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The rising incidence of metabolic diseases worldwide has prompted renewed interest in the study of intermediary metabolism and cellular bioenergetics. The application of modern biochemical methods for quantitating fuel substrate metabolism with advanced mouse genetic approaches has greatly increased understanding of the mechanisms that integrate energy metabolism in the whole organism. Examination of the intermediary metabolism of skeletal cells has been sparked by a series of unanticipated observations in genetically modified mice that suggest the existence of novel endocrine pathways through which bone cells communicate their energy status to other centers of metabolic control. The recognition of this expanded role of the skeleton has in turn led to new lines of inquiry directed at defining the fuel requirements and bioenergetic properties of bone cells. This article provides a comprehensive review of historical and contemporary studies on the metabolic properties of bone cells and the mechanisms that control energy substrate utilization and bioenergetics. Special attention is devoted to identifying gaps in our current understanding of this new area of skeletal biology that will require additional research to better define the physiological significance of skeletal cell bioenergetics in human health and disease. [ABSTRACT FROM AUTHOR]

Cardiovascular function in dinosaurs can be inferred from fossil evidence with knowledge of how metabolic rate, blood flow rate, blood pressure, and heart size are related to body size in living animals. Skeletal stature and nutrient foramen size in fossil femora provide direct evidence of a high arterial blood pressure, a large four-chambered heart, a high aerobic metabolic rate, and intense locomotion. But was the heart of a huge, long-necked sauropod dinosaur able to pump blood up 9 m to its head?. [ABSTRACT FROM AUTHOR]

It is known that arterial pressure correlates positively with body height in males, and it has been suggested that this is due to the increasing vertical hydrostatic gradient from the heart to the carotid baroreceptors. Therefore, we tested the hypothesis that a higher gravito-inertial stress induced by the use of a human centrifuge would increase mean arterial pressure (MAP) more in tall than in short males in the seated position. In short (162-171 cm; n = 8) and tall (194-203 cm; n = 10) healthy males (18-41 yr), brachial arterial pressure, heart rate (HR), and cardiac output were measured during +2G centrifugation, while they were seated upright with the legs kept horizontal (+2Gz). In a separate experiment, the same measurements were done with the subjects supine (+2Gx). During +2Gz MAP increased in the short (22 ± 2 mmHg, P < 0.0001) and tall (23 ± 2 mmHg, P < 0.0001) males, with no significant difference between the groups. HR increased more (P = 0.05) in the tall than in the short group (14 ± 2 vs. 7 ± 2 bpm). Stroke volume (SV) decreased in the short group (26 ± 4 ml, P = 0.001) and more so in the tall group (39 ± 5 ml, P < 0.0001; short vs. tall, P = 0.047). During +2Gx, systolic arterial pressure increased (P < 0.001) and SV (P = 0.012) decreased in the tall group only. In conclusion, during +2Gz, MAP increased in both short and tall males, with no difference between the groups. However, in the tall group, HR increased more during +2Gz, which could be caused by a larger hydrostatic pressure gradient from heart to head, leading to greater inhibition of the carotid baroreceptors. [ABSTRACT FROM AUTHOR]

Ischemic preconditioning (IP) is a cardioprotective mechanism against myocellular death and cardiac dysfunction resulting from reperfusion of the ischemic heart. At present, the precise list of mediators involved in IP and the pathways of their mechanisms of action are not completely known. The aim of the present study was to investigate the role of platelet-activating factor (PAF), a phospholipid mediator that is known to be released by the ischemic-reperfused heart, as a possible endogenous agent involved in IP. Experiments were performed on Langendorff-perfused rat hearts undergoing 30 min of ischemia followed by 2 h of reperfusion. Treatment with a low concentration of PAF (2 × 10-11 M) before ischemia reduced the extension of infarct size and improved the recovery of left ventricular developed pressure during reperfusion. The cardioprotective effect of PAF was comparable to that observed in hearts in which IP was induced by three brief (3 min) periods of ischemia separated by 5-min reperfusion intervals. The PAF receptor antagonist WEB-2170 (1 × 10-9 M) abrogated the cardioprotective effect induced by both PAF and IP. The protein kinase C (PKC) inhibitor chelerythrine (5 × 10-6 M) or the phosphoinositide 3-kinase (P13K) inhibitor LY-294002 (5 × 10-5 M) also reduced the cardioprotective effect of PAF. Western blot analysis revealed that following IP treatment or PAF infusion, the phosphorylation of PKC-ε and Akt (the downstream target of PI3K) was higher than that in control hearts. The present data indicate that exogenous applications of low quantities of PAF induce a cardioprotective effect through PI3K and PKC activation, similar to that afforded by IP. Moreover, the study suggests that endogenous release of PAF, induced by brief periods of ischemia and reperfusion, may participate to the triggering of the IP of the heart. [ABSTRACT FROM AUTHOR]

Analyzes the thyroid-stimulating hormones (TSH) and thyroid-stimulating hormone receptor structure-function relationship. Molecular biology of TSH; Evolutionary adaptation of TSH bioactivity; Design of TSH analogs.

Studies the role of platelet-activating factor (PAF) in cardiovascular pathophysiology. Definition of PAF; Molecular heterogeneity of PAF and functional implications; Metabolism of PAF; PAF receptors and signal transduction; Cardiovascular responses to PAF; Effect of PAF on the heart and endothelial cells; Involvement of PAF in cardiovascular pathophysiological processes.

Presents information on a study which determined the localization, neurochemical phenotype and electrophysiological properties of neurons of the inferior mesenteric ganglion. Retrograde tracing; Characterization of firing pattern; Immunohistochemistry of vascular neurons.

Presents information on a study that characterize thrombin-stimulated phospholipase A2 activity and the resultant release of lysophospholipids from endothelial cells. Methodology; Results of the study; Discussion of the study.

Presents a study on the organ and cell cultures of the small intestines of mice as model for programmed cell death (PCD). Composition pattern of the intestinal epithelium of a mouse; Methodology; Results.

Examines the cellular aspects of the carotid body function. Structural organization; Biochemical properties of carotid body tissue; Input-output relationships in carotid body chemoreceptors; Electrical properties of chemoreceptor cells; Transduction of natural stimuli in chemoreceptor cells; Neurotransmission at the chemoreceptor cell-sensory nerve ending synapse.

Presents a study which examined the reflex vascular responses to large rapid increases and decreases in carotid sinus pressure. Steady-state responses to changes in carotid sinus pressure; Vascular responses to single pulse changes in carotid pressure of various durations; Responses of efferent sympathetic nervous discharge.

Investigates the effect of beta- and alpha-adrenoreceptors in the total vascular capacitance responses to changing pressure in vascularly isolated carotid sinuses of anesthesized dogs. Efficacy and selectivity of beta-adrenergic antagonists; Effect of adrenoreceptor antagonist on capacitance responses to unloading of the carotid baroreceptors.

Investigates the invariance of the control of the carotid sinus baroreflex system over the resistance to venous return (RVR) in mongrel dogs. Four-parameter lumped model of the systemic circulation; Compliance-weighted average of vascular resistances.

Investigates reflex vascular responses to abdominal venous distensions in the anesthetized dog. Importance of splanchnic congestion in the maintenance of blood pressure during gravitational stress; Vasoconstriction and augmentation of the carotid baroreflex.