Sticks, Stones, and So-Called Judges: Why the Era of Trump Necessitates Revisiting Presidential Influence on the Courts

This Note will be primarily divided into three main sections. Part I of this Note will begin by discussing the importance of judicial independence in modern society and the role of elected officials in shaping the public perception of the courts. Additionally, as problems of judicial legitimacy are age-old and date back to America’s founding, Part I will include a brief discussion of an early clash between President Thomas Jefferson and the courts. Parts II and III of this Note will seek to place President Trump’s conduct towards the judicial branch within the proper historical context. Part II examines the ways in which Presidents have been able to significantly alter the makeup of the judiciary while in office. For considerations of brevity, this section will include a few illustrative examples in which Presidents have sought to alter the makeup of the courts, and each will be discussed in the context of the actions of President Trump. Part III will explore instances of Presidents undermining the legitimacy of the judiciary by making comments about pending and past court cases, particularly using examples from more recent administrations. This Note concludes that, while President Trump’s behavior regarding the judiciary has been the subject of intense media scrutiny during his first two years in office, it is important to place his comments and actions in a historical context by looking at the examples set by past Presidents. Through this frame of analysis, this Note concludes that, although President Trump’s rhetorical attacks on the independence of the judiciary—particularly in the criminal context and in targeting individual judges—have been numerous and unprecedented, President Trump is also quietly shaping the makeup of the judiciary in a way that could become even more drastic if his administration embraces a modern Court-packing plan or continues to make judicial appointments at staggering rates

Quail Genomics: a knowledgebase for Northern bobwhite

<p>Abstract</p> <p>Background</p> <p>The Quail Genomics knowledgebase (<url>http://www.quailgenomics.info</url>) has been initiated to share and develop functional genomic data for Northern bobwhite (<it>Colinus virginianus</it>). This web-based platform has been designed to allow researchers to perform analysis and curate genomic information for this non-model species that has little supporting information in GenBank.</p> <p>Description</p> <p>A multi-tissue, normalized cDNA library generated for Northern bobwhite was sequenced using 454 Life Sciences next generation sequencing. The Quail Genomics knowledgebase represents the 478,142 raw ESTs generated from the sequencing effort in addition to assembled nucleotide and protein sequences including 21,980 unigenes annotated with meta-data. A normalized MySQL relational database was established to provide comprehensive search parameters where meta-data can be retrieved using functional and structural information annotation such as gene name, pathways and protein domain. Additionally, blast hit cutoff levels and microarray expression data are available for batch searches. A Gene Ontology (GO) browser from Amigo is locally hosted providing 8,825 unigenes that are putative orthologs to chicken genes. In an effort to address over abundance of Northern bobwhite unigenes (71,384) caused by non-overlapping contigs and singletons, we have built a pipeline that generates scaffolds/supercontigs by aligning partial sequence fragments against the indexed protein database of chicken to build longer sequences that can be visualized in a web browser. </p> <p>Conclusion</p> <p>Our effort provides a central repository for storage and a platform for functional interrogation of the Northern bobwhite sequences providing comprehensive GO annotations, meta-data and a scaffold building pipeline. The Quail Genomics knowledgebase will be integrated with Japanese quail (<it>Coturnix coturnix</it>) data in future builds and incorporate a broader platform for these avian species. </p

Effects of river water and salinity on the toxicity of deltamethrin to freshwater shrimp, cladoceran, and fish

Deltamethrin is a pyrethroid insecticide used extensively to control invertebrate pests on cotton and other crops. It is acutely toxic to nontarget aquatic organisms, but existing toxicity data are mostly from toxicity tests using purified laboratory water that differs greatly from the turbid, high-conductivity rivers in the cotton-growing regions of Australia. The aim of this study was to determine whether the water quality variables conductivity, suspended particles, and dissolved organic matter alter the toxicity of deltamethrin to freshwater crustaceans and a fish. We tested three Australian native species: a cladoceran (Ceriodaphnia cf. dubia), a freshwater shrimp (Paratya australiensis), and larvae of the eastern rainbow fish (Melanotaenia duboulayi). Conductivity of the test solutions ranged from 200 to 750 μS/cm, but such changes did not modify the toxicity of deltamethrin to any of the test species. However, the toxicity of deltamethrin to C. cf. dubia and P. australiensis in river water was significantly decreased (1.8-fold to 6.3-fold reduction) compared to that in laboratory water. Variability in the toxicity data limited our ability to detect differences between laboratory and river water for M. duboulayi. Despite reductions in toxicity in natural waters, deltamethrin remained highly toxic [all L(E)C50 values <0.26 μg/L] to all organisms tested; thus, further investigation of the hazard of deltamethrin is warranted. © 2008 Springer Science+Business Media, LLC

State of the Antarctic and Southern Ocean Climate System

This paper reviews developments in our understanding of the state of the Antarctic and Southern Ocean climate and its relation to the global climate system over the last few millennia. Climate over this and earlier periods has not been stable, as evidenced by the occurrence of abrupt changes in atmospheric circulation and temperature recorded in Antarctic ice core proxies for past climate. Two of the most prominent abrupt climate change events are characterized by intensification of the circumpolar westerlies (also known as the Southern Annular Mode) between ∼6000 and 5000 years ago and since 1200–1000 years ago. Following the last of these is a period of major trans-Antarctic reorganization of atmospheric circulation and temperature between A.D. 1700 and 1850. The two earlier Antarctic abrupt climate change events appear linked to but predate by several centuries even more abrupt climate change in the North Atlantic, and the end of the more recent event is coincident with reorganization of atmospheric circulation in the North Pacific. Improved understanding of such events and of the associations between abrupt climate change events recorded in both hemispheres is critical to predicting the impact and timing of future abrupt climate change events potentially forced by anthropogenic changes in greenhouse gases and aerosols. Special attention is given to the climate of the past 200 years, which was recorded by a network of recently available shallow firn cores, and to that of the past 50 years, which was monitored by the continuous instrumental record. Significant regional climate changes have taken place in the Antarctic during the past 50 years. Atmospheric temperatures have increased markedly over the Antarctic Peninsula, linked to nearby ocean warming and intensification of the circumpolar westerlies. Glaciers are retreating on the peninsula, in Patagonia, on the sub-Antarctic islands, and in West Antarctica adjacent to the peninsula. The penetration of marine air masses has become more pronounced over parts of West Antarctica. Above the surface, the Antarctic troposphere has warmed during winter while the stratosphere has cooled year-round. The upper kilometer of the circumpolar Southern Ocean has warmed, Antarctic Bottom Water across a wide sector off East Antarctica has freshened, and the densest bottom water in the Weddell Sea has warmed. In contrast to these regional climate changes, over most of Antarctica, near-surface temperature and snowfall have not increased significantly during at least the past 50 years, and proxy data suggest that the atmospheric circulation over the interior has remained in a similar state for at least the past 200 years. Furthermore, the total sea ice cover around Antarctica has exhibited no significant overall change since reliable satellite monitoring began in the late 1970s, despite large but compensating regional changes. The inhomogeneity of Antarctic climate in space and time implies that recent Antarctic climate changes are due on the one hand to a combination of strong multidecadal variability and anthropogenic effects and, as demonstrated by the paleoclimate record, on the other hand to multidecadal to millennial scale and longer natural variability forced through changes in orbital insolation, greenhouse gases, solar variability, ice dynamics, and aerosols. Model projections suggest that over the 21st century the Antarctic interior will warm by 3.4° ± 1°C, and sea ice extent will decrease by ∼30%. Ice sheet models are not yet adequate enough to answer pressing questions about the effect of projected warming on mass balance and sea level. Considering the potentially major impacts of a warming climate on Antarctica, vigorous efforts are needed to better understand all aspects of the highly coupled Antarctic climate system as well as its influence on the Earth\u27s climate and oceans

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Sticks, Stones, and So-Called Judges: Why the Era of Trump Necessitates Revisiting Presidential Influence on the Courts

This Note will be primarily divided into three main sections. Part I of this Note will begin by discussing the importance of judicial independence in modern society and the role of elected officials in shaping the public perception of the courts. Additionally, as problems of judicial legitimacy are age-old and date back to America’s founding, Part I will include a brief discussion of an early clash between President Thomas Jefferson and the courts. Parts II and III of this Note will seek to place President Trump’s conduct towards the judicial branch within the proper historical context. Part II examines the ways in which Presidents have been able to significantly alter the makeup of the judiciary while in office. For considerations of brevity, this section will include a few illustrative examples in which Presidents have sought to alter the makeup of the courts, and each will be discussed in the context of the actions of President Trump. Part III will explore instances of Presidents undermining the legitimacy of the judiciary by making comments about pending and past court cases, particularly using examples from more recent administrations. This Note concludes that, while President Trump’s behavior regarding the judiciary has been the subject of intense media scrutiny during his first two years in office, it is important to place his comments and actions in a historical context by looking at the examples set by past Presidents. Through this frame of analysis, this Note concludes that, although President Trump’s rhetorical attacks on the independence of the judiciary—particularly in the criminal context and in targeting individual judges—have been numerous and unprecedented, President Trump is also quietly shaping the makeup of the judiciary in a way that could become even more drastic if his administration embraces a modern Court-packing plan or continues to make judicial appointments at staggering rates

Coral-Based Climate Variability in the Western Pacific Warm Pool since 1867

We have generated monthly resolved, stable isotope (δ18O and δ13C) and Sr/Ca time series from a massive Porites coral from Rabaul (4°S, 152°E): a site located in the warmest sector of the Western Pacific Warm Pool (WPWP). The coral δ18O and Sr/Ca time series are well correlated to each other and positive excursions in both records coincide with times of ENSO warm phase events. These time series contain abundant interannual variability that exhibits the well‐recognized pattern of low amplitude ENSO variation between ∼1920–1960 and high amplitude ENSO variation between 1880–1920 and 1960–1997. The ENSO‐filtered coral δ18O and Sr/Ca time series are well matched to each other (r = 0.73) and to similarly filtered coral δ18O records from Papua New Guinea (r \u3e 0.56). There is no long‐term trend in the coral δ18O record, but there is a long‐term trend of increasing coral Sr/Ca from 1867 to 1997. This trend in coral Sr/Ca suggests a cooling of ∼0.7°C, which is rather unlikely and implies that factors other than SST may be influencing the coral Sr/Ca record. The trend in coral Sr/Ca is not an analytical artifact, nor a product of time varying riverine input, nor a product of skeletal diagenesis, nor the results of kinetic effects, but may reflect surface‐water variability in Sr/Ca. Despite the presence of a nonclimatic trend in coral Sr/Ca, the Rabaul coral records contain abundant interannual‐ to multidecadal‐scale variability, much of which is coherent with other proxy records from the WPWP and with instrumental records of ENSO variability