Re-assessing global water storage trends from GRACE time series

Monitoring changes in freshwater availability is critical for human society and sustainable economic development. To identify regions experiencing secular change in their water resources, many studies compute linear trends in the total water storage (TWS) anomaly derived from the Gravity Recovery and Climate Experiment (GRACE) mission data. Such analyses suggest that several major water systems are under stress (Rodell et al 2009 Nature 460 999–1002; Long et al 2013 Geophys. Res. Lett. 40 3395–401; Richey et al 2015 Water Resour. Res. 51 5217–38; Voss et al 2013 Water Resour. Res. 49 904–14; Famiglietti 2014 Nat. Clim. Change. 4 945–8; Rodell et al 2018 Nature 557 651–9). TWS varies in space and time due to low frequency natural variability, anthropogenic intervention, and climate-change (Hamlington et al 2017 Sci. Rep. 7 995; Nerem et al 2018 Proc. Natl Acad. Sci.). Therefore, linear trends from a short time series can only be interpreted in a meaningful way after accounting for natural spatiotemporal variability in TWS (Paolo et al 2015 Science 348 327–31; Edward 2012 Geophys. Res. Lett. 39 L01702). In this study, we first show that GRACE TWS trends from a short time series cannot determine conclusively if an observed change is unprecedented or severe. To address this limitation, we develop a novel metric, trend to variability ratio (TVR), that assesses the severity of TWS trends observed by GRACE from 2003 to 2015 relative to the multi-decadal climate-driven variability. We demonstrate that the TVR combined with the trend provides a more informative and complete assessment of water storage change. We show that similar trends imply markedly different severity of TWS change, depending on location. Currently more than 3.2 billion people are living in regions facing severe water storage depletion w.r.t. past decades. Furthermore, nearly 36% of hydrological catchments losing water in the last decade have suffered from unprecedented loss. Inferences from this study can better inform water resource management

Can we resolve the basin-scale sea-level trend budget from GRACE ocean mass?

Understanding sea level changes at a regional scale is important for improving local sea level projections and coastal management planning. Sea level budget (SLB) estimates derived from the sum of observation of each component close for the global mean. The sum of steric and Gravity Recovery and Climate Experiment (GRACE) ocean mass contributions to sea level calculated from measurements does not match the spatial patterns of sea surface height trends from satellite altimetry at 1° grid resolution over the period 2005–2015. We investigate potential drivers of this mismatch aggregating to subbasin regions and find that the steric plus GRACE ocean mass observations do not represent the small-scale features seen in the satellite altimetry. In addition, there are discrepancies with large variance apparent at the global and hemispheric scale. Thus, the SLB closure on the global scale to some extent represents a cancelation of errors. The SLB is also sensitive to the glacial isostatic adjustment correction for GRACE and to altimery orbital altitude. Discrepancies in the SLB are largest for the Indian-South Pacific Ocean region. Taking the spread of plausible sea level trends, the SLB closes at the ocean-basin scale ( ) but with large spread of magnitude, one third or more of the trend signal. Using the most up-to-date observation products, our ocean-region SLB does not close everywhere, and consideration of systematic uncertainties diminishes what information can be gained from the SLB about sea level processes, quantifying contributions, and validating Earth observation systems

Can GPS and GRACE data be used to separate past and present-day surface loading in a data-driven approach?

Glacial isostatic adjustment (GIA) and the hydrological cycle are both associated with mass changes and vertical land motion (VLM), which are observed by GRACE and GPS, respectively. Hydrology-related VLM results from the instantaneous response of the elastic solid Earth to surface loading by freshwater, whereas GIA-related VLM reveals the long-term response of the viscoelastic Earth mantle to past ice loading history. Thus, observations of mass changes and VLM are interrelated, making GIA and hydrology difficult to quantify and study independently. In this work, we investigate the feasibility of separating these processes based on GRACE and GPS observations, in a fully data-driven and physically consistent approach. We take advantage of the differences in the spatio-temporal characteristics of the GIA and hydrology fields to estimate the respective contributions of each component using a Bayesian hierarchical modelling framework. A closed-loop synthetic test confirms that our method successfully solves this source separation problem. However, there are significant challenges when applying the same approach with actual observations and the answer to the main question of this study is more nuanced. In particular, in regions where GPS station coverage is sparse, the lack of informative data becomes a limiting factor

The scope of the Kalman filter for spatio-temporal applications in environmental science

The Kalman filter is a workhorse of dynamical modeling. But there are challenges when using the Kalman filter in environmental science: the complexity of environmental processes, the complicated and irregular nature of many environmental datasets, and the scale of environmental datasets, which may comprise many thousands of observations per time-step. We show how these challenges can be met within the Kalman filter, identifying some situations which are relatively easy to handle, such as datasets which are high-resolution in time, and some which are hard, like areal observations on small contiguous polygons. Overall, we conclude that many applications in environmental science are within the scope of the Kalman filter, or its generalizations

Polymorphisms at codons 108 and 189 in murine PrP play distinct roles in the control of scrapie incubation time

Rona Barron - ORCID: 0000-0003-4512-9177 https://orcid.org/0000-0003-4512-9177Item not available from this repository.Susceptibility to transmissible spongiform encephalopathies (TSEs) is associated strongly with PrP polymorphisms in humans, sheep and rodents. In mice, scrapie incubation time is controlled by polymorphisms at PrP codons 108 (leucine or phenylalanine) and 189 (threonine or valine), but the precise role of each polymorphism in the control of disease is unknown. The L108F and T189V polymorphisms are present in distinct structural regions of PrP and thus provide an excellent model with which to investigate the role of PrP structure and gene variation in TSEs. Two unique lines of transgenic mice, in which 108F and 189V have been targeted separately into the endogenous murine Prnp a gene, have been produced. TSE inoculation of inbred lines of mice expressing all allelic combinations at codons 108 and 189 has revealed a complex relationship between PrP allele and incubation time. It has been established that both codons 108 and 189 control TSE incubation time, and that each polymorphism plays a distinct role in the disease process. Comparison of ME7 incubation times in mouse lines that are heterozygous at both codons has also identified a previously unrecognized intramolecular interaction between PrP codons 108 and 189.https://doi.org/10.1099/vir.0.80525-086pubpub

A polymorphism in the regulatory region of PRNP is associated with increased risk of sporadic Creutzfeldt-Jakob disease

Background: Creutzfeldt-Jakob disease (CJD) is a rare transmissible neurodegenerative disorder. An important determinant for CJD risk and phenotype is the M129V polymorphism of the human prion protein gene (PRNP), but there are also other coding and non-coding polymorphisms inside this gene.Methods: We tested whether three non-coding polymorphism located inside the PRNP regulatory region (C-101G, G310C and T385C) were associated with risk of CJD and with age at onset in a United Kingdom population-based sample of 131 sporadic CJD (sCJD) patients and 194 controls.Results: We found no disease association for either PRNP C-101G or PRNP T385C. Although the crude analysis did not show a significant association between PRNP G310C and sCJD (OR: 1.5; 95%CI = 0.7 to 2.9), after adjusting by PRNP M129V genotype, it resulted that being a C allele carrier at PRNP G310C was significantly (p = 0.03) associated with a 2.4 fold increased risk of developing sCJD (95%CI = 1.1 to 5.4). Additionally, haplotypes carrying PRNP 310C coupled with PRNP 129M were significantly overrepresented in patients (p = 0.02) compared to controls. Cases of sCJD carrying a PRNP 310C allele presented at a younger age (on average 8.9 years younger than those without this allele), which was of statistical significance (p = 0.05). As expected, methionine and valine homozygosity at PRNP M129V increased significantly the risk of sCJD, alone and adjusted by PRNP G310C (OR MM/MV = 7.3; 95%CI 3.9 to 13.5 and OR VV/MV = 4.0; 95%CI 1.7 to 9.3).Conclusions: Our findings support the hypothesis that genetic variations in the PRNP promoter may have a role in the pathogenesis of sCJD

A reassessment of the early archaeological record at Leang Burung 2, a Late Pleistocene rock-shelter site on the Indonesian island of Sulawesi

This paper presents a reassessment of the archaeological record at Leang Burung 2, a key early human occupation site in the Late Pleistocene of Southeast Asia. Excavated originally by Ian Glover in 1975, this limestone rock-shelter in the Maros karsts of Sulawesi, Indonesia, has long held significance in our understanding of early human dispersals into \u27Wallacea\u27, the vast zone of oceanic islands between continental Asia and Australia. We present new stratigraphic information and dating evidence from Leang Burung 2 collected during the course of our excavations at this site in 2007 and 2011-13. Our findings suggest that the classic Late Pleistocene modern human occupation sequence identified previously at Leang Burung 2, and proposed to span around 31,000 to 19,000 conventional 14C years BP (~35-24 ka cal BP), may actually represent an amalgam of reworked archaeological materials. Sources for cultural materials of mixed ages comprise breccias from the rear wall of the rock-shelter-remnants of older, eroded deposits dated to 35-23 ka cal BP-and cultural remains of early Holocene antiquity. Below the upper levels affected by the mass loss of Late Pleistocene deposits, our deep-trench excavations uncovered evidence for an earlier hominin presence at the site. These findings include fossils of now-extinct proboscideans and other \u27megafauna\u27 in stratified context, as well as a cobble-based stone artifact technology comparable to that produced by late Middle Pleistocene hominins elsewhere on Sulawesi

Rapid End-Point Quantitation of Prion Seeding Activity with Sensitivity Comparable to Bioassays

A major problem for the effective diagnosis and management of prion diseases is the lack of rapid high-throughput assays to measure low levels of prions. Such measurements have typically required prolonged bioassays in animals. Highly sensitive, but generally non-quantitative, prion detection methods have been developed based on prions' ability to seed the conversion of normally soluble protease-sensitive forms of prion protein to protease-resistant and/or amyloid fibrillar forms. Here we describe an approach for estimating the relative amount of prions using a new prion seeding assay called real-time quaking induced conversion assay (RT-QuIC). The underlying reaction blends aspects of the previously described quaking-induced conversion (QuIC) and amyloid seeding assay (ASA) methods and involves prion-seeded conversion of the alpha helix-rich form of bacterially expressed recombinant PrPC to a beta sheet-rich amyloid fibrillar form. The RT-QuIC is as sensitive as the animal bioassay, but can be accomplished in 2 days or less. Analogous to end-point dilution animal bioassays, this approach involves testing of serial dilutions of samples and statistically estimating the seeding dose (SD) giving positive responses in 50% of replicate reactions (SD50). Brain tissue from 263K scrapie-affected hamsters gave SD50 values of 1011-1012/g, making the RT-QuIC similar in sensitivity to end-point dilution bioassays. Analysis of bioassay-positive nasal lavages from hamsters affected with transmissible mink encephalopathy gave SD50 values of 103.5–105.7/ml, showing that nasal cavities release substantial prion infectivity that can be rapidly detected. Cerebral spinal fluid from 263K scrapie-affected hamsters contained prion SD50 values of 102.0–102.9/ml. RT-QuIC assay also discriminated deer chronic wasting disease and sheep scrapie brain samples from normal control samples. In principle, end-point dilution quantitation can be applied to many types of prion and amyloid seeding assays. End point dilution RT-QuIC provides a sensitive, rapid, quantitative, and high throughput assay of prion seeding activity

Lack of association between PRNP 1368 polymorphism and Alzheimer's disease or vascular dementia

<p>Abstract</p> <p>Background</p> <p>Polymorphisms of the prion protein gene (<it>PRNP</it>) at codons 129 and 219 play an important role in the susceptibility to Creutzfeldt-Jakob disease (CJD), and might be associated with other neurodegenerative disorders. Several recent reports indicate that polymorphisms outside the coding region of <it>PRNP </it>modulate the expression of prion protein and are associated with sporadic CJD, although other studies failed to show an association. These reports involved the polymorphism <it>PRNP </it>1368 which is located upstream from <it>PRNP </it>exon 1. In a case-controlled protocol, we assessed the possible association between the <it>PRNP </it>1368 polymorphism and either Alzheimer's disease (AD) or vascular dementia (VaD).</p> <p>Methods</p> <p>To investigate whether the <it>PRNP </it>1368 polymorphism is associated with the occurrence of AD or VaD in the Korean population, we compared the genotype, allele, and haplotype frequencies of the <it>PRNP </it>1368 polymorphism in 152 AD patients and 192 VaD patients with frequencies in 268 healthy Koreans.</p> <p>Results and conclusion</p> <p>Significant differences in genotype, allele and haplotype frequencies of <it>PRNP </it>1368 polymorphism were not observed between AD and normal controls. There were no significant differences in the genotype and allele frequencies of the <it>PRNP </it>1368 polymorphism between Korean VaD patients and normal controls. However, in the haplotype analysis, haplotype Ht5 was significantly over-represented in Korean VaD patients. This was the first genetic association study of a polymorphism outside the coding region of <it>PRNP </it>in relation to AD and VaD.</p

Prion Shedding from Olfactory Neurons into Nasal Secretions

This study investigated the role of prion infection of the olfactory mucosa in the shedding of prion infectivity into nasal secretions. Prion infection with the HY strain of the transmissible mink encephalopathy (TME) agent resulted in a prominent infection of the olfactory bulb and the olfactory sensory epithelium including the olfactory receptor neurons (ORNs) and vomeronasal receptor neurons (VRNs), whose axons comprise the two olfactory cranial nerves. A distinct glycoform of the disease-specific isoform of the prion protein, PrPSc, was found in the olfactory mucosa compared to the olfactory bulb, but the total amount of HY TME infectivity in the nasal turbinates was within 100-fold of the titer in the olfactory bulb. PrPSc co-localized with olfactory marker protein in the soma and dendrites of ORNs and VRNs and also with adenylyl cyclase III, which is present in the sensory cilia of ORNs that project into the lumen of the nasal airway. Nasal lavages from HY TME-infected hamsters contained prion titers as high as 103.9 median lethal doses per ml, which would be up to 500-fold more infectious in undiluted nasal fluids. These findings were confirmed using the rapid PrPSc amplification QuIC assay, indicating that nasal swabs have the potential to be used for prion diagnostics. These studies demonstrate that prion infection in the olfactory epithelium is likely due to retrograde spread from the olfactory bulb along the olfactory and vomeronasal axons to the soma, dendrites, and cilia of these peripheral neurons. Since prions can replicate to high levels in neurons, we propose that ORNs can release prion infectivity into nasal fluids. The continual turnover and replacement of mature ORNs throughout the adult lifespan may also contribute to prion shedding from the nasal passage and could play a role in transmission of natural prion diseases in domestic and free-ranging ruminants