PubMed Health⌕ Search

Biomedical subjects

C Pereira

Publications and source records attributed to C Pereira.

At least 19 recordsLinked to original sources
PubMed2006

Iberian study of aeroallergens sensitisation in allergic rhinitis.

BACKGROUND: Allergic rhinitis (AR) is a prevalent allergic disease in Iberian countries, but there are no recent epidemiological studies that characterize this pathology according to clinical classification and aeroallergens sensitisation. This is a clinical study, representative of each country METHODS: Descriptive, observational cross-sectional, population-based study carried-out in Portugal and Spain. 3397 consecutive patients (5 regions in Spain and 3 regions in Portugal) were selected for clinical observation and skin prick tests were carried out using the same panel of standardized aeroallergens. RESULTS: 3225 patients (aged 10-50 years old) completed the study (IC 95%, SE 15). Intermittent rhinitis makes up 36% of the entire sample. Of them, intermittent AR mild forms represented 82% in Spain and 92% in Portugal that is, 87% for Iberian countries. Persistent types of rhinitis showed exactly the same rate of severity in Portugal and Spain, 44% mild and 56% moderate/severe. Seasonal forms represent 37% while 63% were perennial. BA was present in 49% of AR patients. There were significant differences between aeroallergens according to the different regions considered. Mites and grass pollens are the most relevant aeroallergens in Spanish and Portuguese AR patients, while Alternaria showed higher positive rates among 10-20 year old patients. CONCLUSIONS: This study characterizes the AR patients in Iberian countries according to the ARIA classification. No correlation was observed between this classification and the conventional (seasonal/perennial). Our results also characterize the allergic cutaneous pattern of aeroallergen sensitisation using the same panel of standardized allergens and show differences between the different regions analysed.

Adolescent↗
PubMed2005

Protective effect of zinc on amyloid-beta 25-35 and 1-40 mediated toxicity.

Amyloid beta-peptide (Abeta) is widely held to be associated with Alzheimer's disease, the insoluble aggregates of the peptide being the major constituents of senile plaques. In this study, we evaluated the effect of Zn(2+) (5, 50 and 200 microM) on Abeta induced toxicity using the human teratocarcinome (NT2) cell line. Our results proved that 50 and 200 microM Zn(2+) protected NT2 cells from Abeta 25-35 toxicity. Zinc was also shown to be effective by preventing the loss of mitochondrial membrane potential (DeltaPsi(m)) induced by Abeta 25-35, not allowing cytochrome c release from mitochondria, and subsequently, caspase 3 activation. However, when the cells were treated with Abeta 1-40, only Zn(2+) 5 microM had a protective effect. We have further observed that 5 microM Zn(2+) prevented Abeta 1-40 aggregation into a beta-sheet structure. Considering the results presented, we argue that Zn(2+) has a concentration-dependent protective effect.

Amyloid beta-Peptides↗
PubMed2005

mtDNA single macrodeletions associated with myopathies: absence of haplogroup-related increased risk.

As for any non-recombining genome, any mutation at mtDNA, if not recurrent, appears on a particular haplotype background, allowing its detection by haplogroup association studies. It has been shown that the propensity for occurrence of single macrodeletions at a level beyond the pathological threshold is associated with super-haplogroup U/K. However, in this report, we present evidence for the absence of preferential haplogroup backgrounds for single macrodeletions. We have analysed how haplogroup diagnostic polymorphisms could disrupt direct repeats usually flanking the deleted segment, and we have concluded that for the Common Deletion, no such polymorphisms are observed in humans, but they do occur in other primates. Furthermore, we also report five new single macrodeletions.

Adolescent↗
PubMed2005

Neurodegenerative pathways in Parkinson's disease: therapeutic strategies.

Parkinson's disease (PD), considered one of the major neurological disorders, is characterized by the loss of dopaminergic neurons in the pars compacta of the substantia nigra and by the presence of intraneuronal cytoplasmic inclusions called Lewy bodies. The causes for degeneration of PD neurons remain unclear, however, recent findings contributed to clarify this issue. This review will discuss the current understanding of the mechanisms underlying Parkinson's disease pathogenesis, focusing on the current and potential therapeutic strategies for human treatment.

Animals↗
PubMed2005

Alzheimer's disease-associated neurotoxic mechanisms and neuroprotective strategies.

The characteristic hallmarks of Alzheimer's disease (AD), the most common form of dementia in the elderly, include senile plaques, mainly composed of beta-amyloid (Abeta) peptide, neurofibrillary tangles and selective synaptic and neuronal loss in brain regions involved in learning and memory. Genetic studies, together with the demonstration of Abeta neurotoxicity, led to the development of the amyloid cascade hypothesis to explain the AD-associated neurodegenerative process. However, a modified version of this hypothesis has emerged, the Abeta cascade hypothesis, which takes into account the fact that soluble oligomeric forms and protofibrils of Abeta and its intraneuronal accumulation also play a key role in the pathogenesis of the disease. Recent evidence posit that synaptic dysfunction triggered by non fibrillar Abeta species is an early event involved in memory decline in AD. The current understanding of the molecular mechanisms responsible for impaired synaptic function and cognitive deficits is outlined in this review, focusing on oxidative stress and disturbed metal ion homeostasis, Ca(2+) dysregulation, mitochondria and endoplasmic reticulum dysfunction, cholesterol dyshomeostasis and impaired neurotransmission. The activation of apoptotic cell death as a mechanism of neuronal loss in AD, and the prominent role of neuroinflammation in this neurodegenerative disorder, are also reviewed herein. Furthermore, we will focus on the more relevant therapeutical strategies currently used, namely those involving antioxidants, drugs for neurotransmission improvement, hormonal replacement, gamma- and beta- secretase inhibitors, Abeta clearance agents (Abeta immunization, disruption of Abeta fibrils, modulation of the cholesterol-mediated Abeta transport), non-steroidal anti-inflammatory drugs (NSAIDs), microtubules stabilizing drugs and kinase inhibitors.

Alzheimer Disease↗
PubMed2005

Development of new IgE specificities to hymenoptera allergens during venom-specific immunotherapy.

BACKGROUND: Despite the benefits of specific immunotherapy (SIT) being clinically well documented for allergic diseases, new IgE specificities to SIT extract allergens could be induced during the treatment. The authors evaluated these changes in patients allergic to Hymenoptera. METHODS: Six patients allergic to Hymenoptera venom were included in the study. Specific IgE (sIgE) levels determination and IgE immunoblots to Apis mellifera, Vespula spp. and Polistes spp. venom were performed before and after one year of SIT. RESULTS: All patients had sIgE levels reduction, after the first year of treatment, except one in whom there was an increase in sIgE levels to Apis mellifera venom, and two patients that maintained a similar value for Vespula spp. venom sIgE before and after one year of treatment. The immunoblot analysis revealed that most of the bands detected before beginning SIT, decreased in intensity or disappeared after one year of treatment. 3/6 patients developed new IgE specificities to venom extracts: one patient to the venom allergens in the treatment, other patient to allergens in other venom and another patient to both. After one year of treatment one of these patients tolerated a field sting by the corresponding insect. The newly recognised proteins were all minor allergens. CONCLUSION: These results confirm that sIgE levels tend to reduce during SIT, and the bands identifying some allergens in the blot tend to decrease or disappear. Nonetheless venom SIT can be responsible for the induction of new sensitisations to other venom allergens, apparently without clinical relevance.

Adult↗
PubMed2005

Urban versus rural environment--any differences in aeroallergens sensitization in an allergic population of Cova da Beira, Portugal?

Cova da Beira is an interior central region of Portugal, with a population of 93000 inhabitants divided in urban and rural living areas. The aim of this study was to access the prevalence of aeroallergens sensitisation in an allergic population, according to the urban and the rural environmental exposure and according to age. 1096 patients observed for suspected allergic symptoms, for a five-year period (1995-2000) were submitted to skin prick tests and were included in this study. They were divided in two environmental exposure groups (A: urban; B: rural) and in to four age subgroups (subgroup I: < or = 10yr; subgroup II: 11-20yr; subgroup III: 21-40yr; subgroup IV: >40yr). The total population included 444 male (40.5%) and 652 female (59.4%) with an average age of 26.5 +/- 17.2 yr. 83% of the 1096 performed SPT were positive. The frequency of aeroallergens sensitisation, comparing the urban versus the rural environment, was respectively: D. pteronyssinus 32% and 34.7%, D. farinae 28.5% and 30.7%, moulds mixture 15.3% and 12%, cat dander 17.1% and 15.2%, dog dander 11% and 10%, grasses mixture 51.3% and 36.4%, Parietaria judaica 29.4% and 14%, Olea europea 30.2% and 23.3%. The sensitisation to indoor aeroallergens, was similar in all the age subgroups and it was lower than that to pollens. There were important differences concerning the pollen sensitisation, when comparing the urban and the rural environmental exposure. We admit that pollution could enhance the sensitisation to pollens in the urban environment.

Adolescent↗
PubMed2004

Kinetics and dynamic evaluation of specific immunotherapy.

UNLABELLED: Specific immunotherapy (SIT) is frequently used in the treatment of allergic diseases. However, the mechanisms by which SIT achieves clinical improvement remained unclear. We decided to study the in vivo kinetics of this therapy, using a nuclear medicine approach (leukocytes labelled with 99mTc-HMPAO) in patients on maintenance doses of specific immunotherapy with confirmed clinical efficacy. MATERIAL AND METHODS: We studied 13 allergic patients grouped according to different treatment schedules: subcutaneous aqueous allergenic extract (3 latex and 2 hymenoptera venom), subcutaneous depot extract (2 house dust mite and 2 pollens), subcutaneous modified allergens (2 pollens), sublingual extract (2 house dust mites). The control group included two allergic patients submitted to subcutaneous injections of bacterial extract (1 patient--positive control), and aqueous solution (1 patient). At the same time that the therapeutic allergen was administered subcutaneously, the autologous labelled white cells were injected intravenously in a peripheral vein in the contralateral arm. A thoracic dynamic acquisition of 60 mins, 64x64 matrix, 2 frame/min, in anterior view was performed. Static acquisition for 256x256 matrix, during 5 mins each at 60, 90, 120, 180, 240, 300 and 360 mins after the administration of the radiolabelled leukocytes, in thoracic (anterior and posterior), and abdominal view were performed. During the examination, the local erythema was monitored. A similar procedure was undertaken for Sublingual administration of immunotherapy. RESULTS: The inflammatory activity at the site of SIT injection (aqueous depot extract) started in the first hour and the increase was time related. For modified allergen extract and sublingual SIT the activity was present since the beginning of the administration. The ascendant lymphatic drainage, which was directed to the homolateral axillary region, to the lymphoid tissue of the upper mediastinum and to the anterior region of the neck began earlier. Thoracic focalisations were present for all the patients, whereas bowel focalisations were only observed for the subcutaneous route of administration. Sublingual SIT did not induce axillary or intestinal inflammatory focalisations, even though the patients had swallowed the allergenic extract. The uptake coefficient in individualized areas corrected to the uptake coefficient background was also studied. CONCLUSIONS: For the subcutaneous route of administration, except for glutaraldehyde-modified allergen, the local inflammatory activity at the allergenic injection site was significantly higher in depth and was time dependent, maintaining activity even after complete disappearance of the erythema and/or wheal. These results express a prompt inflammatory involvement of the immune system with this allergenic therapy, which was unexpected until now. We also observed differences concerning allergic diseases, the type of allergenic extracts and routes of administration.

Administration, Sublingual↗
PubMed2003

Specific immunotherapy for severe latex allergy.

We studied 4 patients (3 adult females + 13y old boy) with latex allergy. All patients had anaphylaxis related with latex and oral-latex-fruit syndrome. All 3 females had severe symptoms in the workplace. The boy had spina bifida with 9 previous surgeries and needed further surgical interventions. Positive skin prick tests (SPT), the presence of serum latex specific IgE (CAP-RAST, Pharmacia-Upjohn, Sweden- class 3 in the 3 females and class 4 in the boy) demonstrated the sensitisation. All 4 patients were treated with specific immunotherapy (SIT) with aqueous extract (ALK-ALK-ABELLO SA, Spain) administered subcutaneously at the hospital, by a modified rush schedule. A maintenance dose (MD) of 0.35_g protein was established according to the magnitude of local reactions (LRs). In one patient a higher dose induced the appearance of a systemic reaction (SR) 40 min after administration, which promptly remitted with treatment. After reaching MD, all 3 females remained assymptomatic at workplace. A challenge test with latex gloves was performed. Two months after MD was reached 2 females had no symptoms and one other had mild symptoms of rhinoconjunctivitis. The boy was subjected to a surgical intervention with no allergic reaction. We also observed a reduction on skin reactivity to latex in all patients by prick tests. We consider SIT with latex to be highly effective, safe and well tolerated provided we use this dose of the allergenic extract.

Adolescent↗
PubMed2002

Blood group antigen profile predicted by molecular biology-use of real-time polymerase chain reaction to genotype important KEL, JK,RHD, and RHCE alleles.

The most clinically important blood group systems in transfusion medicine, excluding the ABO system, are the RH, Kell, and Kidd systems. Alloantibodies to antigens of these systems may be produced following blood transfusion or during pregnancy and can result in serious hemolytic transfusion reactions and hemolytic disease of the newborn. We developed rapid and robust techniques for RHD, RHCE, KEL, and JK genotyping with the use of a real-time polymerase chain reaction instrument. Two fluorescence-based methods for the detection of amplification products were used: for KEL1/KEL2, JK1/JK2, and RHE/RHe (exon 5) we used the hybridization probes protocol; for RHC/RHc the analysis was done in sequences of exon 1 for RHC and exon 2 for RHc; and for RHD, analysis was done in sequences of intron 4, exon 7, and exon 4 pseudogene using the SYBR Green I protocol. The genotyping tests were validated with samples from 85 Caucasian Portuguese and 15 Black European blood donors. Complete phenotype-genotype correlations were obtained. The potential use of the presented methods can be predicted in clinical transfusion medicine, allowing appropriate monitoring, early intervention, and improved care. When blood group genotyping techniques are necessary, this methodology is highly competitive for a routine laboratory.

Journal Article↗
PubMed2001

The alpha-linolenic acid content of green vegetables commonly available in Australia.

Green vegetable consumption has long been considered to have health benefits mainly due to the vitamins, minerals and phytonutrients (such as vitamin C, folate, antioxidants etc) contained in a vegetable-rich diet. Additionally, green vegetables are known to contain a relatively high proportion of omega-3 polyunsaturated fatty acids (PUFAs), primarily in the form of alpha-linolenic acid (18:3n-3). However, there are no data available on the fatty acid composition and concentration of green vegetables commonly consumed in Australia. The present study determined the fatty acid content of 11 green vegetables that are commonly available in Australia. The total fatty acid concentrations of the vegetables under study ranged from 44 mg/100 g wet weight in Chinese cabbage to 372 mg/100 g in watercress. There were three PUFAs in all vegetables analyzed; these were 16:3n-3, 18:2n-6, and 18:3n-3 fatty acids. Sample vegetables contained significant quantities of 16:3n-3 and 18:3n-3, ranging from 23 to 225 mg/100 g. Watercress and mint contained the highest amounts of 16:3n-3 and 18:3n-3, and parsley had the highest amount of 18:2n-6 in both percentage composition and concentration. Mint had the highest concentration of 18:3n-3 with a value of 195 mg/100 g, while watercress contained the highest concentration of 16:3n-3 at 45 mg/100 g. All 11 green vegetables contained a high proportion of PUFAs, ranging from 59 to 72% of total fatty acids. The omega-3 PUFA composition ranged from 40 to 62% of total fatty acids. Monounsaturated fatty acid composition was less than 6% of total fatty acids. The proportion of saturated fatty acids ranged from 21% in watercress and mint to 32% of total fatty acids in Brussels sprouts. No eicosapentaenoic and docosahexaenoic acids were detected in any of the samples. Consumption of green vegetables could contribute to 18:3n-3 PUFA intake, especially for vegetarian populations.

Australia↗
PubMed2001

Effect of a complex environmental mixture from coal tar containing polycyclic aromatic hydrocarbons (PAH) on the tumor initiation, PAH-DNA binding and metabolic activation of carcinogenic PAH in mouse epidermis.

Human exposure to polycyclic aromatic hydrocarbons (PAH) occurs through complex mixtures such as coal tar. The effect of complex PAH mixtures on the activation of carcinogenic PAH to DNA-binding derivatives and carcinogenesis were investigated in mice treated topically with NIST (National Institute of Standards and Technology) Standard Reference Material 1597 (SRM), a complex mixture of PAH extracted from coal tar, and either additional benzo[a]pyrene (B[a]P) or dibenzo[a,l]pyrene (DB[a,l]P). In an initiation-promotion study using 12-O-tetradecanoylphorbol-13-acetate as the promoter for 25 weeks, the SRM and B[a]P co-treated mice had a similar incidence of papillomas per mouse compared with the group exposed to B[a]P alone as the initiator. PAH-DNA adduct analysis of epidermal DNA by 33P-post-labeling and reversed-phase high-performance liquid chromatography found the SRM co-treatment led to a significant decrease in the total level of DNA adducts and B[a]P-DNA adducts to less than that observed in mice treated with B[a]P alone at 6, 12 and 72 h exposure. After 24 and 48 h exposure, there was no significant difference in the levels of adducts between these groups. In the DB[a,l]P initiation-promotion study, the co-treated group had significantly fewer papillomas per mouse than mice treated with DB[a,l]P alone as initiator. Averaging over the times of exposure gave strong evidence that mice co-treated with SRM and DB[a,l]P had a significantly lower level of PAH-DNA adducts than mice treated with DB[a,l]P alone. Western immunoblots showed that both cytochrome P450 (CYP) 1A1 and 1B1 were induced by the SRM. These results are consistent with the hypothesis that two major factors determining the carcinogenic activity of PAH within a complex mixture are (i) the persistence of certain PAH-DNA adducts as well as total adduct levels, and (ii) the ability of the components present in the mixture to inhibit the activation of carcinogenic PAH by the induced CYP enzymes.

Animals↗