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The demand for treating diseases using yoga therapy, a Complementary and Alternative Medicine (CAM) treatment, has increased globally. An increase in the research in this yoga area from fewer than 10 research publications per year in the 1990s to at least 20 per year after 2010 is evidence of this change in treatment needs over time. The beneficial effect of yoga therapy has been limited to practice in acute care despite its remarkable success in this domain. This is due to many factors that impact the therapy's effectiveness, irrespective of disease indications. However, the prime challenges for its effectiveness lie with the reliability of the yoga trial outcome and reporting. There is a great need to reevaluate the yoga trials' reporting for the reliability of their outcome. This study attempts to address the issue by studying challenges for presbyopia with yoga interventions. Among many indications, progressive vision loss (presbyopia), which occurs due to refractive errors in the ocular region, has scope to be treated effectively with yoga therapies. However, trials for yoga interventions for treating refractive errors have not been studied well. This study was conducted to understand the challenges in yoga therapy trials and its potential to treat presbyopia. The CLARIFY guidelines were used to understand the challenges and factors that impact effective treatment in the current research landscape. We found that trials conducted are not in compliance with the reporting guidelines. Adaptation of CLARIFY guidelines is essential to produce reliable evidence to prescribe yoga therapies to treat refractive errors.

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Context: Yoga is beneficial in enhancing mental health and consequently cognitive growth. Some studies have show that yoga practice can improve cognitive functioning in children. Objective: The study intended to evaluate the effectiveness of a school-based yoga intervention on the cognitive abilities-attention and memory-of adolescents. Design: The research team conducted a one-group, pretest-posttest study. Setting: The study occurred at a rural residential school in Udupi, Karnataka, and South India. Participants: Participants were a convenience sample of 36 adolescents, with a mean age of 12.19 ± 0.4 years, in the seventh grade at the school. Intervention: A senior yoga expert prepared a structured, yoga-intervention module, which was implemented, with each session lasting one hour and occurring five days a week for 12 weeks. Outcome Measures: The Digit Span Forward (DSF) and Digit Span Backward (DSB) tests and Letter-Number Sequencing (LNS) test were used by a trained research examiner to evaluate cognition. Results: Comparing the mean DSB, total digit span score, and LNS at baseline and postintervention showed significantly higher posttest scores than pretest ones, with P = .005, P = .005, and P = .001, respectively. Conclusions: Yoga training improves cognitive functions and is a simple, low-cost, and effective adjuvant modality.

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Neurological disorders (NLDs) are among the top leading causes for disability worldwide. Dramatic changes in the epigenetic topography of the brain and nervous system have been found in many NLDs. Histone lysine acetylation has prevailed as one of the well characterised epigenetic modifications in these diseases. Two instrumental components of the acetylation machinery are the evolutionarily conserved Bromodomain and PHD finger containing (BRPF) and Bromo and Extra terminal domain (BET) family of proteins, also referred to as acetylation 'readers'. Several reasons, including their distinct mechanisms of modulation of gene expression and their property of being highly tractable small molecule targets, have increased their translational relevance. Thus, compounds which demonstrated promising results in targeting these proteins have advanced to clinical trials. They have been established as key role players in pathologies of cancer, cardiac diseases, renal diseases and rheumatic diseases. In addition, studies implicating the role of these bromodomains in NLDs are gaining pace. In this review, we highlight the findings of these studies, and reason for the plausible roles of all BET and BRPF members in NLDs. A comprehensive understanding of their multifaceted functions would be radical in the development of therapeutic interventions.

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Depression, anxiety and related mood disorders are major psychiatric illnesses worldwide, and chronic stress appears to be one of the primary underlying causes. Therapeutics to treat these debilitating disorders without a relapse are limited due to the incomplete molecular understanding of their etiopathology. In addition to the well-studied genetic component, research in the past two decades has implicated diverse epigenetic mechanisms in mediating the negative effects of chronic stressful events on neural circuits. This includes the cognitive circuitry, where the dynamic hippocampal dentate gyrus (DG) neurogenesis gets affected in depression and related affective disorders. Most of these epigenetic studies have focused on the impact of acetylation/deacetylation and methylation of several histone lysine residues on neural gene expression. However, there is a dearth of investigation into the role of demethylation of these lysine residues in chronic stress-induced changes in neurogenesis that results in altered behaviour. Here, using the chronic social defeat stress (CSDS) paradigm to induce depression and anxiety in C57BL/6 mice and ex vivo DG neural stem/progenitor cell (NSCs/NPCs) culture we show the role of the members of the JMJD2/KDM4 family of histone lysine demethylases (KDMs) in mediating stress-induced changes in DG neurogenesis and mood disorders. The study suggests a critical role of JMJD2D in DG neurogenesis. Altered enrichment of JMJD2D on the promoters of Id2 (inhibitor of differentiation 2) and Sox2 (SRY-Box Transcription Factor 2) was observed during proliferation and differentiation of NSCs/NPCs obtained from the DG. This would affect the demethylation of repressive epigenetic mark H3K9, thus activating or repressing these and possibly other genes involved in regulating proliferation and differentiation of DG NSCs/NPCs. Treatment of the NSCs/NPCs culture with Dimethyloxallyl Glycine (DMOG), an inhibitor of JMJDs, led to attenuation in their proliferation capacity. Additionally, systemic administration of DMOG in mice for 10 days induced depression-like and anxiety-like phenotype without any stress exposure.