bluuebunny/crossref_metadata_2025_split huggingface dataset:
Shifting Pacific storm tracks as stressors to ecosystems of western North America
Authors: Dannenberg Matthew P. , Wise Erika K. 
Published: May 2017

AbstractMuch of the precipitation delivered to western North America arrives during the cool season via midlatitude Pacific storm tracks, which may experience future shifts in response to climate change. Here, we assess the sensitivity of the hydroclimate and ecosystems of western North America to the latitudinal position of cool‐season Pacific storm tracks. We calculated correlations between storm track variability and three hydroclimatic variables: gridded cool‐season standardized precipitation‐evapotranspiration index, April snow water equivalent, and water year streamflow from a network of USGS stream gauges. To assess how historical storm track variability affected ecosystem processes, we derived forest growth estimates from a large network of tree‐ring widths and land surface phenology and wildfire estimates from remote sensing. From 1980 to 2014, cool‐season storm tracks entered western North America between approximately 41°N and 53°N. Cool‐season moisture supply and snowpack responded strongly to storm track position, with positive correlations to storm track latitude in eastern Alaska and northwestern Canada but negative correlations in the northwestern U.S. Ecosystems of the western United States were greener and more productive following winters with south‐shifted storm tracks, while Canadian ecosystems were greener in years when the cool‐season storm track was shifted to the north. On average, larger areas of the northwestern United States were burned by moderate to high severity wildfires when storm tracks were displaced north, and the average burn area per fire also tended to be higher in years with north‐shifted storm tracks. These results suggest that projected shifts of Pacific storm tracks over the 21st century would likely alter hydroclimatic and ecological regimes in western North America, particularly in the northwestern United States, where moisture supply and ecosystem processes are highly sensitive to the position of cool‐season storm tracks.
Estimating Groundwater Mounding in Sloping Aquifers for Managed Aquifer Recharge
Authors: Zlotnik Vitaly A. , Kacimov Anvar , Al‐Maktoumi Ali 
Published: May 2017

AbstractDesign of managed aquifer recharge (MAR) for augmentation of groundwater resources often lacks detailed data, and simple diagnostic tools for evaluation of the water table in a broad range of parameters are needed. In many large‐scale MAR projects, the effect of a regional aquifer base dip cannot be ignored due to the scale of recharge sources (e.g., wadis, streams, reservoirs). However, Hantush's (1967) solution for a horizontal aquifer base is commonly used. To address sloping aquifers, a new closed‐form analytical solution for water table mound accounts for the geometry and orientation of recharge sources at the land surface with respect to the aquifer base dip. The solution, based on the Dupiuit‐Forchheimer approximation, Green's function method, and coordinate transformations is convenient for computing. This solution reveals important MAR traits in variance with Hantush's solution: mounding is limited in time and space; elevation of the mound is strongly affected by the dip angle; and the peak of the mound moves over time. These findings have important practical implications for assessment of various MAR scenarios, including waterlogging potential and determining proper rates of recharge. Computations are illustrated for several characteristic MAR settings.
Optimization strategies aimed to increase the efficacy of H. pylori eradication therapies
Authors: Gisbert Javier P. , McNicholl Adrian G. 
Published: May 2017

AbstractBackgroundAs with any other infectious disease, we should aim for treatments offering ≥90% Helicobacter pylori eradication rates in clinical practice.AimTo summarize optimization strategies aimed to increase the efficacy of H. pylori eradication therapies.MethodsA systematic bibliographic search (in PubMed up to August 2016) was designed to identify studies investigating optimization strategies aimed to increase the efficacy of H. pylori eradication therapies.ResultsThe most direct way to optimize a treatment is using higher doses of drugs unless it has been shown that lower doses are equally effective. Similarly, prescriptions should use 14‐day duration unless a shorter scheme has been shown locally to be equally effective. Double‐dose proton‐pump inhibitor therapy is recommended for triple therapy and may probably increase the efficacy of nonbismuth concomitant regimen as well. The efficacy of triple therapies in the presence of resistance can be significantly improved by the addition of bismuth salts, which offer an additive effect in combination with antibiotics. Overall, probiotics seem to reduce antibiotic side effects, but the increase in eradication rates is not so evident; therefore, they cannot be generally recommended for clinical practice yet.ConclusionsUsing potent acid inhibition and/or higher antibiotic doses—especially by increasing the number of daily intakes—and lengthening treatments up to 14 days improves efficacy in most regimens and should be generally recommended. Triple therapies can be efficiently improved by the addition of bismuth salts, turning them into quadruple therapies. Finally, some treatments will require a combination of optimization strategies to significantly improve results.
Examination of PHOX2B in adult neuroendocrine neoplasms reveals relatively frequent expression in phaeochromocytomas and paragangliomas
Authors: Lee John P , Hung Yin P , O'Dorisio Thomas M , Howe James R , Hornick Jason L , Bellizzi Andrew M 
Published: May 2017

AimsPaired‐like homeobox 2b (PHOX2B) is a transcription factor with expression outside of the central nervous system restricted to neurons and chromaffin cells of the autonomic nervous system. Germline mutations cause congenital central hypoventilation syndrome and predispose to neuroblastoma and Hirschsprung disease. Among paediatric small round cell tumours, PHOX2B is neuroblastoma‐specific. Two studies of adult autonomic nervous system tumours (n = 62) produced conflicting results (all tumours stained in one; expression restricted to 40% of paragangliomas in the other). We examined PHOX2B expression in a large cohort of phaeochromocytomas and paragangliomas, as well as well‐differentiated neuroendocrine tumours (WDNETs) and poorly differentiated neuroendocrine carcinomas (PDNECs).Methods and resultsTissue microarrays (TMAs) were constructed from 609 tumours: 111 phaeochromocytomas, 146 paragangliomas, 250 WDNETs, and 102 PDNECs. PHOX2B immunohistochemistry was scored for extent (%) and intensity (0–3+), and an H‐score (extent × intensity) was calculated. PHOX2B expression was seen in 32% of phaeochromocytomas and in 47% of paragangliomas. Mean/median H‐scores for these tumours were in the 30–55 range (i.e. weak to moderate staining). No WDNETs and only 7% of PDNECs stained, the latter often strongly. In a representative cohort of corresponding whole sections (n = 55), the results in WDNETs and PDNECs were unchanged, whereas half of the phaeochromocytomas/paragangliomas that were negative on TMAs became focally, weakly positive.ConclusionsWe found frequent, weak to moderate PHOX2B expression in phaeochromocytomas/paragangliomas and no expression in WDNETs, which could be diagnostically useful in the distinction of these tumours. Expression in a minority of PDNECs probably reflects the transcription factor lineage infidelity that is characteristic of this tumour class.
HMGA2 is a specific immunohistochemical marker for pleomorphic adenoma and carcinoma ex‐pleomorphic adenoma
Authors: Mito Jeffrey K , Jo Vickie Y , Chiosea Simion I , Dal Cin Paola , Krane Jeffrey F 
Published: May 2017

AimsAccurate classification of salivary gland neoplasms may be challenging, owing to morphological overlap, particularly in small biopsies. Recurrent translocations involving the high‐mobility group AT‐hook 2 (HMGA2) gene are present in a subset of pleomorphic adenomas (PAs) and carcinoma ex‐pleomorphic adenomas (CA ex‐PAs). The aim of this study was to evaluate immunohistochemical HMGA2 expression in 225 salivary gland tumours, including 56 PAs, 37 CA ex‐PAs, and 132 potential histological mimics, to determine its diagnostic utility.Methods and resultsHMGA2 expression was identified in 19 PAs (33.9%) and nine CA ex‐PAs (24.3%). Expression was strong and diffuse throughout all PAs, and in four of nine positive CA ex‐PAs. In five CA ex‐PAs, HMGA2 showed weak‐to‐strong multifocal staining within the carcinomatous component, and strong diffuse HMGA2 expression in the residual PA. Among histological mimics, six de‐novo salivary duct carcinomas (28.5%), three epithelial–myoepithelial carcinomas (33.3%) and one case each of myoepithelioma and basal cell adenoma expressed HMGA2. Fluorescence in‐situ hybridization for HMGA2 rearrangement performed on a subset of tumours that showed diffuse HMGA2 expression in PAs and CA ex‐PAs was frequently associated with rearrangement of the HMGA2 locus, whereas cases of de‐novo salivary duct carcinoma, or CA ex‐PA with limited or no HMGA2 expression, had an intact HMGA2 locus.ConclusionsHMGA2 expression is a highly specific (96.2%), but low‐sensitivity (29.8%), marker for PA and CA ex‐PA when compared with histological mimics, and is frequently associated with rearrangement of the HMGA2 locus.
Elimination of GPR146‐mediated antiviral function through IRF3/HES1‐signalling pathway
Authors: Huang Hongjun , Zhang Na , Xiong Qingqing , Chen Ruoyu , Zhang Chengfei , Wang Ning , Wang Li , Ren Hua , Liu Mingyao , Qian Min , Du Bing 
Published: May 2017

SummaryAs the most important host defence against viral infection, interferon (IFN) stimulates hundreds of antiviral genes (ISGs) that together establish an ‘antiviral state’. However, the antiviral function of most ISGs in viral infection still need further exploration. Here, we demonstrated that the expression of G‐protein‐coupled receptor 146 (GPR146) is highly increased by both IFN‐β and IFN‐γ in a signal transducer and activator of transcription 1‐dependent signalling pathway. Most importantly, overexpression of GPR146 protects the host cells from vesicular stomatitis virus and Newcastle disease virus infection but not from infection by herpes simplex virus. In contrast, the virus‐induced IFN‐β production changed little in Gpr146‐knockout cells. Furthermore, the Gpr146‐deficient mice showed similar susceptibility to wild‐type mice with vesicular stomatitis virus infection. Interestingly, the expression of GPR146 in virus‐infected cells was strikingly reduced and can partially explain why the viral infection was little influenced in Gpr146‐knockout mice. Surprisingly, virus‐activated IFN regulatory factor 3 (IRF3) signalling not only induces the expression of IFN but also represses GPR146 expression through HES1 (hairy and enhancer of split‐1)‐mediated transcriptional activity to establish a dynamic equilibrium between pro‐viral and antiviral stages in host cells. Taken together, these data reveal the antiviral role of GPR146 in fighting viral infection although the GPR146‐mediated protection is eliminated by IRF3/HES1‐signalling, which suggests a potential therapeutic significance of both GPR146 and HES1 signalling in viral infection.
Cell death and thymic tolerance
Authors: Daley Stephen R. , Teh Charis , Hu Daniel Y. , Strasser Andreas , Gray Daniel H.D. 
Published: May 2017

SummaryThe differentiation of hematopoietic precursors into the many functionally distinct T‐cell types produced by the thymus is a complex process. It proceeds through a series of stages orchestrated by a variety of thymic microenvironments that shape the T‐cell developmental processes. Numerous cytokine and cell surface receptors direct thymocyte differentiation but the primary determinant of cell fate is the engagement of the T‐cell antigen receptor (TCR). The strength of the TCR signal and the maturation stage of the thymocyte receiving it can direct the various differentiation programs or, alternatively, end the process by inducing cell death. The regulation of thymocyte death is critical for the efficiency of thymic T‐cell differentiation and the preservation of immune tolerance. A detailed knowledge of mechanisms that eliminate thymocytes from the T‐cell repertoire is essential to understand the “logic” of T‐cell selection in the thymus. This review focuses on the central role of the BCL‐2 family of proteins in the apoptotic checkpoints that punctuate thymocyte differentiation and the consequences of defects in these processes.
Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases
Authors: Man Si Ming , Karki Rajendra , Kanneganti Thirumala‐Devi 
Published: May 2017

SummaryCell death is a fundamental biological phenomenon that is essential for the survival and development of an organism. Emerging evidence also indicates that cell death contributes to immune defense against infectious diseases. Pyroptosis is a form of inflammatory programmed cell death pathway activated by human and mouse caspase‐1, human caspase‐4 and caspase‐5, or mouse caspase‐11. These inflammatory caspases are used by the host to control bacterial, viral, fungal, or protozoan pathogens. Pyroptosis requires cleavage and activation of the pore‐forming effector protein gasdermin D by inflammatory caspases. Physical rupture of the cell causes release of the pro‐inflammatory cytokines IL‐1β and IL‐18, alarmins and endogenous danger‐associated molecular patterns, signifying the inflammatory potential of pyroptosis. Here, we describe the central role of inflammatory caspases and pyroptosis in mediating immunity to infection and clearance of pathogens.
Restimulation‐induced cell death: new medical and research perspectives
Authors: Zheng Lixin , Li Jian , Lenardo Michael 
Published: May 2017

SummaryIn the periphery, homeostasis of the immune system depends on the equilibrium of expanding and contracting T lymphocytes during immune response. An important mechanism of lymphocyte contraction is clonal depletion of activated T cells by cytokine withdrawal induced death (CWID) and TCR restimulation induced cell death (RICD). Deficiencies in signaling components for CWID and RICD leads to autoimmunune lymphoproliferative disorders in mouse and human. The most important feature of CWID and RICD is clonal specificity, which lends great appeal as a strategy for targeted tolerance induction and treatment of autoimmune diseases, allergic disorders, and graft rejection by depleting undesired disease‐causing T cells while keeping the overall host immunity intact.
RIPK3 in cell death and inflammation: the good, the bad, and the ugly
Authors: Orozco Susana , Oberst Andrew 
Published: May 2017

SummaryNecroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases‐1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro‐apoptotic protease caspase‐8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions. Interestingly, accumulating evidence suggests that RIPK3 has functions beyond the induction of necroptotic cell death, especially in the areas of tissue injury and sterile inflammation. Here, we will discuss the role of RIPK3 in a variety of physiological conditions, including necroptotic and non‐necroptotic cell death, in the context of viral and bacterial infections, tissue damage, and inflammation.
Dying to protect: cell death and the control of T‐cell homeostasis
Authors: Li Kun‐Po , Shanmuganad Sharmila , Carroll Kaitlin , Katz Jonathan D. , Jordan Michael B. , Hildeman David A. 
Published: May 2017

SummaryT cells play a critical role in immune responses as they specifically recognize peptide/MHC complexes with their T‐cell receptors and initiate adaptive immune responses. While T cells are critical for performing appropriate effector functions and maintaining immune memory, they also can cause autoimmunity or neoplasia if misdirected or dysregulated. Thus, T cells must be tightly regulated from their development onward. Maintenance of appropriate T‐cell homeostasis is essential to promote protective immunity and limit autoimmunity and neoplasia. This review will focus on the role of cell death in maintenance of T‐cell homeostasis and outline novel therapeutic strategies tailored to manipulate cell death to limit T‐cell survival (eg, autoimmunity and transplantation) or enhance T‐cell survival (eg, vaccination and immune deficiency).
Caspase‐8: regulating life and death
Authors: Tummers Bart , Green Douglas R. 
Published: May 2017

SummaryRoles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best‐known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis. Of the two best understood pathways of apoptosis, the extrinsic and intrinsic (mitochondrial) pathways, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) superfamily. Ligation of these death receptors can also induce necroptosis. The extrinsic apoptosis and necroptosis pathways regulate each other and their balance determines whether cells live. Integral in the regulation and initiation of death receptor‐mediated activation of programmed cell death is the aspartate‐specific cysteine protease (caspase)‐8. This review describes the role of caspase‐8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase‐8 inhibits necroptosis. The importance of caspase‐8 in the development and homeostasis and the way that dysfunctional caspase‐8 may contribute to the development of malignancies in mice and humans are also explored.
Augmentation programme for the endangered Ozark hellbender Cryptobranchus alleganiensis bishopi in Missouri
Authors: Ettling J. A. , Wanner M. D. , Pedigo A. S. , Kenkel J. L. , Noble K. R. , Briggler J. T. 
Published: May 2017

The Ozark hellbender Cryptobranchus alleganiensis bishopi is an endangered aquatic salamander that inhabits cold‐water streams in the Ozark Highlands of Missouri and Arkansas in the USA. As a result of the drastic population declines over the past 40+ years, with a prominent shift in age structure (large, mature individuals predominate; young classes virtually absent), the Ozark Hellbender Working Group (OHWG) was established in 2001 to develop a conservation strategy for the species. The OHWG comprises representatives from state and federal agencies, Saint Louis Zoo (MO, USA), universities and interested individuals. Based on data from the Hellbender Population and Viability Assessment it was determined that without intervention, including a captive‐propagation, head‐start and augmentation programme, it was highly likely (>96% probability) that the species would go extinct within the next 75 years. Inter‐agency collaboration has facilitated significant progress since the inception of the captive‐propagation programme in 2002. The joint strategy of the world's first captive breeding of Ozark hellbenders in 2011 and subsequent captive breeding in the 2012–2015 period, together with the hatching and rearing of wild‐collected eggs, means 6737 larvae/juveniles have been produced and/or reared at the Saint Louis Zoo. Since 2008, 3138 juvenile Ozark hellbenders reared at Saint Louis Zoo have been released into the wild in Missouri to augment remaining populations in four different streams (Bryant Creek, North Fork of the White River, Current River and Eleven Point River). Based on the success of the captive‐propagation programme, post‐release survival and dedicated individuals of various organizations the future of the Ozark hellbender is looking optimistic.
Physical performances of alkali‐activated portland cement‐glass‐limestone blends
Authors: Thomsen René Mossing , Garzón Sergio Ferreiro , Herfort Duncan , Skibsted Jørgen , Yue Yuanzheng 
Published: May 2017

AbstractThe potential of calcium aluminosilicate (CAS) glasses as supplementary cementitious materials is studied in terms of the development of compressive strength for mortars containing a mixture of portland cement, CAS glass, and limestone. In addition, the impact of internal and external alkali activation of the cementitious systems on the mortar performances is investigated. Internal alkali activation is obtained by adding alkali oxides to the CAS glass system, whereas external alkali activation is realized by hydration of the blended cements containing alkali‐free CAS glasses using alkaline solutions. For the internally alkali‐activated systems and the alkali‐free mortars, higher strengths are achieved in comparison to the reference mortar prepared from plain ordinary portland cement. In contrast, the externally alkali‐activated mortars exhibit lower compressive strengths, implying the importance of both the immediate availability of alkali ions in the cementitious system and the increased dissolution rate of the glass particles caused by the network depolymerization. The glasses are also studied by thermal analysis and the results are used to calculate the theoretical CO2 emissions. The lowest embodied CO2 emission is estimated for the blends containing alkali‐activated CAS glasses.
Selection of core animals in the Algorithm for Proven and Young using a simulation model
Authors: Bradford H.L. , Pocrnić I. , Fragomeni B.O. , Lourenco D.A.L. , Misztal I. 
Published: May 2017

SummaryThe Algorithm for Proven and Young (APY) enables the implementation of single‐step genomic BLUP (ssGBLUP) in large, genotyped populations by separating genotyped animals into core and non‐core subsets and creating a computationally efficient inverse for the genomic relationship matrix (G). As APY became the choice for large‐scale genomic evaluations in BLUP‐based methods, a common question is how to choose the animals in the core subset. We compared several core definitions to answer this question. Simulations comprised a moderately heritable trait for 95,010 animals and 50,000 genotypes for animals across five generations. Genotypes consisted of 25,500 SNP distributed across 15 chromosomes. Genotyping errors and missing pedigree were also mimicked. Core animals were defined based on individual generations, equal representation across generations, and at random. For a sufficiently large core size, core definitions had the same accuracies and biases, even if the core animals had imperfect genotypes. When genotyped animals had unknown parents, accuracy and bias were significantly better (p ≤ .05) for random and across generation core definitions.