88 research outputs found
Antibody reactivity against potato apyrase, a protein that shares epitopes with Schistosoma mansoni ATP diphosphohydrolase isoforms, in acute and chronically infected mice, after chemotherapy and reinfection
Schistosoma mansoni ATP diphosphohydrolase isoforms and potato apyrase share conserved epitopes. By enzyme-linked immunosorbent assays, elevated levels of IgM, IgG2a and IgG1 antibody reactivity against potato apyrase were observed in S. mansoni-infected BALB/c mice during the acute phase of infection, while only IgM and IgG1 antibody reactivity levels maintained elevated during the chronic phase of infection. Antibody reactivity against potato apyrase was monitored over an 11-month period in chronically-infected mice treated with oxamniquine. Eleven months later, the level of seropositive IgM decreased significantly (~30%) compared to the level found in untreated, infected mice. The level of seropositive IgG1 decreased significantly four months after treatment (MAT) (61%) and remained at this level even after 11 months. The IgG2a reactivity against potato apyrase, although unchanged during chronic phase to 11 MAT, appeared elevated again in re-infected mice suggesting a response similar to that found during the acute phase. BALB/c mouse polyclonal anti-potato apyrase IgG reacted with soluble egg antigens probably due to the recognition of parasite ATP diphosphohydrolase. This study, for the first time, showed that the IgG2a antibody from S. mansoni-infected BALB mice cross-reacts with potato apyrase and the level of IgG2a in infected mice differentiates disease phases. The results also suggest that different conserved-epitopes contribute to the immune response in schistosomiasis
Angiotensin Converting Enzyme Gene Polymorphisms and Coronary Risk in a Portuguese Population
Introdução: A história familiar de doença das
artérias coronárias (DAC) constitui um
poderoso marcador de risco de DAC,
independente dos factores de risco
tradicionais. Poderá ser descodificado
reconhecendo os polimorfismos associados ao
aumento de risco. Têm surgido resultados
contraditórios em relação à ligação entre os
polimorfismos do gene da enzima de conver são da angiotensina (ECA) e o risco de DAC.
Objectivo: Com o presente trabalho
pretendemos avaliar se os polimorfismos do
gene da ECA constituem factor de risco de
doença das artérias coronárias.
Métodos: Estudo caso-controlo, incluindo
517 controlos escolhidos aleatoriamente dos
cadernos eleitorais, sem história sugestiva de
DAC e 301 doentes com história de enfarte
agudo do miocárdio ou doença coronária
confirmada por coronariografia, com pelo
menos 75 % de obstrução de um dos vasos
coronários. Tentou-se que os casos e controlos
não fossem significativamente diferentes em
termos de sexo e idade.
Os polimorfismos dialélicos do gene da ECA
foram tipados por amplificação por PCR. Os
produtos de amplificação eram identificados
em gel de poliacrilamida, por electroforese.
Os dados foram avaliados recorrendo ao SPSS
for Windows,Background: A family history of coronary
heart disease (CHD) is a strong risk marker
for the disease, independently of classical
risk factors. It could be decoded by
recognizing the polymorphisms associated
with increased risk. Renin-angiotensin
system genes are candidate genes in CHD
and the deletion allele of the angiotensin
converting enzyme (ACE) has been reported
as deleterious. However, there is
disagreement as to the role of the
insertion/deletion polymorphism of the ACE
gene in coronary risk.
Aim: To evaluate whether ACE gene
polymorphisms constitute a CHD risk factor.
Methods: We conducted a population-based
case-control study of 301 subjects with a
history of myocardial infarction or
angiographic evidence of coronary heart
disease and 510 age- and gender-matched
controls, without CHD, living in a region with
high CHD mortality rates. Blood samples
were taken, DNA extracted and genotypes
determined by the polymerase chain reaction
(PCR). Amplification products were identified
by agarose gel electrophoresis.info:eu-repo/semantics/publishedVersio
Polymorphism of the ACE Gene is Associated with Extent and Severity of Coronary Disease
Introdução: Os doentes com doença das
artérias coronárias (DAC) apresentam
extensão da doença e evolução muito
variáveis, que muito vezes nos escapam e que
ultrapassam os factores de risco tradicionais.
As diferenças poderão, pelo menos em parte,
ser explicáveis por polimorfismos genéticos
menos favoráveis que lhe estejam associados.
Os polimorfismos do gene da ECA têm sido
profusamente avaliados, embora se
desconheça a ligação entre estes
polimorfismos e a extensão da DAC.
Objectivo: Os autores pretendem avaliar se os
polimorfismos do gene da enzima de conver são da Angiotensina I (ECA) constituem um
marcador da extensão e gravidade da DAC.
Métodos: Estudo descritivo, em 296 doentes
com história de enfarte do miocárdio ou
doença coronária confirmada por
coronariografia, com pelo menos 75 % de
obstrução de um dos vasos coronários.
A quantificação da gravidade e extensão, foi
feita segundo o score de Leaman, de acordo
com o número de artérias com redução do
diâmetro superior a 75 %, e com o número de
segmentos coronários afectados.
Os genotipos do ECA, foram tipados por
amplificação por PCR e os produtos de
amplificação separados por electroforese em
gel de poliacrilamida. Calculou-se a média e desvio padrão dos
scores coronários dos três polimorfismos e os
valores foram comparados estatisticamente
recorrendo ao teste T de Student para
amostras independentes.
Resultados e Conclusão: O genotipo DD
aparece neste estudo claramente ligado Ã
extensão da DAC, com um alto grau de
significância. A confirmar-se este conceito,
poderá justificar-se fazer uma prevenção
secundária particularmente cuidadosa nos
doentes vasculares portadores deste genotipo.Background: The progression and extent of
coronary heart disease (CHD) are extremely
variable and in many instances independent
of conventional risk factors.
The differences may be partly explained by
less favorable genetic polymorphisms that are
associated with them. The polymorphisms of
the angiotensin I converting enzyme (ACE)
gene have been thoroughly evaluated, but the
connection between them and the extent of
CHD is unknown.
Aims: Our study is aimed at determining
whether any or all of the polymorphisms of
the ACE gene are markers of the extent and
severity of CHD.
Methods: This was a descriptive study of 296
patients with a history of myocardial
infarction or with coronary disease confirmed
by coronary angiography. The severity of
CHD was quantified according to Leaman’s
score (based on the number of arteries with
more than 75 % reduction in diameter and the
number of affected coronary segments). The
ACE genotypes were determined by specific
polymerase chain reaction amplification and
the segments were subjected to
polyacrylamide gel electrophoresis. The mean coronary score and standard deviation of the
three polymorphisms were calculated and the
values statistically compared using the
Student’s t test for independent samples.
Results: 296 patients with a mean age of
5510.3 years, 234 male, were evaluated.
Conclusion: The study clearly shows that the
DD genotype is linked to the extent of CHD,
with a high level of significance. If this is
confirmed, careful secondary prevention is
indicated in patients with this genotype.info:eu-repo/semantics/publishedVersio
IRAK4 gene polymorphism and odontogenic maxillary sinusitis
Objectives This study aimed to evaluate whether a specific interleukin-1 receptor-associated kinase-4 (IRAK4) gene polymorphism had any influence on the development of changes in maxillary sinus, particularly in the presence of etiological factors of dental origin.Materials and methods The study population included 153 Portuguese Caucasians that were selected from a database of 504 retrospectively analysed computed tomography (CT) scans. A genetic test was performed, and a model was created through logistic analysis and regression coefficients. The statistical methodologies included were the independent Chi test, Fisher's exact test, binary logistic regression and the receiver operating characteristic (ROC) curve.Results The estimated prevalence of IRAK4 gene polymorphism found in a Portuguese Caucasian population was 26.8 % (CI 95 %) [20.1, 34.7 %]. A model to predict the inflammatory response in the maxillary sinus in the presence etiological factors of dental origin was constructed. This model had the following as variables: previously diagnosed sinusitis, sinus pressure symptoms, cortical bone loss observed on CT, positive genetic test result and radiographic examination that revealed the roots of the teeth communication with the maxillary sinus, which are interpreted as risk factors.Conclusions The constructed model should be considered an initial clinical tool. The area under the ROC curve found, AUC=0.91, revealed that the model correctly predicts the outcome in 91.1 % of cases.info:eu-repo/semantics/publishedVersio
Outcome in patients perceived as receiving excessive care across different ethical climates: a prospective study in 68 intensive care units in Europe and the USA
Purpose: Whether the quality of the ethical climate in the intensive care unit (ICU) improves the identification of patients receiving excessive care and affects patient outcomes is unknown. Methods: In this prospective observational study, perceptions of excessive care (PECs) by clinicians working in 68 ICUs in Europe and the USA were collected daily during a 28-day period. The quality of the ethical climate in the ICUs was assessed via a validated questionnaire. We compared the combined endpoint (death, not at home or poor quality of life at 1 year) of patients with PECs and the time from PECs until written treatment-limitation decisions (TLDs) and death across the four climates defined via cluster analysis. Results: Of the 4747 eligible clinicians, 2992 (63%) evaluated the ethical climate in their ICU. Of the 321 and 623 patients not admitted for monitoring only in ICUs with a good (n = 12, 18%) and poor (n = 24, 35%) climate, 36 (11%) and 74 (12%), respectively were identified with PECs by at least two clinicians. Of the 35 and 71 identified patients with an available combined endpoint, 100% (95% CI 90.0–1.00) and 85.9% (75.4–92.0) (P = 0.02) attained that endpoint. The risk of death (HR 1.88, 95% CI 1.20–2.92) or receiving a written TLD (HR 2.32, CI 1.11–4.85) in patients with PECs by at least two clinicians was higher in ICUs with a good climate than in those with a poor one. The differences between ICUs with an average climate, with (n = 12, 18%) or without (n = 20, 29%) nursing involvement at the end of life, and ICUs with a poor climate were less obvious but still in favour of the former. Conclusion: Enhancing the quality of the ethical climate in the ICU may improve both the identification of patients receiving excessive care and the decision-making process at the end of life
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