Microcytic anemia factor no estudo das anemias microcíticas

A anemia ferropénica e a β-Talassemia menor são as anemias microcíticas mais frequentes na prática laboratorial, sendo o seu diagnóstico de extrema importância clínica. O objectivo deste estudo consistiu na análise do poder discriminatório do MAF na caracterização destas anamias. Foi desenvolvido um estudo caso-controlo, tendo sido analisados os hemogramas de um grupo de 47 indivíduos com anemia ferropénica e 37 com β-talassemia, e de um grupo controlo constituído por 58 indivíduos saudáveis. Na diferenciação dos grupos patológicos, apenas a Hemoglobina, o VGM e o RDW apresentaram diferenças significativas. O MAF não demonstrou poder discriminatório relativamente às anemias microcíticas.

Stability of the Transthyretin Molecule as a Key Factor in

Transthyretin (TTR) protects against A-Beta toxicity by binding the peptide thus inhibiting its aggregation. Previous work showed different TTR mutations interact differently with A-Beta, with increasing affinities correlating with decreasing amyloidogenecity of the TTR mutant; this did not impact on the levels of inhibition of A-Beta aggregation, as assessed by transmission electron microscopy. Our work aimed at probing differences in binding to A-Beta by WT, T119M and L55P TTR using quantitative assays, and at identifying factors affecting this interaction. We addressed the impact of such factors in TTR ability to degrade A-Beta. Using a dot blot approach with the anti-oligomeric antibody A11, we showed that A-Beta formed oligomers transiently, indicating aggregation and fibril formation, whereas in the presence of WT and T119M TTR the oligomers persisted longer, indicative that these variants avoided further aggregation into fibrils. In contrast, L55PTTR was not able to inhibit oligomerization or to prevent evolution to aggregates and fibrils. Furthermore, apoptosis assessment showed WT and T119M TTR were able to protect against A-Beta toxicity. Because the amyloidogenic potential of TTR is inversely correlated with its stability, the use of drugs able to stabilize TTR tetrameric fold could result in increased TTR/ABeta binding. Here we showed that iododiflunisal, 3-dinitrophenol, resveratrol, [2-(3,5-dichlorophenyl)amino] (DCPA) and [4- (3,5-difluorophenyl)] (DFPB) were able to increase TTR binding to A-Beta; however only DCPA and DFPB improved TTR proteolytic activity. Thyroxine, a TTR ligand, did not influence TTR/A-Beta interaction and A-Beta degradation by TTR, whereas RBP, another TTR ligand, not only obstructed the interaction but also inhibited TTR proteolytic activity. Our results showed differences between WT and T119M TTR, and L55PTTR mutant regarding their interaction with A-Beta and prompt the stability of TTR as a key factor in this interaction, which may be relevant in AD pathogenesis and for the design of therapeutic TTR-based therapies.

Postaerobic Exercise Blood Pressure Reduction in Very Old Persons With Hypertension.

BACKGROUND AND PURPOSE: A single bout of aerobic exercise acutely decreases blood pressure, even in older adults with hypertension. Nonetheless, blood pressure responses to aerobic exercise in very old adults with hypertension have not yet been documented. Therefore, this study aimed to assess the effect of a single session of aerobic exercise on postexercise blood pressure in very old adults with hypertension. METHODS: Eighteen older adults with essential hypertension were randomized into exercise (N = 9, age: 83.4 ± 3.2 years old) or control (N = 9, age: 82.7 ± 2.5 years old) groups. The exercise group performed a session of aerobic exercise constituting 2 periods of 10 minutes of walking at an intensity of 40% to 60% of the heart rate reserve. The control group rested for the same period of time. Anthropometric variables and medication status were evaluated at baseline. Heart rate and systolic and diastolic blood pressures were measured at baseline, after exercise, and at 20 and 40 minutes postexercise. RESULTS: Systolic blood pressure showed a significant interaction for group × time (F3,24 = 6.698; P = .002; ηp = 0.153). In the exercise group, the systolic blood pressure at 20 (127.3 ± 20.9 mm Hg) and 40 minutes (123.7 ± 21.0 mm Hg) postexercise was significantly lower in comparison with baseline (135.6 ± 20.6 mm Hg). Diastolic blood pressure did not change. Heart rate was significantly higher after the exercise session. In the control group, no significant differences were observed. CONCLUSIONS: A single session of aerobic exercise acutely reduces blood pressure in very old adults with hypertension and may be considered an important nonpharmacological strategy to control hypertension in this age group.