Secretor status and ankylosing spondylitis

Objective. To assess the genetic association between secretor status and ankylosing spondylitis (AS). Methods. A restriction digest method for determining secretor status was developed; 166 patients with AS and 216 healthy British white controls were typed for secretor status using this method. Results. The frequency of nonsecretors among patients with AS (47/166, 28%) was not significantly different from controls (72/216, 33%). Conclusion. Secretor status does not influence susceptibility to AS.

Lewis phenotype, secretor status, and coeliac disease

Patients who cannot secrete ABO and Lewis blood group antigens into body fluids, an ability controlled by a single gene on chromosome 19, are known to be at increased risk of certain autoimmune diseases associated with human leucocyte antigen (HLA) markers. This study investigated the possibility of an association with coeliac disease using red cell Lewis (Le) blood group phenotype to infer secretor status. Among 73 patients with coeliac disease who had Le a or b antigen, 48% were non-secretors (Le a + b-) compared with 27% of 137 blood donors (p = 0.004: odds ratio 2.49, 95% confidence intervals 1.37 to 4.51) and 26% of 62 medical and nursing staff controls (p = 0.014: odds ratio 2.65, 95% confidence intervals 1.27 to 5.50). Clinical characteristics did not differ between secretors and non-secretors with coeliac disease. Thus, the non-secretor state is significantly associated with coeliac disease, suggesting that genes on chromosome 19 may directly or indirectly participate in conferring susceptibility.

Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease

The hypothesis that non-secretors of ABO blood group antigens, a group shown to be more susceptible to certain bacterial infections, may be at greater risk of gastroduodenal disease because of increased susceptibility to Helicobacter pylori infection was investigated. Of 101 patients with symptoms of dyspepsia who were undergoing endoscopy, 32% were non-secretors (determined from Lewis blood group phenotype), 36% had endoscopically visible gastroduodenal disease (antral gastritis, gastric ulcer, erosive duodenitis, duodenal ulcer or some combination), and 58% had H pylori detected in antral biopsy specimens. Non-secretors and patients with H pylori infection were significantly more likely to have gastroduodenal disease (p = 0.02 and p = 0.002 respectively). There was, however, no significant association between secretor status and H pylori infection, logistic regression analysis confirming that these were independently associated with gastroduodenal disease. Overall, the relative risk of gastroduodenal disease for non-secretors compared with secretors was 1.9 (95% confidence intervals 1.2, 3.2). Non-secretion of ABO blood group antigens is not related to H pylori infection but is independently and significantly associated with endoscopic gastroduodenal disease. The mechanism of this remains to be explained.

Polymorphisms of Lewis and Secretor genes are related to breast cancer and metastasis in axillary lymph nodes

ABH and Lewis antigen expression has been associated with cancer development and prognosis, tumor differentiation, and metastasis. Considering that invasive ductal breast carcinoma (IDC) presents multiple molecular alterations, the aim of the present study was to determine whether the polymorphism of ABO, Lewis, and Secretor genes, as well as ABO phenotyping, could be associated with tumor differentiation and lymph nodes metastasis. Seventy-six women with IDC and 78 healthy female blood donors were submitted to ABO phenotyping/genotyping and Lewis and Secretor genotyping. Phenotyping was performed by hemagglutination and genotyping by the polymerase chain reaction with sequence-specific primers. ABO, Lewis, and Secretor genes were classified by individual single nucleotide polymorphism at sites 59, 1067, 202, and 314 of the Lewis gene, 428 of the Secretor gene, and 261 (O1 allele), 526 (O2 and B allele), and 703 (B allele). No association was found between breast cancer and ABO antigen expression (P = 0.9323) or genotype (P = 0.9356). Lewis-negative genotype was associated with IDC (P = 0.0126) but not with anatomoclinical parameters. Nonsecretor genotype was associated with axillary lymph node metastasis (P = 0.0149). In conclusion, Lewis and Secretor genotyping could be useful to predict respectively breast cancer susceptibility and axillary lymph nodes metastasis.

Lack of association between ABO histo-blood groups, secretor and non-secretor phenotypes, and anti-Toxoplasma gondii antibodies among pregnant women from the northwestern region of São Paulo State, Brazil

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

ABO, Lewis, secretor and non-secretor phenotypes in patients infected or uninfected by the Helicobacter pylori bacillus

CONTEXT: Epidemiological studies have demonstrated higher frequencies of the O blood group and the non-secretor phenotype of ABH antigens among patients suffering from peptic ulcers. Since Helicobacter pylori has been established as the main etiological factor in this disease, controversies about the associations of the ABO and Lewis blood group phenotypes and secretor and non-secretor phenotypes in relation to susceptibility towards infection by this bacillus have been presented. OBJECTIVE: To verify the frequencies of ABO, Lewis blood group phenotypes, secretor and non-secretor phenotypes in patients infected or uninfected by H. pylori. DESIGN: Cross-sectional study. SETTING: Outpatient clinic. PARTICIPANTS: One hundred and twenty patients with dyspeptic symptoms who underwent endoscopy. MAIN MEASUREMENTS: ABO and Lewis blood group phenotypes were determined by a standard hemagglutination test and the secretor and non-secretor phenotypes were evaluated by saliva samples using the inhibitor hemagglutination test. RESULTS: The diagnosis of infection, made via breath and urea tests and confirmed using polymerase chain reaction (PCR) in gastric biopsy fragments, showed the presence of H. pylori in 61.7% of the patients and absence in 38.3%. The differences between the frequencies of the ABO blood group phenotypes among infected (A 27.0%; B 12.2%; AB 4.0% and O 56.8%) and uninfected patients (A 58.7%; B 13.0%; AB 4.3% and O 24.0%) were significant. The Lewis blood type, secretor and non-secretor phenotypes showed homogeneous distribution between the groups of patients analyzed. CONCLUSIONS: Our results suggest that the infection of H. pylori can be related to ABO blood groups but not to the Lewis blood group nor to secretor and non-secretor phenotypes. Copyright©2002, Associação Paulista de Medicina.

Caracterização histoquímica e determinação do ciclo secretor da glândula salivar do tórax de Polistes versicolor (Olivier, 1791) (Hymenoptera: vespidae)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Sistema histo-sangüíneo ABO, status Secretor e anticorpos anti-Toxoplasma gondii em gestação da região Noroeste do Estado de São Paulo: um estudo de associação

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Estudo das glândulas salivares de fêmeas e de machos de carrapatos Rhipicephalus sanguineus (Latreille, 1806) (Acari, Ixodidae): caracterização do ciclo secretor com ênfase no processo de degenaração

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Polimorfismo dos genes ABO, Lewis e Secretor correlacionados com o câncer de mama

Pós-graduação em Biociências e Biotecnologia Aplicadas à Farmácia - FCFAR

Avaliação do estado secretor ABH e Lewis em mulheres não grávidas com e sem risco de desenvolver vulvovaginite por Candida sp

Um estudo epidemiológico da prevalência da infecção por Candida sp. em mulheres não grávidas foi realizado em uma população do Norte do Brasil (Belém-Pará, 2002). Este estudo teve como objetivo principal contribuir para esclarecer os mecanismos de infecção por Candida sp e sua possível associação com os antígenos de grupos sangüíneos ABO e Lewis e estado secretor de substâncias ABH. Tal estudo compreendeu um total de 165 mulheres, atendidas no Ambulatório do Hospital da Polícia Militar e Laboratório de Análises Clínicas do centro de Ciências Biológicas da Universidade Federal do Pará, que procuraram essas unidades para a realização de exames ginecológicos, das quais foram coletadas amostras de sangue, saliva e muco vaginal. A presença da infecção por Candida sp foi feita através do exame a fresco de secreção vaginal e bacterioscopia da secreção vaginal. A identificação dos fenótipos ABH e Lewis no sangue foi determinada pelos testes de hemaglutinação direta e na saliva pelo dot-blot Elisa. Aplicou-se um questionário padrão para obtenção das informações epidemiológicas. A prevalência da infecção por Candida sp foi de 47,9%. Dentre os sintomas mais comumente associados à infecção por Candida sp, destacaram-se o prurido e corrimento. Mulheres com idade inferior a 40 anos, que não faziam uso de preservativo e que já tiveram infecções anteriores apresentaram um maior risco de infecção vulvovaginal por Candida sp. Mulheres infectadas e não infectadas por Candida sp tiveram distribuição similares para os fenótipos de grupos sangüíneos ABO, Lewis e estado secretor de substâncias ABH. E na comparação da expressão dos antígenos Lewis no sangue, saliva e muco vaginal, verificou-se que ambas as secreções expressavam antígenos Lewis sem qualquer estreita correlação dos fenótipos eritrocitários Lewis. Neste contexto, considera-se que a natureza da diversidade genética na interação entre hospedeiro e Candida sp requer estudos complementares envolvendo a identificação de diferentes cepas para determinar estas prováveis associações entre os fenótipos de grupo sangüíneos ABH e Lewis com candidíase.

Fenofibrato (agonista PPAR-alfa) induz a formação de células beges no tecido adiposo branco subcutâneo em camundongos obesos induzidos por dieta

O atual quadro de obesidade instalado no mundo estimula o estudo em busca de seu tratamento. O fenofibrato, um agonista PPAR-α, é usado atualmente para tratar a dislipidemia. No entanto, efeitos pleiotrópicos sobre a perda de massa corporal (MC) e redução nos depósitos de gordura necessitam de maiores estudos. O objetivo do trabalho foi examinar os efeitos do agonista PPAR-α fenofibrato sobre o gasto energético, MC, metabolismo de carboidratos, perfil secretor de adipocinas, plasticidade e termogênese do tecido adiposo branco subcutâneo (TABs) em camundongos com obesidade induzida por dieta. Este experimento foi aprovado pelo Comitê de Ética para Experimentação Animal local sob o protocolo CEUA/032/2013. Camundongos machos C57BL/6 de 3 meses foram divididos em dois grupos: dieta padrão (SC, 10% lipídios) e dieta hiperlipídica (HF, 50% de lipídios), as quais foram administradas durante 10 semanas para induzir o sobrepeso. Em seguida, foi iniciado o tratamento com fenofibrato (100 mg/kg MC, adicionado à dieta), formando quatro grupos: SC, SC-F, HF, HF-F. O tratamento teve duração de cinco semanas, com o total de 15 semanas de experimento. A análise estatística utilizou teste t de student no pré-tratamento e one way ANOVA seguida pelo pós-teste de Holm-Sidak durante o tratamento. O two way ANOVA foi utilizado para testar possíveis interações entre dieta e tratamento. O nível de significância P<0,05 foi considerado estatisticamente significativo. O grupo HF apresentou sobrepeso, resistência à insulina, além de remodelamento do tecido adiposo branco subcutâneo (TABs). O fenofibrato atenuou significativamente estes parâmetros (P<0,05). Os grupos tratados apresentaram formação de células beges no TABs, confirmado através de maior expressão gênica do PPAR-α, PPAR-β, PGC1-α, BMP8, UCP-1, PRDM16 e FNDC5/Irisina nos grupos tratados do que em suas contrapartes (P<0,05). O tratamento com fenofibrato também foi capaz de aumentar os niveis plasmáticos de FNDC5/Irisina em ambos os grupos tratados (P<0,005). Os grupos SC-F e HF-F apresentaram aumento do gasto energético, a produção de CO2 e consumo de O2 após o tratamento com fenofibrato (P<0,05). A ativação do PPAR-α parece ser fundamental para provocar browning através da indução da irisina e da transcrição de UCP-1. O fenofibrato restaurou a MC, a sensibilidade à insulina e a morfometria do TABs. Relevantemente, o fenofibrato aumentou a expressão de genes tipicamente expressos no tecido adiposo marrom no TABs, evidenciando a plasticidade do TABs em células beges com capacidade termogênica, caracterizando o browning.

The role of glycans in the development and progression of prostate cancer

Prostate cancer is a unique and heterogeneous disease. Currently, a major unmet clinical need exists to develop biomarkers that enable indolent disease to be distinguished from aggressive disease. The prostate is an abundant secretor of glycoproteins of all types, and alterations in glycans are, therefore, attractive as potential biomarkers and therapeutic targets. Despite progress over the past decade in profiling the genome and proteome, the prostate cancer glycoproteome remains relatively understudied. A wide range of alterations in the glycoproteins on prostate cancer cells can occur, including increased sialylation and fucosylation, increased O-β-N-acetylglucosamine (GlcNAc) conjugation, the emergence of cryptic and high-mannose N-glycans and alterations to proteoglycans. Glycosylation can alter protein function and has a key role in many important biological processes in cancer including cell adhesion, migration, interactions with the cell matrix, immune surveillance, cell signalling and cellular metabolism; altered glycosylation in prostate cancer might modify some, or all of these processes. In the past three years, powerful tools such as glycosylation-specific antibodies and glycosylation gene signatures have been developed, which enable detailed analyses of changes in glycosylation. Thus, emerging data on these often overlooked modifications have the potential to improve risk stratification and therapeutic strategies in patients with prostate cancer.

Influence of the lateral pterygoid muscle on the growth of the mandibular condilar cartilage

At the end of the last century, a model to explain clinical observations related to the mandibular growth was developed. According to it, the lateral pterigoid muscle (LPM) was one of the main modulators of the differentiation of mesenquimal cells inside the condyle to condroblasts or osteoblasts, and therefore of the growth of the mandibular condilar cartilage (CCM). The main components of the model were the humoral and the mechanical. Nowadays, the humoral would include growth factors such as IGF-I, FGF-2 and VEGF, which seem to be involved in mandibular growth. Since skeletal muscle can secrete these growth factors, there is a possibility that LPM modulates the growth of CCM by a paracrine or endocrine mechanism. The mechanical component derived from the observations that both the blood flow inside the temporomandibular joint (ATM) and the action of the retrodiscal pad on the growth of the CCM, depend, in part, on the contractile activity of the LPM. Despite the fact that there are some results suggesting  hat LPM is activated under conditions of mandibular protrusion, there is no full agreement on whether this can stimulate the growth of CCM. In this review, the contributions and limitations of the works related to mandibular growth are discussed and a model which integrates the available information to explain the role of the LPM in the growth of the CCM is proposed.