32 research outputs found

    Tribe’s Trajectory & LGBTQ Rights

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    I’m not sure I’ll ever live it down. I actually said—out loud, to his face, a full ten minutes into our very first conversation—“Holy smokes, you’re Larry Tribe!” I was in Cambridge that day as a newly admitted student. Somehow, inexplicably (it’s not that big of a campus), I got lost. Very lost. Fortunately, a passerby professor took mercy and steered me to his office. In a bid to regain my composure, and to seem like a plausible future law student, I jumped straight to explaining why I was there: I wanted to be a civil rights lawyer. To prove it, I recounted a paper I’d just delivered, entitled “Sodomy and the Supremes.” I brightly added that the hero of this tale—a certain Larry Tribe—must be a colleague of his. “Oh,” he said gently, “that’s me.” To which I replied . . . well, you already know. In my defense, “holy smokes” is a justified reaction to Laurence H. Tribe. By virtually any measure, he ranks among the greatest and most influential legal scholars and advocates in U.S. history. He has written constitutions into existence. He has ad-vised world leaders on matters of historic import. And, in exploring the U.S. Constitution, he has mapped “constellations where the rest of us saw only a random collection of stars.” Among his towering achievements—perhaps first among them, in my (admittedly biased) view—stand Tribe’s contributions to the early and continuing progress of LGBTQ rights in the United States. The story of that struggle is vast. Its cast of characters numbers in the millions: people from all walks of life who reshaped society from the top down and the bottom up and the closet out. As Tribe is quick to emphasize, most who have fought for LGBTQ rights lacked the privilege and security he enjoyed in doing so; some were literally fighting for their lives, their safety, their homes, or their jobs, while many others fought for the most basic opportunities to flourish and form families. It would be mistaken and reductionist to address this history without emphasizing the critically important role that so many people, of all sexual orientations and gender identities, played in the story. Yet there is no denying the special significance of Tribe’s role in the legal campaign for LGBTQ civil rights. From the outset, this has been one of his main projects as a scholar and advocate. And a review of his writings reveals a fascinating tale. At least as early as 1978, Tribe intuitively grasped the profound connection between same-sex intimacy and the realization of personal identity. He also perceived that the Constitution protected gays and lesbians from laws that made their existence a crime. But he recognized that a decisive majority of the Supreme Court lacked such vision. This tension drove decades of generative and intensely strategic advocacy. Tribe reached new heights of brilliance in articulating principles designed to persuade a conservative Court to protect the rights of LGBTQ people. By design, however, these frameworks lacked something essential: a grounding in the integrity and humanity of LGBTQ identity, experience, and relationships. Even as Tribe’s deep reservoir of empathy powered this constitutional project—and shone through in his relationships with LGBTQ friends and students—he kept it carefully closeted in his legal filings. There, he adhered to broad, universal claims about the meaning of free speech, privacy, dignity, and equality. At stake were the rights of all Americans, he insisted, not just LGBTQ people and their allies (whose presence and collective stake in the outcome were downplayed in service of litigation strategy). Only after substantial judicial and popular evolution did Tribe finally adopt a different approach, submitting an amicus brief in Lawrence v. Texas that spoke in far more particularized, meaningful ways about the rights of LGBTQ people—and the constitutional sin that rendered them outlaws. This brief hearkened back to Tribe’s earliest exploration of the rights of “homosexuals.” It also marked a pivot toward his pathmarking exploration of the liberty/equality dyad that would drive the case for marriage equality through United States v. Windsor and Obergefell v. Hodges. In this short Essay, I’ll survey Tribe’s fight for LGBTQ rights, drawing on his early writings and several interviews with him conducted in March and April 2021

    Brief for Plaintiff-Appellee, Carroll v. Trump, No. 20-3977 (2nd Cir. Apr. 16, 2021)

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    Introduction In June 2019, E. Jean Carroll revealed that former President Donald J. Trump had sexually assaulted her decades earlier. Trump denied it, saying he did not know who Carroll was and had never met her. But he did not stop there. He launched a series of vicious, personal attacks. He implied that she was too ugly to rape; that she had falsely accused other men of sexual assault; and that she had invented her story for money, or to sell books, or to advance a political plot. None of this was true. Trump knew that he had assaulted Carroll. He knew who she was. And he knew what he was doing when he went on a defamation rampage designed to crush her— to punish and retaliate against her—for daring to reveal his decades-old crime. Faced with this staggering onslaught, Carroll sought relief in court and sued Trump for defamation. Her case proceeded in New York state court for ten months. Trump did everything he could to stall, but his efforts ultimately failed. Just as the parties were about to engage in merits discovery, the White House prevailed upon the Department of Justice (DOJ) to intercede. Following a certification under the Westfall Act, 28 U.S.C. § 2679(d), DOJ lawyers removed the case to federal court and sought to substitute the United States as the defendant. They took the position that Trump was just doing his job—i.e., that he was acting within the scope of his employment—when he repeatedly slandered a private citizen who was no longer willing to hide the fact that he had raped her long before taking office. On two separate grounds, Judge Kaplan denied DOJ’s motion to substitute. He first held that the statute invoked by DOJ in support of substitution—the Federal Tort Claims Act (FTCA), 28 U.S.C. §§ 1346, 2671, as amended by the Westfall Act—does not apply to the President. That conclusion is compelled by the FTCA’s text and structure, as well as a host of constitutional, legislative, and judicial authorities, all of which confirm that the FTCA does not apply to the President. On appeal, DOJ (joined by Trump) seeks to show otherwise, but their arguments make a mess of the statute and offend settled separation-of-powers principles. In the alternative, Judge Kaplan concluded Trump was not acting within the scope of his employment when he defamed Carroll. This commonsense conclusion follows directly from the evidence before the Court and from longstanding principles of respondeat superior liability. On appeal, DOJ and Trump offer no basis to disturb that finding. Indeed, there is almost nothing in their briefs that discusses the facts at all. Instead, they urge the Court to adopt a new rule that would create categorical immunity for any federal official who defames anyone while speaking to the press or responding to perceived critics. That rule is both wrong and dangerous, and this Court should reject Appellants’ effort to avoid answering for Trump’s conduct. “Public office does not carry with it a license to defame at will, for even the highest officers exist to serve the public, not to denigrate its members.” Clark v. McGee, 49 N.Y.2d 613, 618-19 (1980). If accepted, Appellants’ extreme position would distort precedent, dishonor the Office of the Presidency, and give succor to the view that our most powerful political leaders stand entirely above the law. This Court should therefore affirm the denial of DOJ’s motion to substitute. Statement of the issues: 1. Is the President an “employee of the government” as that term is defined in the Federal Tort Claims Act (FTCA), 28 U.S.C. § 2671? 2. Assuming the President is an “employee of the government” under the FTCA, did Donald J. Trump act within the scope of his employment when he subjected E. Jean Carroll to willful, outrageous defamatory attacks in retaliation for revealing that he had sexually assaulted her decades before he was elected President

    Noah's Sons

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    Genesis 5–10 gives Noah’s three sons Shem, Ham, and Japheth great significance by presenting them as the three ancestors of postdiluvian humanity. Within this section two literary units focus on them: the story of Noah’s vineyard and drunkenness in Gen 9:18–27 and the Table of Nations in Gen 10. Whereas the first account describes a hierarchical relationship between the three ancestors (and their respective descendants), the second one, in the form of a segmented genealogy, shows the ancestors’ equal dispersion over the world and their inner differentiation into nations, tribes, and languages. Noah’s sons are furthermore mentioned at the end of the genealogy in Gen 5 and in the flood narrative

    Netrin-3 Signals Through Serine Phosphorylation in Tetrahymena thermophila

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    The netrin family of proteins are structurally related to laminin and, while first discovered in the nematode Caenorhabditis elegans, are now known to be present in species throughout the animal kingdom, including humans. These proteins also have a wide variety of roles that include inhibition of apoptosis, chemorepulsion, and axonal guidance. Due to the results of previous studies involving netrin-1 in vertebrate systems, the current prevailing assumption is that netrins, when acting as chemorepellents, signal using tyrosine kinases. However, data that we gathered through phosphoserine-targeting ELISA assays and immunofluorescence microscopy demonstrates that the netrin-3 peptides signal Tetrahymena thermophila through serine phosphorylation instead, causing the ciliate protists to avoid netrin-3 peptides in response. Treatment with netrin-3 peptides also seems to cause mitotic inhibition in Tetrahymena, which can be reversed by addition of a serine kinase inhibitor. This new information suggests that netrin-3 may have physiological roles that have previously been unexplored

    Biofilm Development on Caenorhabditis elegans by Yersinia Is Facilitated by Quorum Sensing-Dependent Repression of Type III Secretion

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    Yersinia pseudotuberculosis forms biofilms on Caenorhabditis elegans which block nematode feeding. This genetically amenable host-pathogen model has important implications for biofilm development on living, motile surfaces. Here we show that Y. pseudotuberculosis biofilm development on C. elegans is governed by N-acylhomoserine lactone (AHL)-mediated quorum sensing (QS) since (i) AHLs are produced in nematode associated biofilms and (ii) Y. pseudotuberculosis strains expressing an AHL-degrading enzyme or in which the AHL synthase (ypsI and ytbI) or response regulator (ypsR and ytbR) genes have been mutated, are attenuated. Although biofilm formation is also attenuated in Y. pseudotuberculosis strains carrying mutations in the QS-controlled motility regulator genes, flhDC and fliA, and the flagellin export gene, flhA, flagella are not required since fliC mutants form normal biofilms. However, in contrast to the parent and fliC mutant, Yop virulon proteins are up-regulated in flhDC, fliA and flhA mutants in a temperature and calcium independent manner. Similar observations were found for the Y. pseudotuberculosis QS mutants, indicating that the Yop virulon is repressed by QS via the master motility regulator, flhDC. By curing the pYV virulence plasmid from the ypsI/ytbI mutant, by growing YpIII under conditions permissive for type III needle formation but not Yop secretion and by mutating the type III secretion apparatus gene, yscJ, we show that biofilm formation can be restored in flhDC and ypsI/ytbI mutants. These data demonstrate that type III secretion blocks biofilm formation and is reciprocally regulated with motility via QS

    Development of Gene Expression Markers of Acute Heat-Light Stress in Reef-Building Corals of the Genus Porites

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    Coral reefs are declining worldwide due to increased incidence of climate-induced coral bleaching, which will have widespread biodiversity and economic impacts. A simple method to measure the sub-bleaching level of heat-light stress experienced by corals would greatly inform reef management practices by making it possible to assess the distribution of bleaching risks among individual reef sites. Gene expression analysis based on quantitative PCR (qPCR) can be used as a diagnostic tool to determine coral condition in situ. We evaluated the expression of 13 candidate genes during heat-light stress in a common Caribbean coral Porites astreoides, and observed strong and consistent changes in gene expression in two independent experiments. Furthermore, we found that the apparent return to baseline expression levels during a recovery phase was rapid, despite visible signs of colony bleaching. We show that the response to acute heat-light stress in P. astreoides can be monitored by measuring the difference in expression of only two genes: Hsp16 and actin. We demonstrate that this assay discriminates between corals sampled from two field sites experiencing different temperatures. We also show that the assay is applicable to an Indo-Pacific congener, P. lobata, and therefore could potentially be used to diagnose acute heat-light stress on coral reefs worldwide

    Peptidoglycan-Modifying Enzyme Pgp1 Is Required for Helical Cell Shape and Pathogenicity Traits in Campylobacter jejuni

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    The impact of bacterial morphology on virulence and transmission attributes of pathogens is poorly understood. The prevalent enteric pathogen Campylobacter jejuni displays a helical shape postulated as important for colonization and host interactions. However, this had not previously been demonstrated experimentally. C. jejuni is thus a good organism for exploring the role of factors modulating helical morphology on pathogenesis. We identified an uncharacterized gene, designated pgp1 (peptidoglycan peptidase 1), in a calcofluor white-based screen to explore cell envelope properties important for C. jejuni virulence and stress survival. Bioinformatics showed that Pgp1 is conserved primarily in curved and helical bacteria. Deletion of pgp1 resulted in a striking, rod-shaped morphology, making pgp1 the first C. jejuni gene shown to be involved in maintenance of C. jejuni cell shape. Pgp1 contributes to key pathogenic and cell envelope phenotypes. In comparison to wild type, the rod-shaped pgp1 mutant was deficient in chick colonization by over three orders of magnitude and elicited enhanced secretion of the chemokine IL-8 in epithelial cell infections. Both the pgp1 mutant and a pgp1 overexpressing strain – which similarly produced straight or kinked cells – exhibited biofilm and motility defects. Detailed peptidoglycan analyses via HPLC and mass spectrometry, as well as Pgp1 enzyme assays, confirmed Pgp1 as a novel peptidoglycan DL-carboxypeptidase cleaving monomeric tripeptides to dipeptides. Peptidoglycan from the pgp1 mutant activated the host cell receptor Nod1 to a greater extent than did that of wild type. This work provides the first link between a C. jejuni gene and morphology, peptidoglycan biosynthesis, and key host- and transmission-related characteristics

    Aligning the Goals of Learning Analytics with its Research Scholarship: An Open Peer Commentary Approach

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    To promote cross-community dialogue on matters of significance within the field of learning analytics (LA), we as editors-in-chief of the Journal of Learning Analytics (JLA) have introduced a section for papers that are open to peer commentary. An invitation to submit proposals for commentaries on the paper was released, and 12 of these proposals were accepted. The 26 authors of the accepted commentaries are based in Europe, North America, and Australia. They range in experience from PhD students and early-career researchers to some of the longest-standing, most senior members of the learning analytics community. This paper brings those commentaries together, and we recommend reading it as a companion piece to the original paper by Motz et al. (2023), which also appears in this issu
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