18 research outputs found

    An exploration into the occupational identity of women following breast cancer and treatment: A qualitative study

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    Introduction: The number of women surviving after breast cancer is increasing, along with the length of time they are living with the after-effects of treatment. Although the treatment’s effects are known to impact occupational participation, little is known about how breast cancer could affect occupational identity. This study aims to illuminate the lived experience of women long-term after breast cancer treatment through an occupational perspective in order to explore how they perceive their occupational identity. Methods: A qualitative study with semi-structured interviews was conducted with six women, who had all received a diagnosis of breast cancer and treatment for longer than a year. Reflexive Thematic Analysis was used to analyse the data. Findings: Three intertwined themes describe the participants’ experience. (1) ‘Disruptions in daily life and Environmental support’, (2) ‘Be able to do’ and identity, and (3) ‘Doing what matters and is possible’. Findings revealed that the occupational identities of the participants were maintained. Cancer treatment effects appear to impact occupational competence that corresponded to participants’ occupational identities, suggesting difficulties in the order of occupational adaptation. Conclusion: Our findings contribute to understanding the challenges to occupational participation related to the occupational identity of women following breast cancer and treatment

    The pore-forming subunit MCU of the mitochondrial Ca2+ uniporter is required for normal glucose-stimulated insulin secretion in vitro and in vivo in mice

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    Aims/hypothesis Mitochondrial oxidative metabolism is central to glucose-stimulated insulin secretion (GSIS). Whether Ca2+ uptake into pancreatic beta cell mitochondria potentiates or antagonises this process is still a matter of debate. Although the mitochondrial Ca2+ importer (MCU) complex is thought to represent the main route for Ca2+ transport across the inner mitochondrial membrane, its role in beta cells has not previously been examined in vivo. Methods Here, we inactivated the pore-forming subunit of the MCU, encoded by Mcu, selectively in mouse beta cells using Ins1Cre-mediated recombination. Whole or dissociated pancreatic islets were isolated and used for live beta cell fluorescence imaging of cytosolic or mitochondrial Ca2+ concentration and ATP production in response to increasing glucose concentrations. Electrophysiological recordings were also performed on whole islets. Serum and blood samples were collected to examine oral and i.p. glucose tolerance. Results Glucose-stimulated mitochondrial Ca2+ accumulation (p< 0.05), ATP production (p< 0.05) and insulin secretion (p< 0.01) were strongly inhibited in beta cell-specific Mcu-null (βMcu-KO) animals, in vitro, as compared with wild-type (WT) mice. Interestingly, cytosolic Ca2+ concentrations increased (p< 0.001), whereas mitochondrial membrane depolarisation improved in βMcu-KO animals. βMcu-KO mice displayed impaired in vivo insulin secretion at 5 min (p< 0.001) but not 15 min post-i.p. injection of glucose, whilst the opposite phenomenon was observed following an oral gavage at 5 min. Unexpectedly, glucose tolerance was improved (p< 0.05) in young βMcu-KO (<12 weeks), but not in older animals vs WT mice. Conclusions/interpretation MCU is crucial for mitochondrial Ca2+ uptake in pancreatic beta cells and is required for normal GSIS. The apparent compensatory mechanisms that maintain glucose tolerance in βMcu-KO mice remain to be established

    Beta Cell Hubs Dictate Pancreatic Islet Responses to Glucose

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    N.R.J. was supported by a Diabetes UK RW and JM Collins Studentship (12/0004601). J.B. was supported by a European Foundation for the Study of Diabetes (EFSD) Albert Renold Young Scientist Fellowship and a Studienstiftung des deutschen Volkes PhD Studentship. D.T. was supported by an Advanced Grant from the European Research Commission (268795). G.A.R. was supported by Wellcome Trust Senior Investigator (WT098424AIA) and Royal Society Wolfson Research Merit Awards, and by MRC Programme (MR/J0003042/1), Biological and Biotechnology Research Council (BB/J015873/1), and Diabetes UK Project (11/0004210) grants. G.A.R. and M.W. acknowledge COST Action TD1304 Zinc-Net. D.J.H. was supported by Diabetes UK R.D. Lawrence (12/0004431), EFSD/Novo Nordisk Rising Star and Birmingham Fellowships, a Wellcome Trust Institutional Support Award, and an MRC Project Grant (MR/N00275X/1) with G.A.R. D.J.H and G.A.R. were supported by Imperial Confidence in Concept (ICiC) Grants. J.F. was supported by an MRC Programme grant (MR/L02036X/1). L.P. provided human islets through collaboration with the Diabetes Research Institute, IRCCS San Raffaele Scientific Institute (Milan), within the European islet distribution program for basic research supported by JDRF (1-RSC-2014-90-I-X). P.M. and M.B. were supported by the Innovative Medicine Initiative Joint Undertaking under grant agreement no. 155005 (IMIDIA), resources of which are composed of financial contribution from the European Union’s Seventh Framework Programme (FP7/2007-2013) and EFPIA companies in kind contribution, and by the Italian Ministry of University and Research (PRIN 2010-2012). D.B. and E.B. provided human islets through the European Consortium for Islet Transplantation sponsored by JDRF (1-RSC-2014-100-I-X)

    Occupational therapy interventions for adults with learning disabilities: evaluating referrals received pre and during the height of the COVID-19 pandemic

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    Introduction The COVID-19 pandemic has significantly impacted on service provision for adults who have a learning disability, resulting in reduced occupational activities, routine, and social contact. Objective To analyse referrals received for Occupational Therapy intervention for adults who have a learning disability pre-COVID-19 (2019) and during COVID-19 (2020). Method This is a descriptive study conducted as a service evaluation with an NHS Trust Clinical Effectiveness Team in a city in the North of England. The data source was obtained from referral documentation. Quantitative and qualitative data were extracted from a data Performa and analysed using descriptive statistics (mean, median, mode, and standard deviation) performed by the Software Microsoft Excel. Results The total number of cases used in this evaluation was 274. There was an increase in referrals during the COVID-19 pandemic, the greatest increase was for Occupational Therapy intervention focusing on engagement in meaningful occupation. Over both years the predominant referrals were for equipment reviews. Conclusion Data collected captures a broad range of information regarding Occupational Therapy service provision pre and during the COVID-19 pandemic and puts this in the context of future considerations regarding the Occupational Therapy services for adults who have a learning disability

    Dysregulation of glucagon secretion by hyperglycemia-induced sodium-dependent reduction of ATP production

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    Diabetes is a bihormonal disorder resulting from combined insulin and glucagon secretion defects. Mice lacking fumarase (Fh1) in their β cells (Fh1βKO mice) develop progressive hyperglycemia and dysregulated glucagon secretion similar to that seen in diabetic patients (too much at high glucose and too little at low glucose). The glucagon secretion defects are corrected by low concentrations of tolbutamide and prevented by the sodium-glucose transport (SGLT) inhibitor phlorizin. These data link hyperglycemia, intracellular Na+ accumulation, and acidification to impaired mitochondrial metabolism, reduced ATP production, and dysregulated glucagon secretion. Protein succination, reflecting reduced activity of fumarase, is observed in α cells from hyperglycemic Fh1βKO and β-V59M gain-of-function KATP channel mice, diabetic Goto-Kakizaki rats, and patients with type 2 diabetes. Succination is also observed in renal tubular cells and cardiomyocytes from hyperglycemic Fh1βKO mice, suggesting that the model can be extended to other SGLT-expressing cells and may explain part of the spectrum of diabetic complications
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