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Biomedical subjects

A Camacho

Publications and source records attributed to A Camacho.

At least 19 recordsLinked to original sources

The anion channel blocker, 4,4'-dinitrostilbene-2,2'-disulfonic acid prevents neuronal death and excitatory amino acid release during glycolysis inhibition in the hippocampus in vivo.

Neuronal death associated with cerebral ischemia and hypoglycemia is related to increased release of excitatory amino acids (EAA) and energy failure. The intrahippocampal administration of the glycolysis inhibitor, iodoacetate (IOA), induces the accumulation of EAA and neuronal death. We have investigated by microdialysis the role of exocytosis, glutamate transporters and volume-sensitive organic anion channel (VSOAC) on IOA-induced EAA release. Results show that the early component of EAA release is inhibited by riluzole, a voltage-dependent sodium channel blocker, and by the VSOAC blocker, tamoxifen, while the early and late components are blocked by the glutamate transport inhibitors, L-trans-pyrrolidine 2,4-dicarboxylate (PDC) and DL-threo-beta-benzyloxyaspartate (DL-TBOA); and by the VSOAC blocker 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS). Riluzole, DL-TBOA and tamoxifen did not prevent IOA-induced neuronal death, while PDC and DNDS did. The VSOAC blockers 5-nitro-2-(3-phenylpropyl-amino) benzoic acid (NPPB) and phloretin had no effect either on EAA efflux or neuronal damage. Results suggest that acute inhibition of glycolytic metabolism promotes the accumulation of EAA by exocytosis, impairment or reverse action of glutamate transporters and activation of a DNDS-sensitive mechanism. The latest is substantially involved in the triggering of neuronal death. To our knowledge, this is the first study to show protection of neuronal death by DNDS in an in vivo model of neuronal damage, associated with deficient energy metabolism and EAA release, two conditions involved in some pathological states such as ischemia and hypoglycemia.

Animals↗

Effect of temperature and organic nutrients on the biodegradation of linear alkylbenzene sulfonate (LAS) during the composting of anaerobically digested sludge from a wastewater treatment plant.

Limits on the application of biosolids (anaerobically processed sludges from wastewater treatment plants) as fertilizers for the amendment of soil are becoming greater because of the accumulation of recalcitrant substances, making necessary the use of techniques that bring the concentration of xenobiotics to lower concentrations than those permitted. In general, the biosolids composting process is sufficient to reduce the usual concentration of linear alkylbenzene sulfonates (LAS) to low levels. In this work, an assessment is made on the effect of temperature in the capacity of enriched bacterial populations to biodegrade LAS, together with the influence that the available nutrients may have in the biodegradation of these compounds. The results show that the microbial metabolism of LAS was not observed in the thermophilic range. The optimum temperature for the biodegradation of LAS appears to be around 40 degrees C, this is, the lowest assayed here, and at this temperature the differences in the biodegradation of LAS among the nutritionally supplemented cultures are small.

Alkanesulfonic Acids↗

Differential effects of the substrate inhibitor l-trans-pyrrolidine-2,4-dicarboxylate (PDC) and the non-substrate inhibitor DL-threo-beta-benzyloxyaspartate (DL-TBOA) of glutamate transporters on neuronal damage and extracellular amino acid levels in rat brain in vivo.

The extracellular concentration of glutamate is highly regulated by transporter proteins, due to its neurotoxic properties. Dysfunction or reverse activation of these transporters is related to the extracellular accumulation of excitatory amino acids and neuronal damage associated with ischemia and hypoglycemia. We have investigated by microdialysis the effects of the substrate and the non-substrate inhibitors of glutamate transporters, l-trans-2,4-pyrrolidine dicarboxylate (PDC) and DL-threo-beta-benzyloxyaspartate (DL-TBOA), respectively, on the extracellular levels of amino acids in the rat hippocampus in vivo. In addition, we have studied the effect of both inhibitors on neuronal damage after direct administration into the hippocampus and striatum. Electroencephalographic activity was recorded after the intrahippocampal infusion of DL-TBOA or PDC. Microdialysis administration of 500 microM DL-TBOA into the hippocampus increased 3.4- and nine-fold the extracellular levels of aspartate and glutamate, respectively. Upon stereotaxic administration it induced neuronal damage dose-dependently in CA1 and dentate gyrus, and convulsive behavior. Electroencephalographic recording showed the appearance of limbic seizures in the hippocampus after DL-TBOA infusion. In the striatum it also induced dose-dependent neuronal damage. These effects were prevented by the i.p. administration of the glutamate receptor antagonists (+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-iminemaleate and 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)-quinoxaline. In contrast to dl-TBOA, PDC (500 microM) induced a more discrete elevation of excitatory amino acids levels (2.6- and three-fold in aspartate and glutamate, respectively), no neuronal damage or behavioral changes, and no alterations in electroencephalographic activity. The differential results obtained with DL-TBOA and PDC might be attributed to their distinct effects on the extracellular concentration of amino acids. Results are relevant to the understanding of the role of glutamate transporters in amino acid removal or release and the induction of excitotoxic cell death.

Animals↗

[Neurological emergencies in a university hospital].

INTRODUCTION: We analyze the demand and to describe the neurological assistance in a university hospital. MATERIAL AND METHODS: We have performed a retrospective and descriptive study of patients attended in the emergency services by neurologists from June 2000 to May 2001. The inventory and analysis has been carried out across a database in which we codify the reports of the patients diagnosed by means of CIE-9. We have been selected one month where we have collected all calls that neurologist have received, not only those of which reports was realized and codified. RESULT: The total number of neurological patients attended in a year was 1,864 representing 2.85% of all emergencies. The most frequent diagnostic were: cerebrovascular stroke (24.57%), epilepsy (13.06%) and headache (6.07%). Few seasonal variation was noted. There was no difference for sex. In the month's study there were 426 patients, which represented 7.78% of all medical urgencies. The most frequent calls came from internal medicine (65.02%). CONCLUSION: Neurological emergencies constitute a large percentage of third level hospital's emergencies which justify a neurologist in the medical emergencies team.

Emergency Service, Hospital↗

Synthesis and characterization of quantum dot superlattices.

Gold nanoparticles have been synthesized using n-alkylthiol molecules as a passivating agent. By fixing the length of the thiol chain, it is possible to produce nanocrystal arrays, such as 1D chains, 2D arrays of chains and 3D crystals.

Crystallization↗

Bioavailability of ranitidine in healthy Mexican volunteers: effect of food.

Is well known that food can affect the bioavailability of several drugs, its impact is major for those drugs that have to act near of drug absorption. Documentation about alterations of ranitidine bioavailability by effect of food is poor. The purpose of this work was to evaluate the effect of food over the bioavailability of ranitidine. Twenty healthy Mexican volunteers were included for the study. The study was made in two stages, in the first one the volunteers had 12 hour fast and took a 300 mg of oral dose of ranitidine (without food, WOF) and blood samples were drawn. Two weeks later, the volunteers took a normal diet just before ranitidine intake (with food, WF). The area under the curve (AUC) was 30% greater in WOF, Cmax was 921.5 ng/ml (WF) vs. 1685.2 (WOF), and t1/2 was 2.70 +/- 1.38 (WF) h vs 3.66 +/- 1.34 (WOF). The AUC, Cmax and t1/2 were statistically different. It is evident that there are differences in the drug disposition due to the presence of food, then, it is possible that the efficacy of ranitidine as inhibitor of gastric secretion being limited by food.

Adolescent↗

Mechanism for the switch of phi29 DNA early to late transcription by regulatory protein p4 and histone-like protein p6.

Bacteriophage phi29 gene expression takes place from four major promoters, three of them (A2b, A2c and A3) clustered within 219 bp at a central region of the genome. Transcription regulation of these promoters involves both a highly specific DNA-binding protein (p4) and a low specificity DNA-binding protein (p6) functionally related to prokaryotic histone-like proteins. Protein p6 forms extended oligomeric arrays along the phage DNA. In contrast, protein p4 binds specifically upstream of late promoter A3 and early promoter A2c. We have analysed the concomitant binding of p6 and p4 and found that the proteins cooperate with each other in the binding to the central region of the genome, resulting in a ternary p4-p6-DNA complex that affects local DNA topology. Through this complex, protein p6 exerts a direct role in the repression of promoter A2c, impeding unwinding of the DNA strands needed for open complex formation. In contrast, protein p6 functions by reinforcing the positioning of protein p4 in the repression of promoter A2b and activation of promoter A3, thereby facilitating p4-mediated transcription regulation.

Bacillus Phages↗

In vivo hydroxyl radical formation after quinolinic acid infusion into rat corpus striatum.

We studied the effect of an acute infusion of quinolinic acid (QUIN) on in vivo hydroxyl radical (.OH) formation in the striatum of awake rats. Using the microdialysis technique, the generation of.OH was assessed through electrochemical detection of the salicylate hydroxylation product 2,3-dihydroxybenzoic acid (2,3-DHBA). The .OH extracellular levels increased up to 30 times over basal levels after QUIN infusion (240 nmol/microl), returning to the baseline 2 h later. This response was attenuated, but not abolished, by pretreatment with the NMDA receptor antagonist MK-801 (10 mg/kg, i.p.) 60 min before QUIN infusion. The mitochondrial toxin 3-nitropropionic acid (3-NPA, 500 nmol/microl) had stronger effects than QUIN on .OH generation, as well as on other markers of oxidative stress explored as potential consequences of .OH increased levels. These results support the hypothesis that early .OH generation contributes to the pattern of toxicity elicited by QUIN. The partial protection by MK-801 suggests that QUIN neurotoxicity is not completely explained through NMDA receptor overactivation, but it may also involve intrinsic QUIN oxidative properties.

Animals↗

Repression of bacteriophage phi 29 early promoter C2 by viral protein p6 is due to impairment of closed complex.

Bacillus subtilis phage phi 29 encodes a very abundant protein, p6, which is a non sequence-specific DNA-binding protein. Protein p6 has the potential to bind cooperatively to the phage genome, forming a nucleoprotein complex in which the DNA adopts a right-handed toroidal conformation winding around a protein core. The formation of this complex at the right end of the phage genome where the early promoter C2 is located affects local topology, which may contribute to the promoter repression, although the underlying molecular mechanism of this repression is not presently known. In this study, we analyzed the effect of the p6 nucleoprotein complex on the formation of transcription complexes at the C2 promoter. The results obtained indicate that the nucleoprotein complex does not occlude promoter C2 to RNA polymerase because both proteins can bind to the same DNA molecule. Protein p6 binds along the fragment including the sequence adjacent to the bound polymerase, altering the structure of the transcriptional complex and affecting specifically the stability of the closed complex. The findings presented might help to answer some of the open questions about the concerted molecular mechanisms of histone-like proteins as transcriptional silencers.

Bacillus Phages↗

Spontaneous carotid and vertebral artery dissection in children.

Carotid and vertebral artery dissection is a rarely reported cause of stroke in childhood and adolescence, especially if there is not a direct trauma to the neck. Four patients, under 15 years of age, presented with an internal carotid artery dissection, and one patient presented with a vertebral artery dissection. They were all making a physical effort when the event occurred. The five patients had ischemic symptoms, and in two the events were preceded by transient ischemic attacks. Headache was associated in four patients. The diagnosis was made by magnetic resonance imaging and angiography, which included transfemoral angiography in two patients. All improved before leaving the hospital, and four patients did not suffer recurrent episodes. The diagnostic accuracy of artery dissection has improved because of noninvasive neuroimaging testing, but it should still be suspected in any pediatric ischemic stroke, especially if there is headache or cervical pain associated.

Adolescent↗

Zinc intervention on macrophages and lymphocytes response.

Normal zinc levels are essential for the development and maintenance of immune functions; Zn deficiency is detrimental to the embryo and offspring of experimental animals, especially concerning immune development. It is known that Zn supplementation improves immune responses. To further explore the relation between Zn administration and the metal in vitro effects, we studied zinc (500 mg/l) supplementation impact on lymphocytes and macrophages and zinc in vitro effects, in BALB/c mice supplemented from gestation to lactation. Results show a significant increase in proliferation (assessed by 3H incorporation) in lymphocytes exposed to Zn (0.1 mM) in vitro, in 3-wk-old mice; this effect is annulled when the supplementation period is lengthened, indicating saturation of the mechanisms involved in zinc induced stimulation. Macrophages functional capacity assessed by erythrophagocytosis was also improved by Zn supplementation and furthermore by the in vitro exposure to the metal, in mice 3 wk old, this was also depressed by Zn accumulation due to the supplementation period extension (9 weeks). Results show an improvement in the immune parameters analysed due to zinc supplementation and to zinc in vitro exposure. Results also suggest the accumulation of zinc as a result of prolonged supplementation periods, suppresses the cells response to zinc in vitro.

Animals↗

[Nonconvulsive status epilepticus: experience in 33 patients].

BACKGROUND: To review the nonconvulsive status epilepticus diagnosed in a general hospital in order to identify its frequency, electroclinical characteristics and response to medical treatment. PATIENTS ANTS AND METHODS: A retrospective study of 33 cases of nonconvulsive status epilepticus was undertaken. The diagnosis was based on clinical and EEG manifestations. Data regarding their clinical presentation, previous epilepsy, etiology of the status, its medical management and outcome were analysed. RESULTS: The 33 patients comprising the study included 20 men and 13 women. The medium age was 49.8 years. A previous history of epilepsy was present in 51.5% of them. Most of the patients presented impaired consciousness (39.4%) or confusional state (36%). The mean duration of the disorder did not exceed 24 hours (64.5%). There were five cases of absence status and 28 of complex partial status, two of them with secondary generalization. A precipitating factor was found in 80% of the patients and the cerebrovascular etiology was the most frequent. There was a good response to phenytoin (80%), although in the first month death was the final outcome for 25% of them. CONCLUSIONS: Nonconvulsive status epilepticus is an underdiagnosed medical emergency because of its different manifestations, similar to confusional or psyquiatric states. The precipitating factor determines its outcome. A high index of suspicion is needed in order to make a faster diagnosis and treatment.

Adult↗

Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum.

The response of endogenous antioxidants to the N-methyl-D-aspartate (NMDA) receptor agonist and excitotoxin, quinolinic acid (QUIN), was investigated in rat corpus striatum. Animals treated with QUIN (240 nmol/microl), were sacrificed at 120 min after a single intrastriatal injection to examine the alterations in the levels of both reduced (GSH) and oxidized (GSSG) glutathione, and the activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (Gpx). Changes in the rate of lipid peroxidation (LP) were also measured after exposure to different doses of QUIN (60, 120, 240 and 480 nmol/microl) as an index of oxidative stress. When compared to control, lipid peroxidation was increased at QUIN doses of 240 and 480 nmol/microl. Striatal levels of GSH and GSSG were decreased and increased, respectively, after QUIN injection; whereas GPx activity was unchanged. Cytosolic copper/zinc SOD (CuZn-SOD) activity decreased after treatment, while mitochondrial manganese SOD (Mn-SOD) was unchanged. The alterations observed on these antioxidant systems suggest that QUIN toxicity is mediated by specific mechanisms leading to oxidative stress.

Animals↗

Properties of Leishmania major dUTP nucleotidohydrolase, a distinct nucleotide-hydrolysing enzyme in kinetoplastids.

We have previously reported the presence, in the parasitic protozoan Leishmania major, of an enzyme involved in controlling intracellular dUTP levels. The gene encoding this enzyme has now been overexpressed in Escherichia coli, and the recombinant enzyme was purified to homogeneity. Biochemical and enzymic analyses of the Leishmania enzyme show that it is a novel nucleotidohydrolase highly specific for deoxyuridine 5'-triphosphate. The enzyme has proved to be a dimer by gel filtration and is able to hydrolyse both dUTP and dUDP quite efficiently, acting as a dUTP nucleotidohydrolase (dUTPase)-dUDP nucleotidohydrolase but has a limited capacity to act upon other nucleoside di- or triphosphates. The reaction products are dUMP and PP(i) when dUTP is the substrate and dUMP and P(i) in the case of dUDP. The enzyme is sensitive to inhibition by the reaction product dUMP but not by PP(i). dUTPase activity is highly dependent on Mg(2+) concentrations and markedly sensitive to the phosphatase inhibitor, NaF. In summary, Leishmania dUTPase appears to be markedly different to other proteins characterized previously that accomplish the same function.

Animals↗

Serum levels of coenzyme Q10 in patients with Parkinson's disease.

We compared serum levels of coenzyme Q10 and the coenzyme Q10/cholesterol ratio in 33 patients with Parkinson's disease (PD) and 31 matched controls. The mean serum coenzyme Q10 levels did not differ significantly between the 2 study groups. Coenzyme Q10 levels were not correlated with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale (UPDRS) or the Hoehn and Yahr staging in the PD group. The coenzyme Q10/cholesterol ratio had a significant correlation (although low) with duration of the disease (r = -0.46), total UPDRS score (r = -0.39), motor examination of the UPDRS (r = 0.45). These values were not influenced significantly by therapy with levodopa or dopamine agonists. The normality of serum coenzyme Q10 and coenzyme Q10/cholesterol ratio suggest that these values are not related with the risk for PD.

Age of Onset↗

Normal cerebrospinal fluid levels of insulin in patients with Parkinson's disease.

We compared CSF levels insulin, measured by a Radioimmunoanalysis method, in 24 patients with Parkinson's disease (PD) and 21 matched controls. The CSF insulin levels did not differ significantly between PD patients and controls. CSF insulin levels were not correlated with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale of the Hoehn and Yahr staging in the PD group. Antiparkinsonian therapy did not influence significantly and CSF levels of insulin. These results suggest that CSF insulin concentrations are not a biological marker of PD and its severity.

Aged↗