tbuckley/cabot-search huggingface dataset:
Long-term exposure to close-proximity air pollution and asthma and allergies in urban children
Authors: C. Pénard-Morand, C. Raherison, D. Charpin, C. Kopferschmitt, F. Lavaud, D. Caillaud, I. Annesi-Maesano
Journal: European Respiratory Journal (2010)

The aim of this study was to evaluate the impact of urban air pollution, assessed through reliable indicators of exposure, on asthma and allergies in schoolchildren. A validated dispersion model combining data on traffic conditions, topography, meteorology and background pollution was used to relate 3-yrs averaged concentrations of major urban pollutants at the sites of schools to skin prick tests, exercise-induced asthma and reported asthma and allergies in 6,683 children (9–11 yrs) attending 108 schools randomly selected in six French communities. For the 4,907 children who had resided at their current address for the past 3 yrs, asthma (exercise induced, past year and lifetime) was significantly positively associated with benzene, SO 2 , particles with a 50% cut-off aerodynamic diameter of 10 μm (PM 10 ), nitrogen oxides (NO x ) and CO. In the same children, eczema (lifetime and past year) was significantly positively associated with benzene, PM 10 , NO 2 , NO x and CO, lifetime allergic rhinitis with PM 10 and sensitisation to pollens with benzene and PM 10 . Among the 2,213 children residing at their current address since birth, the associations persisted for lifetime asthma with benzene (adjusted OR per interquartile range (95% CI) 1.3 (1.0–1.9)) and PM 10 (1.4 (1.0–2.0)), and for sensitisation to pollens with volatile organic compounds (1.3 (1.0–1.9)) and PM 10 (1.2 (1.0–1.9)). Accurately modelled urban air pollution was associated with some measures of childhood asthma and allergies.
Selective Upregulation of Cardiac Endothelin System in Patients With Ischemic but Not Idiopathic Dilated Cardiomyopathy
Authors: Gian Gastone Neri Serneri, Ilaria Cecioni, Simone Vanni, Rita Paniccia, Brunella Bandinelli, Annamaria Vetere, Xiao Janming, Iacopo Bertolozzi, Maria Boddi, Gian Franco Lisi, Guido Sani, Pietro Amedeo Modesti
Journal: Circulation Research (2000)

Abstract —Only scarce information is available on the activity and modifications of the cardiac endothelin (ET)–1 system in heart failure due to ischemic (ICM) or idiopathic dilated (DCM) cardiomyopathy. The activity of the ET-1 system was investigated by measuring cardiac ET-1 and big ET-1 formation and quantifying cardiac mRNA for prepro–ET-1 (ppET-1), ET-converting enzyme-1, and ET A and ET B receptors both in myocardium and in isolated myocytes using Northern blot, reverse transcription–polymerase chain reaction, and in situ hybridization in 22 patients with DCM and 20 with ICM who underwent cardiac transplantation and in 7 potential heart transplant donors (nonfailing hearts). Notwithstanding a similar increase of plasma ET-1 in the 2 groups, cardiac ET formation, mRNA levels for ppET-1, and ET A and ET B receptors were higher on both the myocardium and isolated myocytes from ICM than on those from DCM hearts ( P &lt;0.001 for all). ppET-1 and ET-converting enzyme-1 mRNAs were expressed on myocytes and endothelial and interstitial cells in ICM, whereas in DCM and nonfailing hearts they were mainly expressed on nonmyocyte cells. In both ICM and DCM, the ET A mRNA signal was expressed on both myocytes and nonmyocyte cells, whereas ET B mRNA was almost exclusively localized on nonmyocyte cells. ET A - and ET B -specific receptor binding was increased on both myocytes and cardiac membranes, showing a positive correlation with left ventricular ejection fraction in ICM ( r =0.78 and 0.70) but not in DCM patients. The present results show that human ventricular myocytes express all of the components of the ET-1 system, which is selectively upregulated in ICM patients and appears to be functionally important in the maintenance of cardiac function.
Brain Circuits for the Internal Monitoring of Movements
Authors: Marc A. Sommer, Robert H. Wurtz
Journal: Annual Review of Neuroscience (2008)

Each movement we make activates our own sensory receptors, thus causing a problem for the brain: the spurious, movement-related sensations must be discriminated from the sensory inputs that really matter, those representing our environment. Here we consider circuits for solving this problem in the primate brain. Such circuits convey a copy of each motor command, known as a corollary discharge (CD), to brain regions that use sensory input. In the visual system, CD signals may help to produce a stable visual percept from the jumpy images resulting from our rapid eye movements. A candidate pathway for providing CD for vision ascends from the superior colliculus to the frontal cortex in the primate brain. This circuit conveys warning signals about impending eye movements that are used for planning subsequent movements and analyzing the visual world. Identifying this circuit has provided a model for studying CD in other primate sensory systems and may lead to a better understanding of motor and mental disorders.
Utilization of an alternative open reading frame of a normal gene in generating a novel human cancer antigen.
Authors: R F Wang, M R Parkhurst, Y Kawakami, P F Robbins, S A Rosenberg
Journal: The Journal of Experimental Medicine (1996)

Tumor infiltrating lymphocytes (TILs) derived from tumor-bearing patients recognize tumor-associated antigens presented by major histocompatibility complex (MHC) class I molecules. The infusion of TIL586 along with interleukin (IL) 2 into an autologous patient with metastatic melanoma resulted in the objective regression of tumor. A gene encoding a tumor antigen recognized by TIL586 was recently isolated and shown to encode gp75. Here we report that an antigenic peptide, MSLQRQFLR, recognized by TIL586 was not derived from the normal gp75 protein. Instead, this nonamer peptide resulted from translation of an alternative open reading frame of the same gene. Thus, the gp75 gene encodes two completely different polypeptides, gp75 as an antigen recognized by immunoglobulin G antibodies in sera from a patient with cancer, and a 24-amino acid product as a tumor rejection antigen recognized by T cells. This represents the first demonstration that a human tumor rejection antigen can be generated from a normal cellular gene using an open reading frame other than that used to encode the normal protein. These findings revealed a novel mechanism for generating tumor antigens, which may be useful as vaccines to induce tumor-specific cell-mediated immunity against cancer.
High Incidence of Childhood Type 1 Diabetes in Liguria, Italy, From 1989 to 1998
Authors: Mario Cotellessa, Paola Barbieri, Massimo Mazzella, Stefano Bonassi, Laura Minicucci, Renata Lorini
Journal: Diabetes Care (2003)

OBJECTIVE—Assessing updated incidence of type 1 diabetes in 0- to 14-year-old children in Liguria, a Northwest region of Italy. RESEARCH DESIGN AND METHODS—Incident cases were recorded prospectively from 1989 to 1998. Incidence rates (IRs) were standardized to the 1999 world population using the direct method. The independent effect of sex, age, residence, and calendar year was estimated with Poisson regression model. The degree of ascertainment was calculated in accordance to capture/recapture method. RESULTS—During 10 full calendar years, 219 new cases of type 1 diabetes in children were diagnosed in Liguria. The standardized IR over the 10-year period was 12.56 cases per 100,000 per year (95% CI 11.0–14.3). The sex-specific IR among men and women was 14.15 and 10.88, respectively. The age-specific IR was higher in the 10- to 14-year-old age-group (15.01/100,000) than in 0- to 4-year-old age-group (9.01/100,000) and in the 5- to 9-year-old age-group (13.03/100,000). CONCLUSIONS—The IR of type 1 diabetes in Liguria is among the highest in Southern Europe and approaches IRs of Northern European countries. In particular it is much higher than those reported in the surrounding Italian regions except for Sardinia. Therefore, the geographical distribution of type 1 diabetes does not seem to reflect the simple North-South gradient reported in several previous works.
Hsa-mir-125b-2 is highly expressed in childhood ETV6/RUNX1 (TEL/AML1) leukemias and confers survival advantage to growth inhibitory signals independent of p53
Authors: Nir Gefen, Vera Binder, Marketa Zaliova, Yvonne Linka, Michelle Morrow, Astrid Novosel, Liat Edry, Libi Hertzberg, Noam Shomron, Owen Williams, Jan Trka, Arndt Borkhardt, Shai Izraeli
Journal: Leukemia (2009)
Integrated Single-Photon Emission Computed Tomography and Computed Tomography Coronary Angiography for the Assessment of Hemodynamically Significant Coronary Artery Lesions
Authors: Shmuel Rispler, Zohar Keidar, Eduard Ghersin, Ariel Roguin, Adrian Soil, Robert Dragu, Diana Litmanovich, Alex Frenkel, Doron Aronson, Ahuva Engel, Rafael Beyar, Ora Israel
Journal: Journal of the American College of Cardiology (2007)
Macrolide effects on the prevention of COPD exacerbations
Authors: Mutsuo Yamaya, Arata Azuma, Hajime Takizawa, Jun-ichi Kadota, Jun Tamaoki, Shoji Kudoh
Journal: European Respiratory Journal (2012)

The number of senile patients with chronic obstructive pulmonary disease (COPD) has recently increased due to an increase in life expectancy, the habit of smoking and the inhalation of toxic particles. COPD exacerbations are caused by airway bacterial and viral infections, as well as the inhalation of oxidative substrates. COPD exacerbations are associated with the worsening of symptoms and quality of life, as well as an increased mortality rate. Several drugs, including long-acting anti-cholinergic agents, long-acting β 2 -agonists and inhaled corticosteroids, have been developed to improve symptoms in COPD patients and to prevent COPD exacerbations. Treatment with macrolide antibiotics has been reported to prevent COPD exacerbations and improve patient quality of life and symptoms, especially in those patients who have frequent exacerbations. In addition to their antimicrobial effects, macrolides have a variety of physiological functions, such as anti-inflammatory and anti-viral effects, reduced sputum production, the inhibition of biofilm formation and the inhibition of bacterial virulence factor production. These unique activities may relate to the prevention of exacerbations in COPD patients who receive macrolides. Herein, we review the inhibitory effects that macrolides have on COPD exacerbations and explore the possible mechanisms of these effects.
Maternal deprivation alters epithelial secretory cell lineages in rat duodenum: role of CRF-related peptides
Authors: M. Estienne, J. Claustre, G. Clain-Gardechaux, A. Paquet, Y. Tache, J. Fioramonti, P. Plaisancie
Journal: Gut (2010)

Chronic psychological stress is associated with development of intestinal barrier dysfunction and impairs host defence mechanisms. The intestinal epithelium, consisting of enterocytes, endocrine cells, goblet cells and Paneth cells, is an important component of this barrier. In the present study, the impact of maternal deprivation (MD) on secretory lineages of duodenal epithelium and the involvement of the peripheral corticotropin-releasing factor (CRF) pathway were investigated.Rat pups were deprived of their dam for 3 h/day (days 5-20). Non-deprived pups served as controls. On days 8, 13, 20, 24, 34, 44 and 84, duodenal tissues were collected for quantitative real-time PCR and immunohistochemistry studies.MD induced a sustained decrease in the number of Paneth and goblet cells but hyperplasia of endocrine cells. These alterations were associated with a duodenal increase of CRF, urocortin 2 and CRF receptor subtype 2 (CRFR(2)) mRNA, whereas CRFR(1) expression was decreased. The effects of MD on intestinal epithelium were inhibited by the CRFR(1)/R(2) antagonist astressin injected daily before MD. Studies using specific receptor antagonists in rats subjected to MD revealed that CRFR(1) was involved in the hyperplasia of endocrine cells and CRFR(2) in the depletion of Paneth cells. Conversely, daily injection of CRF and of the CRFR(2) agonist urocortin 2 in control rats resulted in changes in epithelial differentiation similar to MD.The activation of CRFR(1) and CRFR(2) induced by MD markedly altered the quantitative distribution of secretory cells of the intestinal epithelium. These alterations, in particular the depletion of Paneth and goblet cells, may create conditions leading to the development of an epithelial barrier defect.
Metabolic and Hemodynamic Changes Induced by the Prolonged Administration of Dextran
Authors: JOHN R. JAENIKE, CHRISTINE WATERHOUSE
Journal: Circulation (1955)

Large amounts of dextran were administered to human subjects under standardized metabolic conditions, with the following results: Dextran is a potent osmotic substance which produces marked salt and water retention and rapid plasma volume expansion. About 50 per cent of the amount given is excreted in the urine during the injection period. Nitrogen and phosphorus sparing and an antiketogenic effect are produced during the period of administration. A fraction of the dextran remains circulating for a prolonged period of time and is associated with a sustained depression of venous hematocrit. Metabolism of this fraction cannot be demonstrated, and its ultimate fate in the body is unknown.
NEUROMETABOLIC DEFICIENCY IN OLD AGE. (SENILE ENCEPHALOMYELOSIS.)
Authors: ERWIN WEXBERG
Journal: American Journal of Psychiatry (1941)

1. A series of observations carried out on clinical material seems to justify the delimitation of a clinical picture for which the name of senile encephalomyelosis is suggested. 2. The symptoms of senile encephalomyelosis are acute or sub- acute mental disturbances of the organic reaction type, usually associated with posterolateral sclerosis (rarely transverse myelitis or spastic spinal paralysis), sometimes associated with polyneuritis and very often associated with hypochromic or hyperchromic anemia, with or without gastric anacidity (hypoacidity). 3. Senile encephalomyelosis appears to be much more frequent in women than in men. 4. The relationship of senile encephalomyelosis to senile anorexia, primary cachexia, senile hypochromic achylic anemia and pernicious anemia can be established. 5. Hypervitaminization, particularly treatment with vitamin B1, liver extract and nicotinic acid, seems to give very good results. 6. Every case of so-called senile delirium or of the apparent confusional and hallucinatory type of senile dementia should be examined from this point of view and tentative hypervitaminization should be instituted. 7. The pathogenesis of senile encephalomyelosis is unknown. A possible hypothesis, however, is that hormonal and more especially, pituitary disturbances might be responsible.
Multifunctional Pattern-Generating Circuits
Authors: K.L. Briggman, W.B. Kristan
Journal: Annual Review of Neuroscience (2008)

The ability of distinct anatomical circuits to generate multiple behavioral patterns is widespread among vertebrate and invertebrate species. These multifunctional neuronal circuits are the result of multistable neural dynamics and modular organization. The evidence suggests multifunctional circuits can be classified by distinct architectures, yet the activity patterns of individual neurons involved in more than one behavior can vary dramatically. Several mechanisms, including sensory input, the parallel activity of projection neurons, neuromodulation, and biomechanics, are responsible for the switching between patterns. Recent advances in both analytical and experimental tools have aided the study of these complex circuits.
Leucopenia after gold and sulphasalazine treatment.
Authors: K L Schmidt
Journal: Annals of the Rheumatic Diseases (1990)

<h3>Abstract</h3> Withdrawal of the growth factor interleukin 3 from IL3-dependent myeloid cells causes them to undergo Bax/Bak1-dependent apoptosis, whereas factor-deprived <i>Bax</i><sup>-/-</sup><i>Bak1</i><sup>-/-</sup> cells remain viable, but arrest and shrink. It was reported that withdrawal of IL3 from <i>Bax</i><sup>-/-</sup><i>Bak1</i><sup>-/-</sup> cells caused decreased expression of the glucose transporter Glut1, leading to reduced glucose uptake, so that arrested cells required Atg5-dependent autophagy for long-term survival. In other cell types, a decrease in Glut1 is mediated by the thioredoxin-interacting protein Txnip, which is induced in IL3-dependent myeloid cells when growth factor is removed. We mutated <i>Atg5</i> and <i>Txnip</i> by CRISPR/Cas9 and found that Atg5-dependent autophagy was not necessary for the long-term viability of cycling or arrested <i>Bax</i><sup>-/-</sup><i>Bak1</i><sup>-/-</sup> cells, and that Txnip was not required for the decrease in Glut1 expression in response to IL3 withdrawal. Surprisingly, Atg5-deficient <i>Bax/Bak1</i> double mutant cells survived for several weeks in medium supplemented with 10% fetal bovine serum (FBS), without high concentrations of added glucose or glutamine. When serum was withdrawn, the provision of an equivalent amount of glucose present in 10% FBS (~0.5 mM) was sufficient to support cell survival for more than a week, in the presence or absence of IL3. Thus, <i>Bax</i><sup>-/-</sup><i>Bak1</i><sup>-/-</sup> myeloid cells deprived of growth factor consume extracellular glucose to maintain long-term viability, without a requirement for Atg5-dependent autophagy.
Uric Acid and Cardiovascular Events
Authors: Marcus E. Kleber, Graciela Delgado, Tanja B. Grammer, Günther Silbernagel, Jie Huang, Bernhard K. Krämer, Eberhard Ritz, Winfried März
Journal: Journal of the American Society of Nephrology (2015)

Obesity and diets rich in uric acid–raising components appear to account for the increased prevalence of hyperuricemia in Westernized populations. Prevalence rates of hypertension, diabetes mellitus, CKD, and cardiovascular disease are also increasing. We used Mendelian randomization to examine whether uric acid is an independent and causal cardiovascular risk factor. Serum uric acid was measured in 3315 patients of the Ludwigshafen Risk and Cardiovascular Health Study. We calculated a weighted genetic risk score (GRS) for uric acid concentration based on eight uric acid–regulating single nucleotide polymorphisms. Causal odds ratios and causal hazard ratios (HRs) were calculated using a two-stage regression estimate with the GRS as the instrumental variable to examine associations with cardiometabolic phenotypes (cross-sectional) and mortality (prospectively) by logistic regression and Cox regression, respectively. Our GRS was not consistently associated with any biochemical marker except for uric acid, arguing against pleiotropy. Uric acid was associated with a range of prevalent diseases, including coronary artery disease. Uric acid and the GRS were both associated with cardiovascular death and sudden cardiac death. In a multivariate model adjusted for factors including medication, causal HRs corresponding to each 1-mg/dl increase in genetically predicted uric acid concentration were significant for cardiovascular death (HR, 1.77; 95% confidence interval, 1.12 to 2.81) and sudden cardiac death (HR, 2.41; 95% confidence interval, 1.16 to 5.00). These results suggest that high uric acid is causally related to adverse cardiovascular outcomes, especially sudden cardiac death.
A Critical Appraisal of the Continuous Glucose–Error Grid Analysis
Authors: Iris M. Wentholt, Joost B. Hoekstra, J. Hans DeVries
Journal: Diabetes Care (2006)

There is no consensus on how to optimally assess the accuracy of continuous glucose sensors. We examined the continuous glucose-error grid analysis (CG-EGA) and compared it with classical accuracy assessment methods, using data from a previously reported study comparing two different continuous glucose sensors in type 1 diabetic patients.Drift, delay, mean absolute difference (MAD), sensitivity, and specificity for detecting hypo- and hyperglycemia were calculated, and a Clarke error grid and a CG-EGA were constructed for both sensors, also including an examination of the influence of choosing different time intervals for paired sensor and reference glucose values.For sensor II, there was a delay between blood glucose and sensed glucose (7.1 min, P < 0.001). Sensor II was more accurate than sensor I during hypo- and hyperglycemia (e.g., smaller MAD, P = 0.011 and P = 0.024, respectively; better sensitivity for detecting hypoglycemia, P = 0.018). Correction for the 7-min delay improved sensor II MAD with 2.2% in every range. In contrast, CG-EGA did not reveal a difference in accuracy between the sensors. Paradoxically, CG-EGA results for sensor II deteriorated when corrected for the delay. CG-EGA calculated with shorter time intervals resulted in worsening accuracy for both sensors.CG-EGA did not detect differences in accuracy whereas conventional methods did. CG-EGA is time demanding; results are hard to interpret and seem to vary with chosen time intervals. At present, CG-EGA does not contribute to a combination of various established assessment methods.
Phasic blood flow velocity pattern in epimyocardial microvessels in the beating canine left ventricle.
Authors: K Ashikawa, H Kanatsuka, T Suzuki, T Takishima
Journal: Circulation Research (1986)

We quantitated phasic epimyocardial microcirculatory coronary blood flow velocity patterns in the beating left ventricle. Using a newly developed floating objective and high-speed cinematography, red cell velocities in small arterioles, capillaries, and small venules and microvascular diameters in the superficial layer of the epimyocardium of beating left ventricle were determined throughout the entire cardiac cycle in open-chest anesthetized dogs. Heart rate was maintained at 140 beats/min by means of left atrial pacing. Peak red cell velocity was observed in midsystole in small arterioles and capillaries, and in late systole in small venules. Abrupt decline in red cell velocity and, in many cases, a momentary cessation or reverse of flow, was observed in these microvessels during the pre-ejection period. The internal diameter of small venule was increased in late systole, while that of small arteriole remained almost constant during the cardiac cycle. Furthermore, in these epimyocardial microvessels, a higher percentage of the total area under the velocity curve occurred during the ejection phase; 51% in small arterioles, 43% in capillaries, and 40% in small venules. These findings indicate that the phasic blood flow pattern is markedly different in the subepimyocardial microvessels from that in the large epicardial artery and the septal artery. During vasodilation following dilazep (50 micrograms/kg, i.v.), an adenosine potentiator, red cell velocity increased throughout the entire cardiac cycle in epimyocardial microvessels with significant increases in the total area under the velocity curves accompanied by significant dilation of the arterioles. The present data will provide information useful in predicting or simulating transmural differences in the phasic blood flow pattern.