个人简介
Sandra gained her B.Sc. from the University of Leeds; followed by her Ph.D. from the University of Liverpool which studied ‘the impact and mechanisms of ageing’ and initiated her interest in the area of ageing research. Sandra returned to Leeds University for her first post-doctoral position, where the foundations of her on-going research focus ‘ageing and the heart’ emerged. This was further developed during a second, senior post-doctoral position as principle investigator, followed by a short-term Lectureship in Physiology. She was appointed to a Lectureship in Biomedical Science at the University of Hull in 2007, and is also a member of the Centre for Cardiovascular and Metabolic Research’ at Hull York Medical School. [http://research.hyms.ac.uk/researchcentres/ccmr/home
Her cardiovascular-focussed teaching is included at all levels of several B.Sc. programmes as well as an undergraduate Masters and taught Masters programme. Sandra’s research revolves around causes of cardiac dysfunction, particularly dysfunction associated with the normal ageing process. She pursues this using a combination of techniques including electrophysiology, proteomics (western blot and confocal immunocytochemistry) and genomics (PCR and qPCR).
研究领域
Ageing of the heart
Age is the single biggest risk factor for cardiac dysfunction. My groups’ main research focus is to describe the changes occurring in the heart with progressive ageing that predispose to cardiac problems. By detailed assessment of changes in the function, proteomics and genomics of the heart associated with ageing we aim to identify key mechanisms and changes which are important for developing methods to support the ageing heart and ensure optimal therapeutic delivery to the elderly suffering from cardiac problems. Key findings have included detailed analysis of the ventricles, atria and sinoatrial node (the pacemaker of the heart) identifying changes predisposing to cardiac arrhythmias and mechanistic signalling pathways regulating these changes.
Innovative tools for clinical cardiology
We aim to extend “Telehealth” beyond currently available tests and methodologies. There is a need to make rapid analytical measurements away from clinical pathology laboratories to expedite diagnosis and treatment as well as provide rapid characterisation to develop use of personalised medicine. On-going studies are developing microfluidic devices for sample manipulation and detection of cardiac biomarkers using a paper device to allow rapid screening of cardiac problems; as well as in-vitro heart tissue characterisation using lab-on-a-chip technology to permit rapid assessment of cardiac function and response in small biopsy samples.
Endogenous stem cells in the heart and their newly-derived myocytes.
The adult heart possesses stem cells that reside within the tissue, known as ‘cardiac progenitor cells’ (CPCs), capable of hyperplasia and repair. Many of their properties and the mechanisms that may potentially allow them to instigate cardiac regeneration are however not well described. Limited data is also available on CPCs in the ageing heart and data on the activity of CPCs in the aged heart is controversial and conflicting. My laboratory aims to increase our understanding of CPCs in the heart across the lifespan, characterising their prevalence and properties of cells arising from their activation. Our studies aim to enable the manipulation and recruitment of active endogenous CPCs in the aged heart creating a possible therapeutic route to allow an old heart to regenerate following damage and adapt to stress.
Interactions of exercise-training with cardiac ageing.
Exercise is known to encourage long-term cardiovascular health however exercise can be a double edged sword for the heart with exercise stress being a potent trigger for cardiac problems acutely as well as evidence that high levels of exercise may also associate with long-term deleterious effects. These long-term deleterious effects have been associated with increased problems of the cardiac conduction system in old age but the specific mechanisms triggering these issues remain largely unidentified. By identifying changes in the heart associated with acute and chronic exercise we aim to identify the consequences of exercise for ageing of the heart, negative and positive.
近期论文
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Walton RD, Jones SA, Rostron KA, Kayani AC, Close GL, McArdle A & Lancaster MK. Interactions of short-term and chronic treadmill training with aging of the left ventricle of the heart. Journal of Gerontology: Biological Sciences. 2015;1-10 (published online, awaiting publication in paper version of journal)
Jones SA & Lancaster MK. Progressive age-associated activation of JNK leads to conduction disruption in the ageing atrium. Mechanisms of ageing and development. 2015:146;72-80.
Choisy SCM, Kim SJ, Hancox JC, Jones SA & James AF. Effects of candesartan, an angiotensin II receptor type I blocker, on atrial remodelling in spontaneously hypertensive rats. Physiology Reports 2015:3(1); e12274.
Kim SJ, Choisy SCM, Barman P, Zhang H, Hancox JC, Jones SA & James AF. Atrial remodelling and the substrate for atrial fibrillation in hearts with elevated afterload. Circulation: arrhythmia_and Electrophysiology 2011;4:761-769.
Hatch F, Lancaster MK & Jones SA. Aging is a primary risk factor for cardiac arrhythmias: disruption of intracellular Ca2+ regulation as a key suspect. Expert Review of Cardiovascular Therapy 2011;9:1059-67.
Jones SA, Yamamoto M, Tellez JO, Billeter R, Boyett MR Honjo H & Lancaster MK. Distinguishing properties of cells from the myocardial sleeves of the pulmonary veins; a comparison of normal and abnormal pacemakers. Circulation: Arrhythmia & Electrophysiology 2008;1:39-48
Jones SA, Boyett MR & Lancaster MK. Declining into failure: The age-dependent loss of the L-type calcium channel within the sinoatrial node. Circulation 2007;115:1183-90.
Yoo S, Dobrzynski H, Yamanushi TT, Fedorov VV, Nikolski VP, Jones SA, Xu SZ, Yamamoto M, Efimov IR & Boyett MR. Localisation of sodium channel isoforms at the Atrioventricular junction and atrioventricular node. Circulation 2006;114:1360-71.
Dobrzynski H, Li J, Tellez J, Greener ID, Nikolski VP, Wright SE, Parson SH, Jones SA, Lancaster MK, Yamamoto M, Honjo H, Takagishi Y, Kodama I, Efimov, Billeter R & Boyett MR. Computer 3-D reconstruction of the sinoatrial node. Circulation 2005:111:846-54.
Jones SA, Lancaster MK & Boyett MR. Age-related changes of connexins and conduction within the sinoatrial node. Journal of Physiology 2004;560:429-37.
Lei M, Jones SA, Liu J, Lancaster MK, Fung SM, Dobrzynski H, Camelitti P, Maier SKG, Noble D & Boyett MR. Requirement of neuronal- and cardiac-type sodium channels for sinoatrial node pacemaking. Journal of Physiology 2004;559:835-48.
Lancaster MK, Jones SA & Boyett MR. Heterogeneous regulation of intracellular Ca2+ within the sino-atrial node. Journal of Physiology 2004;556:481-94.
Nikolski V, Jones SA, Lancaster MK, Boyett MR & Efimov IR. Connexin43 staining reveals the substrate for AV-nodal pathway conduction. Circulation Research 2003;92:469-75.
Jones SA, McArdle A, McArdle F, Jack CIA & Jackson MJ. Lack of protection of prior heat shock against UV-induced oxidative stress in human skin fibroblasts. Redox Reports 2003;8:198-203.
Boyett MR, Dobrzynski H, Lancaster MK, Jones SA, Honjo H & Kodama I. Sophisticated architecture is required for the sinoatrial node to perform its normal pacemaker function. Journal of Cardiovascular Electrophysiology 2003;14:104-6.
Honjo H, Inada S, Lancaster MK, Yamamoto M, Niwa R, Jones SA, Shibata N, Mitsui K, Boyett MR, Kamiya K & Kodama I. SR Ca2+ release is not a dominating factor in sinoatrial node pacemaker activity. Circulation Research 2003;92:e41-4.
Zhang H, Noble D, Cannell M, Orchard C, Lancaster MK, Jones SA, Boyett MR, Holden AV, Jafri MS, Sobie EA, Lederer WJ, Demir S, Michailova A, Delprincipe F, Egger M, Niggli, Smith GL, Loughery CM, Macquaide N, Dempster J & Trafford AW. Dynamics of intracellular: Calcium handling-from experiments to virtual cells. International Journal of Bifurcation and chaos 2003;13:3535-78.
Dobrzynski H, Lei M, Jones SA, Lancaster MK & Boyett MR. The gradient model of the rabbit sinoatrial node. Korean Journal of Physiology & Pharmacology 2002;6:173-81.
Musa H, Lei M, Honjo H, Jones SA, Dobrzynski H, Lancaster MK, Takagishi Y, Henderson Z, Kodama I & Boyett MR. Heterogeneous expression of Ca2+ handling proteins in the sinoatrial node. Journal of Histochemistry & Cytochemistry 2002;50:311-24.
Jones SA, Morton MJ, Hunter M and Boyett MR. Expression of TASK-1, a pH-sensitive, twin-pore domain K+ channel in rat myocytes. American Journal of Physiology - Heart 2002;283:H181-5.
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