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  1. AU="Nawazish Naqvi"
  2. AU="Marquardt, Viktoria"
  3. AU="Watts, Robyn"
  4. AU="Caballero, Susana J"
  5. AU="van Dijk, J Hessel M"
  6. AU=Della Guardia Lucio
  7. AU="Zhilich V.N."
  8. AU="George, Darren"
  9. AU=Lin Xiukun
  10. AU="Kanwal Gujral"
  11. AU="Christian Young"
  12. AU=Takeuchi Kaoru
  13. AU="Wiślicki, W."
  14. AU="Veiga, Susana"
  15. AU="Reynolds, Matthew W."
  16. AU="Oates, Stephen B"
  17. AU=Okubo K
  18. AU="Behnood, Sanaz"

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  1. Artikel ; Online: Mechanism-Based Cardiac Regeneration Strategies in Mammals

    Nawazish Naqvi / Siiri E. Iismaa / Robert M. Graham / Ahsan Husain

    Frontiers in Cell and Developmental Biology, Vol

    2021  Band 9

    Abstract: Heart failure in adults is a leading cause of morbidity and mortality worldwide. It can arise from a variety of diseases, with most resulting in a loss of cardiomyocytes that cannot be replaced due to their inability to replicate, as well as to a lack of ...

    Abstract Heart failure in adults is a leading cause of morbidity and mortality worldwide. It can arise from a variety of diseases, with most resulting in a loss of cardiomyocytes that cannot be replaced due to their inability to replicate, as well as to a lack of resident cardiomyocyte progenitor cells in the adult heart. Identifying and exploiting mechanisms underlying loss of developmental cardiomyocyte replicative capacity has proved to be useful in developing therapeutics to effect adult cardiac regeneration. Of course, effective regeneration of myocardium after injury requires not just expansion of cardiomyocytes, but also neovascularization to allow appropriate perfusion and resolution of injury-induced inflammation and interstitial fibrosis, but also reversal of adverse left ventricular remodeling. In addition to overcoming these challenges, a regenerative therapy needs to be safe and easily translatable. Failure to address these critical issues will delay the translation of regenerative approaches. This review critically analyzes current regenerative approaches while also providing a framework for future experimental studies aimed at enhancing success in regenerating the injured heart.
    Schlagwörter heart failure ; ischemic injury ; cardiomyocyte proliferation ; cardioprotection ; cardiac regeneration ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2021-10-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Remuscularization with triiodothyronine and β1-blocker therapy reverses post-ischemic left ventricular dysfunction and adverse remodeling

    Nikolay Bogush / Lin Tan / Emmen Naqvi / John W. Calvert / Robert M. Graham / W. Robert Taylor / Nawazish Naqvi / Ahsan Husain

    Scientific Reports, Vol 12, Iss 1, Pp 1-

    2022  Band 16

    Abstract: Abstract Renewal of the myocardium by preexisting cardiomyocytes is a powerful strategy for restoring the architecture and function of hearts injured by myocardial infarction. To advance this strategy, we show that combining two clinically approved drugs, ...

    Abstract Abstract Renewal of the myocardium by preexisting cardiomyocytes is a powerful strategy for restoring the architecture and function of hearts injured by myocardial infarction. To advance this strategy, we show that combining two clinically approved drugs, but neither alone, muscularizes the heart through cardiomyocyte proliferation. Specifically, in adult murine cardiomyocytes, metoprolol, a cardioselective β1-adrenergic receptor blocker, when given with triiodothyronine (T3, a thyroid hormone) accentuates the ability of T3 to stimulate ERK1/2 phosphorylation and proliferative signaling by inhibiting expression of the nuclear phospho-ERK1/2-specific phosphatase, dual-specificity phosphatase-5. While short-duration metoprolol plus T3 therapy generates new heart muscle in healthy mice, in mice with myocardial infarction-induced left ventricular dysfunction and pathological remodeling, it remuscularizes the heart, restores contractile function and reverses chamber dilatation; outcomes that are enduring. If the beneficial effects of metoprolol plus T3 are replicated in humans, this therapeutic strategy has the potential to definitively address ischemic heart failure.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2022-05-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Murradambirra Dhangaang (make food secure)

    Simone Sherriff / Deanna Kalucy / Allison Tong / Nawazish Naqvi / Janice Nixon / Sandra Eades / Tangerene Ingram / Kym Slater / Michelle Dickson / Amanda Lee / Sumithra Muthayya

    BMC Public Health, Vol 22, Iss 1, Pp 1-

    Aboriginal community and stakeholder perspectives on food insecurity in urban and regional Australia

    2022  Band 17

    Abstract: Abstract Background It is widely acknowledged that the invasion by colonial powers of the Australian continent had profound and detrimental impacts on Aboriginal Communities, including food security. Policies of successive governments since European ... ...

    Abstract Abstract Background It is widely acknowledged that the invasion by colonial powers of the Australian continent had profound and detrimental impacts on Aboriginal Communities, including food security. Policies of successive governments since European arrival have since further exacerbated the situation, with food insecurity now affecting 20–25% of Aboriginal and Torres Strait Islander people. Food insecurity contributes to long-term impacts on health, in particular diet-sensitive chronic diseases. This study aimed to describe Aboriginal community and stakeholder perspectives on food insecurity to get a better understanding of the key contributing factors and recommendations for potential strategies to address this issue in Aboriginal communities in urban and regional Australia. Methods Semi-structured interviews were conducted with 44 participants who were purposively selected. This included Aboriginal people in two communities and both Aboriginal and non-Aboriginal stakeholders from local food relief agencies, food suppliers, schools, and government in an urban and regional location in NSW. A conceptual framework was developed from literature on food security, and sensitizing concepts of availability, affordability, accessibility and acceptability or the lack thereof of healthy food were used to elicit responses from the participants. Interview transcripts were analysed thematically. Results All participants felt strongly that food insecurity was a major problem experienced in their local Aboriginal communities. Five core areas impacting on food security were identified: trapped in financial disadvantage; gaps in the local food system; limitations of non-Aboriginal food relief services; on-going impacts of colonization; and maintaining family, cultural and community commitments and responsibilities. Participants suggested a number of actions that could help ease food insecurity and emphasized that Aboriginal values and culture must be strongly embedded in potential programs. Conclusions This study found ...
    Schlagwörter Food insecurity ; Diet inequality ; Aboriginal and Torres Strait Islander ; Indigenous ; Stakeholders ; Food systems ; Public aspects of medicine ; RA1-1270
    Sprache Englisch
    Erscheinungsdatum 2022-05-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Evaluation of the Fracture Liaison Service within the Canadian Healthcare Setting

    Matthew Wong-Pack / Nawazish Naqvi / George Ioannidis / Ramy Khalil / Alexandra Papaioannou / Jonathan Adachi / Arthur N. Lau

    Journal of Osteoporosis, Vol

    2020  Band 2020

    Abstract: Previous studies evaluating fracture liaison service (FLS) programs have found them to be cost-effective, efficient, and reduce the risk of fracture. However, few studies have evaluated the clinical effectiveness of these programs. We compared the ... ...

    Abstract Previous studies evaluating fracture liaison service (FLS) programs have found them to be cost-effective, efficient, and reduce the risk of fracture. However, few studies have evaluated the clinical effectiveness of these programs. We compared the patient populations of those referred for osteoporosis management by FLS to those referred by primary care physicians (PCP), within the Canadian healthcare system in the province of Ontario. Specifically, we investigated if a referral from FLS is similarly effective as PCP at identifying patients at risk for future osteoporotic fractures and if osteoporosis therapies have been previously initiated. A retrospective chart review of patients assessed by a single Ontario rheumatology practice affiliated with FLS between January 1, 2014, and December 31, 2017, was performed identifying two groups: those referred by FLS within Hamilton and those referred by their PCP for osteoporosis management. Fracture risk of each patient was determined using FRAX. A total of 573 patients (n = 225 (FLS group) and n = 227 (PCP group)) were evaluated. Between the FLS and PCP groups, there were no significant differences in the absolute 10-year risk of a major osteoporotic fracture (15.6% (SD = 10.2) vs 15.3% (SD = 10.3)) and 10-year risk of hip fracture (4.7% (SD = 8.3) vs 4.7% (SD = 6.8)), respectively. 10.7% of patients referred by FLS and 40.5% of patients referred by their PCP were on osteoporosis medication prior to fracture. Our study suggests that referral from FLS is similarly effective as PCP at identifying patients at risk for future osteoporotic fractures, and clinically effective at identifying the care gap with the previous use of targeted osteoporosis therapies from referral from PCP being low and much lower in those referred by FLS. Interventional programs such as FLS can help close the treatment gap by providing appropriate care to patients that were not previously identified to be at risk for fracture by their primary care physician and initiate proper medical management.
    Schlagwörter Medicine ; R
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Hindawi Limited
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: DUSP5 expression in left ventricular cardiomyocytes of young hearts regulates thyroid hormone (T3)-induced proliferative ERK1/2 signaling

    Nikolay Bogush / Lin Tan / Hussain Naib / Ebrahim Faizullabhoy / John W. Calvert / Siiri E. Iismaa / Ankan Gupta / Ramani Ramchandran / David I. K. Martin / Robert M. Graham / Ahsan Husain / Nawazish Naqvi

    Scientific Reports, Vol 10, Iss 1, Pp 1-

    2020  Band 14

    Abstract: Abstract Cardiomyocytes of newborn mice proliferate after injury or exposure to growth factors. However, these responses are diminished after postnatal day-6 (P6), representing a barrier to building new cardiac muscle in adults. We have previously shown ... ...

    Abstract Abstract Cardiomyocytes of newborn mice proliferate after injury or exposure to growth factors. However, these responses are diminished after postnatal day-6 (P6), representing a barrier to building new cardiac muscle in adults. We have previously shown that exogenous thyroid hormone (T3) stimulates cardiomyocyte proliferation in P2 cardiomyocytes, by activating insulin-like growth factor-1 receptor (IGF-1R)-mediated ERK1/2 signaling. But whether exogenous T3 functions as a mitogen in post-P6 murine hearts is not known. Here, we show that exogenous T3 increases the cardiomyocyte endowment of P8 hearts, but the proliferative response is confined to cardiomyocytes of the left ventricular (LV) apex. Exogenous T3 stimulates proliferative ERK1/2 signaling in apical cardiomyocytes, but not in those of the LV base, which is inhibited by expression of the nuclear phospho-ERK1/2-specific dual-specificity phosphatase, DUSP5. Developmentally, between P7 and P14, DUSP5 expression increases in the myocardium from the LV base to its apex; after this period, it is uniformly expressed throughout the LV. In young adult hearts, exogenous T3 increases cardiomyocyte numbers after DUSP5 depletion, which might be useful for eliciting cardiac regeneration.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-12-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Redox activation of JNK2α2 mediates thyroid hormone-stimulated proliferation of neonatal murine cardiomyocytes

    Lin Tan / Nikolay Bogush / Hussain Naib / Jennifer Perry / John W. Calvert / David I. K. Martin / Robert M. Graham / Nawazish Naqvi / Ahsan Husain

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Band 15

    Abstract: Abstract Mitochondria-generated reactive oxygen species (mROS) are frequently associated with DNA damage and cell cycle arrest, but physiological increases in mROS serve to regulate specific cell functions. T3 is a major regulator of mROS, including ... ...

    Abstract Abstract Mitochondria-generated reactive oxygen species (mROS) are frequently associated with DNA damage and cell cycle arrest, but physiological increases in mROS serve to regulate specific cell functions. T3 is a major regulator of mROS, including hydrogen peroxide (H2O2). Here we show that exogenous thyroid hormone (T3) administration increases cardiomyocyte numbers in neonatal murine hearts. The mechanism involves signaling by mitochondria-generated H2O2 (mH2O2) acting via the redox sensor, peroxiredoxin-1, a thiol peroxidase with high reactivity towards H2O2 that activates c-Jun N-terminal kinase-2α2 (JNK2α2). JNK2α2, a relatively rare member of the JNK family of mitogen-activated protein kinases (MAPK), phosphorylates c-Jun, a component of the activator protein 1 (AP-1) early response transcription factor, resulting in enhanced insulin-like growth factor 1 (IGF-1) expression and activation of proliferative ERK1/2 signaling. This non-canonical mechanism of MAPK activation couples T3 actions on mitochondria to cell cycle activation. Although T3 is regarded as a maturation factor for cardiomyocytes, these studies identify a novel redox pathway that is permissive for T3-mediated cardiomyocyte proliferation—this because of the expression of a pro-proliferative JNK isoform that results in growth factor elaboration and ERK1/2 cell cycle activation.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2019-11-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Thyroid hormone action in postnatal heart development

    Ming Li / Siiri E. Iismaa / Nawazish Naqvi / Amy Nicks / Ahsan Husain / Robert M. Graham

    Stem Cell Research, Vol 13, Iss 3, Pp 582-

    2014  Band 591

    Abstract: Thyroid hormone is a critical regulator of cardiac growth and development, both in fetal life and postnatally. Here we review the role of thyroid hormone in postnatal cardiac development, given recent insights into its role in stimulating a burst of ... ...

    Abstract Thyroid hormone is a critical regulator of cardiac growth and development, both in fetal life and postnatally. Here we review the role of thyroid hormone in postnatal cardiac development, given recent insights into its role in stimulating a burst of cardiomyocyte proliferation in the murine heart in preadolescence; a response required to meet the massive increase in circulatory demand predicated by an almost quadrupling of body weight during a period of about 21 days from birth to adolescence. Importantly, thyroid hormone metabolism is altered by chronic diseases, such as heart failure and ischemic heart disease, as well as in very sick children requiring surgery for congenital heart diseases, which results in low T3 syndrome that impairs cardiovascular function and is associated with a poor prognosis. Therapy with T3 or thyroid hormone analogs has been shown to improve cardiac contractility; however, the mechanism is as yet unknown. Given the postnatal cardiomyocyte mitogenic potential of T3, its ability to enhance cardiac function by promoting cardiomyocyte proliferation warrants further consideration.
    Schlagwörter Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2014-11-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Comparative regenerative mechanisms across different mammalian tissues

    Siiri E. Iismaa / Xenia Kaidonis / Amy M. Nicks / Nikolay Bogush / Kazu Kikuchi / Nawazish Naqvi / Richard P. Harvey / Ahsan Husain / Robert M. Graham

    npj Regenerative Medicine, Vol 3, Iss 1, Pp 1-

    2018  Band 20

    Abstract: Abstract Stimulating regeneration of complex tissues and organs after injury to effect complete structural and functional repair, is an attractive therapeutic option that would revolutionize clinical medicine. Compared to many metazoan phyla that show ... ...

    Abstract Abstract Stimulating regeneration of complex tissues and organs after injury to effect complete structural and functional repair, is an attractive therapeutic option that would revolutionize clinical medicine. Compared to many metazoan phyla that show extraordinary regenerative capacity, which in some instances persists throughout life, regeneration in mammalians, particularly humans, is limited or absent. Here we consider recent insights in the elucidation of molecular mechanisms of regeneration that have come from studies of tissue homeostasis and injury repair in mammalian tissues that span the spectrum from little or no self-renewal, to those showing active cell turnover throughout life. These studies highlight the diversity of factors that constrain regeneration, including immune responses, extracellular matrix composition, age, injury type, physiological adaptation, and angiogenic and neurogenic capacity. Despite these constraints, much progress has been made in elucidating key molecular mechanisms that may provide therapeutic targets for the development of future regenerative therapies, as well as previously unidentified developmental paradigms and windows-of-opportunity for improved regenerative repair.
    Schlagwörter Medicine ; R
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2018-02-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Cardiac hypertrophy limits infarct expansion after myocardial infarction in mice

    Siiri E. Iismaa / Ming Li / Scott Kesteven / Jianxin Wu / Andrea Y. Chan / Sara R. Holman / John W. Calvert / Ahtesham ul Haq / Amy M. Nicks / Nawazish Naqvi / Ahsan Husain / Michael P. Feneley / Robert M. Graham

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Band 13

    Abstract: Abstract We have previously demonstrated that adult transgenic C57BL/6J mice with CM-restricted overexpression of the dominant negative W v mutant protein (dn-c-kit-Tg) respond to pressure overload with robust cardiomyocyte (CM) cell cycle entry. Here, ... ...

    Abstract Abstract We have previously demonstrated that adult transgenic C57BL/6J mice with CM-restricted overexpression of the dominant negative W v mutant protein (dn-c-kit-Tg) respond to pressure overload with robust cardiomyocyte (CM) cell cycle entry. Here, we tested if outcomes after myocardial infarction (MI) due to coronary artery ligation are improved in this transgenic model. Compared to non-transgenic littermates (NTLs), adult male dn-c-kit-Tg mice displayed CM hypertrophy and concentric left ventricular (LV) hypertrophy in the absence of an increase in workload. Stroke volume and cardiac output were preserved and LV wall stress was markedly lower than that in NTLs, leading to a more energy-efficient heart. In response to MI, infarct size in adult (16-week old) dn-c-kit-Tg hearts was similar to that of NTL after 24 h but was half that in NTL hearts 12 weeks post-MI. Cumulative CM cell cycle entry was only modestly increased in dn-c-kit-Tg hearts. However, dn-c-kit-Tg mice were more resistant to infarct expansion, adverse LV remodelling and contractile dysfunction, and suffered no early death from LV rupture, relative to NTL mice. Thus, pre-existing cardiac hypertrophy lowers wall stress in dn-c-kit-Tg hearts, limits infarct expansion and prevents death from myocardial rupture.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2018-04-01T00:00:00Z
    Verlag Nature Publishing Group
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    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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