6 research outputs found

    Blood Pressure And Cardiac Autonomic Modulation At Rest, During Exercise And Recovery Time In The Young Overweight

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    This study aimed to assess the blood pressure (BP), cardiac autonomic modulation at rest, in physical exercise and in the recovery in untrained eutrophic (E) and overweight (O) youth. The body mass index (BMI), waist circumference (WC), systolic BP-SBP (E: 109.80 ± 10.05; O: 121.85 ± 6.98 mmHg) and diastolic BP DBP (E: 65.90 ± 7.28; O: 73.14 ± 12.22 mmHg) were higher in overweight and the heart rate recovery (%HRR) was lower as compared with E volunteers. The BMI was associated with SBP (r= 0.54), DBP (r= 0.65), load on the heart rate variability threshold-HRVT (r=-0.46), %HRR2' (r=-0.48) and %HRR 5′ (r=-0.48), and WC was associated with SBP (r= 0.54), DBP (r= 0.64) and HRR2' (r=-0.49). The %HRR was associated to SBP, DBP and HRVT. In summary, the anthropometric variables, BP and cardiac autonomic modulation in the recovery are altered in overweight youth.221273

    Understanding The Function Of Conserved Variations In The Catalytic Loops Of Fungal Glycoside Hydrolase Family 12

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    Enzymes that cleave the xyloglucan backbone at unbranched glucose residues have been identified in GH families 5, 7, 12, 16, 44, and 74. Fungi produce enzymes that populate 20 of 22 families that are considered critical for plant biomass deconstruction. We searched for GH12-encoding genes in 27 Eurotiomycetes genomes. After analyzing 50 GH12-related sequences, the conserved variations of the amino acid sequences were examined. Compared to the endoglucanases, the endo-xyloglucanase-associated YSG deletion at the negative subsites of the catalytic cleft with a SST insertion at the reducing end of the substrate-binding crevice is highly conserved. In addition, a highly conserved alanine residue was identified in all xyloglucan-specific enzymes, and this residue is substituted by arginine in more promiscuous glucanases. To understand the basis for the xyloglucan specificity displayed by certain GH12 enzymes, two fungal GH12 endoglucanases were chosen for mutagenesis and functional studies: an endo-xyloglucanase from Aspergillus clavatus (AclaXegA) and an endoglucanase from A. terreus (AtEglD). Comprehensive molecular docking studies and biochemical analyses were performed, revealing that mutations at the entrance of the catalytic cleft in AtEglD result in a wider binding cleft and the alteration of the substrate-cleavage pattern, implying that a trio of residues coordinates the interactions and binding to linear glycans. The loop insertion at the crevice-reducing end of AclaXegA is critical for catalytic efficiency to hydrolyze xyloglucan. 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    CHRONIC CHAGASIC CARDIOPATHY: THE PRODUCT OF A TURBULENT HOST-PARASITE RELATIONSHIP

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    The pathogenesis of chronic chagasic cardiopathy is still a debated matter. In this review, the main theories raised about it since the first description of the disease in 1909 by Carlos Chagas, are considered. The scarcity of T.cruzi parasites into the myocardium and the apparent lack of correlation between their presence and the occurrence of myocardial inflammatory infiltrate, have originated many theories indicating that chronic Chagas' cardiopathy is an autoimmune disease. Recently however, papers using immunohistochemical technique or PCR have demonstrated a strong association between moderate or severe myocarditis and presence of T.cruzi Ags, indicating a direct participation of the parasite in the genesis of chronic chagasic myocarditis. Different patterns of cytokine production seem to have important role in the outcome of the disease. Participation of the microcirculatory alterations and fibrosis as well as the relationship with the parasite are also emphasized. Finally, the author suggests that the indeterminate form of the disease occurs when the host immunological response against the parasite is more efficient while the chronic cardiopathy occurs in patients with hyperergic and inefficient immune response<br>A patogênese da cardiopatia crônica chagásica ainda é assunto controverso. Na presente revisão as principais teorias patogenéticas propostas, desde a descrição da doença por Carlos Chagas em 1909, são abordadas. A escassez de parasitas do T.cruzi no miocárdio e a aparente falta de correlação entre sua presença e a ocorrência de infiltrado inflamatório no miocárdio originaram várias teorias de autoimunidade na patogênese da cardiopatia crônica chagásica. Entretanto, trabalhos recentes têm demonstratado a presença de Ags do T.cruzi em associação com infiltrado inflamatório chagásico através de técnicas de imunoperoxidase e de PCR, sugerindo fortemente uma participação direta do parasita na gênese dessa miocardite. Diferentes padrões de produção de citocinas parecem desempenhar importante papel na evolução da doença. Ressalta-se também a possível participação do parasita em lesões da microcirculação e fibrose. Finalmente, o autor sugere que a forma indeterminada ocorre em pacientes cuja resposta imunológica contra o T.cruzi é mais efficente, enquanto que pacientes com cardiopatia crônica são aqueles com resposta contra o parasita ineficiente e hiperérgic
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