tbuckley/cabot-search huggingface dataset:
Congenital cystic adenomatoid malformation of the lung
Authors: M. W. Moncreieff, A. H. Cameron, R. Astley, K. D. Roberts, L. D. Abrams, J. R. Mann
Journal: Thorax (1969)

Nine cases of congenital cystic adenomatoid malformation of the lung are described. One was stillborn: two presented in the newborn period (one of them surviving after a lobectomy), and the remaining six were older children all of whom survived after lobectomy. There have been only three cases previously reported in children outside the newborn period. The pathological, clinical, and radiological features are discussed and compared with previously reported cases.
Complications of alcoholic liver cirrhosis: Active assessment by endoscopy and sonography
Authors: Yi-Wen Huang, Jui-Ting Hu, Sien-Sing Yang
Journal: Hepatology (2010)

We read with interest the article by Jepsen et al.1 on a Danish population–based cohort study of the clinical course of alcoholic liver cirrhosis. Their study assessed three complications (i.e., ascites, variceal hemorrhage, and hepatic encephalopathy) at the diagnosis of cirrhosis for the prediction of mortality. This population-based cohort revealed the outcomes of complications during the clinical course of alcoholic cirrhosis; however, several issues need to be discussed. The diagnosis of cirrhosis in this study was mainly based on clinical, biochemical, image, and hemodynamic findings, which are useful in patients with advanced liver cirrhosis. Only 6% of their patients were confirmed by liver histology. Those with a less severe degree of cirrhosis may have been underdiagnosed. Furthermore, alcoholic hepatitis may share similar clinical features with alcoholic cirrhosis, which needs to be differentiated by liver histology.2-5 The detection of ascites and varices in patients with cirrhosis is important in predicting the prognosis.6 In Jepsen et al.'s study,1 ascites was defined mainly by physical findings. Patients with cirrhosis and lesser amounts of ascites could have been underdiagnosed. Sonography has been widely used for the early detection of ascites. We analyzed 141 patients with alcoholic liver disease between July 2005 and March 2008. We evaluated the presence of complications in 83 patients with alcoholic cirrhosis; liver histology provided confirmation for 54%. Liver histology may not be available for patients with decompensated liver function and coagulopathy. All patients underwent an ultrasound examination to confirm the presence of ascites, and 76 patients (92%) underwent endoscopy to confirm the presence of varices. Figure 1 shows the prevalence of major complications in our patients with alcoholic cirrhosis. Our recent study indeed confirmed that endoscopic findings of varices, with or without hemorrhaging, predict mortality in patients with alcoholic cirrhosis with or without alcoholic hepatitis.7 Therefore, the active assessment of patients for varices and ascites may allow an early prediction of mortality. Prevalence of complications in 83 patients with alcoholic cirrhosis. Yi-Wen Huang M.D.* , Jui-Ting Hu M.D.* , Sien-Sing Yang M.D.* , * Liver Unit, Cathay General Hospital Medical Center, Taipei, Taiwan, Division of Gastroenterology, Department of Internal Medicine, National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan, Faculty of Medicine, Fu-Jen Catholic University College of Medicine, Taipei, Taiwan.
Anthony John Fogarty
Authors: K. Fogarty
Journal: BMJ (2008)

<i>Abstract.</i> Endothelin (ET-1) acts as a potent vasoconstrictor in the human kidney, and this vasoconstriction could contribute to the ischemia seen in acute renal failure. In animal studies, the vasoactive properties of ET-1 are known to be ET<sub>A</sub> receptor-and/or ET<sub>B</sub> receptor-mediated; however, the receptor subtype involved in the human kidney remains to be defined. In a phase I, single-center, double-blind, randomized, three-period, crossover design, the effects of orally administered ABT-627, a selective ET<sub>A</sub> receptor antagonist, on renal hemodynamics during ET-1 infusion were evaluated. Two doses of ABT-627 (5 and 20 mg) were compared with placebo and nifedipine. For each dose level of ABT-627, a cohort of nine subjects was studied. A para-aminohippuric acid/inulin clearance test was performed once at the end of each 7-d treatment period. Infusion of ET-1 significantly decreased effective renal plasma flow, GFR, sodium excretion, and urine flow. Pretreatment with 20 mg of ABT-627 significantly decreased mean arterial pressure. In constrast, 7 d of treatment with both doses of ABT-627 did not affect baseline renal parameters. However, because mean arterial pressure decreased, a tendency toward a reduction of renal vascular resistance could indeed be demonstrated. Compared with placebo, both doses of ABT-627 were equally effective in blocking all renal effects caused by ET-1 infusion. In the model of exogenous ET-1 infusion, ABT-627 had a tendency to prevent ET-1-induced renal changes more effectively compared with nifedipine. The contribution of endogenous ET-1 and the ET<sub>A</sub> receptor in maintaining basal renal vascular tone in the human kidney is small. In addition, compared with placebo, selective ET<sub>A</sub> receptor antagonism with both doses of ABT-627 completely prevented all renal changes caused by ET-1 infusion.
Electron Microscopy of Human Bronchial Mucosa
Authors: Geoffrey L. Brinkman
Journal: JAMA (1965)

Whereasg visible light in conjunction with optical staining techniques is useful for studying structures as small as 1,500 Angstrom units (1 A =0.0001α, 1α=0.0001 cm) in biological tissues, or light microscopy using ultraviolet radiation is useful for structures as small as 1,000 A units, electron microscopy, because of its higher resolution in conjunction with heavy metal staining, permits visualization of dimensions as small as 5 A units. Thus, in cytology the electron microscopy is capable of demonstrating the tiniest intercellular structures, the ultrafine structure of the cell walls and membranes and indeed, of reaching down into the molecular level itself. This power of the electron microscope must be used with caution insofar as interpretation of a whole organ is concerned because of the extremely minute areas of tissue which it examines in any single field. Also, because the internal cellular structure is seen in such detail, changes due to autolysis,
Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK–positive anaplastic large-cell lymphoma
Authors: Christine Damm-Welk, Kerstin Busch, Birgit Burkhardt, Jutta Schieferstein, Susanne Viehmann, Ilske Oschlies, Wolfram Klapper, Martin Zimmermann, Jochen Harbott, Alfred Reiter, Willi Woessmann
Journal: Blood (2007)
Differential Expression of Matrix Metalloproteinases After Stent Implantation and Balloon Angioplasty in the Hypercholesterolemic Rabbit
Authors: Laurent J. Feldman, Mikael Mazighi, Aliocha Scheuble, Jean-François Deux, Edoardo De Benedetti, Cécile Badier-Commander, Elisabeth Brambilla, Dominique Henin, P. Gabriel Steg, Marie-Paule Jacob
Journal: Circulation (2001)

Background —Intimal hyperplasia is the principal mechanism of in-stent restenosis. Matrix metalloproteinases (MMPs) play a key role in intimal growth after balloon angioplasty (BA). Little is known, however, about MMP expression after stent implantation (ST). We investigated whether MMP9 and MMP2 are differentially expressed after ST and BA. Methods and Results —Hypercholesterolemic rabbits underwent ST and BA in the right and left iliac arteries, respectively. The expression of MMPs and their inhibitors (TIMPs) was studied at various time points in the injured arteries by use of zymography, reverse transcription–polymerase chain reaction, and immunohistochemistry. MMP2, but not MMP9, was constitutively expressed in uninjured arteries. MMP9 expression was rapidly induced after injury, whereas the increase in MMP2 expression was delayed. At all time points, pro-MMP9 activity and MMP9 mRNA levels were ≥2-fold (ANOVA, P =0.002) and ≥3-fold ( P &lt;0.0001) higher after ST than after BA, respectively. Active MMP9 was detected only after ST. Although the increases in MMP2 mRNA levels were of similar magnitudes after ST and BA, pro-MMP2 activity was slightly higher 7 and 30 days after ST, and MMP2 activity was ≥2-fold higher 7 to 60 days after ST ( P =0.002). No difference in TIMP expression was observed between stented and balloon-injured arteries. Cellular distributions of MMPs and TIMP1 were similar after ST and BA. Early inflammatory cell recruitment and 30-day intimal growth were more severe after ST. Conclusions —Stent implantation results in more intense and sustained expression of MMP9 and activation of MMP2 than balloon angioplasty.
Queen's Speech promises libel reform and bill on adult social care
Authors: N. Hawkes
Journal: BMJ (2012)

Campaigners have welcomed a commitment by the government to reform the libel laws in England and Wales. Defamation will be deemed to have occurred only if “serious harm” has been caused, and the rules will be tightened to avoid libel tourism, under which foreign plaintiffs bring actions that would be unlikely to succeed in their home countries.

The announcement, made in the Queen’s Speech to parliament, which outlines the government’s intended legislation, is a response to a large campaign launched after the law was used in an attempt to silence critics.

One of them, science writer Simon Singh, who was sued by the British Chiropractic Association for an article he wrote, said: “The reform promised in the Queen’s Speech today is a welcome response to the intolerable effects of the current laws. I hope the government will now move forward rapidly to bring forward a bill that protects those writing about serious …
<i>Gadd45a</i> Functions as a Promoter or Suppressor of Breast Cancer Dependent on the Oncogenic Stress
Authors: Jennifer S. Tront, Yajue Huang, Albert A. Fornace, Barbara Hoffman, Dan A. Liebermann
Journal: Cancer Research (2010)

Gadd45a plays a pivotal role as a stress sensor that modulates cellular responses to various stress stimuli including oncogenic stress. We reported that the stress sensor Gadd45a gene functions as a tumor suppressor in Ras-driven breast tumorigenesis via increasing JNK-mediated apoptosis and p38-mediated senescence. In contrast, here, we show that Gadd45a promotes Myc-driven breast cancer by negatively regulating MMP10 via GSK3 β/β-catenin signaling, resulting in increased tumor vascularization and growth. These novel findings indicate that Gadd45a functions as either tumor promoter or suppressor, is dependent on the oncogenic stress, and is mediated via distinct signaling pathways. Collectively, these novel findings highlight the significance of the type of oncogenic alteration on how stress response genes function during initiation and progression of tumorigenesis. Because Gadd45a is a target for BRCA1 and p53, these findings have implications regarding BRCA1/p53 tumor suppressor functions.
SOME ADVANCES IN RENAL AND URETERAL DIAGNOSIS.
Authors: CHARLES LESTER LEONARD
Journal: JAMA (1907)

The uncertainties that frequently surrounded the diagnosis of lesions in the deeper urinary tract have been materially lessened by recent advances in the physical methods of diagnosis. This is particularly true of the intrarenal and intraureteral disorders, where improvements in diagnosis have resulted in a clearer differentiation between the symptoms of conditions that had been grouped as identical; in a more exact determination of the character and location of the lesion; and hence in a more accurate analysis of the indications for treatment, resulting in valuable modifications, more precise operative intervention, and, finally, a marked betterment in results. The facts that have led to a differentiation in the symptomatology and a more accurate localizing of intrarenal and intraureteral lesions have been derived from the study of the symptoms after an accurate localization of a calculus has been made by the Roentgen method of diagnosis. Thus the localizing symptoms observed as
Some clarification needed
Authors: R. G. Richards
Journal: BMJ (2010)

<h3>Background</h3> Although recent reports suggest that the incidence of parapneumonic empyema has increased in several regions of the USA, national trends in disease burden are unknown. National trends in the incidence of parapneumonic empyema hospitalisations and changes in empyema by associated pathogens were examined. <h3>Methods</h3> National hospitalisation data (1996–2008) were analysed and rates estimated using census estimates as denominators. Incidence rate ratios (IRR) compared 2008 with 1996 rates. Discharge diagnosis codes were used to characterise pathogens associated with empyema hospitalisations. <h3>Results</h3> Overall, national parapneumonic empyema-related hospitalisation rates increased from 3.04 per 100 000 in 1996 to 5.98 per 100 000 in 2008, a 2.0-fold increase (95% CI 1.8 to 2.1). The increases were observed among children (IRR 1.9 (95% CI 1.4 to 2.7)) and adults aged 18–39, 40–64 and ≥65 years (IRR 1.8 (95% CI 1.5 to 2.1), 2.0 (95% CI 1.6 to 3.1) and 1.7 (95% CI 1.5 to 2.0), respectively). Overall, pneumococcal empyema rates remained relatively stable in all age groups whereas streptococcal- (non-pneumococcal) and staphylococcal-related empyema rates increased 1.9-fold and 3.3-fold, respectively, with consistent increases across age groups. The overall in-hospital case fatality ratio for parapneumonic empyema-related hospitalisations was 8.0% (95% CI 6.4% to 9.5%) in 1996 and 7.2% (95% CI 6.3% to 8.1%) in 2008 (p=0.395). Of the empyemas where study pathogens were listed (37.6%), staphylococcal-related empyema had the largest absolute increases across age groups and was associated with longer hospital stay and higher in-hospital mortality than other empyemas. <h3>Conclusions</h3> Although parapneumonic empyema-related hospitalisations remained relatively rare, they increased substantially during the study period. A number of pathogens, especially staphylococcus, contributed to this increase.
The flow cytometric analysis of telomere length in antigen-specific CD8+ T cells during acute Epstein-Barr virus infection
Authors: Fiona J. Plunkett, Maria Vieira D. Soares, Nicola Annels, Andrew Hislop, Kamal Ivory, Mark Lowdell, Mike Salmon, Alan Rickinson, Arne N. Akbar
Journal: Blood (2001)
A trans-acting mechanism represses the expression of the major transplantation antigens in mouse hybrid thymoma cell lines.
Authors: P Baldacci, C Transy, M Cochet, C Penit, A Israel, P Kourilsky
Journal: The Journal of Experimental Medicine (1986)

We have fused an H-2- thymoma (BM5R.9) with an H-2+ thymoma (BW5147) and have found that many of the resulting hybrids exhibit an H-2- phenotype. In several hybrids that were analyzed in detail, this phenotype is related to the absence of steady-state H-2 mRNA and shows some instability, possibly related to the loss of chromosomes in segregants. We conclude from our studies that BM5R.9 cells display a trans-acting mechanism that can repress the expression of H-2 antigens, and that the gene(s) causing the repression are not located on chromosome 17. This mechanism is not sufficient to explain the H-2- phenotype of BM5R.9, for which an additional, cis-acting process, must be postulated. We discuss these results in the context of the regulation of expression of the major class I transplantation antigens.
Embolism and Secondary Thrombosis of the Bifurcation of the Aorta
Authors: R. B. T. Baldwin, D. F. Thomas
Journal: BMJ (1954)

MEDICAL MEMORANDA rence of jaundice in these reactions suggests that more often the shock-organ is the liver, probably because of the part played by that organ in the breakdown of the drug.It is, however, of interest to note that in two of the earliest descriptions of P.A.S. sensitivity reactions (Home, 1949; Hemming and Stewart, 1949) one of the outstanding symptoms was an intractable dry cough; unfortunately, these patients were not x-rayed during their reactions.The finding of cold agglutinins in the blood of the case reported above is of interest in view of the possible relationship suggested by Crofton et al. (1952) between Lbffler's syndrome and other conditions, including tropical eosinophilia, which are characterized by the presence of pulmonary infiltrations and blood eosinophilia.Thus Viswanathan (1948) has drawn attention to the presence of cold agglutinins in the blood in tropical eosinophilia.I wish to thank Dr. A. M.
Accommodating the Effect of Ancient DNA Damage on Inferences of Demographic Histories
Authors: A. Rambaut, S. Y.W. Ho, A. J. Drummond, B. Shapiro
Journal: Molecular Biology and Evolution (2008)

DNA sequences extracted from ancient remains are increasingly used to generate large population data sets, often spanning tens of thousands of years of population history. Bayesian coalescent methods such as those implemented in the software package BEAST can be used to estimate the demographic history of these populations, sometimes resulting in complex scenarios of fluctuations in population size, which can be correlated with the timing of environmental events, such as glaciations. Recently, however, Axelsson et al. (Axelsson E, Willerslev E, Gilbert MTP, Nielsen R. 2008. The effect of ancient DNA damage on inferences of demographic histories. Mol Biol Evol 25:2181–2187.) claimed that many of these complex demographic trends are likely to be the result of postmortem DNA damage, a problem that they investigate by removing all sites involving transitions from ancient sequences prior to analysis. When this solution is applied to a previously published data set of Pleistocene bison, they show that the demographic signal of population expansion and decline disappears. Although some apparently segregating mutations in ancient sequences may be due to postmortem damage, we argue that discarding the data will result in loss of power to detect patterns of population change. Instead, to accommodate this problem, we implement a model in which sequences are the result of a joint process of molecular evolution and postmortem DNA damage within a probabilistic inference framework. Through simulation, we demonstrate the ability of this model to accurately recover evolutionary parameters, demographic history, and DNA damage rates. When this model is applied to the bison data set, we find that the rate of DNA damage is significant but low and that the reconstruction of population size history is nearly identical to previously published estimates.
Illuminating the future of DNA sequencing
Authors: Mick Watson
Journal: Genome biology (2014)

Human (clinical) genome sequencing is the biggest potential market in DNA sequencing, and it is this market that all of the sequencing companies are striving to capture. In another article in this issue of Genome Biology, Neil Hall expresses some concern over the limitation of Illumina's newly announced Hiseq X Ten platform to human indeed, at face value this does appear strange. The fact that Illumina have presented PhiX data from the X Ten confirms that there is no limitation inherent to the technology. The limitation is one of licensing. However, those involved in human genome sequencing will not be surprised by the move.
Identification of a Metalloprotease-Chemokine Signaling System in the Ovarian Cancer Microenvironment: Implications for Antiangiogenic Therapy
Authors: Anika Agarwal, Sarah L. Tressel, Rajani Kaimal, Marianthi Balla, Francis H. Lam, Lidija Covic, Athan Kuliopulos
Journal: Cancer Research (2010)

Abstract Ovarian cancer is a lethal gynecologic malignancy that may benefit from new therapies that block key paracrine pathways involved in tumor-stromal interactions and tumor vascularity. It was recently shown that matrix metalloprotease-1 (MMP1) activation of the G protein–coupled receptor protease-activated receptor-1 (PAR1) is an important stimulator of angiogenesis and metastasis in peritoneal mouse models of ovarian cancer. In the present study, we tested the hypothesis that MMP1-PAR1 promotes angiogenesis through its paracrine control of angiogenic chemokine receptors. We found that MMP1-PAR1 activation induces the secretion of several angiogenic factors from ovarian carcinoma cells, most prominently interleukin (IL)-8, growth-regulated oncogene-α (GRO-α), and monocyte chemoattractant protein-1. The secreted IL-8 and GRO-α acts on endothelial CXCR1/2 receptors in a paracrine manner to cause robust endothelial cell proliferation, tube formation, and migration. A cell-penetrating pepducin, X1/2pal-i3, which targets the conserved third intracellular loop of both CXCR1 and CXCR2 receptors, significantly inhibited endothelial cell proliferation, tube formation, angiogenesis, and ovarian tumor growth in mice. Matrigel plugs mixed with MMP1-stimulated, OVCAR-4–conditioned media showed a dramatic 33-fold increase in blood vessel formation in mice. The X1/2pal-i3 pepducin completely inhibited MMP1-dependent angiogenesis compared with a negative control pepducin or vehicle. Conversely, a vascular endothelial growth factor–directed antibody, Avastin, suppressed angiogenesis in mice but, as expected, was unable to inhibit IL-8 and GRO-α–dependent endothelial tube formation in vitro. These studies identify a critical MMP1-PAR1-CXCR1/2 paracrine pathway that might be therapeutically targeted for ovarian cancer treatment. Cancer Res; 70(14); 5880–90. ©2010 AACR.
A Statewide Collaborative Initiative to Improve the Quality of Care for Patients With Acute Myocardial Infarction and Heart Failure
Authors: John E. Brush, Edna Rensing, Frank Song, Sallie Cook, Janet Lynch, Leroy Thacker, Sarat Gurram, Robert O. Bonow, Joani Brough, C. Michael Valentine
Journal: Circulation (2009)

To enhance quality improvement, we created a unique statewide collaboration among 3 organizations: the Virginia Health Quality Center (Virginia's Medicare Quality Improvement Organization), the American College of Cardiology, and the American Heart Association. The goal was to improve discharge measures for acute myocardial infarction and heart failure.In 2004, 29 hospitals participated in the collaborative initiative. Using Medicare data submitted from 2004 through the second quarter of 2006, we analyzed adherence to individual discharge measures and all-or-none appropriate care measures for acute myocardial infarction, heart failure, and both. To control for differences in hospital characteristics, we were able to match 21 of the participating hospitals with 21 similar nonparticipating hospitals. In this paired analysis, the total appropriate care measure increased from 61% to 77% in participating hospitals compared with an increase from 51% to 60% in nonparticipating hospitals (P<0.0001). A generalized linear mixed model examining the full data set at the patient level failed to show a clear advantage among participating hospitals. Participating hospitals had higher baseline rates for most quality measures, suggesting a possible effect of a prior collaborative. Further analysis of only hospitals that participated in a prior collaborative showed that participants in the current collaborative initiative had higher rates of improvement for 7 of 10 quality measures and appropriate care measures for heart failure, acute myocardial infarction, or both (all P<0.05).We report a unique collaboration of a Medicare Quality Improvement Organization and 2 national organizations to address quality of care for acute myocardial infarction and heart failure. A composite measure of quality (the total appropriate care measure) improved more in the participating hospitals during the timeframe of the intervention, although the greater improvement in this and other measures in the participating hospitals appeared to be dependent on participation in a prior collaborative initiative.