminals after a toxic drug exposure by in vivo MPP(+) perfusion. The possibility to extend this neurotoxic study to another neurotransmitter systems is suggested.

1-Methyl-4-phenylpyridinium↗
PubMed2001

The utilization of classical spin Monte Carlo methods to simulate the magnetic behavior of extended three-dimensional cubic networks incorporating M(II) ions with an S = 5/2 ground state spin.

The numerical simulations of the magnetic properties of extended three-dimensional networks containing M(II) ions with an S = 5/2 ground-state spin have been carried out within the framework of the isotropic Heisenberg model. Analytical expressions fitting the numerical simulations for the primitive cubic, diamond, together with (10-3) cubic networks have all been derived. With these empirical formulas in hands, we can now extract the interaction between the magnetic ions from the experimental data for these networks. In the case of the primitive cubic network, these expressions are directly compared with those from the high-temperature expansions of the partition function. A fit of the experimental data for three complexes, namely [(N(CH(3))(4)][Mn(N(3))] 1, [Mn(CN(4))](n)() 2, and [Fe(II)(bipy)(3)][Mn(II)(2)(ox)(3)] 3, has been carried out. The best fits were those obtained using the following parameters, J = -3.5 cm(-)(1), g = 2.01 (1); J = -8.3 cm(-)(1), g = 1.95 (2); and J = -2.0 cm(-)(1), g = 1.95 (3).

Journal Article↗
PubMed2001

Light- and thermal-induced spin crossover in [Fe(abpt)2(N(CN)2)2]. Synthesis, structure, magnetic properties, and high-spin<-->low spin relaxation studies.

[Fe(abpt)2(N(CN)2)2] (abpt = 4-amino-3,5-bis(pyridin-2-yl)-1,2,4-triazole) represents the first example of an iron(II) spin-crossover compound containing dicyanamide ligand, [N(CN)(2)](-), as a counterion. It shows an incomplete two-step spin transition with around 37% of HS molecules trapped in the low-temperature region when standard cooling or warming modes, i.e., 1-2 K min(-)(1), were used. The temperature, T(1/2) approximately 86 K, at which 50% of the conversion takes place, is one of the lowest temperatures observed for an iron(II) spin-crossover compound. Quenching experiments at low temperatures have shown that the incomplete character of the conversion is a consequence of slow kinetics. The quenched HS state relaxes back to the LS state displaying noticeable deviation from a single-exponential law. The rate of relaxation was evaluated in the range of temperatures 10-60 K. In the upper limit of temperatures, where thermal activation predominates, the activation energy and the pre-exponential parameter were estimated as E(a) approximately 280 cm(-)(1) and A(HL) approximately 10 s(-)(1), respectively. The lowest value of k(HL) around 1.2 x 10(-)(4) s(-)(1) (T = 10 K) was obtained in the region of temperatures where tunneling predominates. A quantitative light induced excited spin state trapping (LIESST) effect was observed, and the HS --> LS relaxation in the range of temperatures 5-52.5 K was studied. From the Arrhenius plot the two above-mentioned characteristic regimes, thermal-activated (E(a) approximately 431 cm(-)(1) and A(HL) approximately 144 s(-)(1)) and tunneling (k(HL) approximately 1.7 x 10(-)(6) s(-)(1) at 5 K), were characterized. The crystal structure was solved at room temperature. It crystallizes in the triclinic P_1 space group, and the unit cell contains a centrosymmetric mononuclear unit. Each iron atom is in a distorted octahedral environment with bond distances Fe-N(1) = 2.216(2) A, Fe-N(2) = 2.121(2) A, and Fe-N(3) = 2.160(2) A for the pyridine, triazole, and dicyanamide ligands, respectively.

Journal Article↗
PubMed2001

Potential role of endogenous brain-derived neurotrophic factor in long-term neuronal reorganization of the superior colliculus after bilateral visual deprivation.

The role of the brain-derived neurotrophic factor (BDNF), the BDNF receptor (TrkB), and the glutamic acid decarboxylase (GAD67) after neonatal, bilateral nerve deafferentiation during postnatal development was investigated in the rat superior colliculus (SC). BDNF and GAD67 mRNA expression were significantly increased in optic (Op) and intermediate gray (InG) layers at 5, 8, 15, and 21 days after birth, but not in adult animals. However, TrkB mRNA expression was not modified at any time tested. At 15 days, where changes in BDNF and GAD67 mRNAs were more evident, an upregulation of the NMDAR(1A) mRNA glutamate receptor in the Op and InG, a modification in the pattern of synaptic zinc in the superficial layers of SC, and an increased synaptophysin immunoreactivity in the Op was found. This indicates the existence of a synergic mechanism between BDNF and NMDA to determine refinement of connections after the loss of visual input in SC.

Animals↗
PubMed2001

Aquaporins in the central nervous system.

In this review, we have tried to summarize most available data dealing with the aquaporin (AQP) family of water channels in the CNS. Two aquaporins have been identified so far in the CNS, AQP1 and AQP4. AQP1 is restricted to the choroid plexus of the lateral ventricles, which raises a role for this aquaporin in cerebrospinal fluid formation. AQP4 is the predominant water channel in the brain and it is more widely distributed than originally believed, with a marked prevalence over periventricular areas. In the first part of this review, we examine the complete distribution pattern of AQP4 in the CNS including its rostro-caudal localization to end with its subcellular location. After discussing scarce data dealing with regulation of aquaporins in the CNS, we focus in potential roles for aquaporins. Novel recent data highlights very important roles for this aquaporin in the normal and pathological brain including, among others, role in potassium buffering, body fluid homeostasis, central osmoreception and development and restoration of brain edema.

Animals↗
PubMed2001

Long-lasting induction of brain-derived neurotrophic factor is restricted to resistant cell populations in an animal model of status epilepticus.

We have recently characterized an animal model of status epilepticus induced by a single intraseptal injection of kainate. Under these conditions, there is a delayed expanding apoptotic hippocampal and amygdalar cell death. In order to further characterize this animal model, we have performed a detailed time-course analysis of the appearance of cell death, brain-derived neurotrophic factor messenger RNA expression and astroglial and microglial response in different brain areas related to the limbic system. We found a long-lasting delayed apoptotic cell death in the hippocampal formation, amygdala, medial thalamus, dorsal endopiriform nucleus and multiple cortical areas from two to 21 days post-injection. There was a spatiotemporal correlation between the appearance of cell death and induction of brain-derived neurotrophic factor messenger RNA expression in the areas studied, and interestingly this induction was found in non-degenerating cells. We conclude that our animal model of status epilepticus exhibits remarkable features of recurrent seizure activity and provides evidence for a neuroprotective role of brain-derived neurotrophic factor against seizure-induced apoptotic cell death.

Animals↗