title: Mindful publishing in the AI era: An editor’s perspective on trends, challenges, and insights in mindfulness research

authors: Medvedev, Oleg N.

abstract: In an age where AI influences many facets of academic pursuit, the dissemination of mindfulness research is undergoing significant transformation. This keynote delivers an editor's perspective on the latest trends in mindfulness research, navigating through the possibilities and perils that AI presents to scholarly publishing.
The talk will cover the core trends revolutionizing how mindfulness research reaches academic and public domains. It will also elaborate on how AI impacts the success rates of paper acceptance and publication, and the broader implications for researchers striving to contribute novel insights in a highly competitive space. This discussion will outline the increased efficiency and new opportunities for disseminating research findings, while also considering the challenges of maintaining rigorous peer-review standards in the fast-paced digital era.
From an editorial vantage point, we share insights on harnessing AI to enhance the visibility and impact of mindfulness studies, and how this influences the themes and narratives that gain prominence in the literature. The talk will reflect on the emerging challenges such as ensuring the ethical use of AI, addressing the digital divide in research accessibility, and preserving the integrity of mindfulness as a discipline amidst rapid technological change.
This keynote presentation aims to equip researchers with an understanding of current publishing trends in mindfulness research, stimulate discussion on overcoming associated challenges, and inspire innovative approaches to sharing their work effectively. Attendees will leave with a clearer vision for navigating the evolving landscape of mindfulness research publication in the era of AI integration.

text: Mindful publishing in the AI era: An editor’s perspective on trends, challenges, and insights in mindfulness research In an age where AI influences many facets of academic pursuit, the dissemination of mindfulness research is undergoing significant transformation. This keynote delivers an editor's perspective on the latest trends in mindfulness research, navigating through the possibilities and perils that AI presents to scholarly publishing.
The talk will cover the core trends revolutionizing how mindfulness research reaches academic and public domains. It will also elaborate on how AI impacts the success rates of paper acceptance and publication, and the broader implications for researchers striving to contribute novel insights in a highly competitive space. This discussion will outline the increased efficiency and new opportunities for disseminating research findings, while also considering the challenges of maintaining rigorous peer-review standards in the fast-paced digital era.
From an editorial vantage point, we share insights on harnessing AI to enhance the visibility and impact of mindfulness studies, and how this influences the themes and narratives that gain prominence in the literature. The talk will reflect on the emerging challenges such as ensuring the ethical use of AI, addressing the digital divide in research accessibility, and preserving the integrity of mindfulness as a discipline amidst rapid technological change.
This keynote presentation aims to equip researchers with an understanding of current publishing trends in mindfulness research, stimulate discussion on overcoming associated challenges, and inspire innovative approaches to sharing their work effectively. Attendees will leave with a clearer vision for navigating the evolving landscape of mindfulness research publication in the era of AI integration.

year: 2024

title: The role of myostatin during postnatal myogenesis and sarcopenia

authors: Siriett, Victoria Katherine

subjects: myostatin

abstract: Myostatin, a TGF-β superfamily member, is a key negative regulator of embryonic and postnatal muscle growth. In order to further elucidate the role of myostatin during postnatal growth, several lines of investigation were undertaken in mice. Analysis of myostatin downstream target genes identified several known and unknown genes. From these, the regulation of an androgen receptor binding co-factor, ARA70, was selected for further investigation. Reverse Northern analysis on the differentially expressed cDNA library indicated an increased expression of ARA70 in myostatin-null muscles, which was later confirmed by Northern blot and semi-quantitative PCR analysis. In corroboration, treatment of myoblast cultures with exogenous myostatin resulted in the down-regulation of ARA70, confirming that myostatin is a negative regulator of ARA70 gene expression. The role of myostatin during sarcopenia, a progressive age-related loss of skeletal muscle mass and strength, was also investigated. The atrophy associated with sarcopenia is frequently correlated with insufficient muscle regeneration, resulting from an impaired propensity of satellite cells to activate and a subsequent decline in myogenesis. Myostatin is a known inhibitor of postnatal satellite cell activation and muscle regeneration, thus muscle mass and regeneration, and satellite cell behaviour were examined in young and aged myostatin-null mice. Myostatin-null mice had increased individual muscle weights, as a consequence of massive fibre hypertrophy and hyperplasia, and an increased proportion of type IIB fibres. Aging induced oxidative fibre type changes and atrophy in the wild-type muscle while no fibre type switching was observed in the myostatin-null muscle and atrophy was minimal. No decrease in satellite cell numbers was observed with aging in both genotypes; though a gradual decline in the number of activated satellite cells was noted during aging. However, both young and aged myostatin-null mice displayed increased satellite cells and activation compared to wild-type mice, suggesting a greater myogenic potential in the myostatin-null satellite cells. Consistent with this, aged myostatin-null myoblasts proliferated faster and displayed a higher fusion index during differentiation than the aged wild-type myoblasts, confirming that the reduced sarcopenia in the myostatin-null mice was due to a preserved increase in the myoblast myogenic activity. An increase in a Pax7-only myoblast population from myostatin-null muscle indicated an enhanced satellite cell self-renewal process, consistent with the increased satellite cell number observed on the myostatin-null muscle fibres. Additionally, muscle regeneration of aged myostatin-null muscle following notexin injury was accelerated, and fibre hypertrophy and type were recovered with regeneration, unlike the aged wild-type muscle. Testing the therapeutic value of a myostatin antagonist, Mstn-ant1, indicated that a short term blockade of myostatin by the antagonist significantly enhanced muscle regeneration in aged mice after injury and during sarcopenia. Antagonism of myostatin led to satellite cell activation, increased Pax7 and MyoD protein levels, and greater myoblast and macrophage cell migration culminating in enhanced muscle regeneration in the aged mice. 
In conclusion, the hypertrophic phenotype associated with myostatin-null mice may in part result from increased androgen receptor (AR) activity due to the up-regulation of ARA70, given that increased expression of the AR leads to hypertrophy. Additionally, the increased muscle mass in myostatin-null mice is likely to result from an augmented myogenic potential and self-renewal process. Overall, a prolonged absence of myostatin reduced sarcopenia and the associated loss of muscle regenerative capacity. Furthermore, the antagonism of myostatin displayed significant therapeutic potential in the alleviation of sarcopenia, through the restoration of the myogenic and inflammatory responses in the aged environment. Thus, the research work clearly demonstrates the role of myostatin in sarcopenia, and documents for the first time a valid therapeutic for alleviating sarcopenia.

text: The role of myostatin during postnatal myogenesis and sarcopenia Myostatin, a TGF-β superfamily member, is a key negative regulator of embryonic and postnatal muscle growth. In order to further elucidate the role of myostatin during postnatal growth, several lines of investigation were undertaken in mice. Analysis of myostatin downstream target genes identified several known and unknown genes. From these, the regulation of an androgen receptor binding co-factor, ARA70, was selected for further investigation. Reverse Northern analysis on the differentially expressed cDNA library indicated an increased expression of ARA70 in myostatin-null muscles, which was later confirmed by Northern blot and semi-quantitative PCR analysis. In corroboration, treatment of myoblast cultures with exogenous myostatin resulted in the down-regulation of ARA70, confirming that myostatin is a negative regulator of ARA70 gene expression. The role of myostatin during sarcopenia, a progressive age-related loss of skeletal muscle mass and strength, was also investigated. The atrophy associated with sarcopenia is frequently correlated with insufficient muscle regeneration, resulting from an impaired propensity of satellite cells to activate and a subsequent decline in myogenesis. Myostatin is a known inhibitor of postnatal satellite cell activation and muscle regeneration, thus muscle mass and regeneration, and satellite cell behaviour were examined in young and aged myostatin-null mice. Myostatin-null mice had increased individual muscle weights, as a consequence of massive fibre hypertrophy and hyperplasia, and an increased proportion of type IIB fibres. Aging induced oxidative fibre type changes and atrophy in the wild-type muscle while no fibre type switching was observed in the myostatin-null muscle and atrophy was minimal. No decrease in satellite cell numbers was observed with aging in both genotypes; though a gradual decline in the number of activated satellite cells was noted during aging. However, both young and aged myostatin-null mice displayed increased satellite cells and activation compared to wild-type mice, suggesting a greater myogenic potential in the myostatin-null satellite cells. Consistent with this, aged myostatin-null myoblasts proliferated faster and displayed a higher fusion index during differentiation than the aged wild-type myoblasts, confirming that the reduced sarcopenia in the myostatin-null mice was due to a preserved increase in the myoblast myogenic activity. An increase in a Pax7-only myoblast population from myostatin-null muscle indicated an enhanced satellite cell self-renewal process, consistent with the increased satellite cell number observed on the myostatin-null muscle fibres. Additionally, muscle regeneration of aged myostatin-null muscle following notexin injury was accelerated, and fibre hypertrophy and type were recovered with regeneration, unlike the aged wild-type muscle. Testing the therapeutic value of a myostatin antagonist, Mstn-ant1, indicated that a short term blockade of myostatin by the antagonist significantly enhanced muscle regeneration in aged mice after injury and during sarcopenia. Antagonism of myostatin led to satellite cell activation, increased Pax7 and MyoD protein levels, and greater myoblast and macrophage cell migration culminating in enhanced muscle regeneration in the aged mice. 
In conclusion, the hypertrophic phenotype associated with myostatin-null mice may in part result from increased androgen receptor (AR) activity due to the up-regulation of ARA70, given that increased expression of the AR leads to hypertrophy. Additionally, the increased muscle mass in myostatin-null mice is likely to result from an augmented myogenic potential and self-renewal process. Overall, a prolonged absence of myostatin reduced sarcopenia and the associated loss of muscle regenerative capacity. Furthermore, the antagonism of myostatin displayed significant therapeutic potential in the alleviation of sarcopenia, through the restoration of the myogenic and inflammatory responses in the aged environment. Thus, the research work clearly demonstrates the role of myostatin in sarcopenia, and documents for the first time a valid therapeutic for alleviating sarcopenia.

year: 2007

title: HE PI KA RERE 'An Early Childhood Approach to a Cultural Milieu'

authors: Karu, Joceleen Helen

subjects: Early childhood education

abstract: This study explores the issues surrounding the inculcation of te reo me ngā tikanga Māori, Māori language customs and values among early childhood teacher educators in a tertiary setting and how these academics go about preparing students with limited or sufficient knowledge of te reo Māori (Māori language) me ngā tikanga Māori (Māori cultural practices) to meet expectations. Te Whāriki, the early childhood curriculum is a curriculum commonly referred to as a bicultural curriculum that contains two expressions of the curriculum, one for general early childhood centres and another for kōhanga reo, neither of which are translations of one another and further asserts the importance of Te Tiriti o Waitangi/ the Treaty of Waitangi and the responsibility of teachers for bicultural development in the education of all children. Equally important, Te Whāriki acknowledges the dual heritage existent within Aotearoa/ New Zealand and further encourages teachers in early childhood settings to have knowledge of te reo and tikanga Māori. Policy imperatives reflected within the New Zealand Graduating Teaching Standards (New Zealand Teachers Council, 2010) and the Ministry of Education’s document Tātaiako/ Cultural Competencies (2011) place further emphasis on the need for those in initial teacher education to demonstrate their conversancy with te reo me ngā tikanga Māori.
The purpose of this study is to provide a narrative of the ways in which the early childhood initial teacher education programme prepares students to use te reo and tikanga Māori. It offers a premise to engage in further discussion of the continued effectiveness of early childhood teacher educators in the maintenance and delivery of te reo me ngā tikanga Māori and sets in motion a cyclical platform for further research from a traditional worldview which reflects and embodies the Māori language, culture and identity through a Kaupapa Māori philosophy and praxis.

text: HE PI KA RERE 'An Early Childhood Approach to a Cultural Milieu' This study explores the issues surrounding the inculcation of te reo me ngā tikanga Māori, Māori language customs and values among early childhood teacher educators in a tertiary setting and how these academics go about preparing students with limited or sufficient knowledge of te reo Māori (Māori language) me ngā tikanga Māori (Māori cultural practices) to meet expectations. Te Whāriki, the early childhood curriculum is a curriculum commonly referred to as a bicultural curriculum that contains two expressions of the curriculum, one for general early childhood centres and another for kōhanga reo, neither of which are translations of one another and further asserts the importance of Te Tiriti o Waitangi/ the Treaty of Waitangi and the responsibility of teachers for bicultural development in the education of all children. Equally important, Te Whāriki acknowledges the dual heritage existent within Aotearoa/ New Zealand and further encourages teachers in early childhood settings to have knowledge of te reo and tikanga Māori. Policy imperatives reflected within the New Zealand Graduating Teaching Standards (New Zealand Teachers Council, 2010) and the Ministry of Education’s document Tātaiako/ Cultural Competencies (2011) place further emphasis on the need for those in initial teacher education to demonstrate their conversancy with te reo me ngā tikanga Māori.
The purpose of this study is to provide a narrative of the ways in which the early childhood initial teacher education programme prepares students to use te reo and tikanga Māori. It offers a premise to engage in further discussion of the continued effectiveness of early childhood teacher educators in the maintenance and delivery of te reo me ngā tikanga Māori and sets in motion a cyclical platform for further research from a traditional worldview which reflects and embodies the Māori language, culture and identity through a Kaupapa Māori philosophy and praxis.

year: 2015