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Biomedical subjects

M Santos

Publications and source records attributed to M Santos.

At least 109 records · Page 6Linked to original sources
PubMed1997

Corticosterone induces hypoactivity of prolactin-immunoreactive cells.

In order to determine whether corticosterone regulates activity of rat lactotrophs by acting directly at the pituitary level, immunohistochemical studies were carried out in adrenalectomized rats, subjected or not to treatment with corticosterone or colchicine, and in monolayer cultures after incubation with corticosterone. Adrenalectomy increased cellular and nuclear areas (p<0.01) of prolactin-immunoreactive cells without affecting their cytoplasmic area. Similar results were found in adrenalectomized and colchicine-treated animals. Corticosterone reversed the effects of adrenalectomy, although normal values were partially reversed. In cultured pituitary cells, exposure to corticosterone reduced numerical density and cellular, cytoplasmic and nuclear areas with respect to control dishes. Morphological differences in shape, arrangement and nuclear features were observed after treatment with corticosterone. These results demonstrate an inhibitory effect of corticosterone on the activity of rat pituitary prolactin cells and suggest that corticosterone induces hypoactivity by acting on the pituitary prolactin cells of male rats.

Adrenalectomy↗
PubMed1997

Pulmonary infection with Nocardia species: a report of 10 cases and review.

Pulmonary nocardiosis (PN) is an infrequent and severe infection due to Nocardia spp., microorganisms that may behave both as opportunists and as primary pathogens. The aim of this study and review was to evaluate the clinical features, evolution and prognostic factors of PN. The study group comprised 10 consecutive patients with pulmonary nocardiosis acquired in a community setting, diagnosed and followed in a tertiary teaching hospital. Chronic obstructive pulmonary disease (COPD), neoplastic disease and human immunodeficiency virus (HIV) infection were the most frequent predisposing factors. Four patients were receiving corticosteroid treatment. Clinical course was chronic and diagnosis was delayed 3 weeks or more in seven of the patients. Lobar or multilobar condensation was the most frequent radiographic pattern. Antimicrobial susceptibility testing showed: 100% sensitivity for amikacin; 83% for imipenem; 71% for cefotaxime; and 71% for trimethoprim-sulphamethoxazole. The disease remained localized in the lung in five cases, with a trend toward chronicity in one with bronchiectasis. In the other five, the disease disseminated, affecting subcutaneous tissue, the central nervous system and the kidney. Three patients died, one with disseminated disease and two who were receiving corticosteroid therapy. The following conclusions were reached: 1) pulmonary nocardiosis is difficult to diagnose, diagnosis is frequently delayed and a high level of suspicion is, thus, required in patients with underlying diseases or chronic corticosteroid therapy; 2) there is frequent dissemination and high mortality; and 3) antimicrobial combinations with proven synergy, such as imipenem and amikacin, are recommended for initial therapy.

Adult↗
PubMed1997

In vivo mucosal uptake, mucosal transfer and retention of iron in mice.

An improved and sensitive method for studying iron absorption in mice with alterations in body iron stores is described. Mice with varying iron status were given a double isotope-labelled test dose containing 59Fe and 51Cr as a non-absorbable indicator, via an oroesophageal needle. Using a whole-body counter it was possible to measure in vivo the initial mucosal iron uptake and long-term iron retention and to calculate mucosal iron transfer. A significant difference was demonstrated between normal and both anaemic and dietary iron-loaded mice with regard to the various steps of iron absorption. When mice were tested twice for iron absorption, the results were highly reproducible. In conjunction with other parameters, the method described is useful in studying the mechanism and the regulation of iron absorption in mice.

Absorption↗
PubMed1997

Actions of xylazine in young swine.

OBJECTIVE: To determine sedative, analgesic, and basic cardiovascular effects of xylazine administered to pigs. ANIMALS: 6 two-month-old Landrace x Large White pigs. PROCEDURE: Xylazine was administered i.v. at increasing dosages (1, 2, 4, 8, and 16 mg/kg of body weight) to otherwise unmedicated, conscious pigs, and the aforementioned effects were determined before xylazine administration and 2, 5, 10, and 15 minutes later. Then a higher xylazine dosage was given after the 15-minute measurements were taken. RESULTS: None of the xylazine dosages induced sufficient analgesia to prevent painful response to tail clamping; considerable excitation with vocalization and without appreciable sedative effect was observed at all dosages. At lower dosages, cardiovascular effects were characterized by bradycardia and biphasic blood pressure response; initial hypertension was followed by hypotension. At higher dosages, severe hypotension with moderate bradycardia was followed by marked bradycardia and return to normal baseline values or slight increase in blood pressure. CONCLUSION: Xylazine did not induce adequate sedative or analgesic effects in pigs at any dosage tested; however, cardiovascular effects were considerable. These effects of xylazine differ from those observed in other domestic species.

Analgesics↗
PubMed1997

[Acute epiglottitis caused by Haemophilus influenzae type b in children: presentation of 21 cases].

BACKGROUND: The aim of this paper is to review the epidemiological, clinical and therapeutical characteristics of Haemophilus influenzae type b (Hib) epiglottitis in children at a time when an efficient and safe vaccination is available. METHODS: The clinical histories of 21 children admitted to Children's Hospital La Fe (1971-1996) with a clinical diagnosis of epiglottitis and isolation of the microorganism in blood cultures (20 cases) and surface culture of the epiglotis (one case) are reviewed. RESULTS: The annual average was 4/100,000 children under 5 years of age. Evolution prior to diagnosis was > 12 hours in 52.4% of the cases. More males were affected (52.4% vs 47.6%). All the children except one (95.2%) were under 5 years of age; 81% were under 3 years of age and 1 child was 6 years and 8 months old. Respiratory distress (100%) and fever > or = 38 degrees C (85.7%) were the most common clinical manifestations. General health was affected in 71.4% of the cases and 66.7% had leucocytosis on admission. The clinical diagnosis was confirmed by direct visualization of the epiglotis in 76.1% of the cases. Hib was isolated in blood culture in 20 cases (95.2%). The strains produced beta-lactamases and were ampicillin-resistant in 57.1%. 19 children (90.5%) required endotracheal intubation. Initial empiric antibiotic therapy was third generation cephalosporins (cefotaxime or ceftriaxone) alone or combined with ampicillin. One child died (4.8%). CONCLUSIONS: Pediatricians must still be aware of this serious infection in order to diagnosis and treat it as early as possible.

Acute Disease↗
PubMed1996

Defective iron homeostasis in beta 2-microglobulin knockout mice recapitulates hereditary hemochromatosis in man.

Previously, hepatic iron overload resembling that in hereditary hemachromatosis (HH) has been found in beta 2-microglobulin knockout (beta 2m-/-) mice. We have now characterized iron metabolism in beta 2m-/- mice. The mutant mice fail to limit the transfer of iron from mucosal cells into the plasma. Transferrin saturation is abnormally high. Pathologic iron depositions occur predominantly in liver parenchymal cells. Reconstitution with normal hematopoietic cells redistributes the iron from parenchymal to Kupffer cells, but does not correct the mucosal defect. We conclude that (a) iron metabolism is defective in the gut mucosa as well as the liver of beta 2m-/- mice; and (b) a beta 2m-dependent gene product is involved in iron homeostasis. Recently, a novel gene of the major histocompatibility complex class I family, HLA-H, has been found to be mutated in a large proportion of HH patients. Our data provide functional support for the proposed causative role of HLA-H mutations in HH.

Absorption↗
PubMed1996

An autonomously replicating plasmid transforms Botrytis cinerea to phleomycin resistance.

A transformation system has been developed for the pathogen fungus Botrytis cinerea, based on the utilization of the wide host plasmid pUT737 that contains the Sh ble gene, conferring resistance to phleomycin. Transformed protoplasts were regenerated at 10-25 micrograms ml(-1) of phleomycin, at a frequency of 25-40 transformants per microgram of DNA, and they were resistant up to 50 micrograms ml(-1). Southern hybridization using undigested and digested total DNA showed the presence of circular autonomously replicating plasmid pUT737 in the transformants. Reisolated plasmid from transformed fungus transformed E. coli and rescued plasmid was identified as PUT737. Transformants were grown for four generations under non-selective conditions and replicative plasmids were still detected. Plasmids present in all transformants at this stage had been modified from native pUT737 and showed the same size and configuration indicating that selection through stabilizing plasmid forms has happened.

Antifungal Agents↗
PubMed1996

Effects of nitric oxide donors sodium nitroprusside and 3-morpholino-sydnonimine on prolactin secretion in conscious rats.

In the present study, we have examined the possible involvement of the central nitric oxide (NO) pathway in the control of prolactin secretion in vivo. The effects of intracerebroventricular (i.c.v.) injections of L-arginine (L-Arg), a precursor of NO, N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase (NOS), and of sodium nitroprusside (SNP) and 3-morpholino-sydnonimine (SIN-1), NO donors, on basal prolactin levels were studied in conscious male rats. Microinjections of L-Arg (100 and 500 mu g) or L-NAME (100 and 500 mu g) did not modify plasma prolactin levels, however i.c.v. injections of both SNP (1, 5, 10 and 20 mu g) and SIN-1 (1, 10 and 100 mu g) induced dose-dependent increases in these levels although SNP was much more potent than SIN-1. These results suggest a role of NO in the control of prolactin secretion.

Animals↗
PubMed1996

Beneficial effects of cyclosporine and rapamycin in small bowel ischemic injury.

Gut ischemia has been implicated in the pathogenesis of necrotizing enterocolitis. Cyclosporine A and rapamycin, both potent novel immunosuppressants which act on signal transduction pathways in CD4+ T-cells, could potentially modulate immune/inflammatory cellular reactions involved in tissue ischemia/reperfusion injury. We hypothesized that cyclosporine A and rapamycin would preserve mucosal cell function and attenuate inflammatory T-cell-mediated cellular changes associated with small bowel ischemic injury. Forty Sprague-Dawley rats underwent 60 min of gut ischemia by vascular occlusion of the superior mesenteric vessels. Animals were randomized to four groups (n = 10): cyclosporine A (CSA, 5 mg/kg/day SQ), rapamycin (RAP, 2 mg/kg/day SQ), cyclosporine A and rapamycin (C&R), and vehicle given to controls (CON). Following 1 hr of reperfusion, small bowel was harvested for xanthine oxidase (XO, units/mg protein) and maltase (MALT, mM substrate degraded/min/g protein) assays. Blood was obtained from the portal vein for tumor necrosis factor-alpha (TNF-alpha, pg/ml) assay. The results of the study are presented below (mean +/- SEM, *, P < 0.05 versus controls). (Table in text) The results indicate that cyclosporine and rapamycin each play a significant role in attenuating ischemia/reperfusion injury in the gut. These data suggest that there are cytoprotective and anti-inflammatory mechanisms of these drugs independent of T-cell signal transduction that provide some protective effect in small bowel ischemia. Furthermore, T-cell-mediated immune mechanisms may not be associated with the adverse effects of small bowel ischemia/reperfusion injury. Additional investigation will be necessary in order to define the role of T-cell-mediated immune injury in the gut and how this relates to the beneficial effect of immunosuppression in small bowel mucosal ischemic injury.

Animals↗
PubMed1996

Cytosolic ascorbate peroxidase from Arabidopsis thaliana L. is encoded by a small multigene family.

A second cytosolic ascorbate peroxidase (cAPX; EC 1.11.1.11) gene from Arabidopsis thaliana has been characterised. This second gene (designated APX1b) maps to linkage group 3 and potentially encodes a cAPX as closely related to that from other dicotyledonous species as to the other member of this gene family (Kubo et al., 1993, FEBS Lett 315: 313 317; here designated APX1a), which maps to linkage group 1. In contrast, the lack of sequence similarity in non-coding regions of the genes implies that they are differentially regulated. Under non-stressed conditions only APX1a is expressed. APX1b was identified during low-stringency probing using a cDNA coding for pea cAPX which, in turn, was recovered from a cDNA library by immunoscreening with an antiserum raised against tea plastidial APX (pAPX). No pAPX cDNAs were recovered, despite the antiserum displaying specificity for pAPX in Western blots.

Amino Acid Sequence↗
PubMed1996

Mutation analysis reveals an insertional hotspot in exon 4 of the LDL receptor gene.

Mutation analysis of the low density lipoprotein receptor (LDLR) gene revealed a novel 8-bp duplication after nucleotide 681 in a Costa Rican patient with familial hypercholesterolaemia. The frameshift caused by this mutation results in a premature termination codon in the EGF precursor homology domain of the mature LDLR, whereby a truncated protein of the first 206 residues with an additional 39 abnormal residues would be created. The insertion overlaps with previously described duplications of 18 bp and 21 bp, thus revealing an insertional hotspot in exon 4 of the LDLR gene. We propose that the structural features of this region of the LDLR gene contribute significantly to genetic instability and the subsequent DNA duplication via an endogenous sequence-directed mechanism of mutagenesis.

Amino Acid Sequence↗
PubMed1996

The effect of cyclosporine in gut ischemic injury: a computerized morphometric and enzymatic analysis.

PURPOSE: Gut ischemia has been implicated in the pathogenesis of necrotizing enterocolitis. Cyclosporine A (CSA), a potent immunosuppressant, attenuates immune/inflammatory cellular reactions. CSA also might be useful for inhibiting cellular immune responses involved in tissue ischemia/reperfusion injury. The authors hypothesized that CSA would attenuate inflammatory cellular changes associated with gut ischemic injury and that these effects could be quantified by computerized morphometry. METHODS: Twenty Sprague-Dawley rats underwent 60 minutes of gut ischemia by vascular occlusion of the superior mesenteric vessels. After 1 hour of reperfusion, the ischemic small bowel was harvested for histopathological examination and computerized morphometry, as well as xanthine oxidase (XO, U/mg protein) and maltase (MALT, mmol/L substrate degraded/min/mg protein) assays. CSA (5 mg/kg/d subcutaneously) was given to experimental animals (CSA, n = 10) for 5 days before ischemia, and vehicle was given to controls (CON, n = 10). The computer morphometric parameters studied were: surface index (SI, mucosal surface length per linear unit of intestine), average villous thickness (AVT), and average villous height (AVH). RESULTS: Results are provided in Table 1. CONCLUSION: The results of this study show that CSA may play a role in attenuating ischemia/reperfusion injury in the gut. Enzymatic analysis showed a beneficial role in the preservation of mucosal cell function after gut ischemia/reperfusion injury, as demonstrated by an elevated maltose level. Computerized morphometry demonstrated significant differences in all parameters in the experimental group, showing that CSA does confer gut mucosal protection during ischemia.

Animals↗
PubMed1996

NADPH-diaphorase activity and vasopressin in the paraventricular nucleus of the hypothalamus following adrenalectomy.

In order to investigate novel neuroendocrine functions of the nitric oxide synthesizing enzyme a combined histochemical and immunocytochemical study focused on the paraventricular nucleus of the hypothalamus was conducted to check a possible influence of bilateral adrenalectomy on three different neuronal populations, NADPH diaphorase (ND)-positive, vasopressin (VP)-immunoreactive and neurons expressing both markers. In the adrenalectomized animals, a slight increase (P > 0.05) of the number of ND magnocellular neurons was detected, whereas no changes were observed in the ND-parvicellular population and in the neurons showing coexistence (magno- and parvicellular) (P > 0.05). By contrast, following bilateral adrenalectomy, a significant increase (P < 0.05) in the VP-parvicellular population (anterior, medial and periventricular subdivisions) was detected, which was reversed when the animals received daily doses of corticosterone. These results suggest that nitric oxide is not closely related to the hypothalamic regulation of the adenocorticotropin secretion exerted by the paraventricular nucleus.

Adrenal Glands↗
PubMed1996

Dopamine inhibits in vitro release of VIP and proliferation of VIP-immunoreactive pituitary cells.

A double immunohistochemical study for VIP and proliferating cell nuclear antigen (PCNA) was carried out on monolayer cultures from adult male rats pituitary glands treated with dopamine (ranging from 10(-9) to 10(-5) M), in order to establish whether or not dopamine is involved in the regulation of the proliferation rate of pituitary VIP-immunoreactive cells. For all doses of dopamine assayed, the release of VIP to the culture medium, the numerical density of VIP-immunoreactive cells and the percentages of VIP- and PCNA-immunoreactive cells decreased significantly after dopamine treatment. These results suggest that dopamine could be a physiological inhibitor involved in the modulation of pituitary VIP proliferation rate.

Animals↗
PubMed1996

The evolutionary history of Drosophila buzzatii. XXXIII. Are Opuntia hosts a selective factor for the inversion polymorphism?

Previous work has shown fitness differences among chromosomal arrangements by means of selection component analysis in two Drosophila buzzatii natural populations, one of which is native to Argentina and the other a colonized population from Carboneras, Spain. Founder effects or niche shifts were proposed to explain the differences observed in the pattern of pleiotropic effects of inversions on fitness components. In this paper, we address the possible role of niche shifts by determining whether differential attraction to, oviposition on, or utilization of the rotting cladodes of two different Opuntia species (O. quimilo and O. ficus-indica) occurred among individuals carrying different second chromosome karyotypes in a natural Argentinian population. Through the analysis of more than 2500 individuals comprising five different life cycle stages associated with the necroses of these two cactus species, we found that the distributions of inversion frequencies in samples of adult flies, third instar larvae and emerging adults collected on both Opuntia species were not significantly different. Likewise, no evidence of differential oviposition was observed. These findings suggest that niche shifts cannot, solely, account for the changes observed in the Carboneras population. In addition, the selection component analysis did not reveal any significant relationship between chromosomal arrangements and the fitness components tested. These results suggest either that fitness differences might be too small to be detected or that the assumptions of the model concerning the mode of selection may not be tenable in the studied population.

Animals↗
PubMed1996

[Lung diseases due to opportunistic environmental Mycobacteria in patients uninfected with human immunodeficiency virus. Risk factors, clinical and diagnostic aspects and course].

Diseases caused by opportunistic ambient mycobacteria (OAM) are common in HIV-positive patients, although they also occur in immunocompetent individuals. The objective of the present study was to describe the risk factors, clinical signs, course and microbiological spectrum of OAM that cause pulmonary diseases in non HIV-infected individuals in our community. We reviewed 29 consecutive patients with OAM-caused pulmonary disease between 1989-1994 (26 men and 3 women, mean age 58 +/- 14 years). Infections were by Mycobacterium kansasii, 19 (66%) cases; M. avium complex, 7 (24%) cases; M. chelonei, 2 (7%) cases, and M. flavescens, one (3%) case. Risk factors most often associated to infection were smoking and a history of pulmonary disease (chronic obstructive pulmonary disease or residual tuberculosis). Clinical signs were non specific, although toxic syndrome and unproductive cough predominated. Chest films were indistinguishable from those for infection by M. tuberculosis, with cavitated alveolar fibrosis being the main pattern. In vitro drug sensitivity tests showed that all strains were resistant to isoniazid, and that M. avium complex and M. chelonei strains were resistant to rifampicin, streptomycin and, to a lesser degree, to ethambutol. With prolonged medical treatment lasting from 12 to 24 months with first line drugs, outcome was good for the 17 patients for whom full follow-up information was available. Therapy failed to eradicate the bacteria in only 2 patients.

Adult↗