646 research outputs found

    Making SDGs work for climate change hotspots

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    The impacts of climate change on people's livelihoods have been widely documented. It is expected that climate and environmental change will hamper poverty reduction, or even exacerbate poverty in some or all of its dimensions. Changes in the biophysical environment, such as droughts, flooding, water quantity and quality, and degrading ecosystems, are expected to affect opportunities for people to generate income. These changes, combined with a deficiency in coping strategies and innovation to adapt to particular climate change threats, are in turn likely to lead to increased economic and social vulnerability of households and communities, especially amongst the poorest

    Hyper- and hypo- nutrition studies of the hepatic transcriptome and epigenome suggest that PPARĪ± regulates anaerobic glycolysis

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    Diet plays a crucial role in shaping human health and disease. Diets promoting obesity and insulin resistance can lead to severe metabolic diseases, while calorie-restricted (CR) diets can improve health and extend lifespan. In this work, we fed mice either a chow diet (CD), a 16 week high-fat diet (HFD), or a CR diet to compare and contrast the effects of these diets on mouse liver biology. We collected transcriptomic and epigenomic datasets from these mice using RNA-Seq and DNase-Seq. We found that both CR and HFD induce extensive transcriptional changes, in some cases altering the same genes in the same direction. We used our epigenomic data to infer transcriptional regulatory proteins bound near these genes that likely influence their expression levels. In particular, we found evidence for critical roles played by PPARĪ± and RXRĪ±. We used ChIP-Seq to profile the binding locations for these factors in HFD and CR livers. We found extensive binding of PPARĪ± near genes involved in glycolysis/gluconeogenesis and uncovered a role for this factor in regulating anaerobic glycolysis. Overall, we generated extensive transcriptional and epigenomic datasets from livers of mice fed these diets and uncovered new functions and gene targets for PPARĪ±

    G55.0+0.3: A Highly Evolved Supernova Remnant

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    Multi-frequency analysis has revealed the presence of a new supernova remnant, G55.0+0.3, in the Galactic plane. A kinematic distance of 14 kpc has been measured from HI spectral line data. The faint, clumpy half-shell is non-thermal and has a physical radius of 70 pc. Using an evolutionary model, the age of the remnant is estimated to be on the order of one million years, which exceeds conventional limits by a factor of five. The remnant may be associated with the nearby pulsar J1932+2020, which has a spin-down age of 1.1 million years. This work implies that the radiative lifetimes of remnants could be much longer than previously suggested.Comment: 27 pages, 7 figures in 9 files (figures 1 and 2 require 2 files each), Accepted for publication in The Astrophysical Journal (Jan. 20, 1998 volume

    A life course approach to the relationship between fetal growth and hypothalamic-pituitary-adrenal axis function

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    CONTEXT: Human and animal studies suggest that hypothalamic-pituitary-adrenal axis (HPA-A) function may be programmed in utero; however, these findings are inconsistent. Given the powerful metabolic actions of cortisol, it is important to clarify the influence of early life on adult HPA-A function. OBJECTIVE: To determine the relationship between fetal growth and HPA-A stress response to a psychosocial stressor in young adults. DESIGN: Multigenerational, prospective cohort study (the Raine Study) conducted between 1989 and 1991. SETTING: King Edward Memorial Hospital, Perth, Western Australia, Australia. PARTICIPANTS: A total of 917 participants aged 18 years from Gen2 of the Raine Study. MAIN OUTCOME MEASURES: Measures of hypothalamic-pituitary-adrenal axis function before and after exposure to the Trier Social Stress Test. RESULTS: In fully adjusted models, an inverse linear relationship was observed between birthweight and plasma measures of (1) baseline cortisol (Ī²ā€…=ā€…-0.90%, 95% CI: -1.73 to -0.07; Pā€…=ā€…0.03); (2) peak cortisol (Ī²ā€…=ā€…-0.78%, 95% CI -1.51 to -0.06; Pā€…=ā€…0.03); (3) area under the curve with respect to ground (Ī²ā€…=ā€…-0.89%, 95% CI -1.60 to -0.18; Pā€…=ā€…0.01); and (4) adrenal sensitivity (Ī²ā€…=ā€…-1.02, 95% CI: -1.85 to -0.18; Pā€…=ā€…0.02). Similar results were demonstrated for percent optimal birthweight. No consistent quadratic relationships were identified. No associations were found between measures of fetal adiposity and HPA-A function at age 18 years, or fetal growth and HPA-A response pattern. Removal of anticipatory responders from the models substantially attenuated the observed relationships. CONCLUSION: We observed an inverse linear relationship between fetal growth and HPA-A function at age 18 years. This differs from the inverse parabolic relationship (inverted U curve) reported in adults of advanced age. Altered adrenal sensitivity may underlie this relationship

    In vivo detection of cerebral tau pathology in long-term survivors of traumatic brain injury

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    Traumatic brain injury (TBI) can trigger progressive neurodegeneration, with tau pathology seen years after a single moderate-severe TBI. Identifying this type of posttraumatic pathology in vivo might help to understand the role of tau pathology in TBI pathophysiology. We used flortaucipir positron emission tomography (PET) to investigate whether tau pathology is present many years after a single TBI in humans. We examined PET data in relation to markers of neurodegeneration in the cerebrospinal fluid (CSF), structural magnetic resonance imaging measures, and cognitive performance. Cerebral flortaucipir binding was variable, with many participants with TBI showing increases in cortical and white matter regions. At the group level, flortaucipir binding was increased in the right occipital cortex in TBI when compared to healthy controls. Flortaucipir binding was associated with increased total tau, phosphorylated tau, and ubiquitin carboxyl-terminal hydrolase L1 CSF concentrations, as well as with reduced fractional anisotropy and white matter tissue density in TBI. Apolipoprotein E (APOE) Īµ4 genotype affected the relationship between flortaucipir binding and time since injury, CSF Ī² amyloid 1ā€“42 (AĪ²42) concentration, white matter tissue density, and longitudinal Mini-Mental State Examination scores in TBI. The results demonstrate that tau PET is a promising approach to investigating progressive neurodegeneration associated with tauopathy after TBI
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