tbuckley/cabot-search huggingface dataset:
Association Between State Laws Governing School Meal Nutrition Content and Student Weight Status
Authors: Daniel R. Taber, Jamie F. Chriqui, Lisa Powell, Frank J. Chaloupka
Journal: JAMA Pediatrics (2013)

<h3>Importance</h3>This study assessed whether stronger school meal nutrition standards may improve student weight status. Results have immediate implications because of the ongoing implementation of new nutrition standards for the National School Lunch Program. <h3>Objective</h3>To determine if state laws with stricter school meal nutrition standards are inversely associated with adolescent weight status, while controlling for unmeasured state-level confounders.<h3>Design</h3>Quasi-experiment.<h3>Setting</h3>Public schools.<h3>Participants</h3>Four thousand eight hundred seventy eighth-grade students in 40 states. Students were categorized by type of school lunch they usually obtained (free/reduced price, regular price, or none).<h3>Interventions</h3>State laws governing school meal nutrition standards. States with standards that exceeded US Department of Agriculture (USDA) school meal standards were compared with states that did not exceed USDA standards. The parameter of interest was the interaction between state laws and student lunch participant status, ie, whether disparities in weight status between school lunch participants and nonparticipants were smaller in states with stricter standards.<h3>Main Outcome Measures</h3>Body mass index percentile and obesity status.<h3>Results</h3>In states that exceeded USDA standards, the difference in obesity prevalence between students who obtained free/reduced-price lunches and students who did not obtain school lunches was 12.3 percentage points smaller (95% CI, −21.5 to −3.0) compared with states that did not exceed USDA standards. Likewise, differences in mean body mass index percentile between those student populations were 11 units smaller in states that exceeded USDA standards (95% CI, −17.7 to −4.3). There was little evidence that students compensated for school meal laws by purchasing more sweets, salty snacks, or sugar-sweetened beverages from other school venues (eg, vending machines) or other sources (eg, fast food).<h3>Conclusions and Relevance</h3>Stringent school meal standards that reflect the latest nutrition science may improve weight status among school lunch participants, particularly those eligible for free/reduced-price lunches.
Antisense nonmuscle myosin heavy chain and c-myb oligonucleotides suppress smooth muscle cell proliferation in vitro.
Authors: M Simons, R D Rosenberg
Journal: Circulation Research (1992)

Smooth muscle cell (SMC) proliferation is a poorly understood process that plays a critical role in several pathological states, including atherosclerosis and hypertension. Recent work suggests that the oncogene c-myb and myosin, a ubiquitous cytoskeletal protein, may be directly involved in this process. We have used antisense nonmuscle myosin heavy chain (NMMHC) or c-myb phosphorothiolate oligonucleotides to inhibit proliferation of SMCs in vitro. The suppression of growth is accompanied by reductions in the concentrations of NMMHC and c-myb mRNAs as well as decreases in the levels of the corresponding proteins. The specificity of the antiproliferative effect is underscored by the absence of any detectable growth inhibition with sense NMMHC or c-myb phosphorothiolate oligonucleotides, an antisense c-myb mismatch phosphorothiolate oligonucleotide, or an antisense thrombomodulin phosphorothiolate oligonucleotide. Furthermore, the treatment of SMCs with antisense phosphorothiolate oligonucleotides for as little as 2 hours causes maximal inhibition of cell growth over the next 72 hours. Under these conditions, SMCs attain normal rates of growth over the following 48 hours, which shows that proliferation is suppressed in a reversible fashion by antisense phosphorothiolate oligonucleotides. These experiments indicate that both c-myb and nonmuscle myosin play critical roles in SMC proliferation and that reductions of either mRNA by antisense phosphorothiolate oligonucleotides arrest the process.
Impairment of Suckling Response, Trigeminal Neuronal Pattern Formation, and Hippocampal LTD in NMDA Receptor ε2 Subunit Mutant Mice
Authors: Tatsuya Kutsuwada, Kenji Sakimura, Toshiya Manabe, Chitoshi Takayama, Nobuo Katakura, Etsuko Kushiya, Rie Natsume, Masahiko Watanabe, Yoshiro Inoue, Takeshi Yagi, Shinichi Aizawa, Masaaki Arakawa, Tomoyuki Takahashi, Yoshio Nakamura, Hisashi Mori, Masayoshi Mishina
Journal: Neuron (1996)
Comment on: Jones et al. Testosterone Replacement in Hypogonadal Men With Type 2 Diabetes and/or Metabolic Syndrome (the TIMES2 Study). Diabetes Care 2011;34:828–837
Authors: Alper Sonmez, Abdullah Taslipinar, Serkan Tapan, Muhittin A. Serdar
Journal: Diabetes Care (2011)

The results of the TIMES2 study indicate that a transdermal testosterone regiment improves glucose control, insulin resistance, lipid parameters, and sexual health in hypogonadal men with type 2 diabetes and metabolic syndrome (1). The idea of improving metabolic profile with a bonus of increased libido must be charming for all the physicians working in the field. However, after winnowing the busy data, we noticed several critical problems with the interpretation of the results.

The effects of testosterone on glycemic control and insulin sensitivity seem to be overemphasized. The abstract states a better glycemic control in the 9th month of testosterone treatment. Yet, it is evident that the HbA1c levels do …
Role of Immature Myeloid Gr-1+ Cells in the Development of Antitumor Immunity
Authors: Qingsheng Li, Ping-Ying Pan, Peidi Gu, Dongping Xu, Shu-Hsia Chen
Journal: Cancer Research (2004)

One of the mechanisms by which tumor cells evade the immune system is the lack of proper antigen-presenting cells. Improvement in host immunity against tumor cells can be achieved by promoting the differentiation of dendritic cells (DCs) from immature myeloid cells (Gr-1(+)Ly-6C(+)F4/80(+)) that accumulate in the bone marrow and lymphoid organs of mice with large tumor burdens. The enriched immature myeloid cells inhibit T-cell proliferation and tumor-specific T-cell response, which can be reversed by the differentiation of immature myeloid cells or depletion of F4/80(+) cells. Sorted Gr-1(+)/F4/80(+) immature myeloid cells differentiated into CD11c(+) cells that express CD80 and I-A/I-E (MHC class II) in the presence of recombinant murine granulocyte macrophage colony-stimulating factor (GM-CSF). Furthermore, intratumoral gene delivery of GM-CSF not only promoted the differentiation of carboxyfluoroscein succinimidyl ester-labeled immature myeloid cells into CD11c(+) cells with the characteristics of mature DCs (CD80(+), I-A/I-E(+)) but also enhanced innate natural killer and adaptive cytolytic T-cell activities in mice treated with interleukin (IL)-12 and anti-4-1BB combination therapy. More importantly, intratumoral delivery of GM-CSF and IL-12 genes in combination with 4-1BB costimulation greatly improved the long-term survival rate of mice bearing large tumors and eradicated the untreated existing hepatic tumor. The results suggest that inducing the maturation of immature myeloid cells, thus preventing their inhibitory activity and enhancing their antigen-presenting capability, by GM-CSF gene therapy is a critically important step in the development of effective antitumor responses in hosts with advanced tumors.
Single-Cell Analysis of RNA Virus Infection Identifies Multiple Genetically Diverse Viral Genomes within Single Infectious Units
Authors: Marine Combe, Raquel Garijo, Ron Geller, José M. Cuevas, Rafael Sanjuán
Journal: Cell Host & Microbe (2015)

Genetic diversity enables a virus to colonize novel hosts, evade immunity, and evolve drug resistance. However, viral diversity is typically assessed at the population level. Given the existence of cell-to-cell variation, it is critical to understand viral genetic structure at the single-cell level. By combining single-cell isolation with ultra-deep sequencing, we characterized the genetic structure and diversity of a RNA virus shortly after single-cell bottlenecks. Full-length sequences from 881 viral plaques derived from 90 individual cells reveal that sequence variants pre-existing in different viral genomes can be co-transmitted within the same infectious unit to individual cells. Further, the rate of spontaneous virus mutation varies across individual cells, and early production of diversity depends on the viral yield of the very first infected cell. These results unravel genetic and structural features of a virus at the single-cell level, with implications for viral diversity and evolution.
Davidson's Principles and Practice of Medicine.
Authors: Stanley Davidson, C Haslett
Journal: Annals of Internal Medicine (1985)

Part 1 - Principles of medicine . Good medical practice . Good prescribing . Molecular mechanisms of disease . Immunological factors in disease . Environmental and nutritional factors in disease . Principles of infectious disease . Ageing and disease Part 2 - Practice of medicine . Critical care and emergency medicine . Poisoning . Medical psychiatry . Oncology . Palliative care and pain management . Infectious diseases . Human immunodeficiency virus infection and the human acquired immunodeficiency syndrome . Sexually transmitted infections . Clinical biochemistry and metabolism . Kidney and urinary tract disease . Cardiovascular disease . Respiratory disease . Endocrine disease . Diabetes mellitus . Alimentary tract and pancreatic disease . Liver and biliary tract disease . Blood disorders . Musculoskeletal disorders . Neurological disease . Skin disease . Appendix
The addition of rituximab to CHOP therapy alters the prognostic significance of CD44 expression
Authors: Xiaolei Wei, Meng Xu, Yongqiang Wei, Fen Huang, Tong Zhao, Xiangzhao Li, Ru Feng, B Hilda Ye
Journal: Journal of Hematology & Oncology (2014)

Expression of CD44 splice isoforms has been previously reported to correlate with inferior outcomes in DLBCL patients treated with CHOP therapy. However, it is unclear whether this observation remains valid in the R-CHOP era. In this study, we correlated CD44H and CD44v6 status with survival outcomes among DLBCL patients with an emphasis on the comparison between CHOP- and R-CHOP-treated subgroups. Our results suggest that rituximab has significantly decreased the prognostic value of CD44H. We also observed that the therapeutic benefit of rituximab is largely restricted to CD44H-positive cases in this cohort.
HoxB5 induces endothelial sprouting in vitro and modifies intussusceptive angiogenesis in vivo involving angiopoietin-2
Authors: S. Winnik, M. Klinkert, H. Kurz, C. Zoeller, J. Heinke, Y. Wu, C. Bode, C. Patterson, M. Moser
Journal: Cardiovascular Research (2009)

AimsHomeobox (Hox) proteins are transcriptional regulators in embryonic patterning, cell differentiation, proliferation, and migration in vertebrates and invertebrates. A growing body of evidence suggests that Hox proteins are involved in endothelial cell regulation. We have shown earlier that HoxB5 upregulates vascular endothelial growth factor receptor-2 and thereby contributes to enhanced endothelial precursor cell differentiation. Here we aim to elucidate the role of HoxB5 in angiogenesis.
Broncho-oesophageal fistula with vascular malformation
Authors: G Verleden, J Verschakelen, G Deneffe, M Demedts
Journal: European Respiratory Journal (1988)

We present a patient with a type III congenital broncho-oesophageal fistula and a connection between the systemic and the pulmonary circulation. The congenital fistula caused chronic bronchopulmonary suppuration with bronchiectasis which in turn was the cause of a left-to-right shunt, probably through multiple precapillary or capillary anastomoses.
Six-minute walking versus shuttle walking: responsiveness to bronchodilation in chronic obstructive pulmonary disease
Authors: V. Pepin, J. Brodeur, Y. Lacasse, J. Milot, P. LeBlanc, F. Whittom, F. Maltais
Journal: Thorax (2006)

The responsiveness of the endurance shuttle walk to functional changes following bronchodilation has recently been reported. The current literature suggests that the 6 min walking test (6MWT) is less responsive to bronchodilation than the endurance shuttle walk.
Does Theophylline Potentiate Inhaled β<sub>2</sub>‐Agonists?
Authors: Karin Svedmyr, Nils Svedmyr
Journal: Allergy (1982)

The influence of pretreatment with equipotent bronchodilating doses of intravenous theophyllamine and inhaled terbutaline on the effect of five terbutaline inhalations was investigated in a cross‐over study in six adult asthmatics with stable and reproducible bronchoconstriction. Theophylline in a dose giving a maximal mean plasma concentration of 16.7 ± 1.21 μg/ml (92 μmol/l) gave far from maximal acute bronchodilation as the following five terbutalne inhalations gave the same further bronchodilation. Pretreatment with five terbutaline inhalations induced almost equal bronchodination compared with theophyllamine but the following five inhalations now gave only about one‐fourth of the effects recorded after theophyllamine pretreatment. This potentiation could, however, be due to the different routes of administration oft lie pretreatments. In a randomized, double‐blind, cross‐over study in eight asthmatics, pretreatment with equipotent oral bronchodilating doses of theophylline and terbutaline was shown to give the same potentiation of the following five terbutaline inhalations. Theoyphylline orally as such thus did not potentiate the effect of inhaled β 2 ‐stimulants. It had only the same effect as oral terbutaline, but induced less tremor. This means that the potentiation after intravenous and oral pretreatment was not due to theophylline but to the different routes of administrations. Systemic; administration probably gave a better distribution and thus better effect of the inhaled terbutaline.
THE SPECIFICATION OF DORSAL CELL FATES IN THE VERTEBRATE CENTRAL NERVOUS SYSTEM
Authors: Kevin J. Lee, Thomas M. Jessell
Journal: Annual Review of Neuroscience (1999)

▪ Abstract The generation of distinct classes of neurons at defined positions within the developing vertebrate nervous system depends on inductive signals provided by local cell groups that act as organizing centers. Genetic and embryological studies have begun to elucidate the processes that control the pattern and identity of neuronal cell types. Here we discuss the cellular interactions and molecular mechanisms that direct neuronal cell fates in the dorsal half of the vertebrate central nervous system. The specification of dorsal neuronal cell fates appears to depend on a cascade of inductive signals initiated by cells of the epidermal ectoderm that flank the neural plate and propagated by roof plate cells within the neural tube. Members of the transforming growth factor −β (TGFβ) family of secreted proteins have a prominent role in mediating these dorsalizing signals. Additional signals involving members of the Wnt and fibroblast growth factor (FGF) families may also contribute to the proliferation and differentiation of dorsal neuronal cell types.
A Phase I Pharmacokinetic and Pharmacodynamic Study of PX-12, a Novel Inhibitor of Thioredoxin-1, in Patients with Advanced Solid Tumors
Authors: Ramesh K. Ramanathan, D. Lynn Kirkpatrick, Chandra P. Belani, David Friedland, Sylvan B. Green, H-H. Sherry Chow, Catherine A. Cordova, Steven P. Stratton, Elizabeth R. Sharlow, Amanda Baker, Tomislav Dragovich
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Thioredoxin-1 (Trx-1) is a cellular redox protein that promotes tumor growth, inhibits apoptosis, and up-regulates hypoxia-inducible factor-1α and vascular endothelial growth factor. Objectives of this study were to determine safety, tolerability, pharmacodynamics, and pharmacokinetics of PX-12, a small-molecule inhibitor of Trx-1. Experimental Design: Thirty-eight patients with advanced solid tumors received PX-12 at doses of 9 to 300 mg/m2, as a 1- or 3-h i.v. infusion on days 1 to 5, repeated every 3 weeks. Results: At the 300 mg/m2 dose level, one patient experienced a reversible episode of pneumonitis during the first cycle, and a second patient developed pneumonitis after the second cycle. Doses up to 226 mg/m2 were well tolerated, and grade 3/4 events were uncommon (&amp;lt;3% of patients). The limiting factor on this dosing schedule was pungent odor caused by expired drug metabolite, 2-butanethiol. The best response was stable disease in seven patients (126-332 days). Whereas PX-12 was not detectable following the infusion, the Cmax of its inactive metabolite, 2-mercaptoimidazole, increased linearly with dose. PX-12 treatment lowered plasma Trx-1 concentrations in a dose-dependent manner. Conclusions: PX-12, the first Trx-1 inhibitor to enter clinical trials, was tolerated up to a dose of 226 mg/m2 by a 3-h infusion. Based on pharmacodynamic and pharmacokinetic data, a trial of prolonged infusion schedule of PX-12 has been initiated.
Time Course of Sympathetic Neural Hyperactivity After Uncomplicated Acute Myocardial Infarction
Authors: Lee N. Graham, Paul A. Smith, John B. Stoker, Alan F. Mackintosh, David A.S.G. Mary
Journal: Circulation (2002)

Background— Little information is available on sympathetic activity after acute myocardial infarction (AMI), despite the belief that sympathetic drive is important in relation to morbidity and mortality. Indirect indices such as plasma catecholamines are transiently elevated after uncomplicated AMI, whereas other prognostically important autonomic indices may be affected longer. We planned to quantify central sympathetic output to the periphery after uncomplicated AMI and to investigate its progress over time. Methods and Results— After uncomplicated AMI, 13 patients had muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). Measurements were obtained 2 to 4 days after AMI and were repeated after 3 and 6 months. We also examined 3 matched control groups comprising normal subjects, patients with coronary artery disease, and hospitalized patients without AMI. MSNA and s-MSNA after AMI (84±4.6 bursts/100 beats and 95±5.8 impulses/100 beats) were unchanged at 3 months but decreased ( P &lt;0.01 and P &lt;0.001) after 6 months (75±4.0 bursts/100 beats and 80±4.4 impulses/100 beats). These were still greater (at least P &lt;0.01) than values in normal subjects, patients with coronary artery disease, and hospitalized patients without AMI (51±3.9 bursts/100 beats, 58±4.7 impulses/100 beats ; 56±2.2 bursts/100 beats, 61±2.2 impulses/100 beats; and 55±3.6 bursts/100 beats, 61±3.3 impulses/100 beats, respectively). This sympathetic hyperactivity was inversely correlated to left ventricular ejection fraction but not to changes in blood pressure. Conclusions— A protracted state of sympathetic hyperactivity was shown to occur after uncomplicated AMI. It is suggested that this hyperactivity may explain delayed cardiovascular morbidity and mortality and that it arises because of an impairment of reflexes from cardiac receptors.
Electron Spin Resonance Characterization of Vascular Xanthine and NAD(P)H Oxidase Activity in Patients With Coronary Artery Disease
Authors: Stephan Spiekermann, Ulf Landmesser, Sergey Dikalov, Martin Bredt, Graciela Gamez, Helma Tatge, Nina Reepschläger, Burkhard Hornig, Helmut Drexler, David G. Harrison
Journal: Circulation (2003)

Increased inactivation of nitric oxide by superoxide (O2*-) contributes to endothelial dysfunction in patients with coronary disease (CAD). We therefore characterized the vascular activities of xanthine oxidase and NAD(P)H oxidase, 2 major O2*--producing enzyme systems, and their relationship with flow-dependent, endothelium-mediated vasodilation (FDD) in patients with CAD.Xanthine- and NAD(P)H-mediated O*.- formation was determined in coronary arteries from 10 patients with CAD and 10 controls by using electron spin resonance spectroscopy. Furthermore, activity of endothelium-bound xanthine oxidase in vivo and FDD of the radial artery were determined in 21 patients with CAD and 10 controls. FDD was measured before and after infusion of the antioxidant vitamin C (25 mg/min i.a.) to determine the portion of FDD inhibited by radicals. In coronary arteries from patients with CAD, xanthine- and NAD(P)H-mediated O2*- formation was increased compared with controls (xanthine: 12+/-2 versus 7+/-1 nmol O2*-/ microg protein; NADH: 11+/-1 versus 7+/-1 nmol O2*-/ microg protein; and NADPH: 12+/-2 versus 9+/-1 nmol O2*-/ microg protein; each P<0.05). Endothelium-bound xanthine oxidase activity was increased by >200% in patients with CAD (25+/-4 versus 9+/-1 nmol O2*-/ microL plasma per min; P<0.05) and correlated inversely with FDD (r=-0.55; P<0.05) and positively with the effect of vitamin C on FDD (r=0.54; P<0.05).The present study represents the first electron spin resonance measurements of xanthine and NAD(P)H oxidase activity in human coronary arteries and supports the concept that increased activities of both enzymes contribute to increased vascular oxidant stress in patients with CAD. Furthermore, the present study suggests that increased xanthine oxidase activity contributes to endothelial dysfunction in patients with CAD and may thereby promote the atherosclerotic process.
Targeting Kinin B <sub>1</sub> Receptor for Therapeutic Neovascularization
Authors: Costanza Emanueli, Maria Bonaria Salis, Tiziana Stacca, Gianfranco Pintus, Rudolf Kirchmair, Jeffrey M. Isner, Alessandra Pinna, Leonardo Gaspa, Domenico Regoli, Cecile Cayla, João B. Pesquero, Michael Bader, Paolo Madeddu
Journal: Circulation (2002)

Background — Kinins are modulators of cardiovascular function. After ischemic injury, enhanced kinin generation may contribute in processes responsible for tissue healing. Methods and Results — Using pharmacological and genetic approaches, we investigated the role of kinin B 1 receptor in reparative angiogenesis in a murine model of limb ischemia. The effect of B 1 pharmacological manipulation on human endothelial cell proliferation and apoptosis was also studied in vitro. Abrogation of B 1 signaling dramatically inhibited the native angiogenic response to ischemia, severely compromising blood perfusion recovery. Outcome was especially impaired in B 1 knockouts that showed a very high incidence of limb necrosis, eventually leading to spontaneous auto-amputation. Conversely, local delivery of a long-acting B 1 receptor agonist enhanced collateral vascular growth in ischemic skeletal muscle, accelerated the rate of perfusion recovery, and improved limb salvage. In vitro, B 1 activation stimulated endothelial cell proliferation and survival, whereas B 1 antagonism induced apoptosis. Conclusions — Our results indicate that the B 1 plays an essential role in the host defense response to ischemic injury. B 1 signaling potentiation might be envisaged as a utilitarian target for the treatment of ischemic vascular disease.