tbuckley/cabot-search huggingface dataset:
Role of sputum differential cell count in detecting airway inflammation in patients with chronic bronchial asthma or COPD.
Authors: M. C. Ronchi, C. Piragino, E. Rosi, M. Amendola, R. Duranti, G. Scano
Journal: Thorax (1996)

Sputum may provide an alternative source of bronchial cells to investigate characteristics of airway inflammation and its functional correlates in patients with asthma or chronic obstructive pulmonary disease (COPD).Two groups of clinically stable patients were studied: a group of 43 patients with mild or moderate asthma and a group of 18 patients with COPD. Twenty normal subjects formed a control group. Sputum production was either spontaneous or induced with inhaled hypertonic saline for five minute periods for up to 20 minutes. The concentration of saline was increased at intervals of 10 minutes from 3% to 4%. Plugs from the lower respiratory tract were selected for differential counting in cytocentrifugation preparations. Bronchial provocation tests were performed by inhaling progressive concentrations of histamine from a DeVilbiss 646 nebuliser and the concentration of histamine which caused a 20% fall in the forced expiratory volume in one second (FEV1) was calculated (PC20FEV1).Neutrophils predominated in the sputum of subjects with COPD while eosinophils predominated in the sputum of those with chronic asthma. However, in 28% of asthmatic subjects an increased percentage of neutrophils was found. In asthmatic patients the differential count of eosinophils was inversely related to the FEV1, FEV1/VC, and bronchial hyperresponsiveness, and directly related to clinical scores.The cellular profile of sputum in normal subjects and in patients with asthma and COPD is different. The concentration of eosinophils in the sputum correlates with the severity of asthma.
A Case of Faecal Impaction in an Infant Five Months Old
Authors: A. M. Sheild
Journal: BMJ (1886)

THE child was first seen by me on March 15th, 1886, and this' his- tory obtained.The mother, being unable to nurse, hand-feeding was resorted to at the end. of the second month.'Cow's milk, sweetened, and diluted with water, was at first giv.en,but this was stated to have caused sickness, and was discontinued.A patent farinaceous food was next emplo.yed,slightly mixed with milk; and this, it was related:, was "kept down by the infant, 'who seemed to improve for
How the Doctor Got Gagged
Authors: William R. Archer
Journal: JAMA (1992)

<h3>To the Editor.</h3> —The article by Sugarman and Powers entitled "How the Doctor Got Gagged"<sup>1</sup>incorrectly characterizes the recent Supreme Court decision in<i>Rust v Sullivan</i><sup>2</sup>as a "significant departure from established precedent." Apparently, this "significant departure" follows from their misperception of a general recognition by the judiciary of a right to "unrestricted communication within the physician-patient relationship." In reality, there is a long history of judicial tolerance of governmental regulation of physician-patient communication. Moreover, there is nothing in the constitution that explicitly denies the right of the people to regulate the delivery of medical care. One may ask, wouldn't we be better off if there was a recognized right to privacy in physician-patient communications? Indeed, as a practicing physician, I believe there should be such a right. The recent Supreme Court decision in<i>Rust</i>does not close the door to the establishment of such a right. What
Serological evidence of<i>Legionella</i>species infection in acute exacerbation of COPD
Authors: J. Roig, X. Soler, C. Domingo, G. de Celis
Journal: European Respiratory Journal (2002)

To the Editor: 

We are concerned about the alleged aetiological role of Legionella spp. in acute exacerbations of chronic obstructive pulmonary disease (AECOPD), as has been recently suggested by both Lieberman et al. 1 in their study published in the European Respiratory Journal , and Ewig 2 in an editorial in the same issue 2. To the best of our knowledge, the distinctive results of the study by Lieberman et al. 1 have not been reported in any other aetiological survey of AECOPD. A recent, in-depth review of bacterial infection in chronic obstructive pulmonary disease, by a worldwide expert on this subject, does not even mention any role for Legionella spp. in AECOPD 3. Although attachment to bronchial cells is the first step of Legionella spp. infection, it is well known that the primary pathogenic process takes place at the macrophage cell level. There are no consistent data that might favour a theoretical isolated infectious bronchitis without any pneumonic involvement 4. In …
A TRANSMISSIBLE TUMOR-LIKE CONDITION IN RABBITS
Authors: Richard E. Shope
Journal: The Journal of Experimental Medicine (1932)

A tumor-like condition has been observed in a wild cottontail rabbit and has been found to be transmissible to both wild and domestic rabbits but not to guinea pigs, white rats, white mice, or chickens. The clinical picture of the experimentally produced condition and the pathological picture of the original and experimentally produced tumors have been described. The tumor has the general appearance of a fibroma. Methods used in transmitting the condition and satisfactory routes of inoculation have been described and discussed.
Wnt/β-Catenin Signaling Maintains the Mesenchymal Precursor Pool for Murine Sinus Horn Formation
Authors: Julia Norden, Franziska Greulich, Carsten Rudat, Makoto Mark Taketo, Andreas Kispert
Journal: Circulation Research (2011)

Canonical (β-catenin [Ctnnb1]-dependent) wingless-related MMTV integration site (Wnt) signaling plays an important role in the development of second heart field-derived structures of the heart by regulating precursor cell proliferation. The signaling pathways that regulate the most posterior elongation of the heart, that is, the addition of the systemic venous return from a Tbx18(+) precursor population, have remained elusive.To define the role of Ctnnb1-dependent Wnt signaling in the development of the cardiac venous pole.We show by in situ hybridization analysis that Wnt pathway components are expressed and canonical Wnt signaling is active in the developing sinus horns. We analyzed sinus horn (Tbx18(cre))-specific Ctnnb1 loss- and gain-of-function mutant embryos. In Ctnnb1-deficient embryos, the dorsal part of the sinus horns is not myocardialized but consists of cells with at least partial fibroblast identity; the sinoatrial node is unaffected. Stabilization of Ctnnb1 in this domain results in the formation of undifferentiated cell aggregates. Analysis of cellular changes revealed a role of canonical Wnt signaling in proliferation of the Tbx18(+) mesenchymal progenitor cell population.Wnt/β-catenin signaling maintains the Tbx18(+)Nkx2-5(-) mesenchymal precursor pool for murine sinus horn formation.
Predicting peak cycle work rate from the incremental shuttle walk test in COPD
Authors: Rahizan Zainuldin, Martin Mackey, Nia Luxton, Jennifer Alison
Journal: European Respiratory Journal (2011)

Equations predicting peak work rate (Wpeak) on an incremental cycle test (ICT) from an incremental shuttle walk test (ISWT) have been developed but often overestimate Wpeak. Since peak oxygen consumption (VO2) from the ISWT and ICT have been shown to be equivalent in moderate to severe COPD, it may be possible to use VO2 as the common measure between ISWT and ICT to improve the accuracy of the predictive equations. The study aimed to develop equations to estimate the Wpeak of an ICT from an ISWT using VO2 as the common link. In a prospective study 45 participants with COPD (mean [SD] FEV1 = 57 [18]%predicted) performed an ICT and two ISWTs. Data from the better ISWT were used for analysis. Gas exchange during exercise tests was measured by a portable gas analyser. The analyses performed were: 1) Stepwise multiple regression analysis with independent variables of gender, age, height, FEV1 and ISWwork (product of ISWdistance and weight) used to develop an equation predicting peak VO2 (VO2peak(ICT)); 2) The slopes and intercepts of the relationship between VO2(ICT) and work rate for each participant were averaged to create an equation relating VO2(ICT) and work rate. The mean peak VO2 measured in the ISWT and ICT were not significantly different. From the stepwise analysis, the regression equation was VO2peak(ICT) = 0.016$*$ISWwork + 9.28$*$Ht – 831.6 (r=0.79). A linear relationship between VO2(ICT) and work rate was found, thus an equation to predict peak work rate was developed as: Wpeak = (VO2peak(ICT) – 425)/10.3. The calculation of a Wpeak(ICT) from a clinically available ISWT via these equations may aid prescription of cycle training intensity when an ICT is unavailable.
Plasma and urine neutrophil gelatinase-associated lipocalin in septic versus non-septic acute kidney injury in critical illness
Authors: Sean M. Bagshaw, Michael Bennett, Michael Haase, Anja Haase-Fielitz, Moritoki Egi, Hiroshi Morimatsu, Giuseppe D’amico, Donna Goldsmith, Prasad Devarajan, Rinaldo Bellomo
Journal: Intensive Care Medicine (2009)
Autocrine expression of osteopontin contributes to PDGF-mediated arterial smooth muscle cell migration
Authors: S JALVY, M RENAULT, L LEEN, I BELLOC, J BONNET, A GADEAU, C DESGRANGES
Journal: Cardiovascular Research (2007)

Migration of smooth muscle cells (SMCs) from the media to the intima of arteries is involved in intimal thickening. The platelet-derived growth factor (PDGF) BB is recognized as a major migratory factor for arterial SMCs both in vitro and during neointima formation. Since PDGF acts in synergy with the matrix protein osteopontin (OPN) and also induces its expression, the present study was conceived to explore the role of the OPN produced in an autocrine fashion by PDGF-stimulated SMCs in the migration process and to define regulatory mechanisms of OPN expression.PDGF stimulation of quiescent rat aortic SMCs induced their migration (transfilter assays) and the increase of OPN expression (mRNA and protein assays). Blockade of either OPN expression by a specific short interference RNA (siRNA) or of its function by a blocking antibody decreased the PDGF-stimulated migration by about 70%, demonstrating that autocrine production and excretion of OPN are integral to the PDGF-induced SMC migration. In parallel, SMC stimulation by PDGF also activated the transcription factor CREB essentially through mitogen-activated protein kinase (MAPK) 1/2 and protein kinase A (PKA) pathways. Inhibition of either CREB expression (via siRNA) or function (via dominant-negative CREB) decreased both PDGF-induced SMC migration and OPN expression. SMC transfection with OPN promoter reporter constructs demonstrated that PDGF-induced OPN transcription is mediated by CREB binding to two functional sites of the OPN promoter: a CRE site located at -1403 and an AP-1 site located at -76.The present study demonstrates that the autocrine expression of OPN plays a major role in PDGF-induced SMC migration. It further shows that the transcription factor CREB, activated in PDGF-stimulated SMCs, plays a key role in PDGF-induced SMC migration, probably by regulating OPN expression.
Evolutionary Patterns of MHC Class II B in Owls and Their Implications for the Understanding of Avian MHC Evolution
Authors: Reto Burri, Hélène Niculita Hirzel, Nicolas Salamin, Alexandre Roulin, Luca Fumagalli
Journal: Molecular Biology and Evolution (2008)

Owing to its special mode of evolution and central role in the adaptive immune system, the major histocompatibility complex (MHC) has become the focus of diverse disciplines such as immunology, evolutionary ecology, and molecular evolution. MHC evolution has been studied extensively in diverse vertebrate lineages over the last few decades, and it has been suggested that birds differ from the established mammalian norm. Mammalian MHC genes evolve independently, and duplication history (i.e., orthology) can usually be traced back within lineages. In birds, this has been observed in only 3 pairs of closely related species. Here we report strong evidence for the persistence of orthology of MHC genes throughout an entire avian order. Phylogenetic reconstructions of MHC class II B genes in 14 species of owls trace back orthology over tens of thousands of years in exon 3. Moreover, exon 2 sequences from several species show closer relationships than sequences within species, resembling transspecies evolution typically observed in mammals. Thus, although previous studies suggested that long-term evolutionary dynamics of the avian MHC was characterized by high rates of concerted evolution, resulting in rapid masking of orthology, our results question the generality of this conclusion. The owl MHC thus opens new perspectives for a more comprehensive understanding of avian MHC evolution.
A systematic review of shockwave therapies in soft tissue conditions: focusing on the evidence
Authors: Cathy Speed
Journal: British Journal of Sports Medicine (2013)

Background ‘Shock wave’ therapies are now extensively used in the treatment of musculoskeletal injuries. This systematic review summarises the evidence base for the use of these modalities. Methods A thorough search of the literature was performed to identify studies of adequate quality to assess the evidence base for shockwave therapies on pain in specific soft tissue injuries. Both focused extracorporeal shockwave therapy (F-ESWT) and radial pulse therapy (RPT) were examined. Results 23 appropriate studies were identified. There is evidence for the benefit of F-ESWT and of RPT in a number of soft tissue musculoskeletal conditions, and evidence that both treatment modalities are safe. There is evidence that F-ESWT is effective in the treatment of plantar fasciitis, calcific tendinitis, and that RPT is effective in plantar fasciitis. Where benefit is seen in F-ESWT, it appears to be dose dependent, with greater success seen with higher dose regimes. There is low level evidence for lack of benefit of low-dose F-ESWT and RPT in non-calcific rotator cuff disease and mixed evidence in lateral epicondylitis.
Collateral effects of antibiotics on mammalian gut microbiomes
Authors: Torey Looft, Heather K. Allen
Journal: Gut Microbes (2012)

Antibiotics are an essential component of the modern lifestyle. They improve our lives by treating disease, preventing disease, and in the case of agricultural animals by improving feed efficiency. However, antibiotic usage is not without collateral effects. The development and spread of antibiotic resistance is the most notorious concern associated with antibiotic use. New technologies have enabled the study of how the microbiota responds to the antibiotic disturbance, including how the community recovers after the antibiotic is removed. One common theme in studies of antibiotic effects is a rapid increase in Escherichia coli followed by a gradual decline. Increases in E. coli are also associated with systemic host stresses, and may be an indicator of ecosystem disturbances of the intestinal microbiota. Moreover, recent studies have shown additional effects mediated by antibiotics on the gut microbiota, such as the stimulation of gene transfer among gut bacteria and the reduction of immune responses in peripheral organs. Querying the microbiota after antibiotic treatment has led to intriguing hypotheses regarding predicting or mitigating unfavorable treatment outcomes. Here we explore the varied effects of antibiotics on human and animal microbiotas.
Noradrenaline, infused locally, reduces arrhythmia severity during coronary artery occlusion in anaesthetised dogs
Authors: A Végh
Journal: Cardiovascular Research (2002)

Objective: To contribute to the debate, discussed in an earlier issue, regarding the role of adrenoceptors in the genesis of early, coronary artery occlusion-induced ventricular arrhythmias. Methods: Mongrel dogs anaesthetised with chloralose and urethane were given either noradrenaline (NA, 100 ng kg−1 min−1), phenylephrine (PHE, 200 ng kg−1 min−1) or isoprenaline (ISO 12.5 ng kg−1 min−1) by intracoronary infusion into a side branch of the left anterior descending coronary artery (LAD), commencing 10 min prior to the occlusion and then throughout the 25-min occlusion period. Control dogs were infused for the same period with saline. In another group of dogs noradrenaline was infused intravenously in a dose of 1 and then 2 μg kg−1 min−1 over a period of 60 min, 24 h prior to coronary artery occlusion. Haemodynamic and coronary blood flow changes, as well as changes in the epicardial ST-segment and in the degree of inhomogeneity were continuously recorded. Ventricular arrhythmias were evaluated as ventricular premature beats (VPBs), tachycardiac (VT) episodes and the incidences of VT and ventricular fibrillation (VF) during occlusion and following reperfusion. Results: Compared to the controls, NA markedly reduced the severity of ventricular arrhythmias resulted from coronary artery occlusion and increased survival (to 40%) following reperfusion; there were no survivors in the control group. Noradrenaline released endogenously following guanethidine administration was also protective. Protection was also seen, although to a lesser extent with intracoronary PHE (occlusion VF 20% cp 80% in controls; survival 42%). In contrast, ISO enhanced arrhythmia severity; five out of seven dogs infused with ISO fibrillated within 10 min of the commencement of occlusion and no dog survived reperfusion. Other indices of ischaemia severity (epicardial ST-segment and inhomogeneity) were also reduced by NA and by PHE. NA, infused 24 h prior to occlusion was also protective against ischaemia and reperfusion-induced arrhythmias and ischaemia-induced changes in inhomogeneity. Conclusion: We conclude that exogenously administered NA, or released endogenously by chemical means, reduces the severity of ischaemia and reperfusion-induced ventricular arrhythmias and that this is mediated by α-adrenoceptors, perhaps through presynaptic inhibition of local NA release or by a 'preconditioning' effect presumably mediated by PKC.
The Implications of Regional Variations in Medicare Spending. Part 2: Health Outcomes and Satisfaction with Care
Authors: Elliott S. Fisher, David E. Wennberg, Thrse A. Stukel, Daniel J. Gottlieb, F. L. Lucas, Étoile L. Pinder
Journal: Annals of Internal Medicine (2003)

Background: The health implications of regional differences in Medicare spending are unknown. Objective: To determine whether regions with higher Medicare spending achieve better survival, functional status, or satisfaction with care. Design: Cohort study. Setting: National study of Medicare beneficiaries. Patients: Patients hospitalized between 1993 and 1995 for hip fracture (n = 614 503), colorectal cancer (n = 195 429), or acute myocardial infarction (n = 159 393) and a representative sample (n = 18 190) drawn from the Medicare Current Beneficiary Survey (MCBS) (19921995). Exposure Measurement: End-of-life spending reflects the component of regional variation in Medicare spending that is unrelated to regional differences in illness. Each cohort member's exposure to different levels of spending was therefore defined by the level of end-of-life spending in his or her hospital referral region of residence (n = 306). Outcome Measurements: 5-year mortality rate (all four cohorts), change in functional status (MCBS cohort), and satisfaction (MCBS cohort). Results: Cohort members were similar in baseline health status, but those in regions with higher end-of-life spending received 60% more care. Each 10% increase in regional end-of-life spending was associated with the following relative risks for death: hip fracture cohort, 1.003 (95% CI, 0.999 to 1.006); colorectal cancer cohort, 1.012 (CI, 1.004 to 1.019); acute myocardial infarction cohort, 1.007 (CI, 1.001 to 1.014); and MCBS cohort, 1.01 (CI, 0.99 to 1.03). There were no differences in the rate of decline in functional status across spending levels and no consistent differences in satisfaction. Conclusions: Medicare enrollees in higher-spending regions receive more care than those in lower-spending regions but do not have better health outcomes or satisfaction with care. Efforts to reduce spending should proceed with caution, but policies to better manage further spending growth are warranted.
The Effects of Calcium and Vitamin D Supplementation on Blood Glucose and Markers of Inflammation in Nondiabetic Adults
Authors: Anastassios G. Pittas, Susan S. Harris, Paul C. Stark, Bess Dawson-Hughes
Journal: Diabetes Care (2007)

We sought to compare the effects of combined calcium and vitamin D supplementation versus placebo on blood glucose and markers of inflammation in nondiabetic adults aged > or =65 years.A total of 314 Caucasian adults without diabetes received either 500 mg calcium citrate and 700 IU vitamin D(3) or placebos daily for 3 years in a double-blind, randomized, controlled trial designed for bone-related outcomes. In a post hoc analysis, fasting plasma glucose (FPG), insulin sensitivity (estimated by homeostasis model assessment of insulin resistance [HOMA-IR]), plasma C-reactive protein, and interleukin-6, were measured at baseline and 3 years.The effects of combined calcium-vitamin D supplementation on 3-year change in FPG depended on baseline FPG (P = 0.02 for interaction). Therefore, we conducted analyses separately in participants with normal fasting glucose (NFG) (FPG <5.6 mmol/l, n = 222) and impaired fasting glucose (IFG) (FPG 5.6-6.9 mmol/l, n = 92) at baseline. Among participants with IFG at baseline, those who took combined calcium-vitamin D supplements had a lower rise in FPG at 3 years compared with those on placebo (0.02 mmol/l [0.4 mg/dl] vs. 0.34 mmol/l [6.1 mg/dl], respectively, P = 0.042) and a lower increase in HOMA-IR (0.05 vs. 0.91, P = 0.031). In the NFG subgroup, there was no difference in the change in FPG or HOMA-IR between the two treatment arms. There were no differences in C-reactive protein or interleukin-6 between the two treatment arms in either subgroup.In healthy, older adults with IFG, supplementation with calcium and vitamin D may attenuate increases in glycemia and insulin resistance that occur over time. However, our findings should be considered hypothesis generating and need to be confirmed in randomized trials specifically designed for the outcomes of interest.
New Roles Opined for OPCML
Authors: Sherry Y. Wu, Anil K. Sood
Journal: Cancer Discovery (2012)

Abstract OPCML, frequently inactivated in ovarian tumors, mediates its antitumor effect via binding to the extracellular domains of several important oncogenic receptor tyrosine kinases (RTK). This, in turn, leads to the downregulation of RTKs in tumor cells and results in significant inhibition of tumor growth. Cancer Discovery; 2(2); 115–6. ©2012 AACR. Commentary on McKie et al., p. 156.
Tetracycline-controllable Selection of CD4+ T Cells: Half-Life and Survival Signals in the Absence of Major Histocompatibility Complex Class II Molecules
Authors: Deborah Witherden, Nicolai van Oers, Caroline Waltzinger, Arthur Weiss, Christophe Benoist, Diane Mathis
Journal: The Journal of Experimental Medicine (2000)

A system that allows the study, in a gentle fashion, of the role of MHC molecules in naive T cell survival is described. Major histocompatibility complex class II–deficient mice were engineered to express Eα chains only in thymic epithelial cells in a tetracycline (tet)-controllable manner. This resulted in tet-responsive display of cell surface E complexes, positive selection of CD4+8– thymocytes, and generation of a CD4+ T cell compartment in a class II–barren periphery. Using this system, we have addressed two unresolved issues: the half-life of naive CD4+ T cells in the absence of class II molecules (3–4 wk) and the early signaling events associated with class II molecule engagement by naive CD4+ T cells (partial CD3 ζ chain phosphorylation and ZAP-70 association).
Correlation between virus genotype and chronicity rate in acute hepatitis C
Authors: Pietro Amoroso, Maria Rapicetta, Maria Elena Tosti, Alfonso Mele, Enea Spada, Salvatore Buonocore, Gennaro Lettieri, Paola Pierri, Paola Chionne, Anna Rita Ciccaglione, Luciano Sagliocca
Journal: Journal of Hepatology (1998)