Peter Stanley

Bio: Peter Stanley is an academic researcher from University of Manchester. The author has contributed to research in topics: Thermoelastic damping & Ultimate tensile strength. The author has an hindex of 18, co-authored 47 publications receiving 1497 citations.

MicroRNA-9 regulates axon extension and branching by targeting Map1b in mouse cortical neurons

Abstract: This paper reports that microRNA-9 controls axonal extension and branching of cortical neurons via its actions on the MAP1B protein.

Development and applications of thermoelastic stress analysis

Abstract: The theory of thermoelastic stress analysis is reviewed and the implications of some theoretical developments are assessed. Available instrumentation is described and techniques available for separation of individual stress values are summarized. The scope of the technique is illustrated with reference to a number of applications covering crack-tip stress studies, stress analysis and damage assessment in composite materials, and ‘field’ work on a traffic-loaded road bridge.

Quantitative stress analysis by means of the thermoelastic effect

Abstract: A new non-contact, full-field, stress analysis technique based on the measurement of the intensity of infra-red radiation emitted from the surface of a cyclically loaded body is applied to series of metallic specimens (including beams in bending, the ‘Brazilian’ disc, and a simple pure-shear testpiece) and critically appraised.

Evaluation of Neuromedin U Actions in Energy Homeostasis and Pituitary Function

Abstract: The brain-gut peptide neuromedin U (NMU) has been identified recently as a physiological regulator of food intake. To further investigate the central role of NMU in energy homeostasis, we examined the distribution of NMU transcript and the effect of intracerebroventricular administration on several physiological parameters and on the pattern of c-Fos activation. Here we report that intracerebroventricular administration of NMU to 24-h fasted rats resulted in a decrease in subsequent food intake and body weight gain. NMU administration activated neurons in several brain regions implicated in the regulation of feeding behavior. Activated cells included catecholaminergic neurons of the arcuate nucleus and brain stem. Distribution studies revealed NMU expression in the caudal brain stem (nucleus of the solitary tract and inferior olive) and pituitary, with significant levels in the pars tuberalis. This contradicts earlier published observations. In obese (fa/fa) Zucker rats, decreases in NMU expression were detected in the nucleus of the solitary tract, pars tuberalis, and pars distalis, whereas in the fasted rat, a decrease in NMU transcript was detected in the pars distalis. These results confirm the effects of NMU on feeding and suggest additional roles for NMU in neuroendocrine function.

Calcium Pumps in Health and Disease

Abstract: Ca2+-ATPases (pumps) are key actors in the regulation of Ca2+ in eukaryotic cells and are thus essential to the correct functioning of the cell machinery They have high affinity for Ca2+ and can efficiently regulate it down to very low concentration levels Two of the pumps have been known for decades (the SERCA and PMCA pumps); one (the SPCA pump) has only become known recently Each pump is the product of a multigene family, the number of isoforms being further increased by alternative splicing of the primary transcripts The three pumps share the basic features of the catalytic mechanism but differ in a number of properties related to tissue distribution, regulation, and role in the cellular homeostasis of Ca2+ The molecular understanding of the function of the pumps has received great impetus from the solution of the three-dimensional structure of one of them, the SERCA pump These spectacular advances in the structure and molecular mechanism of the pumps have been accompanied by the emergence and rapid expansion of the topic of pump malfunction, which has paralleled the rapid expansion of knowledge in the topic of Ca2+-signaling dysfunction Most of the pump defects described so far are genetic: when they are very severe, they produce gross and global disturbances of Ca2+ homeostasis that are incompatible with cell life However, pump defects may also be of a type that produce subtler, often tissue-specific disturbances that affect individual components of the Ca2+-controlling and/or processing machinery They do not bring cells to immediate death but seriously compromise their normal functioning

Cation-chloride cotransporters in neuronal development, plasticity and disease

Abstract: Electrical activity in neurons requires a seamless functional coupling between plasmalemmal ion channels and ion transporters. Although ion channels have been studied intensively for several decades, research on ion transporters is in its infancy. In recent years, it has become evident that one family of ion transporters, cation-chloride cotransporters (CCCs), and in particular K(+)-Cl(-) cotransporter 2 (KCC2), have seminal roles in shaping GABAergic signalling and neuronal connectivity. Studying the functions of these transporters may lead to major paradigm shifts in our understanding of the mechanisms underlying brain development and plasticity in health and disease.

Layered reward signalling through octopamine and dopamine in Drosophila

Abstract: Dopamine is synonymous with reward and motivation in mammals. However, only recently has dopamine been linked to motivated behaviour and rewarding reinforcement in fruitflies. Instead, octopamine has historically been considered to be the signal for reward in insects. Here we show, using temporal control of neural function in Drosophila, that only short-term appetitive memory is reinforced by octopamine. Moreover, octopamine-dependent memory formation requires signalling through dopamine neurons. Part of the octopamine signal requires the α-adrenergic-like OAMB receptor in an identified subset of mushroom-body-targeted dopamine neurons. Octopamine triggers an increase in intracellular calcium in these dopamine neurons, and their direct activation can substitute for sugar to form appetitive memory, even in flies lacking octopamine. Analysis of the β-adrenergic-like OCTβ2R receptor reveals that octopamine-dependent reinforcement also requires an interaction with dopamine neurons that control appetitive motivation. These data indicate that sweet taste engages a distributed octopamine signal that reinforces memory through discrete subsets of mushroom-body-targeted dopamine neurons. In addition, they reconcile previous findings with octopamine and dopamine and suggest that reinforcement systems in flies are more similar to mammals than previously thought.

Repair of Acute Myocardial Infarction by Human Stemness Factors Induced Pluripotent Stem Cells

Abstract: Background—Nuclear reprogramming provides an emerging strategy to produce embryo-independent pluripotent stem cells from somatic tissue. Induced pluripotent stem cells (iPS) demonstrate aptitude for de novo cardiac differentiation, yet their potential for heart disease therapy has not been tested. Methods and Results—In this study, fibroblasts transduced with human stemness factors OCT3/4, SOX2, KLF4, and c-MYC converted into an embryonic stem cell–like phenotype and demonstrated the ability to spontaneously assimilate into preimplantation host morula via diploid aggregation, unique to bona fide pluripotent cells. In utero, iPS-derived chimera executed differentiation programs to construct normal heart parenchyma patterning. Within infarcted hearts in the adult, intramyocardial delivery of iPS yielded progeny that properly engrafted without disrupting cytoarchitecture in immunocompetent recipients. In contrast to parental nonreparative fibroblasts, iPS treatment restored postischemic contractile performance, ventricular wall thickness, and electric stability while achieving in situ regeneration of cardiac, smooth muscle, and endothelial tissue. Conclusions—Fibroblasts reprogrammed by human stemness factors thus acquire the potential to repair acute myocardial infarction, establishing iPS in the treatment of heart disease. (Circulation. 2009;120:408-416.)