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Acute megakaryoblastic leukemia is characterized by heterogeneous biology and clinical behavior. Immunophenotypic characteristics include the expression of megakaryocytic differentiation markers (e.g. CD41, CD42a, CD42b, CD61) associated with immaturity markers (CD34, CD117, HLA-DR) and myeloid markers (e.g. CD13, CD33) and even with lymphoid cross-lineage markers (e.g. CD7, CD56). Although the diagnostic immunophenotype has already been well described, given the rarity of the disease, its immunophenotypic heterogeneity and post-therapeutic instability, there is no consensus on the combination of monoclonal markers to detect minimal/measurable residual disease (MRD). Currently, MRD is an important tool for assessing treatment efficacy and prognostic risk. In this study, we evaluated the immunophenotypic profile of MRD in a retrospective cohort of patients diagnosed with acute megakaryoblastic leukemia, to identify which markers, positive or negative, were more stable after treatment and which could be useful for MRD evaluation. The expression profile of each marker was evaluated in sequential MRD samples. In conclusion, the markers evaluated in this study can be combined in an MRD immunophenotypic panel to investigate for megakaryoblastic leukemia. Although this study is retrospective and some data are missing, the information obtained may contribute to prospective studies to validate more specific strategies in the detection of MRD in acute megakaryoblastic leukemia., Competing Interests: Conflicts of interest The authors have no conflicts of interest to declare., (Copyright © 2023 Associação Brasileira de Hematologia, Hemoterapia e Terapia Celular. Published by Elsevier España, S.L.U. All rights reserved.)

The World Health Organization (WHO) created the concept of Integrated Care for Older People and one of its constructs is intrinsic capacity (IC). The study aimed to carry out a screening with the tools designated by the WHO to assess the IC domains and whether they can be used as indicators for decision-making on integrated care for older people based on risk categorization. The interaction between the risk category and the domain scores was verified. One hundred and sixty three (163) community-dwelling older people of both genders were evaluated. Domains assessed: cognitive, psychological, vitality, locomotion, and sensory. Scores indicating a low, moderate and high risk were assigned to each domain. For all domains, there were individuals in all risk groups. Effect of risk on the domains: cognitive [χ 2 (2) = 134.042; p < 0.001], psychological [χ 2 (2) = 92.865; p < 0.001], vitality [χ 2 (2) = 129.564; p < 0.001], locomotion [χ 2 (2) = 144.101; p < 0.001], and sensory [χ 2 (2) = 129.037; p < 0.001]. Scores of the CI domains were affected by the risk category. There were individuals in all risk groups, demonstrating the importance of screening as a public health strategy, making it possible to know which risk category each elderly person belongs to and thus develop strategies in the short-, medium- and long-term.

Background: Exercise oscillatory ventilation (EOV) is an abnormal breathing pattern that occurs in ~20% of patients with heart failure (HF) and is associated with poor prognosis and exercise intolerance. β-blockers (βb) are prescribed for most HF patients; however, their effect on EOV remains unclear. We evaluated the effect of βb on EOV in HF patients with reduced ejection fraction (HFrEF)., Methods: Fifteen patients diagnosed with HF, ejection fraction < 45%, aged from 18 to 65 years, were included before starting βb therapy. Patients underwent clinical evaluation, cardiopulmonary exercise testing, echocardiography, laboratory exams (norepinephrine levels, B type natriuretic peptide) at baseline and after βb therapy optimized for six months. Presence of exercise oscillatory breathing was determined by two experienced observers who were blinded to the moment of the test (pre or post)., Results: Fifteen patients (1 female), aged 49.5 ± 2.5 years, with HFrEF, NYHA I-III enrolled in the study. The etiologies of the HFrEF were idiopathic (n = 8) and hypertensive (n = 7). LVEF increased after βb therapy from 25.9 ± 2.5% to 33 ± 2.6%, P = 0.02; peak VO 2 did not significantly change (21.8 ± 1.7 vs 24.7 ± 1.9, P = 0.4); VE/VCO 2 slope changed from 32.1 ± 10.6-27.5 ± 9.1, P = 0.03. Before βb initiation, nine patients (60%) had EOV, but only two (13%) did after optimized therapy. McNemar test was used to evaluate the significance of the association between the two moments (P = 0.02)., Conclusion: In patients with HF, medical therapy with βb can reverse EOV. This may explain why these patients experience symptom improvement after βb therapy., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

A large body of evidence has suggested the existence of a reflex network that becomes hyperactive secondary to musculoskeletal alterations that occur in heart failure (HF) syndrome. Together with sympathoinhibitory cardiovascular reflexes, suppressed in the presence of the syndrome, heart failure can contribute to physical exercise intolerance. The hyperactivation of signals originated from receptors located in skeletal muscles (mechanoreceptors - metaboreceptors) is a recently proposed hypothesis to explain the origin of fatigue and dyspnea symptoms in HF. In HF, other alterations in the reflex control system, which are not mutually exclusive, contribute to dyspnea. The inappropriate stimulation of the arterial baroreceptors, with the consequent lack of inhibition of the muscle metaboreflex and carotid chemoreflex unloading and the increase in the renal vasoconstriction with angiotensin II release can also be considered. Although the functional alterations of the reflexes were used independently to illustrate the sympathetic excitation observed in HF, the interaction between these reflexes under normal and pathological conditions, especially its contribution to the sympathoexcitatory state found in HF, has not been broadly investigated. Therefore, questions about a possible association between the muscle receptors (mechano and metaboreceptors) in the genesis of the ergoreflex exacerbation, observed in HF, remain. Thus, the objective of this review was to integrate the knowledge on the mechano and metaboreflex (ergoreflex) in HF syndrome, as well as to clarify the influence of HF drug therapy on the ergoreflex.

The heart failure (HF) syndrome can be defined as the final pathway of any type of heart disease. The sympatho-inhibitory cardiovascular reflexes, such as the arterial baroreceptor reflex, are significantly decreased in HF. Patients with HF present higher ventilation for a certain workload when compared with normal individuals. This fact generates low ventilatory efficiency and is related to higher ventilation associated with the carbon dioxide production, which is a predictor of bad prognosis, in addition to being a limiting factor for the practice of exercises. There is evidence that the autonomic imbalance contributes to the pathogenesis and the progression of heart failure. The chemoreflexes are the main mechanisms of control and regulation of the ventilatory responses to the changes in concentrations of arterial oxygen and carbon dioxide. The chemoreflex activation causes an increase in the sympathetic activity, heart rate, arterial pressure and minute volume. However, the increase in the minute volume and the arterial pressure, due to negative feedback, cause inhibition of the sympathetic response at the chemoreflex activation. In spite of the functional alterations of the reflexes, their behavior in normal and pathological conditions, especially their contribution to the sympathoexcitatory state observed in HF has not been broadly studied. Therefore, this review aims at integrating the knowledge on central and peripheral chemoreflexes in HF syndrome, as well as clarifying the influence of the heart failure drug therapy on the chemoreflexes.

The mechanical alterations related to the excessive use of accessory respiratory muscles and the mouth breathing observed in children with asthma may lead to the development of alterations in head posture, shoulders, thoracic region and, consequently, in alterations of body posture. The purpose of this study was to assess body posture changes of children with asthma compared to a non-asthmatic control group matched for gender, age, weight, and height. Thirty children with asthma and 30 non-asthmatic children aged 7 to 12 years were enrolled in this study. Digital photographic records were obtained for analysis of the body posture of the children by computed photogrammetry. The intraclass correlation coefficient and Student's t test (p < 0.05) were used for statistical analysis. There were no significant differences between groups for the angles analyzed, except for the knee flexor angle. These results demonstrate that children with asthma did not present postural alterations compared to non-asthmatic controls since the only angle for which there was a significant difference between groups showed weak reproducibility. The findings of this study do not support the notion that children with asthma present alterations in body posture.