Letter from W[illiam] W[allace] Campbell to John Muir, 1914 Jun 9.

PACIFIC COST COMMITTEEOF THE\u3c br \u3eAMERICAN ASSOCIATION FOR THE ADVANCEMENT OF SCIENCE\u3c br \u3e\u3c br \u3eMt. Hamilton. June 9. 1914. \u3c br \u3e\u3c br \u3eMy dear Dr. Muir:- \u3c br \u3e\u3c br \u3eThe American Association for the Advancement of Science has decided to hold a general meeting of the Association in San Francisco and vicinity on the occasion of the Panama-Pacific International Exposition. In 1915, and has appointed 8 Pacific Coast Committee of thirty-one members to make the necessary arrangements. It has been decided that:\u3c br \u3e1. The sessions of the meeting shall begin on Monday. August 2nd, and terminate on Saturday, August 7th.2. The general sessions of the meeting shall be held in San Francisco. \u3c br \u3e3. The general evening lectures shall be delivered in San Francisco. \u3c br \u3e4. The sessions for the presentation of addresses and papers in the separate divisions of science shall be held chiefly at the University of California. \u3c br \u3e5. Sessions for the presentation of addresses and papers in the separate divisions of science shall be held on one day at Stanford University. \u3c br \u3eThe Pacific Coast Committee desires to have the general support of a Committee of One Hundred, whose members are chosen from amongst those who may be said to represent best the Intellectual life\u3c br \u3e\u3c br \u3e05770 of the Pacific region of North America, from Alaska to Mexico and from the Hooky Mountains to the Philippine Islands. It is not expected that the Committee of One Hundred will meet for active duty. In effect it will compose the background upon which the scientific interests of the Pacific region will on this occasion be seen in projection. Mrs. Phoebe Apperson Hearst has accepted appointment as Honorary President of the Committee. Br. Benjamin Ide Wheeler will be the President, and Dr. John Casper Brenner the Vice-President.In behalf of the Pacific Coast Committee, I respectfully invite you to membership in the Committee of One Hundred as one of about ten Honorary Vice-Presidents, end trust that you will grant us the favor of acceptance. In due time 8 printed list of the members will be sent you. The kindness of an early response is requested. I may say that the American Association for the Advancement of Science is the largest scientific society in America, with membership of approximately ten thousand widely distributed throughout North America and the related islands. About seven hundred members live in the Pacific region. Yours faithfully[illegible] Chairman Pacific Coast Committee. Dr. John Muir, Martinez, California. PACIFIC DIVISIONOF THEAMERICAN ASSOCIATION FOR THE ADVANCEMENTOF SCIENCEPACIFIC COAST COMMITTEEWilliam Wallace Campbell, Chairman Lick Observatory PACIFIC DIVISIONOF THEAMERICAN ASSOCIATION FOR THE ADVANCEMENTOF SCIENCEPACIFIC COAST COMMITTEEWilliam Wallace Campbell, Chairman Lick Observatory, University of California, Mount HamiltonJohn Casper Branner Stanford UniversityWilliam Alanson BryanCollege of Hawaii, HonoluluHenry Smith CarhartThroop College of TechnologyPasadena Charles Lincoln EdwardsLos Angeles William Trufant FosterReed College, Portland George Ellery HaleMount Wilson Solar ObservatoryCarnegie InstitutionPasadena Mellen Woodman HaskellUniversity of California, BerkeleyEugene Woldemar HilgardUniversity of California, BerkeleyGeorge Holmes HowisonUniversity of California, BerkeleyOliver Peebles Jenkins Stanford UniversityDavid Starr JordanStanford UniversityVernon Lyman Kellogg Stanford UniversityCharles Atwood KofoidUniversity of California, BerkeleyAlfred Louis Kroeber John Casper Branner Stanford UniversityWilliam Alanson BryanCollege of Hawaii, HonoluluHenry Smith CarhartThroop College of TechnologyPasadena Charles Lincoln EdwardsLos Angeles William Trufant FosterReed College, Portland George Ellery HaleMount Wilson Solar ObservatoryCarnegie InstitutionPasadena Mellen Woodman HaskellUniversity of California, BerkeleyEugene Woldemar HilgardUniversity of California, BerkeleyGeorge Holmes HowisonUniversity of California, BerkeleyOliver Peebles Jenkins Stanford UniversityDavid Starr JordanStanford UniversityVernon Lyman Kellogg Stanford UniversityCharles Atwood KofoidUniversity of California, BerkeleyAlfred Louis KroeberUniversity of California, BerkeleyAndrew Cowper LawsonUniversity of California, BerkeleyArmin Otto LeuschnerUniversity of California, Berkeley Exum Percival LewisUniversity of California, BerkeleyJames Harvey McBridePasadena Daniel Trembly MacDougalDesert Laboratory, CarnegieInstitution, Tucson Lillien Jane MartinStanford University John Campbell MerriamUniversity of California, Berkeley Agnes Clay pole MoodyBerkeley John MuirMartinez William Emerson RitterScripps Institution for BiologicalResearch, University of CaliforniaLa JollaHarris Joseph RyanStanford University Fernando SanfordStanford University William Albert SetchellUniversity of California, Berkeley John Maxon StillmanStanford UniversityLyman Brumbaugh StookeyUniversity of Southern CaliforniaLos Angeles Benjamin Ide WheelerUniversity of California, Berkele

What Explains the Incidence of the Use of a Common Sediment Control on Lots with Houses Under Construction?

To analyze compliance with one aspect of the regulation of stormwater discharge, we estimate a random-utility model of the probability that a builder uses a silt fence to control sediments on a lot with a house under construction in an urbanizing county of South Carolina. The probability increases if the builder is responsible to the subdivision’s developer or if a homeowners association exists. The probability also increases as the cost to install a silt fence decreases or the number of houses under construction per built house in a subdivision increases. The results can help county officials target inspection to improve compliance.compliance with regulation, erosion and sediment control, filter fabric, management of stormwater runoff, random-utility model, silt fence, storm water pollution prevention plan, Agribusiness, Community/Rural/Urban Development, Demand and Price Analysis, Environmental Economics and Policy, Industrial Organization, Land Economics/Use, Q01, Q24, Q53, Q58,

Passing the buck? Responsibility attribution and cognitive bias in multilevel democracies

<p>This paper explores the effect of national partisanship and Euroscepticism on individuals’ causal responsibility attribution in European multilevel democracies. It is particularly focused on the average differences in responsibility attribution in federal and non-federal states, as well as in countries belonging to different European Union enlargement waves. Using a pooled dataset of the 2004, 2009, and 2014 European Election Studies, results show that when poor economic outcomes are at stake, partisans of the national incumbent in federal states are more likely to assign responsibility to regional governments following a blame-attribution logic, while this logic is absent in non-federal states. Likewise, Eurosceptic individuals are more likely to assign responsibility to European authorities when they hold negative views of the economy and they belong to countries that have been European Union members for a longer period.</p

Single-Cell Characterization of Pulmonary Nodules Implicates Suppression of Immunosurveillance across Early Stages of Lung Adenocarcinoma

UNLABELLED: A greater understanding of molecular, cellular, and immunological changes during the early stages of lung adenocarcinoma development could improve diagnostic and therapeutic approaches in patients with pulmonary nodules at risk for lung cancer. To elucidate the immunopathogenesis of early lung tumorigenesis, we evaluated surgically resected pulmonary nodules representing the spectrum of early lung adenocarcinoma as well as associated normal lung tissues using single-cell RNA sequencing and validated the results by flow cytometry and multiplex immunofluorescence (MIF). Single-cell transcriptomics revealed a significant decrease in gene expression associated with cytolytic activities of tumor-infiltrating natural killer and natural killer T cells. This was accompanied by a reduction in effector T cells and an increase of CD4+ regulatory T cells (Treg) in subsolid nodules. An independent set of resected pulmonary nodules consisting of both adenocarcinomas and associated premalignant lesions corroborated the early increment of Tregs in premalignant lesions compared with the associated normal lung tissues by MIF. Gene expression analysis indicated that cancer-associated alveolar type 2 cells and fibroblasts may contribute to the deregulation of the extracellular matrix, potentially affecting immune infiltration in subsolid nodules through ligand-receptor interactions. These findings suggest that there is a suppression of immune surveillance across the spectrum of early-stage lung adenocarcinoma. SIGNIFICANCE: Analysis of a spectrum of subsolid pulmonary nodules by single-cell RNA sequencing provides insights into the immune regulation and cell-cell interactions in the tumor microenvironment during early lung tumor development

Tissue-specific immunopathology in fatal COVID-19

Funding: Inflammation in COVID-19: Exploration of Critical Aspects of Pathogenesis (ICECAP) receives funding and support from the Chief Scientist Office (RapidResearch in COVID-19 programme [RARC-19] funding call, “Inflammation in Covid-19: Exploration of Critical Aspects of Pathogenesis; COV/EDI/20/10” to D.A.D., C.D.L., C.D.R., J.K.B., and D.J.H.), LifeArc (through the University of Edinburgh STOPCOVID funding award to K.D., D.A.D., and C.D.L.), UK Research and Innovation (UKRI) (Coronavirus Disease [COVID-19] Rapid Response Initiative; MR/V028790/1 to C.D.L., D.A.D., and J.A.H.), and Medical Research Scotland (CVG-1722-2020 to D.A.D., C.D.L., C.D.R., J.K.B., and D.J.H.). C.D.L. is funded by a Wellcome Trust Clinical Career Development Fellowship(206566/Z/17/Z). J.K.B. and C.D.R. are supported by the Medical Research Council (grant MC_PC_19059) as part of the International Severe AcuteRespiratory Infection Consortium Coronavirus Clinical Characterisation Consortium (ISARIC-4C). D.J.H., I.H.U., and M.E. are supported by the Industrial Centre for Artificial Intelligence Research in Digital Diagnostics. S.P. is supported by Kidney Research UK, and G.T. is supported by the Melville Trust for the Cure and Care of Cancer. Identification of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and sequencing work was supported by theU.S. Food and Drug Administration grant HHSF223201510104C (“Ebola Virus Disease: correlates of protection, determinants of outcome and clinicalmanagement”; amended to incorporate urgent COVID-19 studies) and contract 75F40120C00085 (“Characterization of severe coronavirus infection inhumans and model systems for medical countermeasure development and evaluation”; awarded to J.A.H.). J.A.H. is also funded by the Centre of Excellence in Infectious Diseases Research and the Alder Hey Charity. R.P.-R. is directly supported by the Medical Research Council Discovery Medicine North Doctoral Training Partnership. The group of J.A.H. is supported by the National Institute for Health Research Health Protection Research Unit in Emerging and Zoonotic Infections at the University of Liverpool in partnership with Public Health England and in collaboration with Liverpool School of Tropical Medicine and the University of Oxford.Rationale: In life-threatening Covid-19, corticosteroids reduce mortality, suggesting that immune responses have a causal role in death. Whether this deleterious inflammation is primarily a direct reaction to the presence of SARS-CoV-2 or an independent immunopathologic process is unknown. Objectives: To determine SARS-CoV-2 organotropism and organ-specific inflammatory responses, and the relationships between viral presence, inflammation, and organ injury. Methods: Tissue was acquired from eleven detailed post-mortem examinations. SARS-CoV-2 organotropism was mapped by multiplex PCR and sequencing, with cellular resolution achieved by in situ viral spike protein detection. Histological evidence of inflammation was quantified from 37 anatomical sites, and the pulmonary immune response characterized by multiplex immunofluorescence. Measurements and main results: Multiple aberrant immune responses in fatal Covid-19 were found, principally involving the lung and reticuloendothelial system, and these were not clearly topologically associated with the virus. Inflammation and organ dysfunction did not map to the tissue and cellular distribution of SARS-CoV-2 RNA and protein, both between and within tissues. An arteritis was identified in the lung, which was further characterised as a monocyte/myeloid-rich vasculitis, and occurred along with an influx of macrophage/monocyte-lineage cells into the pulmonary parenchyma. In addition, stereotyped abnormal reticulo-endothelial responses, including excessive reactive plasmacytosis and iron-laden macrophages, were present and dissociated from viral presence in lymphoid tissues. Conclusions: Tissue-specific immunopathology occurs in Covid-19, implicating a significant component of immune-mediated, virus-independent immunopathology as a primary mechanism in severe disease. Our data highlight novel immunopathological mechanisms, and validate ongoing and future efforts to therapeutically target aberrant macrophage and plasma cell responses as well as promoting pathogen tolerance in Covid-19.Publisher PDFPeer reviewe

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Defining failed induction of labor

BACKGROUND: While there are well-accepted standards for the diagnosis of arrested active-phase labor, the definition of a "failed" induction of labor remains less certain. One approach to diagnosing a failed induction is based on the duration of the latent phase. However, a standard for the minimum duration that the latent phase of a labor induction should continue, absent acute maternal or fetal indications for cesarean delivery, remains lacking. OBJECTIVE: The objective of this study was to determine the frequency of adverse maternal and perinatal outcomes as a function of the duration of the latent phase among nulliparous women undergoing labor induction. METHODS: This study is based on data from an obstetric cohort of women delivering at 25 U.S. hospitals from 2008-2011. Nulliparous women who had a term singleton gestation in the cephalic presentation were eligible for this analysis if they underwent a labor induction. Consistent with prior studies, the latent phase was determined to begin once cervical ripening had ended, oxytocin was initiated and rupture of membranes (ROM) had occurred, and was determined to end once 5 cm dilation was achieved. The frequencies of cesarean delivery, as well as of adverse maternal (e.g., cesarean delivery, postpartum hemorrhage, chorioamnionitis) and perinatal outcomes (e.g., a composite frequency of either seizures, sepsis, bone or nerve injury, encephalopathy, or death), were compared as a function of the duration of the latent phase (analyzed with time both as a continuous measure and categorized in 3-hour increments). RESULTS: A total of 10,677 women were available for analysis. In the vast majority (96.4%) of women, the active phase had been reached by 15 hours. The longer the duration of a woman's latent phase, the greater her chance of ultimately undergoing a cesarean delivery (P<0.001, for time both as a continuous and categorical independent variable), although more than forty percent of women whose latent phase lasted for 18 or more hours still had a vaginal delivery. Several maternal morbidities, such as postpartum hemorrhage (P < 0.001) and chorioamnionitis (P < 0.001), increased in frequency as the length of latent phase increased. Conversely, the frequencies of most adverse perinatal outcomes were statistically stable over time. CONCLUSION: The large majority of women undergoing labor induction will have entered the active phase by 15 hours after oxytocin has started and rupture of membranes has occurred. Maternal adverse outcomes become statistically more frequent with greater time in the latent phase, although the absolute increase in frequency is relatively small. These data suggest that cesarean delivery should not be undertaken during the latent phase prior to at least 15 hours after oxytocin and rupture of membranes have occurred. The decision to continue labor beyond this point should be individualized, and may take into account factors such as other evidence of labor progress

Preterm neonatal morbidity and mortality by gestational age: a contemporary cohort

Although preterm birth less than 37 weeks gestation is the leading cause of neonatal morbidity and mortality in the United States, the majority of data regarding preterm neonatal outcomes come from older studies, and many reports have been limited to only very preterm neonates. Delineation of neonatal outcomes by delivery gestational age is needed to further clarify the continuum of mortality and morbidity frequencies among preterm neonates

Molecular Poltergeists: Mitochondrial DNA Copies (numts) in Sequenced Nuclear Genomes

The natural transfer of DNA from mitochondria to the nucleus generates nuclear copies of mitochondrial DNA (numts) and is an ongoing evolutionary process, as genome sequences attest. In humans, five different numts cause genetic disease and a dozen human loci are polymorphic for the presence of numts, underscoring the rapid rate at which mitochondrial sequences reach the nucleus over evolutionary time. In the laboratory and in nature, numts enter the nuclear DNA via non-homolgous end joining (NHEJ) at double-strand breaks (DSBs). The frequency of numt insertions among 85 sequenced eukaryotic genomes reveal that numt content is strongly correlated with genome size, suggesting that the numt insertion rate might be limited by DSB frequency. Polymorphic numts in humans link maternally inherited mitochondrial genotypes to nuclear DNA haplotypes during the past, offering new opportunities to associate nuclear markers with mitochondrial markers back in time