tbuckley/cabot-search huggingface dataset:
Abstract 15201: Initial HFrEF Pharmacotherapy Choice is Associated With 2-Year Mortality
Authors: Nancy M Albert, Dana A Drzayich Antol, Adrianne Waldman Casebeer, Richard W DeClue, Yong Li, Engels Obi, Stephen Stemkowski, Chun-Lan Chang
Journal: Circulation (2016)

Introduction: Risk factors associated with increased mortality for patients (pts) with HFrEF have been examined in prior studies, but the impact of real world initial pharmacotherapy (IPT) as a ris...
Regulation of metastatic ability and drug resistance in pulmonary adenocarcinoma by matrix rigidity via activating c-Met and EGFR
Authors: Chih-Cheng Chang, Ting-Lieh Hsieh, Tung-Yu Tiong, Chi-Hao Hsiao, Andrea Tung-Qian Ji, Wei-Tse Hsu, Oscar K. Lee, Jennifer H. Ho
Journal: Biomaterials (2015)
Clinical utility of basophil activation test in diagnosis of fish allergy
Authors: Ryo Imakiire, Tomoki Hattori, Keigo Kainuma, Reiko Tokuda, Keiko Kameda, Naofumi Suzuki, Yu Kuwabara, Taiga Kobori, Mizuho Nagao, Takao Fujisawa
Journal: Journal of Allergy and Clinical Immunology (2018)
Dietary linoleic acid is required for development of experimentally induced alcoholic liver injury
Authors: A A Nanji, S W French
Journal: Hepatology (1988)

We had previously hypothesized that linoleic acid (LA) was essential for development of alcoholic induced liver injury in our rat model. Male Wistar rats were fed a nutritionally adequate diet (25% calories as fat) with ethanol (8-17 g/kg/day). The source of fat was tallow (0.7% LA), lard (2.5% LA) or tallow supplemented with linoleic acid (2.5%). Liver damage was followed monthly by obtaining blood for alanine aminotransferase assay and liver biopsy for assessment of morphologic changes. Enzyme and histologic changes (fatty liver, necrosis and inflammation) in the tallow-linoleic acid-ethanol fed animals were more severe than in the lard-ethanol group. The tallow ethanol group did not show any evidence of liver injury. Our results strongly support our hypothesis that LA is essential for development of alcoholic liver disease in our rat model.
The Mutational Landscape and Immune Microenvironment of Primary Intestinal Follicular Lymphoma (PIFL)
Authors: Johannes Hellmuth, Abner Louissaint, Monika Szczepanowski, Sarah Häbe, Alessandro Pastore, Annette M. Staiger, Sylvia Hartmann, Robert Kridel, Matthew D. Ducar, Peter Koch, Martin Dreyling, Martin-Leo Hansmann, German Ott, Andreas Rosenwald, Randy D. Gascoyne, David M. Weinstock, Wolfgang Hiddemann, Wolfram Klapper, Oliver Weigert
Journal: Blood (2017)
Targeted repair of heart injury by stem cells fused with platelet nanovesicles
Authors: Junnan Tang, Teng Su, Ke Huang, Phuong-Uyen Dinh, Zegen Wang, Adam Vandergriff, Michael T. Hensley, Jhon Cores, Tyler Allen, Taosheng Li, Erin Sproul, Emily Mihalko, Leonard J. Lobo, Laura Ruterbories, Alex Lynch, Ashley Brown, Thomas G. Caranasos, Deliang Shen, George A. Stouffer, Zhen Gu, Jinying Zhang, Ke Cheng
Journal: Nature Biomedical Engineering (2018)
Pooled RCTs: In postmenopausal women, hormone therapy for 6 to 7 years did not affect mortality at 18 years
Authors: Bruce E. Johnson, Cynda Ann Johnson
Journal: Annals of Internal Medicine (2018)

Source Citation Manson JE, Aragaki AK, Rossouw JE, et al; WHI Investigators. Menopausal hormone therapy and long-term all-cause and cause-specific mortality: The Women's Health Initiative randomized trials. JAMA. 2017;318:927-38. 28898378
The Synergistic T-Cell Signal By CD79A/CD40 Costimulatory Endodomain Enhances CD19 Chimeric Antigen Receptor T-Cell Proliferation and Survival
Authors: Jakrawadee Julamanee, Seitaro Terakura, Reona Sakemura, Kotaro Miyao, Shingo Okuno, Sonoko Kamoshita, Erina Takagi, Daisuke Koyama, Tatsunori Goto, Ryo Hanajiri, Tetsuya Nishida, Makoto Murata, Hitoshi Kiyoi
Journal: Blood (2017)
Migrated endoclip removal after cholecystectomy under digital single-operator cholangioscopy guidance
Authors: Takeshi Ogura, Atsushi Okuda, Akira Miyano, Nobu Nishioka, Kazuhide Higuchi
Journal: Endoscopy (2018)

Laparoscopic cholecystectomy is now an established treatment for cholecystolithiasis or acute cholecystitis [1] [2] [3], but adverse events such as endoclip migration into the biliary tract may occur [4]. Usually, migrated endoclips can be removed by standard bile duct stone removal techniques. However, if endoclips have migrated into the intrahepatic bile duct, removal of the endoclip is sometimes challenging. In addition, bile duct injury may occur during removal [5]. Herein, we describe technical tips for the safe removal of a migrated endoclip under direct digital single-operator cholangioscopy guidance.
Positively selected enhancer elements endow osteosarcoma cells with metastatic competence
Authors: James J Morrow, Ian Bayles, Alister P W Funnell, Tyler E Miller, Alina Saiakhova, Michael M Lizardo, Cynthia F Bartels, Maaike Y Kapteijn, Stevephen Hung, Arnulfo Mendoza, Gursimran Dhillon, Daniel R Chee, Jay T Myers, Frederick Allen, Marco Gambarotti, Alberto Righi, Analisa DiFeo, Brian P Rubin, Alex Y Huang, Paul S Meltzer, Lee J Helman, Piero Picci, Henri H Versteeg, John A Stamatoyannopoulos, Chand Khanna, Peter C Scacheri
Journal: Nature Medicine (2018)
Hepatocellular carcinoma–related cyclin D1 is selectively regulated by autophagy degradation system
Authors: Shan‐Ying Wu, Sheng‐Hui Lan, Shang‐Rung Wu, Yen‐Chi Chiu, Xi‐Zhang Lin, Ih‐Jen Su, Ting‐Fen Tsai, Chia‐Jui Yen, Tsung‐Hsueh Lu, Fu‐Wen Liang, Chung‐Yi Li, Huey‐Jen Su, Chun‐Li Su, Hsiao‐Sheng Liu
Journal: Hepatology (2018)

Dysfunction of degradation machineries causes cancers, including hepatocellular carcinoma (HCC). Overexpression of cyclin D1 in HCC has been reported. We previously reported that autophagy preferentially recruits and degrades the oncogenic microRNA (miR)‐224 to prevent HCC. Therefore, in the present study, we attempted to clarify whether cyclin D1 is another oncogenic factor selectively regulated by autophagy in HCC tumorigenesis. Initially, we found an inverse correlation between low autophagic activity and high cyclin D1 expression in tumors of 147 HCC patients and three murine models, and these results taken together revealed a correlation with poor overall survival of HCC patients, indicating the importance of these two events in HCC development. We found that increased autophagic activity leads to cyclin D1 ubiquitination and selective recruitment to the autophagosome (AP) mediated by a specific receptor, sequestosome 1 (SQSTM1), followed by fusion with lysosome and degradation. Autophagy‐selective degradation of ubiquitinated cyclin D1 through SQSTM1 was confirmed using cyclin D1/ubiquitin binding site (K33‐238R) and phosphorylation site (T286A) mutants, lentivirus‐mediated silencing autophagy‐related 5 (ATG5), autophagy‐related 7 (ATG7), and Sqstm1 knockout cells. Functional studies revealed that autophagy‐selective degradation of cyclin D1 plays suppressive roles in cell proliferation, colony, and liver tumor formation. Notably, an increase of autophagic activity by pharmacological inducers (amiodarone and rapamycin) significantly suppressed tumor growth in both the orthotopic liver tumor and subcutaneous tumor xenograft models. Our findings provide evidence of the underlying mechanism involved in the regulation of cyclin D1 by selective autophagy to prevent tumor formation. Conclusion: Taken together, our data demonstrate that autophagic degradation machinery and the cell‐cycle regulator, cyclin D1, are linked to HCC tumorigenesis. We believe these findings may be of value in the development of alternative therapeutics for HCC patients. (Hepatology 2018;68:141‐154).
Overcoming Limitations Inherent in Sulfamidase to Improve Mucopolysaccharidosis IIIA Gene Therapy
Authors: Yonghong Chen, Shujuan Zheng, Luis Tecedor, Beverly L. Davidson
Journal: Molecular Therapy (2018)

Sulfamidase (SGSH) deficiency causes mucopolysaccharidosis type IIIA (MPS IIIA), a lysosomal storage disease (LSD) that affects the CNS. In earlier work in LSD mice and dog models, we exploited the utility of adeno-associated viruses (AAVs) to transduce brain ventricular lining cells (ependyma) for secretion of lysosomal hydrolases into the cerebrospinal fluid (CSF), with subsequent distribution of enzyme throughout the brain resulting in improved cognition and extending lifespan. A critical feature of this approach is efficient secretion of the expressed enzyme from transduced cells, for delivery by CSF to nontransduced cells. Surprisingly, we found that SGSH was poorly secreted from cells, resulting in retention of the expressed product. Using site-directed mutagenesis of native SGSH, we identified an improved secretion variant that also displayed enhanced uptake properties that were mannose-6-phosphate receptor independent. In studies in MPS IIIA-deficient mice, ependymal transduction with AAVs expressing variant SGSH improved spatial learning and reduced memory deficits, substrate accumulation, and astrogliosis. Secondary lysosomal enzyme elevations in the CSF and brain parenchyma were also resolved. In contrast, ependymal transduction with AAVs expressing wild-type SGSH had significantly lower CSF SGSH levels and limited impacts on behavior. These results demonstrate the utility of a previously undescribed SGSH variant for improved MPS IIIA brain gene therapy.
Potential US Population Impact of the 2017 ACC/AHA High Blood Pressure Guideline
Authors: Paul Muntner, Robert M. Carey, Samuel Gidding, Daniel W. Jones, Sandra J. Taler, Jackson T. Wright, Paul K. Whelton
Journal: Circulation (2017)

Background: The 2017 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults provides recommendations for the definition of hypertension, systolic and diastolic blood pressure (BP) thresholds for initiation of antihypertensive medication, and BP target goals. Objectives: This study sought to determine the prevalence of hypertension, implications of recommendations for antihypertensive medication, and prevalence of BP above the treatment goal among US adults using criteria from the 2017 ACC/AHA guideline and the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7). Methods: The authors analyzed data from the 2011 to 2014 National Health and Nutrition Examination Survey (N = 9 623). BP was measured 3 times following a standardized protocol and averaged. Results were weighted to produce US population estimates. Results: According to the 2017 ACC/AHA and JNC7 guidelines, the crude prevalence of hypertension among US adults was 45.6% (95% confidence interval [CI]: 43.6% to 47.6%) and 31.9% (95% CI: 30.1% to 33.7%), respectively, and antihypertensive medication was recommended for 36.2% (95% CI: 34.2% to 38.2%) and 34.3% (95% CI: 32.5% to 36.2%) of US adults, respectively. Nonpharmacological intervention is advised for the 9.4% of US adults with hypertension who are not recommended for antihypertensive medication according to the 2017 ACC/AHA guideline. Among US adults taking antihypertensive medication, 53.4% (95% CI: 49.9% to 56.8%) and 39.0% (95% CI: 36.4% to 41.6%) had BP above the treatment goal according to the 2017 ACC/AHA and JNC7 guidelines, respectively. Conclusions: Compared with the JNC7 guideline, the 2017 ACC/AHA guideline results in a substantial increase in the prevalence of hypertension, a small increase in the percentage of US adults recommended for antihypertensive medication, and more intensive BP lowering for many adults taking antihypertensive medication.
Transitory presence of myeloid-derived suppressor cells in neonates is critical for control of inflammation
Authors: Yu-Mei He, Xing Li, Michela Perego, Yulia Nefedova, Andrew V Kossenkov, Erik A Jensen, Valerian Kagan, Yu-Feng Liu, Shu-Yu Fu, Qing-Jian Ye, Yan-Hong Zhou, Lai Wei, Dmitry I Gabrilovich, Jie Zhou
Journal: Nature Medicine (2018)
Abstract MP43: Electrocardiographic and Blood Pressure Effects of Energy Drinks and Panax Ginseng in Healthy Volunteers: A Randomized Clinical Trial
Authors: Sachin A Shah, Tinh An (April) Nguyen, Andrew Occiano, Amanda Chan, Joseph C Sky, Mouchumi Bhattacharyya, Kate M O’Dell, Allen Shek, Nancy N Nguyen
Journal: Circulation (2016)

Introduction: Energy drink usage has been linked to emergency room visits and deaths. Cardiovascular and neurological adverse effects are among the most frequently reported, warranting further exploration of risk factors and cardiovascular outcomes. Hypothesis: We assessed the hypothesis that energy drinks and panax ginseng may contribute to significant electrocardiographic and blood pressure changes in healthy individuals. Methods: This was a randomized, double blinded, placebo controlled, crossover study where young healthy volunteers consumed 3 different study drinks on different days. The interventions included 32 ounces of an energy drink, control drink with 800 mg of panax ginseng or a matching placebo drink, all of which were consumed over a 45 minute period. Primary endpoints of interest were QTc interval and systolic blood pressure. Secondary endpoints included QT interval, PR interval, QRS duration, heart rate, and diastolic blood pressure. All endpoints were assessed at baseline, 1, 2, 3.5, and 5.5 hours post-study drink administration. Results: Twenty seven volunteers completed the study. A significant increase in QTc interval 2 hours post energy drink consumption was evident when compared to placebo (3.37±10.7 msec and -3.19±11.8 msec respectively; p=0.030). Similarly, systolic blood pressure 2 hours post energy drink consumption increased when compared to placebo (2.00±6.37 mmHg and -2.67±5.83 mmHg respectively; p=0.014). The PR interval significantly reduced over a 2 hour period post energy drink use in a clinically non-meaningful manner. Heart rate at 2 hours was not significantly higher in the energy drink group. The QT interval, QRS interval and diastolic blood pressure were not impacted at any time across groups. Conclusions: In conclusion, certain energy drinks consumed at a high volume can significantly increase the QTc interval and systolic blood pressure by over 6 msec and 4 mmHg respectively. Panax ginseng does not have a significant impact on ECG or blood pressure parameters. Future studies are warranted to delineate the electrophysiological and hemodynamic risks of certain energy drinks consumed at different concentrations and durations.
Chanzyme TRPM7 Mediates the Ca2+ Influx Essential for Lipopolysaccharide-Induced Toll-Like Receptor 4 Endocytosis and Macrophage Activation
Authors: Michael S. Schappe, Kalina Szteyn, Marta E. Stremska, Suresh K. Mendu, Taylor K. Downs, Philip V. Seegren, Michelle A. Mahoney, Sumeet Dixit, Julia K. Krupa, Eric J. Stipes, Jason S. Rogers, Samantha E. Adamson, Norbert Leitinger, Bimal N. Desai
Journal: Immunity (2018)
Erratum: Sorafenib priming may augment salvage chemotherapy in relapsed and refractory FLT3-ITD-positive acute myeloid leukemia
Authors: K D Cummins, S M Jane, S Ninkovic, A Bazargan, R Filshie, G Sutrave, M Hertzberg, A Scott, S Lane, C K Yannakou, D Ritchie, J D'Rozario, J Black, K Bavishi, A Wei
Journal: Blood Cancer Journal (2014)

Correction to: Blood Cancer Journal (2014) 4, e237; doi:10.1038/bcj.2014.59; published online 8 August 2014 Since the publication of this article, the authors have identified an error concerning one of the author names. S Nikovic should have been listed as S Ninkovic The corrected list is shown above.
Sexually transmitted disease surveillance in Britain: 1982.
Journal: BMJ (1984)

The two most notable events of 1982 in Britain were an increase in reports of infections due to 3 lactamase producing Neisseria gonorrhoeae to over 1000, and the detection of cases of the acquired immune deficiency syndrome (AIDS).This report describes the trends in sexually transmitted disease in Britain and then considers these two subjects in more detail.Trends in incidence The total new attendances at sexually transmitted disease clinics in Britain rose to 562 841 in 1982, a rise of 766% compared with 1981 (table I), continuing the upward trend evident since the late 1950s.Data on new attendances are available for England and Wales from 1925 to 1982.The annual numberTABLE I-Sexually transmitted disease: reported new cases 1977-82 in the United Kingdom (from clinic returns to health departments) Diagnosis
Autophagy Sustains Pancreatic Cancer Growth through Both Cell-Autonomous and Nonautonomous Mechanisms
Authors: Annan Yang, Grit Herter-Sprie, Haikuo Zhang, Elaine Y. Lin, Douglas Biancur, Xiaoxu Wang, Jiehui Deng, Josephine Hai, Shenghong Yang, Kwok-Kin Wong, Alec C. Kimmelman
Journal: Cancer Discovery (2018)

Abstract Autophagy has been shown to be elevated in pancreatic ductal adenocarcinoma (PDAC), and its role in promoting established tumor growth has made it a promising therapeutic target. However, due to limitations of prior mouse models as well as the lack of potent and selective autophagy inhibitors, the ability to fully assess the mechanistic basis of how autophagy supports pancreatic cancer has been limited. To test the feasibility of treating PDAC using autophagy inhibition and further our understanding of the mechanisms of protumor effects of autophagy, we developed a mouse model that allowed the acute and reversible inhibition of autophagy. We observed that autophagy inhibition causes significant tumor regression in an autochthonous mouse model of PDAC. A detailed analysis of these effects indicated that the tumor regression was likely multifactorial, involving both tumor cell–intrinsic and host effects. Thus, our study supports that autophagy inhibition in PDAC may have future utility in the treatment of pancreatic cancer and illustrates the importance of assessing complex biological processes in relevant autochthonous models. Significance: This work demonstrates that autophagy is critical pancreatic tumor maintenance through tumor cell–intrinsic and –extrinsic mechanisms. These results have direct clinical relevance to ongoing clinical trials as well as drug-development initiatives. Cancer Discov; 8(3); 276–87. ©2018 AACR. See related commentary by Noguera-Ortega and Amaravadi, p. 266. This article is highlighted in the In This Issue feature, p. 253
Possible Biomarkers of Deadly Ebola
Authors: M.J. Friedrich
Journal: JAMA (2018)

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Abstract 19580: Identification of a Pro-Hypertrophic Pathway With Chamber Specificity for the Right Ventricle; Implications for Right-Heart Dysfunction in Pulmonary Arterial Hypertension
Authors: Imad Al Ghouleh, Daniel Meijles, John Sembrat, Mauricio Rojas, Rebecca R Vanderpool, Jeffrey Baust, Asma Naqvi, Patrick J Pagano
Journal: Circulation (2016)

Introduction: Decompensated right ventricle (RV) hypertrophy and failure is the leading cause of death from pulmonary arterial hypertension (PAH). The mechanisms remain unclear. In this work, we id...
Immune Responses to Retroviruses
Authors: Asier Sáez-Cirión, Nicolas Manel
Journal: Annual Review of Immunology (2018)

Retroviruses are genome invaders that have shared a long history of coevolution with vertebrates and their immune system. Found endogenously in genomes as traces of past invasions, retroviruses are also considerable threats to human health when they exist as exogenous viruses such as HIV. The immune response to retroviruses is engaged by germline-encoded sensors of innate immunity that recognize viral components and damage induced by the infection. This response develops with the induction of antiviral effectors and launching of the clonal adaptive immune response, which can contribute to protective immunity. However, retroviruses efficiently evade the immune response, owing to their rapid evolution. The failure of specialized immune cells to respond, a form of neglect, may also contribute to inadequate antiretroviral immune responses. Here, we discuss the mechanisms by which immune responses to retroviruses are mounted at the molecular, cellular, and organismal levels. We also discuss how intrinsic, innate, and adaptive immunity may cooperate or conflict during the generation of immune responses.
Novel Reversible Model of Atherosclerosis and Regression Using Oligonucleotide Regulation of the LDL Receptor
Authors: Debapriya Basu, Yunying Hu, Lesley-Ann Huggins, Adam E. Mullick, Mark J. Graham, Tomasz Wietecha, Shelley Barnhart, Allison Mogul, Katharina Pfeiffer, Andreas Zirlik, Edward A. Fisher, Karin E. Bornfeldt, Florian Willecke, Ira J. Goldberg
Journal: Circulation Research (2018)

Animal models have been used to explore factors that regulate atherosclerosis. More recently, they have been used to study the factors that promote loss of macrophages and reduction in lesion size after lowering of plasma cholesterol levels. However, current animal models of atherosclerosis regression require challenging surgeries, time-consuming breeding strategies, and methods that block liver lipoprotein secretion.We sought to develop a more direct or time-effective method to create and then reverse hypercholesterolemia and atherosclerosis via transient knockdown of the hepatic LDLR (low-density lipoprotein receptor) followed by its rapid restoration.We used antisense oligonucleotides directed to LDLR mRNA to create hypercholesterolemia in wild-type C57BL/6 mice fed an atherogenic diet. This led to the development of lesions in the aortic root, aortic arch, and brachiocephalic artery. Use of a sense oligonucleotide replicating the targeted sequence region of the LDLR mRNA rapidly reduced circulating cholesterol levels because of recovery of hepatic LDLR expression. This led to a decrease in macrophages within the aortic root plaques and brachiocephalic artery, that is, regression of inflammatory cell content, after a period of 2 to 3 weeks.We have developed an inducible and reversible hepatic LDLR knockdown mouse model of atherosclerosis regression. Although cholesterol reduction decreased early en face lesions in the aortic arches, macrophage area was reduced in both early and late lesions within the aortic sinus after reversal of hypercholesterolemia. Our model circumvents many of the challenges associated with current mouse models of regression. The use of this technology will potentially expedite studies of atherosclerosis and regression without use of mice with genetic defects in lipid metabolism.
Neonatal intestinal colonization with extended-spectrum β-lactamase–producing Enterobacteriaceae—a 5-year follow-up study
Authors: V. Nordberg, K. Jonsson, C.G. Giske, A. Iversen, O. Aspevall, B. Jonsson, A. Camporeale, M. Norman, L. Navér
Journal: Clinical Microbiology and Infection (2018)
Response to ‘Serological diagnostics in the detection of IgG autoantibodies against human collagen VII in epidermolysis bullosa acquisita: a multicentre analysis': reply from authors
Authors: M. Hertl, T. Hashimoto
Journal: British Journal of Dermatology (2018)

Linked Article: Jonkman et al. Br J Dermatol 2018; 178:573.