tbuckley/cabot-search huggingface dataset:
Pizza, beer, amylase, lipase and the acute abdomen
Authors: J. A. Catton, D. N. Lobo
Journal: Gut (2010)

<h3>Abstract</h3> Wearable biosensors and smartphone applications can measure physiological variables over multiple days in free-living conditions, revealing circadian rhythms and responses to external stressors such as meals and physical activity. Here we develop a probabilistic Bayesian framework to learn interpretable, personal parameters from wearable time series data. We measure food and drink ingestion, glucose dynamics, physical activity, heart rate (HR) and heart rate variability (HRV) in 25 healthy participants over 14 days. Modelling ingestion events with glucose reveals that slow glucose decreases are associated with large postprandial glucose spikes, and we uncover a circadian baseline rhythm in glucose levels with high amplitudes in some individuals. Physical activity and circadian rhythms explain 40-65% of HR variance, whereas the variance explained for HRV is more heterogeneous across individuals (20-80%). Finally, incorporating activity, HR and HRV in the modelled glucose explains an additional 10% glucose variability in some individuals, highlighting the relevance of integrating multiple physiological signals for a complete and predictive understanding of glucose dynamics.
Preculture of PBMCs at high cell density increases sensitivity of T-cell responses, revealing cytokine release by CD28 superagonist TGN1412
Authors: Paula S. Römer, Susanne Berr, Elita Avota, Shin-Young Na, Manuela Battaglia, Ineke ten Berge, Hermann Einsele, Thomas Hünig
Journal: Blood (2011)
Stability of Body Weight in Type 2 Diabetes
Authors: Helen C. Looker, William C. Knowler, Robert L. Hanson
Journal: Diabetes Care (2006)

In a recent volume in this journal, Chaudhry et al. (1) reported their findings of weight change in 205 men with diabetes. They conclude that over the course of at least 5 years, modest weight gain is the norm in men with diabetes. In contrast, we have previously published data (2) on 816 adult Pima Indians with diabetes, which showed that the general pattern of weight change after a diagnosis of diabetes was weight loss. These apparently discrepant findings may reflect ethnic differences, but there are a number of other potential reasons for the …
Incidence of anencephaly and other major malformations when oestriol excretion is very low.
Authors: L Dean, D A Abell, N A Beischer
Journal: BMJ (1977)

A study of 533 women with very low urinary oestriol excretion during the third trimester of pregnancy showed an incidence of major fetal malformations among their infants of 7-1% and a perinatal mortality rate of 14-6%. Thirteen of the malformations were cases of anencephaly, and 26 of the 78 perinatal deaths were due to or associated with major fetal malformations. The incidence of these complications was higher when maternal oestriol excretion was lower. Routine screening by urinary oestriol assay, with fetal radiography when values below 20-8 mumol/24 hours (6 mg/24 h) are detected is the most reliable method of detecting anencephaly before birth.
Norman Leonard Paros
Authors: N. Davis
Journal: BMJ (2002)

General practitioner Colchester, Essex (b London 1923; q Queens' College, Cambridge/St Bartholomew's Hospital 1946; FRCGP, DObst RCOG, Cert AvMed, KStJ), d 16 April 2002.

Norman began his career in the Royal Army Medical Corps. He served on troopships from 1947 to 1949 and was at the withdrawal from Palestine and India. He also saw service in the Malaya emergency and was recalled to the 15th Field Ambulance for the Suez campaign of 1956. He initiated GP vocational training in Colchester. Through the St John Ambulance and the British Aeromedical Practitioners Association he combined medicine with his love of travel. He was also a cruise ship doctor, and did public duties at Wimbledon and Lords. Predeceased by his wife, Margaret, and a daughter, he leaves a daughter.
Polymorphisms in Genes Related to Oxidative Stress (<i>MPO, MnSOD, CAT</i>) and Survival After Treatment for Breast Cancer
Authors: Christine B. Ambrosone, Jiyoung Ahn, Keshav K. Singh, Hamed Rezaishiraz, Helena Furberg, Carol Sweeney, Brian Coles, Andrew Trovato
Journal: Cancer Research (2005)

The proximate cause of cancer cell death by radiation therapy and a number of therapeutic agents is through generation of reactive oxygen species, resulting in DNA damage as well as mitochondrial membrane disruption, triggering the apoptotic cascade. Because mitochondrial manganese superoxide dismutase catalyzes conversion of superoxide radicals to H(2)O(2), with catalase neutralizing H(2)O(2) and myeloperoxidase converting H(2)O(2) to highly reactive hypochlorous acid, we hypothesized that gene variants could impact the efficacy of treatment for breast cancer and improve survival. Women who were treated with radiation and/or chemotherapy for incident breast cancer at the Arkansas Cancer Research Center from 1985 to 1996 were identified. DNA was extracted from paraffin-embedded normal tissue (n = 279), and MnSOD, CAT, and MPO genotypes were determined using mass spectrometry. Cox proportional hazards models were adjusted for age, race, stage with node status, and estrogen receptor and progesterone receptor status. Women who were homozygous for MPO G alleles, associated with increased transcription, had better survival (hazard ratio, 0.60; 95% confidence interval, 0.38-0.95; P = 0.03) than those with common alleles. Both CAT TT and MnSOD CC genotypes were associated with nonsignificant reduced hazard of death. When we combined genotypes associated with higher levels of reactive oxygen species for MnSOD and MPO, women with MnSOD CC and MPO GG genotypes had a 3-fold decrease in hazard of death (hazard ratio, 0.33; 95% confidence interval, 0.13-0.80; P = 0.01). These data indicate that gene variants that impact oxidative stress modify prognosis after treatment for breast cancer.
Aberrant and Alternative Splicing in Cancer
Authors: Julian P. Venables
Journal: Cancer Research (2004)

Abstract Pre-mRNA splicing is a sophisticated and ubiquitous nuclear process, which is a natural source of cancer-causing errors in gene expression. Intronic splice site mutations of tumor suppressor genes often cause exon-skipping events that truncate proteins just like classical nonsense mutations. Also, many studies over the last 20 years have reported cancer-specific alternative splicing in the absence of genomic mutations. Affected proteins include transcription factors, cell signal transducers, and components of the extracellular matrix. Antibodies against alternatively spliced products on cancer cells are currently in clinical trials, and competitive reverse transcription-PCR across regions of alternative splicing is being used as a simple diagnostic test. As well as being associated with cancer, the nature of the alternative gene products is usually consistent with an active role in cancer; therefore, the alternative splicing process itself is a potential target for gene therapy.
Characterization and molecular analysis of Adh retrosequences in species of the Drosophila obscura group
Authors: T. Luque, G. Marfany, R. Gonzalez-Duarte
Journal: Molecular Biology and Evolution (1997)

Retrosequences, genes, and pseudogenes originated by retrotranscription are frequent components of vertebrate genomes, but they have only occasionally been described in invertebrates. In Drosophila, very few retrosequences have been reported, among them those of alcohol dehydrogenase (Adh) and phosphoglyceromutase (Pglym). Although 52 Adh gene sequences are available for comparison, Adh retrosequences have been described only in the sibling species D. teissieri and D. yakuba (melanogaster subgroup) and in D. subobscura (obscura subgroup). Here, we report the presence of Adh retrosequences in two closely related species of D. subobscura: D. madeirensis and D. guanche. Extensive sequence comparisons with their functional paralogs suggest separate retrotranscriptional events: one in the melanogaster subgroup in the ancestor of D. teissieri and D. yakuba, and the other in the obscura subgroup before the radiation of the lineages leading to D. subobscura, D. madeirensis, and D. guanche. In the former, the Adh retrotranscript originated a new expressed gene, named jingwei. However, in the obscura Adh retrosequences, retention of codon bias and higher Ks than Ka values, both distinctive evolutionary features supporting functionality, have to be considered together with a frameshift, premature stop codons, and other nucleotide substitutions, which, added to the lack of the original promoter elements, suggest that they are pseudogenes. At least two different Adh retrosequences have been characterized in each of the obscura species, and their phylogenetic analysis indicates that paralogs and their flanking genomic regions share a higher degree of similarity than orthologous sequences. Two alternative hypotheses could explain this current organization and structure: either a multiplication event occurred independently in each species, or gene conversion events should be invoked after a single duplication in the species ancestor. The significance of retrotranscriptional events in the evolution of invertebrate genomes is discussed.
The consequences of tobacco tax on household health and finances in rich and poor smokers in China: an extended cost-effectiveness analysis
Authors: Stéphane Verguet, Cindy L Gauvreau, Sujata Mishra, Mary MacLennan, Shane M Murphy, Elizabeth D Brouwer, Rachel A Nugent, Kun Zhao, Prabhat Jha, Dean T Jamison
Journal: The Lancet Global Health (2015)

BackgroundIn China, there are more than 300 million male smokers. Tobacco taxation reduces smoking-related premature deaths and increases government revenues, but has been criticised for disproportionately affecting poorer people. We assess the distributional consequences (across different wealth quintiles) of a specific excise tax on cigarettes in China in terms of both financial and health outcomes.MethodsWe use extended cost-effectiveness analysis methods to estimate, across income quintiles, the health benefits (years of life gained), the additional tax revenues raised, the net financial consequences for households, and the financial risk protection provided to households, that would be caused by a 50% increase in tobacco price through excise tax fully passed onto tobacco consumers. For our modelling analysis, we used plausible values for key parameters, including an average price elasticity of demand for tobacco of −0·38, which is assumed to vary from −0·64 in the poorest quintile to −0·12 in the richest, and we considered only the male population, which constitutes the overwhelming majority of smokers in China.FindingsOur modelling analysis showed that a 50% increase in tobacco price through excise tax would lead to 231 million years of life gained (95% uncertainty range 194–268 million) over 50 years (a third of which would be gained in the lowest income quintile), a gain of US$703 billion ($616–781 billion) of additional tax revenues from the excise tax (14% of which would come from the lowest income quintile, compared with 24% from the highest income quintile). The excise tax would increase overall household expenditures on tobacco by $376 billion ($232–505 billion), but decrease these expenditures by $21 billion (−$83 to $5 billion) in the lowest income quintile, and would reduce expenditures on tobacco-related disease by $24·0 billion ($17·3–26·3 billion, 28% of which would benefit the lowest income quintile). Finally, it would provide financial risk protection worth $1·8 billion ($1·2–2·3 billion), mainly concentrated (74%) in the lowest income quintile.InterpretationIncreased tobacco taxation can be a pro-poor policy instrument that brings substantial health and financial benefits to households in China.FundingBill & Melinda Gates Foundation and Dalla Lana School of Public Health.
Serotype-specific effectiveness and correlates of protection for the 13-valent pneumococcal conjugate vaccine: a postlicensure indirect cohort study
Authors: Nick J Andrews, Pauline A Waight, Polly Burbidge, Emma Pearce, Lucy Roalfe, Marta Zancolli, Mary Slack, Shamez N Ladhani, Elizabeth Miller, David Goldblatt
Journal: The Lancet Infectious Diseases (2014)
Measurable Urinary Albumin Predicts Cardiovascular Risk among Normoalbuminuric Patients with Type 2 Diabetes
Authors: Piero Ruggenenti, Esteban Porrini, Nicola Motterlini, Annalisa Perna, Aneliya Parvanova Ilieva, Ilian Petrov Iliev, Alessandro Roberto Dodesini, Roberto Trevisan, Antonio Bossi, Giuseppe Sampietro, Enrica Capitoni, Flavio Gaspari, Nadia Rubis, Bogdan Ene-Iordache, Giuseppe Remuzzi
Journal: Journal of the American Society of Nephrology (2012)

Micro- or macroalbuminuria is associated with increased cardiovascular risk factors among patients with type 2 diabetes, but whether albuminuria within the normal range predicts long-term cardiovascular risk is unknown. We evaluated the relationships between albuminuria and cardiovascular events in 1208 hypertensive, normoalbuminuric patients with type 2 diabetes from the BErgamo NEphrologic Diabetes Complication Trial (BENEDICT), all of whom received angiotensin-converting enzyme inhibitor (ACEI) therapy at the end of the trial and were followed for a median of 9.2 years. The main outcome was time to the first of fatal or nonfatal myocardial infarction; stroke; coronary, carotid, or peripheral artery revascularization; or hospitalization for heart failure. Overall, 189 (15.6%) of the patients experienced a main outcome event (2.14 events/100 patient-years); 24 events were fatal. Albuminuria independently predicted events (hazard ratio [HR], 1.05; 95% confidence interval [CI], 1.02-1.08). Second-degree polynomial multivariable analysis showed a continuous nonlinear relationship between albuminuria and events without thresholds. Considering the entire study population, even albuminuria at 1-2 μg/min was significantly associated with increased risk compared with albuminuria <1 μg/min (HR, 1.04; 95% CI, 1.02-1.07). This relationship was similar in the subgroup originally randomly assigned to non-ACEI therapy. Among those originally receiving ACEI therapy, however, the event rate was uniformly low and was not significantly associated with albuminuria. Taken together, among normoalbuminuric patients with type 2 diabetes, any degree of measurable albuminuria bears significant cardiovascular risk. The association with risk is continuous but is lost with early ACEI therapy.
ON BIMOLECULAR LAYERS OF LIPOIDS ON THE CHROMOCYTES OF THE BLOOD
Authors: E. Gorter, F. Grendel
Journal: The Journal of Experimental Medicine (1925)

We have examined the blood of man and of the rabbit, dog, guinea pig, sheep, and goat. There exists a great difference in the size of the red blood cells of these animals, but the total surfaces of the chromocytes See PDF for Structure from 0.1 cc. blood do not show a similarly great divergence, because animals having very small cells (goat and sheep) have much greater quantities of these cells in their blood than animals with blood cells of larger dimensions (dog and rabbit). We give all the results of our experiments, omitting only those in which we were unable to avoid losses in the procedure of evaporation of the acetone. It is clear that all our results fit in well with the supposition that the chromocytes are covered by a layer of fatty substances that is two molecules thick.
MicroRNA-26a Regulates Pathological and Physiological Angiogenesis by Targeting BMP/SMAD1 Signaling
Authors: Basak Icli, A.K.M. Wara, Javid Moslehi, Xinghui Sun, Eva Plovie, Meghan Cahill, Julio F. Marchini, Andrew Schissler, Robert F. Padera, Jianru Shi, Hui-Wen Cheng, Srilatha Raghuram, Zoltan Arany, Ronglih Liao, Kevin Croce, Calum MacRae, Mark W. Feinberg
Journal: Circulation Research (2013)

Rationale : The rapid induction and orchestration of new blood vessels are critical for tissue repair in response to injury, such as myocardial infarction, and for physiological angiogenic responses, such as embryonic development and exercise. Objective : We aimed to identify and characterize microRNAs (miR) that regulate pathological and physiological angiogenesis. Methods and Results : We show that miR-26a regulates pathological and physiological angiogenesis by targeting endothelial cell (EC) bone morphogenic protein/SMAD1 signaling in vitro and in vivo. MiR-26a expression is increased in a model of acute myocardial infarction in mice and in human subjects with acute coronary syndromes. Ectopic expression of miR-26a markedly induced EC cycle arrest and inhibited EC migration, sprouting angiogenesis, and network tube formation in matrigel, whereas blockade of miR-26a had the opposite effects. Mechanistic studies demonstrate that miR-26a inhibits the bone morphogenic protein/SMAD1 signaling pathway in ECs by binding to the SMAD1 3′-untranslated region, an effect that decreased expression of Id1 and increased p21 WAF/CIP and p27. In zebrafish, miR-26a overexpression inhibited formation of the caudal vein plexus, a bone morphogenic protein-responsive process, an effect rescued by ectopic SMAD1 expression. In mice, miR-26a overexpression inhibited EC SMAD1 expression and exercise-induced angiogenesis. Furthermore, systemic intravenous administration of an miR-26a inhibitor, locked nucleic acid-anti–miR-26a, increased SMAD1 expression and rapidly induced robust angiogenesis within 2 days, an effect associated with reduced myocardial infarct size and improved heart function. Conclusions : These findings establish miR-26a as a regulator of bone morphogenic protein/SMAD1-mediated EC angiogenic responses, and that manipulating miR-26a expression could provide a new target for rapid angiogenic therapy in ischemic disease states.
American College of Cardiology/American Heart Association Clinical Competence Statement on Echocardiography
Authors: Miguel A. Quiñones, Pamela S. Douglas, Elyse Foster, John Gorcsan, Jannet F. Lewis, Alan S. Pearlman, Jack Rychik, Ernesto E. Salcedo, James B. Seward, J. Geoffrey Stevenson, Daniel M. Thys, Howard H. Weitz, William A. Zoghbi, Mark A. Creager, William L. Winters, Michael Elnicki, John W. Hirshfeld, Beverly H. Lorell, George P. Rodgers, Cynthia M. Tracy, Howard H. Weitz
Journal: Circulation (2003)
Persistent nuclear ribosomal DNA sequence polymorphism in the Amelanchier agamic complex (Rosaceae)
Authors: C. S. Campbell, M. F. Wojciechowski, B. G. Baldwin, L. A. Alice, M. J. Donoghue
Journal: Molecular Biology and Evolution (1997)

Individual plants of several Amelanchier taxa contain many polymorphic nucleotide sites in the internal transcribed spacers (ITS) of nuclear ribosomal DNA (nrDNA). This polymorphism is unusual because it is not recent in origin and thus has resisted homogenization by concerted evolution. Amelanchier ITS sequence polymorphism is hypothesized to be the result of gene flow between two major North American clades resolved by phylogenetic analysis of ITS sequences. Western North American species plus A. humilis and A. sanguinea of eastern North America form one clade (A), and the remaining eastern North American Amelanchier make up clade B. Five eastern North American taxa are polymorphic at many of the nucleotide sites where clades A and B have diverged and are thought to be of hybrid origin, with A. humilis or A. sanguinea as one parent and various members of clade B as the other parent. Morphological evidence suggests that A. humilis is one of the parents of one of the polymorphic taxa, a microspecies that we refer to informally as A. "erecta." Sequences of 21 cloned copies of the ITS1-5.8S gene-ITS2 region from one A. "erecta" individual are identical to A. humilis sequence or to the clade B consensus sequence, or they are apparent recombinants of A. humilis and clade B ITS repeats. Amelanchier "erecta" and another polymorphic taxon are suspected to be relatively old because both grow several hundred kilometers beyond the range of one of their parents. ITS sequence polymorphisms have apparently persisted in these two taxa perhaps because of polyploidy and/or agamospermy (asexual seed production), which are prevalent in the genus.
Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities.
Authors: Philip J Landrigan, Clyde B Schechter, Jeffrey M Lipton, Marianne C Fahs, Joel Schwartz
Journal: Environmental Health Perspectives (2002)

In this study, we aimed to estimate the contribution of environmental pollutants to the incidence, prevalence, mortality, and costs of pediatric disease in American children. We examined four categories of illness: lead poisoning, asthma, cancer, and neurobehavioral disorders. To estimate the proportion of each attributable to toxins in the environment, we used an environmentally attributable fraction (EAF) model. EAFs for lead poisoning, asthma, and cancer were developed by panels of experts through a Delphi process, whereas that for neurobehavioral disorders was based on data from the National Academy of Sciences. We define environmental pollutants as toxic chemicals of human origin in air, food, water, and communities. To develop estimates of costs, we relied on data from the U.S. Environmental Protection Agency, Centers for Disease Control and Prevention, National Center for Health Statistics, the Bureau of Labor Statistics, the Health Care Financing Agency, and the Practice Management Information Corporation. EAFs were judged to be 100% for lead poisoning, 30% for asthma (range, 10-35%), 5% for cancer (range, 2-10%), and 10% for neurobehavioral disorders (range, 5-20%). Total annual costs are estimated to be $54.9 billion (range $48.8-64.8 billion): $43.4 billion for lead poisoning, $2.0 billion for asthma, $0.3 billion for childhood cancer, and $9.2 billion for neurobehavioral disorders. This sum amounts to 2.8 percent of total U.S. health care costs. This estimate is likely low because it considers only four categories of illness, incorporates conservative assumptions, ignores costs of pain and suffering, and does not include late complications for which etiologic associations are poorly quantified. The costs of pediatric environmental disease are high, in contrast with the limited resources directed to research, tracking, and prevention.
Role of cooling and drying in hyperventilation induced asthma.
Authors: R D Farley, M K Albazzaz, K R Patel
Journal: Thorax (1988)

Respiratory heat loss has been proposed as a mechanism of exercise induced asthma. Whether the predominant stimulus is airway drying or cooling remains unclear. We have measured changes in FEV1 after isocapnic cold air hyperventilation (CAH) (-23.4 degrees (SD 0.43 degrees) C) and dry ambient air hyperventilation (AAH) (18.7 degrees (0.52 degrees)C) in seven asthmatic patients (mean age 31 (SD 9) years and baseline FEV1 3.2(0.9)1) and in seven normal subjects (age 28(6) years and FEV1 3.6(0.7)1). The inspired water content in both cases was 0.3 mg/l air. The rate of respiratory heat exchange per breath was calculated in watts (W) with microcomputer based equipment. Cold air hyperventilation caused a fall in FEV1 almost twice that of ambient air hyperventilation at each level of ventilation: CAH v AAH (% fall) 8.0 (5.1) v 3.9 (4.0) at 15 l/min, 11.6 (7.8) v 7.0 (4.4) at 30 l/min, and 20.7 (10.9) v 12.4 (6.3) at 60 l/min. Identical latent heat loss (evaporative drying) was imposed on the airway during the two challenges. Sensible heat loss (convective cooling) in cold air hyperventilation was 41 W at 15 l/min, 63 W at 30 l/min, and 114 W at 60 l/min; whereas in ambient air hyperventilation the loss was 6, 13, and 23 W respectively. It is concluded that the rate of cooling of the upper airway is the predominant stimulus in hyperventilation induced asthma.