tbuckley/cabot-search huggingface dataset:
Phylogenetic relationships of the enigmatic hoatzin (Opisthocomus hoazin) resolved using mitochondrial and nuclear gene sequences Process Citation]
Authors: J. M. Hughes, A. J. Baker
Journal: Molecular Biology and Evolution (1999)

The hoatzin (Opisthocomus hoazin) is a bizarre, long-tailed, crested bird that inhabits the riparian lowlands of South America. Among its peculiar attributes are (1) microbial foregut fermentation to convert plant cellulose in consumed foliage into simple sugars, (2) a highly modified skeleton to accommodate its large crop, and (3) in the young of this species, wing claws at the wrist joint which are used to climb among the branches of the nest tree. Consequently, the taxonomic position of this unusual bird has perplexed systematists since its description over 200 years ago. Traditionally classified among the fowl-like birds (Galliformes), recent studies have favored its placement with the cuckoos (Cuculiformes: Cuculidae). To help resolve this systematic uncertainty, we sequenced six mitochondrial genes (cytochrome oxidase I, II, and III, ATPase 8, ATPase 6, and cytochrome b) and one nuclear gene (c-mos), totaling 5,487 base pairs. With this large data set and an appropriate range of outgroup taxa, we demonstrate that the hoatzin should not be classified among the cuckoos or Galliformes. Instead, our analyses indicate that the hoatzin is most closely related to the turacos (Musophagiformes: Musophagidae), a small family of arboreal, frugivorous birds inhabiting sub-Saharan Africa. This phylogenetic relationship is also supported by osteological behavioral, and fossil evidence.
Molecular Pathways: Targeting Diacylglycerol Kinase Alpha in Cancer
Authors: Benjamin Purow
Journal: Clinical Cancer Research (2015)

Abstract Lipid kinases have largely been neglected as targets in cancer, and an increasing number of reports suggest diacylglycerol kinase alpha (DGKα) may be one with promising therapeutic potential. DGKα is one of 10 DGK family members that convert diacylglycerol (DAG) to phosphatidic acid (PA), and both DAG and PA are critical lipid second messengers in the plasma membrane. A host of important oncogenic proteins and pathways affect cancer cells in part through DGKα, including the c-Met and VEGF receptors. Others partially mediate the effects of DGKα inhibition in cancer, such as mTOR and HIF-1α. DGKα inhibition can directly impair cancer cell viability, inhibits angiogenesis, and notably may also boost T-cell activation and enhance cancer immunotherapies. Although two structurally similar inhibitors of DGKα were established decades ago, they have seen minimal in vivo usage, and it is unlikely that either of these older DGKα inhibitors will have utility for cancer. An abandoned compound that also inhibits serotonin receptors may have more translational potential as a DGKα inhibitor, but more potent and specific DGKα inhibitors are sorely needed. Other DGK family members may also provide therapeutic targets in cancer, but require further investigation. Clin Cancer Res; 21(22); 5008–12. ©2015 AACR.
The Significance of Electrocardiographic Late Potentials: Predictors of Ventricular Tachycardia
Authors: E J Berbari, R Lazzara
Journal: Annual Review of Medicine (1992)

Advances in human genome editing, in particular the development of the clustered regularly interspaced palindromic repeats (CRISPR)/Cas9 method, have led to increasing concerns about the ethics of editing the human genome. In response, the US National ...Read More
Perspectives on Cost and Value in Cancer Care
Authors: Leonard B. Saltz
Journal: JAMA Oncology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
Response and Long-Term Outcome After Treatment With Third-Party Mesenchymal Stromal Cells - Updated Results In 58 Patients With Steroid-Refractory Acute Graft-Versus Host Disease -
Authors: Felix von Dalowski, Michael Kramer, Martin Wermke, Christoph Röllig, Nael Alakel, Friedrich Stölzel, Stefani Parmentier, Katja Sockel, Mathias Krech, Marc Schmitz, Uwe Platzbecker, Johannes Schetelig, Martin Bornhauser, Malte von Bonin
Journal: Blood (2013)
M4 Muscarinic Receptor Signaling Ameliorates Striatal Plasticity Deficits in Models of L-DOPA-Induced Dyskinesia
Authors: Weixing Shen, Joshua L. Plotkin, Veronica Francardo, Wai Kin D. Ko, Zhong Xie, Qin Li, Tim Fieblinger, Jürgen Wess, Richard R. Neubig, Craig W. Lindsley, P. Jeffrey Conn, Paul Greengard, Erwan Bezard, M. Angela Cenci, D. James Surmeier
Journal: Neuron (2015)
Epidemiological investigation and case–control study: a Legionnaires’ disease outbreak associated with cooling towers in Warstein, Germany, August–September 2013
Authors: Anna Maisa, Ansgar Brockmann, Frank Renken, Christian Lück, Stefan Pleischl, Martin Exner, Inka Daniels-Haardt, Annette Jurke
Journal: Eurosurveillance (2015)

Between 1 August and 6 September 2013, an outbreak of Legionnaires' disease (LD) with 159 suspected cases occurred in Warstein, North Rhine-Westphalia, Germany. The outbreak consisted of 78 laboratory-confirmed cases of LD, including one fatality, with a case fatality rate of 1%. Legionella pneumophila, serogroup 1, subtype Knoxville, sequence type 345, was identified as the epidemic strain. A case-control study was conducted to identify possible sources of infection. In univariable analysis, cases were almost five times more likely to smoke than controls (odds ratio (OR): 4.81; 95% confidence interval (CI): 2.33-9.93; p < 0.0001). Furthermore, cases were twice as likely to live within a 3 km distance from one identified infection source as controls (OR: 2.14; 95% CI: 1.09-4.20; p < 0.027). This is the largest outbreak of LD in Germany to date. Due to a series of uncommon events, this outbreak was most likely caused by multiple sources involving industrial cooling towers. Quick epidemiological assessment, source tracing and shutting down of potential sources as well as rapid laboratory testing and early treatment are necessary to reduce morbidity and mortality. Maintenance of cooling towers must be carried out according to specification to prevent similar LD outbreaks in the future.
Immunologic Aspects of Renal Disease
Authors: C B Carpenter
Journal: Annual Review of Medicine (1970)

Almost a century and a half ago, Richard Bright suggested that in flammation of the kidney in nephritis was a morbid action directly in­ volving the organ, or a consequence of a morbid action elsewhere, resulting in a deposit in the kidney. After a number of years of intensive investigation in experimental animals and man, we now know that the morbid action is an immunological one, and that the kidney may be damaged by the direct assault of antikidney (glomerular basement membrane) antibodies, or by passive deposition of circulating antigen-antibody complexes in the glo­ merular capillaries. Although there are a number of experimental animal models for the production of acute and chronic glomerulonephritis, the immune injury seems always to be a result of either of th ese two patho­ genetic mechanisms [reviewed in (1)]. As detailed immunopathological studies are made of human glomerulonephritis, clear-cut examples of these mechanisms are being obtained, although a number of cases do not fit a clear-cut pattern of either antikidney antibody disease or complex deposit disease. Most naturally occurring nephritis in man now appears to be of the complex type, but little is known of the qualitative and quantitative aspects of the antigens and antibodies involved in such soluble complex formation. Furthermore, in the less frequently occurring cases due to antiglomerular basement membrane antibody, there are few clues as to why such an auto­ immune process can begin. Both pathogenetic mechanisms can result in either an acute massive inflammatory reaction, or an indolent, slowly pro­ gressing one (2). Regardless of the limitations in our understanding of the unusual anti­ body responses in nephritis, considerable insight has been gained into the proximate causes of inflammation and tissue damage which occur once antibody or antigen-antibody complexes become concentrated in the wall of
Comment on Castellaneta et al. High Rate of Spontaneous Normalization of Celiac Serology in a Cohort of 446 Children With Type 1 Diabetes: A Prospective Study. Diabetes Care 2015;38:760–766
Authors: Giulio Maltoni, Silvana Salardi, Stefano Zucchini
Journal: Diabetes Care (2015)

We read with interest the data reported by Castellaneta et al. (1) about the spontaneous normalization of autoantibody markers for celiac disease (CD) in a wide population of children and adolescents with type 1 diabetes mellitus (T1DM). The authors hypothesized that this phenomenon could be related to a state of temporary positivity of celiac serology in children with T1DM. They concluded that a gluten-free diet should be delayed in the absence of clinical signs of CD and that these subjects should be carefully followed up with serological and histological tests for a confirmation of the diagnosis. …
PRMT1-mediated methylation of the EGF receptor regulates signaling and cetuximab response
Authors: Hsin-Wei Liao, Jung-Mao Hsu, Weiya Xia, Hung-Ling Wang, Ying-Nai Wang, Wei-Chao Chang, Stefan T. Arold, Chao-Kai Chou, Pei-Hsiang Tsou, Hirohito Yamaguchi, Yueh-Fu Fang, Hong-Jen Lee, Heng-Huan Lee, Shyh-Kuan Tai, Mhu-Hwa Yang, Maria P. Morelli, Malabika Sen, John E. Ladbury, Chung-Hsuan Chen, Jennifer R. Grandis, Scott Kopetz, Mien-Chie Hung
Journal: Journal of Clinical Investigation (2015)

Posttranslational modifications to the intracellular domain of the EGFR are known to regulate EGFR functions; however, modifications to the extracellular domain and their effects remain relatively unexplored. Here, we determined that methylation at R198 and R200 of the EGFR extracellular domain by protein arginine methyltransferase 1 (PRMT1) enhances binding to EGF and subsequent receptor dimerization and signaling activation. In a mouse orthotopic colorectal cancer xenograft model, expression of a methylation-defective EGFR reduced tumor growth. Moreover, increased EGFR methylation sustained signaling activation and cell proliferation in the presence of the therapeutic EGFR monoclonal antibody cetuximab. In colorectal cancer patients, EGFR methylation level also correlated with a higher recurrence rate after cetuximab treatment and reduced overall survival. Together, these data indicate that R198/R200 methylation of the EGFR plays an important role in regulating EGFR functionality and resistance to cetuximab treatment.
Construction of evidence-based perioperative safety management system in China—an interim report from a multicentre prospective study
Authors: Yuguang Huang, Jingmei Jiang, Guanghua Lei, Guichen Li, Hanzhong Li, Huijun Li, Hong Shang, Hong Sun, Shizheng Wu, Xinjuan Wu, Shijie Xin, Xiaochu Yu, Shengxiu Zhao, Zhe Zheng
Journal: The Lancet (2015)
Prognosis after Recovery from Acute Myocardial Infarction
Authors: J T Bigger, J Coromilas, F M Weld, J A Reiffel, L M Rolnitzky
Journal: Annual Review of Medicine (1984)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Photomediated Reactive Oxygen Species‐Generable Nanoparticles for Triggered Release and Endo/Lysosomal Escape of Drug upon Attenuated Single Light Irradiation
Authors: Eun Ha Seo, Chung‐Sung Lee, Kun Na
Journal: Advanced Healthcare Materials (2015)

Nanoparticles with “smart” stimuli‐responsive materials and multiple therapeutic strategies in a single delivery platform have emerged for highly efficient cancer therapy. Here, photomediated reactive oxygen species (ROS)‐generable nanoparticles are designed that can trigger drug release and endo/lysosomal escape upon attenuated single light irradiation, simultaneously, for synergistic chemo‐photodynamic ablation. In this study, the self‐ROS‐generable nanoparticles (SRNs) are prepared from the polymer based on polysaccharide, chlorin e6 as ROS generator and lipoic acid as ROS scavenger covalently conjugated pullulan with anticancer drug (doxorubicin, DOX) through self‐assembly, and can disassemble via the ROS‐mediated reduction of lipoyl group in response to low level exogenous single light switch. After cellular internalization in hepatic cancer through asialoglycoprotein receptor (ASGPR, as pullulan receptor)‐mediated endocytosis, once irradiated, SRNs are able to produce ROS that can simultaneously induce drug release triggering and endo/lysosomal escape of DOX into cytoplasm as well as directly photodynamic therapy for highly efficient chemo‐photodynamic cancer therapy. This promising delivery system, which has huge potential in biomedical applications, may be optimal for smart delivery platform.
Baseline Characteristics of Patients with Refractory Chronic Idiopathic/Spontaneous Urticaria (CIU/CSU) Enrolled in a Phase III, Randomized, Placebo-Controlled Trial of Omalizumab
Authors: Karin Rosen, Hsin-Ju Hsieh, Panayiotis Georgiou, Thomas Casale, Marcus Maurer
Journal: Journal of Allergy and Clinical Immunology (2013)
Circulatory Adaptation to High Altitude
Authors: H N Hultgren, R F Grover
Journal: Annual Review of Medicine (1968)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Lifitegrast Ophthalmic Solution 5.0% versus Placebo for Treatment of Dry Eye Disease
Authors: Joseph Tauber, Paul Karpecki, Robert Latkany, Jodi Luchs, Joseph Martel, Kenneth Sall, Aparna Raychaudhuri, Valerie Smith, Charles P. Semba
Journal: Ophthalmology (2015)

<h3>Purpose</h3> Lifitegrast is an integrin antagonist that decreases T-cell–mediated inflammation associated with dry eye disease (DED). We report the results of OPUS-2, a phase III study evaluating the efficacy and safety of lifitegrast compared with placebo for the treatment of DED. <h3>Design</h3> A 12-week, multicenter, randomized, prospective, double-masked, placebo-controlled clinical trial. <h3>Participants</h3> Adults aged ≥18 years with use of artificial tears within 30 days, inferior corneal staining score ≥0.5 (0–4 scale), Schirmer tear test (without anesthesia) ≥1 and ≤10 mm, and eye dryness score ≥40 (0–100 visual analogue scale [VAS]). <h3>Methods</h3> Subjects were randomized 1:1 after 14-day placebo run-in to lifitegrast ophthalmic solution 5.0% or placebo twice daily for 84 days. <h3>Main Outcome Measures</h3> Co-primary efficacy end points were change, from baseline to day 84, in eye dryness score (VAS, both eyes) and inferior corneal fluorescein staining score in the designated study eye. Secondary end points were change, from baseline to day 84, in ocular discomfort score (0–4 scale) in study eye, eye discomfort score (VAS), total corneal staining score in the study eye, and nasal conjunctival lissamine green staining score (0–4 scale) in the study eye. Treatment-emergent adverse events (TEAEs) were recorded. <h3>Results</h3> A total of 718 subjects were randomized: placebo, n=360; lifitegrast, n=358 (intent-to-treat population). Lifitegrast-treated subjects experienced greater improvement in eye dryness than placebo-treated subjects (treatment effect, 12.61; 95% confidence interval [CI], 8.51–16.70; <i>P</i> < 0.0001). There was no between-group difference in inferior corneal staining (treatment effect, 0.03; 95% CI, −0.10 to 0.17; <i>P</i> = 0.6186). There was nominally significant improvement of secondary symptom end points among lifitegrast-treated subjects: ocular discomfort (nominal <i>P</i> = 0.0005) and eye discomfort (nominal, <i>P</i> < 0.0001). There were no between-group differences on secondary signs: total corneal staining and nasal lissamine staining. More lifitegrast-treated subjects (33.7%) than placebo-treated subjects (16.4%) experienced ocular TEAEs; no ocular TEAEs were serious. <h3>Conclusions</h3> Lifitegrast met the co-primary symptom end point (eye dryness) but not the co-primary sign end point (inferior corneal staining). Secondary end point findings were consistent with this pattern. Most ocular TEAEs were mild to moderate; there were no unexpected TEAEs. Lifitegrast warrants further consideration as a treatment for DED.
Neonatal circumcision and penile cancer
Authors: E. J Schoen
Journal: BMJ (1996)

Seventeen were resistant to isoniazid, three to rifampicin, two to ethambutol, 19 to streptomy- cin, and six to both isoniazid and streptomycin.'Wo patients had tuberculosis that was resistant to at least three drugs, of whom one repeatedly defaulted from the clinic while the other was a Nigerian with his first presentation ofpulmonary tuberculosis.The pattern of drug resistance was similar to that in a previous study, but the incidence has more than doubled since that study.4Mycobacteria were detectable on sputum examination in 159 patients.Thus within the local urban community there is great potential for transmission of M tuberculosis that is resistant to one drug.In addition, patients may well receive what is effectively two-drug treatment on diagnosis, which will accelerate the emergence of drug resistance.Since multidrug resistance is the result of the sequential acquisition of resistance to single drugs,' treatment strategies must be altered as resistance to single drugs becomes more common and not when multidrug resistance is established.If our findings are con- firmed elsewhere, British policies for treating tuberculosis will need to be revised soon.Four- drug empirical treatment of tuberculosis should then become normal practice, pending definitive results from drug sensitivity tests of the organism being treated.
A Review of: “David H. Smith and Cynthia B. Cohen (eds.), A Christian Response to the New Genetics: Religious, Ethical and Social Issues.”
Authors: Lisa Sowle Cahill
Journal: The American Journal of Bioethics (2006)

"A Review of: “David H. Smith and Cynthia B. Cohen (eds.), A Christian Response to the New Genetics: Religious, Ethical and Social Issues.”." , 6(4), pp. 78–79
TWEAK/Fn14 interaction promotes oxidative stress through NADPH oxidase activation in macrophages
Authors: Julio Madrigal-Matute, Valvanera Fernandez-Laso, Cristina Sastre, Patricia Llamas-Granda, Jesús Egido, José Luis Martin-Ventura, Guillermo Zalba, Luis Miguel Blanco-Colio
Journal: Cardiovascular Research (2015)

The interaction between TNF-like weak inducer of apoptosis (TWEAK, Tnfsf12) and the receptor, fibroblast growth factor-inducible 14 (Fn14), regulates vascular damage through different mechanisms, including inflammation. Oxidative stress plays a major role in inflammation and the development of atherosclerosis, but the relationship between TWEAK and oxidative stress is, however, poorly understood.In this study, we found that TWEAK and Fn14 are co-localized with the NADPH subunits, p22phox and Nox2, in human advanced atherosclerotic plaques. Using primary human macrophages and a murine macrophage cell line, we demonstrate that TWEAK promotes ROS production and enhances NADPH oxidase activity. Hence, we show a direct involvement of the TWEAK-Fn14 axis in oxidative stress, as genetic silencing of Fn14 or Nox2 abrogates the TWEAK-induced ROS production. Furthermore, our results point at Rac1 as an upstream mediator of TWEAK during oxidative stress. Finally, using an in vivo murine model we confirmed the major role of TWEAK in oxidative stress, as genetic silencing of Tnfsf12 in an ApoE(-/-) background reduces the number of DHE and 8-hydroxydeoxyguanosine-positive macrophages by 50%.Our results suggest that TWEAK regulates vascular damage by stimulating ROS production in an Nox2-dependent manner. These new insights into the TWEAK/Fn14 axis underline their potential use as therapeutic targets in atherosclerosis.
Pretreatment with Antioxidants Augments the Acute Arterial Vasoconstriction Caused by Diesel Exhaust Inhalation
Authors: Cora S. Sack, Karen L. Jansen, Kristen E. Cosselman, Carol A. Trenga, Pat L. Stapleton, Jason Allen, Alon Peretz, Casey Olives, Joel D. Kaufman
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Diesel exhaust inhalation, which is the model traffic-related air pollutant exposure, is associated with vascular dysfunction.
Global Transcriptional Profiling of Diapause and Climatic Adaptation in<i>Drosophila melanogaster</i>
Authors: Xiaqing Zhao, Alan O. Bergland, Emily L. Behrman, Brian D. Gregory, Dmitri A. Petrov, Paul S. Schmidt
Journal: Molecular Biology and Evolution (2015)

Wild populations of the model organism Drosophila melanogaster experience highly heterogeneous environments over broad geographical ranges as well as over seasonal and annual timescales. Diapause is a primary adaptation to environmental heterogeneity, and in D. melanogaster the propensity to enter diapause varies predictably with latitude and season. Here we performed global transcriptomic profiling of naturally occurring variation in diapause expression elicited by short day photoperiod and moderately low temperature in two tissue types associated with neuroendocrine and endocrine signaling, heads, and ovaries. We show that diapause in D. melanogaster is an actively regulated phenotype at the transcriptional level, suggesting that diapause is not a simple physiological or reproductive quiescence. Differentially expressed genes and pathways are highly distinct in heads and ovaries, demonstrating that the diapause response is not uniform throughout the soma and suggesting that it may be comprised of functional modules associated with specific tissues. Genes downregulated in heads of diapausing flies are significantly enriched for clinally varying single nucleotide polymorphism (SNPs) and seasonally oscillating SNPs, consistent with the hypothesis that diapause is a driving phenotype of climatic adaptation. We also show that chromosome location-based coregulation of gene expression is present in the transcriptional regulation of diapause. Taken together, these results demonstrate that diapause is a complex phenotype actively regulated in multiple tissues, and support the hypothesis that natural variation in diapause propensity underlies adaptation to spatially and temporally varying selective pressures.