tbuckley/cabot-search huggingface dataset:
Detection and quantitation of myocardial infarction in vivo using transmission computed tomography.
Authors: P W Doherty, M J Lipton, W H Berninger, C G Skioldebrand, E Carlsson, R W Redington
Journal: Circulation (1981)

In vivo studies were performed on 28 dogs to evaluate the usefulness of transmission computed tomography (CT) in the detection and quantitation of experimentally induced myocardial infarction. Intravenously administered contrast material was required to define the internal structure of the heart and to differentiate normal from infarcted tissue. Transmural infarcts with homogeneous central regions were visualized as areas of diminished contrast enhancement compared with the normal myocardium. All transmural infarcts of at least 24 hours' duration showed a surrounding border zone of patchy necrosis that was variable in size and had high CT numbers due to slow washout of the contrast material from this region. Infarct area determined from the images for individual slices correlated well (r = 0.976) with that calculated using pathology. The technique is very sensitive and can detect infarction within a papillary muscle. Nontransmural or patchy infarcts show up as areas of diffuse contrast enhancement without a central core of diminished enhancement. The distribution of the contrast material is similar to that of technetium-99m pyrophosphate in the border zone of the infarct in infusion studies, but in bolus studies it behaves more like thallium-201.
AN EARLY RENAL LESION IN SYSTEMIC LUPUS ERYTHEMATOSUS.
Authors: J. D. EVERALL, R. H. HEPTINSTALL, A. M. JOEKES
Journal: British Journal of Dermatology (1958)

Journal Article AN EARLY RENAL LESION IN SYSTEMIC LUPUS ERYTHEMATOSUS. Get access J. D. EVERALL, M.R.C.P., J. D. EVERALL, M.R.C.P. St. Mary's Hospital, Landon Search for other works by this author on: Oxford Academic Google Scholar R. H. HEPTINSTALL, M.D., and, R. H. HEPTINSTALL, M.D., and St. Mary's Hospital, Landon Search for other works by this author on: Oxford Academic Google Scholar A. M. JOEKES, M.A., B.M., M.R.C.P. A. M. JOEKES, M.A., B.M., M.R.C.P. St. Mary's Hospital, Landon Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 70, Issue 2, 1 February 1958, Pages 44–47, https://doi.org/10.1111/j.1365-2133.1958.tb13290.x Published: 01 February 1958
Accelerated ageing of the lung in COPD: new concepts
Authors: Nicolas Mercado, Kazuhiro Ito, Peter J Barnes
Journal: Thorax (2015)

The rise in life expectancy worldwide has been accompanied by an increased incidence of age-related diseases, representing an enormous burden on healthcare services and society. All vital organs lose function with age, and this is well described in the lung, with a progressive decline in pulmonary function after the age of about 25 years. The lung ages, like any other organ, with progressive functional impairment and reduced capacity to respond to environmental stresses and injury. Normal physiological ageing results in enlarged alveolar spaces and loss of lung elasticity in the elderly known as 'senile emphysema', whereas in COPD there is destruction of the alveolar walls and fibrosis of peripheral airways. However, COPD shows striking age-associated features, such as an increase in cellular senescence, stem cell exhaustion, increased oxidative stress, alteration in the extracellular matrix and a reduction in endogenous antiageing molecules and protective pathways such as autophagy. In this review we discuss the evidence showing how oxidative stress induces accelerated ageing by upregulating the phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mechanistic target of rapamycin signalling pathway resulting in depletion of stem cells, defective autophagy, reduced antioxidant responses and defective mitochondrial function thus generating further oxidative stress. Understanding the mechanisms of accelerated ageing in COPD may identify novel therapeutic approaches.
Crossing the Species Barrier: Genomic Hotspots of Introgression between Two Highly Divergent Ciona intestinalis Species
Authors: Camille Roux, Georgia Tsagkogeorga, Nicolas Bierne, Nicolas Galtier
Journal: Molecular Biology and Evolution (2013)

Inferring a realistic demographic model from genetic data is an important challenge to gain insights into the historical events during the speciation process and to detect molecular signatures of selection along genomes. Recent advances in divergence population genetics have reported that speciation in face of gene flow occurred more frequently than theoretically expected, but the approaches used did not account for genome-wide heterogeneity (GWH) in introgression rates. Here, we investigate the impact of GWH on the inference of divergence with gene flow between two cryptic species of the marine model Ciona intestinalis by analyzing polymorphism and divergence patterns in 852 protein-coding sequence loci. These morphologically similar entities are highly diverged molecular-wise, but evidence of hybridization has been reported in both laboratory and field studies. We compare various speciation models and test for GWH under the approximate Bayesian computation framework. Our results demonstrate the presence of significant extents of gene flow resulting from a recent secondary contact after >3 My of divergence in isolation. The inferred rates of introgression are relatively low, highly variable across loci and mostly unidirectional, which is consistent with the idea that numerous genetic incompatibilities have accumulated over time throughout the genomes of these highly diverged species. A genomic map of the level of gene flow identified two hotspots of introgression, that is, large genome regions of unidirectional introgression. This study clarifies the history and degree of isolation of two cryptic and partially sympatric model species and provides a methodological framework to investigate GWH at various stages of speciation process.
The effect of hydrolyzed cow's milk formula for allergy prevention in the first year of life: The German Infant Nutritional Intervention Study, a randomized double-blind trial
Authors: Andrea von Berg, Sibylle Koletzko, Armin Grübl, Birgit Filipiak-Pittroff, H.-Erich Wichmann, Carl Peter Bauer, Dietrich Reinhardt, Dietrich Berdel
Journal: Journal of Allergy and Clinical Immunology (2003)
Severe surfing-related ocular injuries: the Stanford Northern Californian experience
Authors: C I Zoumalan, M S Blumenkranz, T J McCulley, D M Moshfeghi
Journal: British Journal of Sports Medicine (2008)

There is a growing body of literature describing severe surfing-related ocular injuries that result in permanent vision loss. We describe three severe surfing-related ocular injuries that occurred on beaches in northern California. One particular case stresses the need to tailor treatment to the patient and injury because of the possibility of good outcomes despite severe injury. Attention should also be directed towards commercially available safety gear and providing additional safety measures to prevent other orbital and ocular injuries.
Do patients with invasive lobular breast cancer benefit in terms of adequate change in surgical therapy from a supplementary preoperative breast MRI?
Authors: J. Heil, A. Buehler, M. Golatta, J. Rom, A. Schipp, A. Harcos, A. Schneeweiss, G. Rauch, C. Sohn, H. Junkermann
Journal: Annals of Oncology (2011)
Planar Cell Polarity and the Kidney
Authors: Helen McNeill
Journal: Journal of the American Society of Nephrology (2009)

Planar cell polarity (PCP) is a form of spatial organization in tissue that was first described in Drosophila melanogaster. PCP plays a critical conserved role in several aspects of mammalian development. Exciting data implicate PCP in normal kidney development and suggest the loss of oriented cell division and convergent extension downstream of defective PCP signaling lead to cystic kidney disease in mouse models. In this review, I first cover the current knowledge of PCP signaling in invertebrate and vertebrate models and then explore how loss of PCP might underlie some forms of cystic kidney disease.
Performing Phase I Clinical Trials of Anticancer Agents: Perspectives from within the European Union and Japan
Authors: Martin D. Forster, Nagahiro Saijo, Lesley Seymour, Hilary Calvert
Journal: Clinical Cancer Research (2010)

Drug discovery and early clinical development is an international endeavor, conducted in partnership between commercial entities such as biotechnology and pharmaceutical companies and academic investigators. Although once considered quite disparate, early clinical trials requirements and conduct are largely harmonized between the European Union, Japan, and the United States, increasing the opportunities for productive commercial-academic collaborations.
The Effects of Alternative Resuscitation Strategies on Acute Kidney Injury in Patients with Septic Shock
Authors: John A. Kellum, Lakhmir S. Chawla, Christopher Keener, Kai Singbartl, Paul M. Palevsky, Francis L. Pike, Donald M. Yealy, David T. Huang, Derek C. Angus
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Septic shock is a common cause of acute kidney injury (AKI), and fluid resuscitation is a major part of therapy.To determine if structured resuscitation designed to alter fluid, blood, and vasopressor use affects the development or severity of AKI or outcomes.Ancillary study to the ProCESS (Protocolized Care for Early Septic Shock) trial of alternative resuscitation strategies (two protocols vs. usual care) for septic shock.We studied 1,243 patients and classified AKI using serum creatinine and urine output. We determined recovery status at hospital discharge, examined rates of renal replacement therapy and fluid overload, and measured biomarkers of kidney damage. Among patients without evidence of AKI at enrollment, 37.6% of protocolized care and 38.1% of usual care patients developed kidney injury (P = 0.90). AKI duration (P = 0.59) and rates of renal replacement therapy did not differ between study arms (6.9% for protocolized care and 4.3% for usual care; P = 0.08). Fluid overload occurred in 8.3% of protocolized care and 6.3% of usual care patients (P = 0.26). Among patients with severe AKI, complete and partial recovery was 50.7 and 13.2% for protocolized patients and 49.1 and 13.4% for usual care patients (P = 0.93). Sixty-day hospital mortality was 6.2% for patients without AKI, 16.8% for those with stage 1, and 27.7% for stages 2 to 3.In patients with septic shock, AKI is common and associated with adverse outcomes, but it is not influenced by protocolized resuscitation compared with usual care.
Burkholderia pseudomallei: another emerging pathogen in cystic fibrosis
Authors: M R O'Carroll, T J Kidd, C Coulter, H V Smith, B R Rose, C Harbour, S C Bell
Journal: Thorax (2003)

Burkholderia pseudomallei is an important cause of acute fulminant pneumonia and septicaemia in tropical regions of northern Australia and south east Asia. Subacute and chronic forms of the disease also occur. There have been three recent reports of adults with cystic fibrosis (CF) who presumably acquired B pseudomallei infection during extended vacations or residence in either Thailand or northern Australia.The clinical course, molecular characteristics, serology and response to treatment are described in four adult CF patients infected with B pseudomallei. Polymerase chain reaction (PCR) based methods were used to confirm B pseudomallei and exclude B cepacia complex. Genotyping was performed using randomly amplified polymorphic DNA (RAPD) PCR and pulsed field gel electrophoresis (PFGE).Four patients are described with a mean duration of infection of 32 months. All but one patient lived in tropical Queensland. Two patients (with the longest duration of infection) deteriorated clinically and one subsequently died of respiratory failure. Both responded to intravenous treatment specifically targeting B pseudomallei. Another patient suffered two severe episodes of acute bronchopneumonia following acquisition of B pseudomallei. Eradication of the organism was not possible in any of the cases. PFGE of a sample isolate from each patient revealed the strains to be unique and RAPD analysis showed retention of the same strain within an individual over time.These findings support a potential pathogenic role for B pseudomallei in CF lung disease, producing both chronic infection and possibly acute bronchopneumonia. Identical isolates are retained over time and are unique, consistent with likely environmental acquisition and not person to person spread. B pseudomallei is emerging as a significant pathogen for patients with CF residing and holidaying in the tropics.
Payment to healthcare professionals for patient recruitment to trials: a systematic review
Authors: J Bryant, J Powell
Journal: BMJ (2005)

Establishing the clinical and cost effectiveness of interventions in healthcare largely depends on good quality randomised controlled trials (RCTs).One element of quality in RCTs is the recruitment of sufficient participants to test a priori hypotheses with statistical confidence and to minimise bias. 1 However, many RCTs fail to meet their recruitment targets. 2 One strategy to increase recruitment to trials is to pay healthcare professionals to recruit subjects either by providing financial incentives or by reimbursing excess costs incurred.Many pharmaceutical companies provide inducements but this is not common practice in publicly funded research programmes.Such programmes need to have confidence that payments are worthwhile.We did a systematic review, therefore, to synthesise the evidence on the effectiveness of payment to healthcare professionals for patient recruitment to trials.
Cholestasis shuts down calcium signaling in cholangiocytes
Authors: Juliette Martin, Jean-François Dufour, Hartmut Jaeschke, Kevin Mullen, Darius Moradpour
Journal: Hepatology (2004)

Cholestasis is one of the principal manifestations of liver disease and often results from disorders involving bile duct epithelia rather than hepatocytes. A range of disorders affects biliary epithelia, and no unifying pathophysiologic event in these cells has been identified as the cause of cholestasis. Here we examined the role of the inositol 1,4,5-trisphosphate receptor (InsP3R)/Ca(2+) release channel in Ca(2+) signaling and ductular secretion in animal models of cholestasis and in patients with cholestatic disorders.The expression and distribution of the InsP3R and related proteins were examined in rat cholangiocytes before and after bile duct ligation or treatment with endotoxin. Ca(2+) signaling was examined in isolated bile ducts from these animals, whereas ductular bicarbonate secretion was examined in isolated perfused livers. Confocal immunofluorescence was used to examine cholangiocyte InsP3R expression in human liver biopsy specimens.Expression of the InsP3R was selectively lost from biliary epithelia after bile duct ligation or endotoxin treatment. As a result, Ca(2+) signaling and Ca(2+)-mediated bicarbonate secretion were lost as well, although other components of the Ca(2+) signaling pathway and adenosine 3',5'-cyclic monophosphate (cAMP)-mediated bicarbonate secretion both were preserved. Examination of human liver biopsy specimens showed that InsP3Rs also were lost from bile duct epithelia in a range of human cholestatic disorders, although InsP3R expression was intact in noncholestatic liver disease.InsP3R-mediated Ca(2+) signaling in bile duct epithelia appears to be important for normal bile secretion in the liver, and loss of InsP3Rs may be a final common pathway for cholestasis.
Correlation of Vectorcardiographic Criteria for Myocardial Infarction with Autopsy Findings
Authors: ROLF M. GUNNAR, RAYMOND J. PIETRAS, JORGE BLACKALLER, STEWART E. DADMUN, PAUL B. SZANTO, JOHN R. TOBIN
Journal: Circulation (1967)

One hundred eight patients who had had vectorcardiograms and electrocardiograms recorded were followed to autopsy, and their hearts were carefully studied postmortem. Vectorcardiographic criteria previously proposed using the Frank corrected lead system were tested against the anatomic findings. These criteria correctly predicted the presence of infarction in 49 (92%) of 53 hearts and correctly localized the infarct in 39 (74%). In four hearts (8%) infarction could not be identified. In 18 (32%) of 55 hearts in which infarcts were not present, these criteria falsely indicated infarction. The reasons for the false positive predictions are discussed. The criteria tested will prove useful in the diagnoses and localizations of myocardial infarcts when the pitfalls of deformities of the vectorcardiogram produced by ventricular hypertrophy and bundle-branch block are avoided.
Cytokines in chronic inflammatory arthritis. IV. Granulocyte/macrophage colony-stimulating factor-mediated induction of class II MHC antigen on human monocytes: a possible role in rheumatoid arthritis.
Authors: J M Alvaro-Gracia, N J Zvaifler, G S Firestein
Journal: The Journal of Experimental Medicine (1989)

Granulocyte/macrophage CSF (GM-CSF) has recently been identified in rheumatoid arthritis (RA) synovial effusions. To study a potential role for GM-CSF and other cytokines on the induction of HLA-DR expression on monocytes and synovial macrophages, we analyzed the relative ability of recombinant human cytokines to induce the surface expression of class II MHC antigens on normal peripheral blood monocytes by FACS analysis. GM-CSF (800 U/ml) (mean fluorescence channel 2.54 +/- 0.33 times the control, p less than 0.001) and IFN-gamma (100 U/ml) (5.14 +/- 0.60, p less than 0.001) were the most potent inducers of HLA-DR. TNF-alpha and IL-4 also increased HLA-DR expression, although to a lesser degree [1.31 +/- 0.06 (p less than 0.02) and 1.20 +/- 0.03 (p less than 0.01), respectively]. IL-1 (40 U/ml), IL-2 (10 ng/ml), IL-3 (50 U/ml), IL-6 (100 U/ml), and CSF-1 (1,000 U/ml) did not affect surface HLA-DR density. GM-CSF also increased HLA-DR mRNA expression and surface HLA-DQ expression, but decreased CD14 (a monocyte/macrophage antigen) expression. The effect of GM-CSF on HLA-DR was not mediated by the generation of IFN-gamma in vitro because it was not blocked by anti-IFN-gamma mAb. GM-CSF was additive with IL-4 and low amounts (less than 3 U/ml) of IFN-gamma and synergistic with TNF-alpha. Because we have recently reported that supernatants of cultured RA synovial cells produce a non-IFN-gamma factor that induces HLA-DR on monocytes, we then attempted to neutralize this factor with specific anti-GM-CSF mAb. Four separate synovial tissue supernatants were studied, and the antibody neutralized the HLA-DR-inducing factor in each (p less than 0.01).
Failure of Higher-Dose Paclitaxel to Improve Outcome in Patients With Metastatic Breast Cancer: Cancer and Leukemia Group B Trial 9342
Authors: Eric P. Winer, Donald A. Berry, Susan Woolf, David Duggan, Alice Kornblith, Lyndsay N. Harris, Richard A. Michaelson, Jeffrey A. Kirshner, Gini F. Fleming, Michael C. Perry, Mark L. Graham, Stewart A. Sharp, Roger Keresztes, I. Craig Henderson, Clifford Hudis, Hyman Muss, Larry Norton
Journal: Journal of Clinical Oncology (2004)

Purpose Cancer and Leukemia Group B Protocol 9342 was initiated to determine the optimal dose of paclitaxel administered as a 3-hour infusion every 3 weeks to women with metastatic breast cancer. Patients and Methods Four hundred seventy-four women with metastatic breast cancer who had received one or no prior chemotherapy regimens were randomly assigned to one of three paclitaxel dosing regimens—175 mg/m 2 , 210 mg/m 2 , or 250 mg/m 2 —each administered as a 3-hour infusion every 3 weeks. Women completed self-administered quality of life and symptom assessment questionnaires at baseline and after three cycles of treatment. Results No evidence of a significant dose-response relationship was demonstrated over the dose range assessed. Response rates were 23%, 26%, and 21% for the three regimens, respectively. A marginally significant association (P = .04) was seen between dose and time to progression; however, in a multivariate analysis, the difference was even less apparent. No statistically significant difference was seen in survival. Neurotoxicity and hematologic toxicity were more severe on the higher dose arms. There was no significant difference in quality of life on the three arms. Conclusion Higher doses of paclitaxel administered as a 3-hour infusion to women with metastatic breast cancer did not improve response rate, survival, or quality of life. There was a slight improvement in time to progression with higher dose therapy, which was offset by greater toxicity. When a 3-hour infusion of paclitaxel is administered every 3 weeks, 175 mg/m 2 should be considered the optimal dose.
Mitral anulus motion. Relation to pulmonary venous and transmitral flows in normal subjects and in patients with dilated cardiomyopathy.
Authors: G Keren, E H Sonnenblick, T H LeJemtel
Journal: Circulation (1988)

The dynamics between mitral anulus motion, and, thus, motion of the base of the heart, and filling of the left atrium and ventricle were studied by Doppler echocardiography in 12 normal subjects and 28 patients with dilated cardiomyopathy. The normal motion of the mitral anulus is associated with two phases of inflow from the pulmonary veins. The first phase (J) of pulmonary venous inflow occurs during ventricular systole, concomitant with the descent of the mitral anulus toward the ventricular apex, the extent of which is 12.8 +/- 1.4 mm. The end of the descent of the anulus occurs at the cessation of aortic ejection. About 100 msec later, a rapid recoil of the mitral anulus toward the atrium coincides with the onset of transmitral filling. This rapid recoil contributes to the displacement of blood from the atria into the ventricles in early diastole. The second phase (K) of pulmonary venous flow begins in early diastole, with its peak occurring about 50 msec after the peak of transmitral flow. During atrial contraction, the mitral anulus moves slightly (2.4 +/- 0.7 mm) toward the atrium and then returns toward its initial position within 120 msec. This motion coincides with the A wave of transmitral flow. In patients with dilated cardiomyopathy, pulmonary venous flow and mitral anulus motion are markedly altered in comparison with normal subjects. In all patients, motion of the mitral anulus is either reduced or absent.(ABSTRACT TRUNCATED AT 250 WORDS)