Biomedical subjects

E C Stevens

Publications and source records attributed to E C Stevens.

10 recordsLinked to original sources

PubMed2005

VO2 response profiles in severe intensity exercise.

AIM: VO2peak can be achieved over the range of intensities that define the severe intensity domain. The purpose of this study was to help characterize the VO2 response during constant-load exercise in this domain. METHODS: Twelve participants performed cycle ergometer tests at 267+/-52 W, 238+/-45 W, and 216+/-37 W, which were individually selected to elicit VO2peak and to cause fatigue in 3 min, 5 min, and 7 min, respectively. RESULTS: Times to fatigue were 201+/-16 s, 301+/-20 s, and 448+/-51 s, respectively. VO2 responded faster at higher work rates, with VO2peak reached after 154+/-25 s, 193+/-35 s, and 206+/-24 s, respectively. Extrapolation of the times to reach VO2peak revealed that 300 W was the highest power, and 151 s was the shortest time, for which VO2peak could be elicited. TheVO2 response was described using a three-component model. Exercise intensity did not affect the speed of the primary response, with time constants of 22+/-3 s, 23+/-4 s, and 23+/-4 s, respectively. However, the size of the primary phase was greater at higher intensities, with amplitudes of 1,798+/-200 mlxmin-1, 1,739+/-267 mlxmin-1, and 1,677+/-254 mlxmin-1, respectively. The amplitude of the slow component was correspondingly smaller at higher intensities. Extrapolation of the slow component amplitudes revealed that 299 W was the highest intensity, and 152(-1)53 s was the shortest time, for which a slow component would be engendered. CONCLUSION: VO2peak is attained faster at higher intensities because the amplitude of the primary response is greater, not because the response is faster. There is a slow component to the VO2 response at all intensities within the severe domain, but not at higher intensities, in the extreme domain, where fatigue occurs before VO2peak can be elicited.

Adult↗

PubMed2002

Growth hormone receptor antagonists: discovery, development, and use in patients with acromegaly.

An understanding of the events that occur during GH receptor (GHR) signaling has facilitated the development of a GHR antagonist (pegvisomant) for use in humans. This molecule has been designed to compete with native GH for the GHR and to prevent its proper or functional dimerization-a process that is critical for GH signal transduction and IGF-I synthesis and secretion. Clinical trials in patients with acromegaly show GHR blockade to be an exciting new mode of therapy for this condition, and pegvisomant may have a therapeutic role in diseases, such as diabetes and malignancy, in which abnormalities of the GH/IGF-I axis have been observed. This review charts the discovery and development of GHR antagonists and details the experience gained in patients with acromegaly.

Acromegaly↗

PubMed2001

The VO(2) response at the onset of severe intensity exercise.

Fourteen participants achieved a peak VO(2) of 2573 +/- 738 ml á min-1 in approximately 3 1/2-min cycle ergometer tests. However, in the first 45 s of exercise, formal description of the phase II of the V(O)2 response indicated that the V(O)2 was projecting toward a value of 3451 +/- 1599 ml x min(-1), well above the peak VO(2)peak and not different from the predicted O(2) demand of 3389 +/- 800 ml x min(-1). We conclude that, at the onset of exercise in the severe intensity domain, VO(2) is initially driven toward the O(2) demand, and then is limited by the achievable VO(2) (VO(2peak)).

Adult↗

PubMed2001

Bone marrow mast cell morphologic features and hematopoietic dyspoiesis in systemic mast cell disease.

Systemic mast cell disease (SMCD) cannot be distinguished from reactive mastocytosis (RM) by quantitation of mast cells in aspirate smears, and few studies have analyzed systematically the morphologic features of mast cells in SMCD vs RM. In addition, although SMCD is associated with myeloproliferative disorders/myelodysplastic syndromes (MPD/MDS), it is not known whether subtle signs of dysplasia or MPD can be found in SMCD, suggesting most cases are part of a dysplastic or myeloproliferative process. We compared 18 bone marrow specimens with SMCD with 10 bone marrow specimens from patients with RM. Mast cells in SMCD were more likely to show cytoplasmic hypogranularity, uneven granule distribution, and fusiform morphologic features. Eight cases of SMCD (44%) demonstrated MPD/MDS, and 9 cases (50%) showed subtle evidence of dyspoiesis, with megaloblastic change, nuclear budding of erythroid precursors, and/or atypical megakaryocytes. Mast cells in SMCD appear morphologically different from those in reactive proliferations. Dyspoietic features were present in most cases of SMCD, suggesting that SMCD is part of a spectrum of chronic myeloproliferative/myelodysplastic disorders.

Adolescent↗

PubMed1986