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Abstract The pituitary functions as a master endocrine gland that secretes hormones critical for regulation of a wide variety of physiological processes including reproduction, growth, metabolism and stress responses. The distinct hormone-producing cell lineages within the pituitary display remarkable levels of cell plasticity that allow remodeling of the relative proportions of each hormone-producing cell population to meet organismal demands. The molecular mechanisms governing pituitary cell plasticity have not been fully elucidated. Our recent studies have implicated a role for the Musashi family of sequence-specific mRNA binding proteins in the control of pituitary hormone production, pituitary responses to hypothalamic stimulation and modulation of pituitary transcription factor expression in response to leptin signaling. To date, these actions of Musashi in the pituitary appear to be mediated through translational repression of the target mRNAs. Here, we report Musashi1 directs the translational activation, rather than repression, of the Prop1, Gata2 and Nr5a1 mRNAs which encode key pituitary lineage specification factors. We observe that Musashi1 further directs the translational activation of the mRNA encoding the glycolipid Neuronatin (Nnat) as determined both in mRNA reporter assays as well as in vivo. Our findings suggest a complex bifunctional role for Musashi1 in the control of pituitary cell function.

Objective Research cannot advance without the voluntary participation of human participants.Summary of arguments Full participation of research participants is often restrained by the traditional research framework, which relegates them to a predefined participant role and allows them only quasi-scripted opportunities to contribute to research processes and outcomes. Terms commonly used to refer to research participants do not reflect their significant role or send a clear message about their value. The authors propose a shift from ‘patient participant’ to ‘participant partner.’ Recognition of the true partnership between the participant and the research team, from the consent process to the trial’s end, will encourage and enable fuller participation.Conclusion Changing the rhetoric of research in the labelling of research participants will require dialogue. ‘Respect for persons’ demands it, and the research process will be better for it.

Tooth morphology is among the most well-studied indicators of ecology. For decades, researchers have examined the gross morphology and wear patterns of teeth as indicators of diet, and recent advances in scanning and computer analysis have allowed the development of new and more quantitative measures of tooth morphology. One of the most popular of these new methods is orientation patch count (OPC). OPC, a measure of surface complexity, was originally developed to distinguish the more complex tooth crowns of herbivores from the less complex tooth crowns of faunivores. OPC and a similar method derived from it, orientation patch count rotated (OPCR), have become commonplace in analyses of both modern and fossil amniote dietary ecology. The widespread use of these techniques makes it possible to now re-assess the utility of OPC and OPCR. Here, we undertake a comprehensive review of OPC(R) and diet and perform a meta-analysis to determine the overall difference in complexity between herbivores and faunivores. We find that the relationship between faunivore and herbivore OPC or OPCR values differs substantially across studies, and although some support the initial assessment of greater complexity in herbivores, others do not. Our meta-analysis does not support an overall pattern of greater complexity in herbivores than faunivores across terrestrial amniotes. It appears that the relationship of OPC or OPCR to diet is taxon-specific and dependent on the type of faunivory of the group in question, with insectivores often having values similar to herbivores. We suggest extreme caution in comparing OPC and OPCR values across studies and offer suggestions for how OPCR can constructively be used in future research.

Abstract β‐islet cell transplantation is a promising proposed treatment for type 1 diabetes mellitus (T1DM) which can provide more physiological glucose control when compared to exogenous insulin therapy and reverse secondary consequences of diabetes. Unfortunately, β‐islet cell transplantation is not a permanent solution for patients with T1DM as 85–90% of β‐islet recipients return to exogenous insulin treatment within 5 years of the transplant. Despite its lack of success, β‐islet cell transplantation still has potential for the treatment of T1DM and significant work has been done to non‐invasively quantify β‐islet cell concentrations in transplantation to better understand the mechanism of β‐islet cell rejection. While several imaging modalities have been utilized, magnetic resonance imaging (MRI) remains at the forefront of β‐islet cell imaging due to its high resolution and lack of radiation exposure to patients. Several MRI contrast agents have been explored for the imaging of β‐islet cells including superparamagnetic iron oxide nanoparticles (SPIONs), gadolinium‐based contrast agents (GBCA), manganese (II), fluorine‐19, and theranostic agents, with SPIONs being the most extensively studied. In this review, we provide an overview of the history, recent progress, and challenges of MRI in islet transplantation with a focus on the molecular imaging agents used.

Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (particulate matter with an aerodynamic diameter < 2.5 μm) exposure is the fifth leading risk factor for death in the world, accounting for 4.2 million deaths and > 103 million disability-adjusted life years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe.

Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (particulate matter with an aerodynamic diameter < 2.5 μm) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.

Tracking error is a ubiquitous tool among active and passive portfolio managers, widely used for fund selection, risk management, and manager compensation. This paper shows that traditional measures of the tracking error are incapable of detecting variations in skewness and kurtosis. As a solution, this paper introduces a new class of Quantile Tracking Errors (QuTE), which measures differences in the quantiles of return distributions between a tracking portfolio and its benchmark. Through an extensive simulation study, this paper shows that QuTE is six times more sensitive than traditional tracking measures to skewness and three times more sensitive to kurtosis. The QuTE statistic is robust to various calibrations and can easily be customized. By using the QuTE tracking measure during the Dot Com bubble and the Great Recession, this paper finds differences between the DIA and its benchmark, the DJIA, that otherwise would have gone undetected. Quantile based tracking provides a robust method for relative performance measurement and index portfolio construction.

Research on NATO burden sharing comprises dozens of works. Since the end of the cold war, NATO adapted, enlarged, and institutionally complexified its mandates and area of operations. Yet, burden sharing research rarely accounts for such aspects given the political and scholarly focus on NATO’s target of 2% of GDP on military spending since the 2000s. This research merges rational institutionalism with collective action models on club goods production to study NATO Centres of Excellence. These 30 institutions are externally funded, independently run, and address the collective strategic problems associated with Alliance Transformation using informal arrangements, the Memorandum of Understanding. The contents of those agreements are compared using rational institutional design theory. This article offers original data reconceptualising the NATO burdens partners undertake beyond military expenditures using COE participation and hosting while offering a framework for a future examination of how the COE institutional agreements manage strategic problems (i.e. enforcement, allocation, uncertainty, etc.) with expanded data. [ABSTRACT FROM AUTHOR]

Disaster can cause several major problems such as food availability (quantity and quality) and mental illness especially in vulnerable group like children, women and the elderly, which in turn will cause disruption to the quality of sleep. Availability of food in good quantity and quality as well as sleep comfort are important factors that cannot be underestimated, especially for children who are still in their first 1000 days of life, because this stage is the golden stage of physical, cognitive, and social-emotional growth and development and would impact their quality of life in the future. Based on that matter, in this paper we will discuss the impact of floods and landslides in Agam Regency, West Sumatra on nutritional status and sleep disturbance in children aged 6-23 months. Sampling was done by consecutive sampling. The children were then asked by their parents to fill out the BISQ (Brief Infant Sleep Questionnaire) questionnaire for ages 6 months to 23 months There were 32,1 % of the infants experienced sleep disturbances. Furthermore, our analysis of nutritional status revealed that of 35,7 % those with nutritional disorders is from the areas prone to flooding and landslides.