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Biomedical subjects

A Alvarez

Publications and source records attributed to A Alvarez.

At least 127 records · Page 7Linked to original sources
PubMed1999

Antigenic and genetic characterization of a putative hybrid transferrin-binding protein B from Neisseria meningitidis.

The transferrin-binding protein Bs (TbpBs) from the bacterium Neisseria meningitidis have been divided into two families according to genetic and antigenic features. TbpB from meningococcal strain B385 showed a molecular mass similar to that exhibited by TbpBs belonging to the high molecular mass family of TbpBs. TbpB was recognized by immunoassay using a specific serum directed against the TbpB of the reference strain for this family (strain M982). It was also recognized by a serum elicited against the TbpB of the reference strain for the low molecular mass family (strain B16B6). The tbpB gene from strain B385 was cloned and sequenced. The highest degree of sequence homology was found to be with the TbpBs belonging to the high molecular mass family, although a region of 14 amino acids that is only present in the TbpB from strain B16B6 was also found. This report illustrates a TbpB that shows hybrid antigenic and genetic behaviour.

Amino Acid Sequence↗
PubMed1998

Prospective study for the detection of Anaplasma marginale Theiler, 1911 (Rickettsiales: Anaplasmataceae) in Costa Rica.

A prospective study was conducted to assess the dynamics of the infection and host response to Anaplasma marginale in one closed herd in the dry tropical forest of Costa Rica. The study subjects were the dams and their calves born during 1 breeding season (1995-1996). All cows were sampled at 3 month intervals for antibody detection using a competitive ELISA (cELISA) and for antigen detection using PCR/nonradioactive probe assay. All 24 calves born during the study were individually identified at birth and subsequently sampled each month for PCR and cELISA. Ticks were identified from all animals throughout the entire study period. The results from this study confirmed that the cELISA is a reliable assay for identifying new and carrier infections and that carrier infections can exist at levels below that detectable by PCR. In addition, it was demonstrated that calves born in this region will most likely be exposed to Anaplasma within the first 6 months of age.

Anaplasma↗
PubMed1998

[Subarachnoid hemorrhage: electrocardiographic, left ventricular wall motion abnormalities and mortality analysis in 14 cases].

BACKGROUND: Electrocardiographic (ECG) changes have been frequently observed in patients with subarachnoid hemorrhage (SAH). Their association with wall motion abnormalities of the left ventricle (LV) have not been well established. PATIENTS AND METHODS: Sixteen patients with SAH were included; 2 patients with previous history of heart disease were subsequently excluded. We studied the neurological damage (Hunt-Hess grading scale), ECG (ST segment, T wave) and echocardiography (LV regional and global contractility) of 14 patients. RESULTS: The ECG was abnormal in 11 patients (T wave: 6 patients; ST segment: 5 patients). Echocardiography showed alterations in 5 patients, all of them with ECG changes (T wave: one patient; ST segment: 4 patients). The neurological lesion was higher in patients with abnormal echocardiogram (Hunt-Hess mean grade: 4.6 vs 2.7 in patients with normal echocardiogram; p < 0.001). An intravenous infusion of dobutamine in a 23 years old male, improved the LV ejection fraction, which was severely depressed at baseline. Mortality, in all cases secondary to the neurological damage, was higher in patients with abnormal ECG (91% vs 0% in patients with normal ECG; p = 0.01) and when the echocardiogram showed alterations although in the last case no statistical differences were found. CONCLUSIONS: Echocardiography abnormalities in patients with SAH and without previous history of heart disease are more frequently related to ECG changes affecting ST segment, and to a higher cerebral damage.

Adult↗
PubMed1998

Stable complexes involving acetylcholinesterase and amyloid-beta peptide change the biochemical properties of the enzyme and increase the neurotoxicity of Alzheimer's fibrils.

Brain acetylcholinesterase (AChE) forms stable complexes with amyloid-beta peptide (Abeta) during its assembly into filaments, in agreement with its colocalization with the Abeta deposits of Alzheimer's brain. The association of the enzyme with nascent Abeta aggregates occurs as early as after 30 min of incubation. Analysis of the catalytic activity of the AChE incorporated into these complexes shows an anomalous behavior reminiscent of the AChE associated with senile plaques, which includes a resistance to low pH, high substrate concentrations, and lower sensitivity to AChE inhibitors. Furthermore, the toxicity of the AChE-amyloid complexes is higher than that of the Abeta aggregates alone. Thus, in addition to its possible role as a heterogeneous nucleator during amyloid formation, AChE, by forming such stable complexes, may increase the neurotoxicity of Abeta fibrils and thus may determine the selective neuronal loss observed in Alzheimer's brain.

Acetylcholinesterase↗
PubMed1998

Necrogenic and regenerative responses of liver of newly weaned rats against a sublethal dose of thioacetamide.

The hepatocellular necrogenic and regenerative responses of newly weaned rats (21 days old) to a sublethal dose of thioacetamide (6.6 mmol kg-1) were studied in comparison to adult (6-month old rats), in terms of liver injury, antioxidant defense systems and cell proliferation. Hepatocellular necrosis, detected by serum aspartate aminotransferase, was less severe in newly weaned rats than in adult animals and was parallel to previous changes in the activity of microsomal FAD monooxygenase system responsible for thioacetamide biotransformation. Liver damage in hepatocytes from newly weaned rats was also detected by the decreased levels of glutathione and protein thiol groups (47%, p < 0.001 and 52%, p < 0.001 vs. untreated, respectively) and by the enhanced malondialdehyde production (334%, p < 0.001) and glutathione S-transferase activity (384%, p < 0.001). No significant differences were detected in these values when compared to adults. Changes in cytosolic and mitochondrial superoxide dismutase and catalase activities in hepatocytes from newly weaned rats at 24 h, following thioacetamide (49%, p < 0.001; 50% and 53%, p < 0.001 vs. untreated, respectively), were less severe against those in adult hepatocytes at 48 h of intoxication, and the increases in glutathione peroxidase and glutathione reductase activities were significantly lowered: 25% (p < 0.001) and 41% (p < 0.001), respectively. Post-necrotic DNA synthesis in hepatocytes from newly weaned rats peaked at 48 h of intoxication, while in adults a more intense peak appeared at 72 h preceded by a sharp decrease in tetraploid population. These differences indicate that the lower necrogenic response against the same dose of thioacetamide in newly weaned rats may be due to the lower rate of thioacetamide biotransformation and to the earlier onset of cell division. Accordingly, the growing liver from newly weaned rats presents advantages against the necrogenic aggression of thioacetamide, first, because the diminished activity of its specific microsomal detoxification system, and second because the earlier increase in the proliferative response prevents the progression of injury permitting an earlier restoration of liver function.

Animals↗
PubMed1998

Flow cytometric studies of nucleoside transport regulation in single chromaffin cells.

The present paper reveals that a fluorescent derivative of nitrobenzylthioinosine, 5-(SAENTA-x8)-fluorescein, is a highly specific inhibitor of the neural NBTI-sensitive nucleoside transporter. 5-(SAENTA-x8)-fluorescein inhibited adenosine transport and [3H]NBTI binding with a Ki of 4 nM in cultured chromaffin cells. Flow cytometry demonstrated that 5-(SAENTA-x8)-fluorescein specifically interacted with the NBTI-sensitive nucleoside transporters with high affinity (K[D] = 6 nM). Activation of protein kinases A and C with forskolin or nicotinic receptor agonists, respectively, resulted in 50% inhibition of the fluorescence bound to the cells. Flow cytometry will allow studying nucleoside transport in single cells from heterogeneous neural cell populations.

Adenosine↗
PubMed1998

Plasticity of Congo red staining displayed by subpopulations of neurons within the rat central nervous system.

We document the presence of subpopulations of neurons within the rat central nervous system that are labelled with a new Congo red staining technique. These neurons (CR neurons) show shrunken somata, and smaller and darker nuclei than Congo red-negative cells (non-CR cells). With the Bielschowsky and the cresyl violet Nissl staining methods, two comparable subpopulations of cells can be distinguished by the same morphometrical criteria as those used for CR and non-CR cells. CR neurons are located preferentially in some brain regions while in others they are virtually absent. Their distribution and proportion varied greatly from animal to animal and after particular treatments. Injections of water that damaged the hippocampal dentate gyrus, cortical lesions or eye enucleation decreased the number of CR-cells in the CA1 subfield, reflected in a shift from the CR-staining subclass to the non-CR subclass. Treatment with 200 mg/kg of CDP-choline also significantly reduced the number of CR cells observed in CA1. In the red nucleus, CR neurons showed a characteristic distribution of beta-amyloid precursor protein (APP) immunoreactivity. The population of dendrites immunolabelled for microtubule-associated protein 2 was markedly decreased in the areas of the hippocampus with high numbers of CR cells. Therefore, it is proposed that neurons labelled with the present Congo red technique might be in a reversible degenerative state or represent a particular physiological state in some areas of the central nervous system.

Amyloid beta-Protein Precursor↗
PubMed1998

Polyploidization and exit from cell cycle as mechanisms of cultured melanoma cell resistance to methotrexate.

Numerous malignant neoplasias are found to contain varying proportions of high-ploidy cells. Although the role they play in the tumor is poorly understood, several lines of evidence suggest that these cells could be especially resistant to various aggressions, a possibility of great interest in cancer treatment. In the present study, we tested this hypothesis through the analysis of the presence of high-ploidy cells following the administration of the chemotherapeutic agent methotrexate. We also determined the expression of two proliferation markers, PCNA and CDK1, after methotrexate-treatment. Cultured cells from the murine melanoma B16F10 were treated with high doses of methotrexate for seven days prior to determination of DNA content and proliferation markers. Our results showed an obvious increase in the mean ploidy of this population. Specifically, there was a dramatic reduction in the proportion of tetraploid cells (predominant in the original population), and an increase in the proportion of cells with higher ploidies, particularly those whose DNA content was greater than 8c, including some cells with ploidies greater than 16c. Furthermore, there was a reduction in the number of PCNA-expressing cells and the reduction was much more marked in the case of CDK1 that was almost absent in the modal-ploidy treated cells. These alterations concerning ploidy and expression of proliferation markers had completely reverted two weeks after withdrawal of the drug. Our results indicate that methotrexate at a high dosage selects a cell population heterogeneous concerning its ploidy level, composed of one subpopulation of high-ploidy cells and another of modal-ploidy cells that, considering its lack of CDK1 expression, would remain in a latent state to evade the effects of the drug.

Animals↗
PubMed1998

Decelerating flow ventilation effects in acute respiratory failure.

PURPOSE: The purpose of this article is to analyze the effect of a pressure-regulated volume-controlled ventilation mode on lung mechanics and gas exchange in patients with acute respiratory failure. MATERIALS AND METHODS: We ventilated 10 patients with two pressure-limited modes: pressure-controlled ventilation (PC) and pressure-regulated volume-controlled ventilation (PRVC) in random order, for 1 hour each. Patients were stabilized on volume-controlled ventilation (VC) for 30 minutes before, between, and at the end of PC and PRVC to reach baseline conditions. At the end of every VC period and at 30 and 60 minutes of PC and PRVC, respiratory mechanics, gasometrics, and hemodynamic parameters were collected. RESULTS: We found no significant differences between the three VC periods. Comparing VC with the two pressure-limited ventilation modes, peak pressure decreased from 29.4+/-9.1 cm H2O (VC) to 25.9+/-8.4 (PC 60 minutes) and 26.1+/-8.2 (PRVC 60 minutes), and PaCO2 decreased significantly from 38.6+/-3.1 mm Hg (VC) to 36.7+/-2.8 (PC 60 minutes) and 36.8+/-2.9 (PRVC 60 minutes). CONCLUSIONS: Pressure-limited ventilation allows mechanical ventilation for the same tidal volume as VC but results in a lower peak inspiratory pressure and a slightly lower PaCO2. The mechanism responsible for this gas exchange effect is unknown but is probably related to a better air distribution of the decelerated flow. The clinical relevance of this phenomenon remains to be established.

Acute Disease↗
PubMed1998

Neuroprotective role of S12024 against neurodegeneration in the rat dentate gyrus.

We assessed the neuroprotective capabilities of S12024 (R,S 1-methyl 8-(2-morpholinylmethoxy)-1,2,3,4-tetrahydroquinoleine methane sulphonate) in a model of neuronal degeneration in the dentate gyrus of the rat hippocampus. Specific degeneration of a large part of neurons in the lateral blade of the gyrus dentatus occurred after small intrahippocampal injections of water with or without amyloid-beta 1-28 fragment. S12024 reduced the number of animals with neuronal loss in the hippocampus, diminished the extent of the lesion, and reversed deficits of passive avoidance learning acquisition in animals with deposits of amyloid-beta 1-28. These results suggest that S12024 has neuroprotective effects on hippocampal cells and that the neurodegeneration by fluid injection combined with deposit of amyloid-beta 1-28 may be used to assay the neuroprotective activity of pharmacological compounds.

Amyloid beta-Peptides↗
PubMed1998

Brain acetylcholinesterase promotes amyloid-beta-peptide aggregation but does not hydrolyze amyloid precursor protein peptides.

It has been suggested that acetylcholinesterase (AChE) has both a putative proteolytic activity against the amyloid precursor protein (APP), and a capacity to accelerate the assembly of amyloid-beta-peptide (Abeta) into Alzheimer's fibrils. Here, we have studied the ability of bovine brain AChE to share both activities. Results indicate that AChE purified through acridinium was able to process the APP peptides, however after further purification by an edrophonium column, the protease activity was lost. Under both conditions the capacity of the enzyme to promote amyloid formation was maintained. Kinetic studies of the Abeta aggregation process using edrophonium-AChE, indicated that the lag phase of the aggregation process was smaller than the one observed with the esterase purified by acridinium alone. Considering that the total amount of amyloid formed, measured by thioflavine-T fluorescence, was similar for both AChE preparations, our results suggest that the edrophonium-AChE possesses an higher intrinsic capacity to stimulate the aggregation of Abeta(1-40) peptide.

Acetylcholinesterase↗
PubMed1998

The distinctive headache of the occipital condyle syndrome: a report of four cases.

Four examples of occipital condyle syndrome, that is, unilateral occipital pain and ipsilateral tongue paralysis due to selective erosion of the occipital condyle, are reported. The four patients complained of a continuous, severe, unilateral, occipital pain which kept them with the head rotated to the side of the pain and held with their hands. The pain became unbearable with head rotation to the nonpainful side and with unilateral suboccipital palpation. The onset of this very characteristic unilateral headache antedated by as long as 2 1/2 months the ipsilateral hypoglossal paralysis. The occipital condyle syndrome may be the first manifestation of cancer or of chronic inflammatory lesions; recognition of this distinctive headache enables the clinical diagnosis to be made.

Aged↗
PubMed1998

Corynebacterium kroppenstedtii sp. nov., a novel corynebacterium that does not contain mycolic acids.

A strain of a hitherto undescribed coryneform bacterium from human clinical material was characterized by phenotypic and molecular taxonomic methods. Comparative 16S rRNA gene sequence analysis demonstrated the strain represents a novel and deep lineage within the genus Corynebacterium sensu stricto. Chemical analyses revealed the unidentified strain was unusual in that it lacked mycolic acids. Based on the phylogenetic and phenotypic distinctiveness of the unknown isolate, it is proposed that the bacterium be classified as a new Corynebacterium species, for which the name Corynebacterium kroppenstedtii sp. nov. is proposed. The type strain is CCUG 35717T.

Aged↗
PubMed1998

Laminin blocks the assembly of wild-type A beta and the Dutch variant peptide into Alzheimer's fibrils.

Amyloid fibril formation is believed to be a nucleation-dependent polymerization process which may be influenced by various other factors with important consequences for the development, prevention or treatment of amyloidosis. We have previously shown that laminin inhibits A beta peptide fibril formation in vitro. Here we present a kinetic study that indicates laminin to be a potent anti-amyloidosis factor, as it not only inhibited A beta 1-40 fibril aggregation, but also inhibited the aggregation of the Dutch A beta 1-40 variant, a peptide with a higher capacity to aggregate than the wild-type A beta 1-40. The inhibitory effect of laminin on amyloid fibril formation was not overcome by the addition of pre-formed A beta fibrils, suggesting that laminin inhibits the fibril elongation process. At the present time, however, we cannot rule out the possibility that laminin also affects the initial nucleation process of A beta fibril formation. On other hand, laminin was not able to counteract the amyloid fibril formation promoted by acetylcholinesterase (AChE), another component of the amyloid deposits found in AD brains. The effect of laminin may be important as an inhibitor of A beta amyloidogenesis in vivo, specifically at the level of cerebral blood vessels.

Acetylcholinesterase↗