tbuckley/cabot-search huggingface dataset:
Pigtail catheter drainage – When to use it
Authors: Jan Plutinsky, Karol Bitter, Zuzana Taligova, Ingrid Libakova, Dalibor Petras, Renata Sabova
Journal: European Respiratory Journal (2011)

Chest drainage for patients (pts) with pneumothorax or various etiology pleural effusions is a method of choice. In some circumstances specialists use a tip with a curled drain-pigtail catheter (PC).   Aim:  To share our experience with pigtail catheter drainage.   Method:  106 pts were drained in 2010. A pigtail catheter was used on 17 pts (16%). PCs 14 or 16 CH were preferred. The site of insertion was determined using a sonography examination. PC with a trocar was inserted into the skin incision. After insertion of the drain the end of the catheter was twisted by pulling back the synthetic fibres and then fixed. The Luer end of drain was connected to a Heimlich valve and then to a urine bag. When production of PE was    Results:  Out of 17 pts, 13 were M, mean age 60 (22-85 yrs), 4 were F, mean age 53.5 (42-69 yrs). The most frequent reason was encapsulated empyema in 8 pts, malignant effusion in 6 pts and TB, haemothorax and non- specific pleuritis in the last 3 pts. In 15 pts (88.2%) chest drainage was successful. 2 pts died during drainage (both from malignant effusion). The median duration of the chest drainage was 9 days (4-21 days).   Conclusions:  The main advantage of using a PC was that the small space in encapsulated empyema is too small for using a conventional drain or when there is a suspicion of septated PE. The disadvantage of pigtail drainage: 1.twisted end impedes the re-expansion of the drained cavity, 2. the system with a trocar is sharp and so careful consideration should be given to the indications (avoid drainage of lung abscess), 3. removing the drains is more painful, 4. is more expensive than a normal catheter.
Low plasma concentrations of interleukin 10 in severe malarial anaemia compared with cerebral and uncomplicated malaria
Authors: Jørgen AL Kurtzhals, Victoria Adabayeri, Bamenla Quarm Goka, Bartholomew D Akanmori, Joseph O Oliver-Commey, Francis K Nkrumah, Charlotte Behr, Lars Hviid
Journal: The Lancet (1998)
Estimated Radiation Dose Associated With Cardiac CT Angiography
Authors: Jörg Hausleiter, Tanja Meyer, Franziska Hermann, Martin Hadamitzky, Markus Krebs, Thomas C Gerber, Cynthia McCollough, Stefan Martinoff, Adnan Kastrati, Albert Schömig, Stephan Achenbach
Journal: JAMA (2009)

Cardiac computed tomography (CT) angiography (CCTA) has emerged as a useful diagnostic imaging modality in the assessment of coronary artery disease. However, the potential risks due to exposure to ionizing radiation associated with CCTA have raised concerns.To estimate the radiation dose of CCTA in routine clinical practice as well as the association of currently available strategies with dose reduction and to identify the independent factors contributing to radiation dose.A cross-sectional, international, multicenter, observational study (50 study sites: 21 university hospitals and 29 community hospitals) of estimated radiation dose in 1965 patients undergoing CCTA between February and December 2007. Linear regression analysis was used to identify independent predictors associated with dose.Dose-length product (DLP) of CCTA.The median DLP of 1965 CCTA examinations performed at 50 study sites was 885 mGy x cm (interquartile range, 568-1259 mGy x cm), which corresponds to an estimated radiation dose of 12 mSv (or 1.2 x the dose of an abdominal CT study or 600 chest x-rays). A high variability in DLP was observed between study sites (range of median DLPs per site, 331-2146 mGy x cm). Independent factors associated with radiation dose were patient weight (relative effect on DLP, 5%; 95% confidence interval [CI], 4%-6%), absence of stable sinus rhythm (10%; 95% CI, 2%-19%), scan length (5%; 95% CI, 4%-6%), electrocardiographically controlled tube current modulation (-25%; 95% CI, -23% to -28%; applied in 73% of patients), 100-kV tube voltage (-46%; 95% CI, -42% to -51%; applied in 5% of patients), sequential scanning (-78%; 95% CI, -77% to -79%; applied in 6% of patients), experience in cardiac CT (-1%; 95% CI, -1% to 0%), number of CCTAs per month (0%; 95% CI, 0%-1%), and type of 64-slice CT system (for highest vs lowest dose system, 97%; 95% CI, 88%-106%). Algorithms for dose reduction were not associated with deteriorated diagnostic image quality in this observational study.Median doses of CCTA differ significantly between study sites and CT systems. Effective strategies to reduce radiation dose are available but some strategies are not frequently used. The comparable diagnostic image quality may support an increased use of dose-saving strategies in adequately selected patients.
Coexistent rheumatoid arthritis and tophaceous gout: a case report.
Authors: D Raman, A M Abdalla, D R Newton, I Haslock
Journal: Annals of the Rheumatic Diseases (1981)

Rheumatoid arthritis and gout are both common rheumatic diseases, but their coincidence is rare. We report the case of a 67-year-old Caucasian woman with rheumatoid arthritis who later developed tophaceous gout. The tophi disappeared with remarkable rapidity on treatment with allopurinol.
Mortality Among Hospitalized Medicare Beneficiaries in the First 2 Years Following ACGME Resident Duty Hour Reform
Authors: Kevin G. Volpp, Amy K. Rosen, Paul R. Rosenbaum, Patrick S. Romano, Orit Even-Shoshan, Yanli Wang, Lisa Bellini, Tiffany Behringer, Jeffrey H. Silber
Journal: JAMA (2007)

The Accreditation Council for Graduate Medical Education (ACGME) implemented duty hour regulations for physicians-in-training throughout the United States on July 1, 2003. The association of duty hour reform with mortality among patients in teaching hospitals nationally has not been well established.To determine whether the change in duty hour regulations was associated with relative changes in mortality among Medicare patients in hospitals of different teaching intensity.An observational study of all unique Medicare patients (N = 8 529 595) admitted to short-term, acute-care, general US nonfederal hospitals (N = 3321) using interrupted time series analysis with data from July 1, 2000, to June 30, 2005. All Medicare patients had principal diagnoses of acute myocardial infarction, congestive heart failure, gastrointestinal bleeding, or stroke or a diagnosis related group classification of general, orthopedic, or vascular surgery. Logistic regression was used to examine the change in mortality for patients in more vs less teaching-intensive hospitals before (academic years 2000-2003) and after (academic years 2003-2005) duty hour reform, adjusting for patient comorbidities, common time trends, and hospital site.All-location mortality within 30 days of hospital admission.In medical and surgical patients, no significant relative increases or decreases in the odds of mortality for more vs less teaching-intensive hospitals were observed in either postreform year 1 (combined medical conditions group: odds ratio [OR], 1.03; 95% confidence interval [CI], 0.98-1.07; and combined surgical categories group: OR, 1.05; 95% CI, 0.98-1.12) or postreform year 2 (combined medical conditions group: OR, 1.03; 95% CI, 0.99-1.08; and combined surgical categories group: OR, 1.01; 95% CI, 0.95-1.08) compared with the prereform years. The only condition for which there was a relative increase in mortality in more teaching-intensive hospitals postreform was stroke, but this association preceded the onset of duty hour reform. Compared with nonteaching hospitals, the most teaching-intensive hospitals had an absolute change in mortality from prereform year 1 to postreform year 2 of 0.42 percentage points (4.4% relative increase) for patients in the combined medical conditions group and 0.05 percentage points (2.3% relative increase) for patients in the combined surgical categories group, neither of which were statistically significant.The ACGME duty hour reform was not associated with either significant worsening or improvement in mortality for Medicare patients in the first 2 years after implementation.
Somatic Mutation and Light Chain Rearrangement Generate Autoimmunity in Anti–Single-Stranded DNA Transgenic Mrl/<i>lpr</i> Mice
Authors: Frederic Brard, Michele Shannon, Eline Luning Prak, Samuel Litwin, Martin Weigert
Journal: The Journal of Experimental Medicine (1999)

Antibodies to single-stranded (ss)DNA are expressed in patients with systemic lupus erythematosus and in lupus-prone mouse models such as the MRL/Mp-lpr/lpr (MRL/lpr) strain. In nonautoimmune mice, B cells bearing immunoglobulin site-directed transgenes (sd-tgs) that code for anti-ssDNA are functionally silenced. In MRL/lpr autoimmune mice, the same sd-tgs are expressed in peripheral B cells and these autoantibodies gain the ability to bind other autoantigens such as double-stranded DNA and cell nuclei. These new specificities arise by somatic mutation of the anti-ssDNA sd-tgs and by secondary light chain rearrangement. Thus, B cells that in normal mice are anergic can be activated in MRL/lpr mice, which can lead to the generation of pathologic autoantibodies. In this paper, we provide the first direct evidence for peripheral rearrangement in vivo.
Targeting PIM Kinases Impairs Survival of Hematopoietic Cells Transformed by Kinase Inhibitor–Sensitive and Kinase Inhibitor–Resistant Forms of Fms-Like Tyrosine Kinase 3 and BCR/ABL
Authors: Myriam Adam, Vanda Pogacic, Marina Bendit, Richard Chappuis, Martijn C. Nawijn, Justus Duyster, Casey J. Fox, Craig B. Thompson, Jan Cools, Juerg Schwaller
Journal: Cancer Research (2006)

Abstract Previous studies have shown that activation of the signal transducer and activator of transcription 5 (STAT5) plays an essential role in leukemogenesis mediated through constitutive activated protein tyrosine kinases (PTK). Because PIM-1 is a STAT5 target gene, we analyzed the role of the family of PIM serine/threonine kinases (PIM-1 to PIM-3) in PTK-mediated transformation of hematopoietic cells. Ba/F3 cells transformed to growth factor independence by various oncogenic PTKs (TEL/JAK2, TEL/TRKC, TEL/ABL, BCR/ABL, FLT3-ITD, and H4/PDGFβR) show abundant expression of PIM-1 and PIM-2. Suppression of PIM-1 activity had a negligible effect on transformation. In contrast, expression of kinase-dead PIM-2 mutant (PIM-2KD) led to a rapid decline of survival in Ba/F3 cells transformed by FLT3-ITD but not by other oncogenic PTKs tested. Coexpression of PIM-1KD and PIM-2KD abrogated growth factor–independent growth of Ba/F3 transformed by several PTKs, including BCR/ABL. Targeted down-regulation of PIM-2 by RNA interference (RNAi) selectively abrogated survival of Ba/F3 cells transformed by various Fms-like tyrosine kinase 3 (FLT3)–activating mutants [internal tandem duplication (ITD) and kinase domain] and attenuated growth of human cell lines containing FLT3 mutations. Interestingly, cells transformed by FLT3 and BCR/ABL mutations that confer resistance to small-molecule tyrosine kinase inhibitors were still sensitive to knockdown of PIM-2, or PIM-1 and PIM-2 by RNAi. Our observations indicate that combined inactivation of PIM-1 and PIM-2 interferes with oncogenic PTKs and suggest that PIMs are alternative therapeutic targets in PTK-mediated leukemia. Targeting the PIM kinase family could provide a new avenue to overcome resistance against small-molecule tyrosine kinase inhibitors. (Cancer Res 2006; 66(7): 3828-35)
Survival analysis and prognostic nomogram for patients undergoing resection of extrahepatic cholangiocarcinoma
Authors: N.A. van der Gaag, J.J. Kloek, J.K. de Bakker, B. Musters, R.B. Geskus, O.R.C. Busch, A. Bosma, D.J. Gouma, T.M. van Gulik
Journal: Annals of Oncology (2012)
ACC/AHA guidelines for ambulatory electrocardiography
Authors: Michael H Crawford, Steven J Bernstein, Prakash C Deedwania, John P DiMarco, Kevin J Ferrick, Arthur Garson, Lee A Green, H.Leon Greene, Michael J Silka, Peter H Stone, Cynthia M Tracy, Raymond J Gibbons, Joseph S Alpert, Kim A Eagle, Timothy J Gardner, Arthur Garson, Gabriel Gregoratos, Richard O Russell, Thomas J Ryan, Sidney C Smith
Journal: Journal of the American College of Cardiology (1999)
Estrogens maintain bile duct mass and reduce apoptosis after biliodigestive anastomosis in bile duct ligated rats
Authors: Gianluca Svegliati-Baroni, Roberto Ghiselli, Marco Marzioni, Domenico Alvaro, Federico Mocchegiani, Stefania Saccomanno, Valerio Sisti, Laura Ugili, Fiorenza Orlando, Gianfranco Alpini, Vittorio Saba, Antonio Benedetti
Journal: Journal of Hepatology (2005)
Rac2-MRC-cIII–generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors
Authors: Margaret Nieborowska-Skorska, Piotr K. Kopinski, Regina Ray, Grazyna Hoser, Danielle Ngaba, Sylwia Flis, Kimberly Cramer, Mamatha M. Reddy, Mateusz Koptyra, Tyrone Penserga, Eliza Glodkowska-Mrowka, Elisabeth Bolton, Tessa L. Holyoake, Connie J. Eaves, Sabine Cerny-Reiterer, Peter Valent, Andreas Hochhaus, Timothy P. Hughes, Heiko van der Kuip, Martin Sattler, Wieslaw Wiktor-Jedrzejczak, Christine Richardson, Adrienne Dorrance, Tomasz Stoklosa, David A. Williams, Tomasz Skorski
Journal: Blood (2012)
Chromosomal Mapping of a Major Quantitative Trait Locus Regulating Compensatory Renal Growth in the Rat
Authors: MICHAL PRAVENEC, VACLAV ZIDEK, ALENA MUSILOVA, VLADIMIR KR[Combining Caron]EN, VLASTA BILA, ROBERT DI NICOLANTONIO
Journal: Journal of the American Society of Nephrology (2000)

Abstract. Despite extensive research conducted over the past century, the mechanisms of compensatory renal growth (CRG) remain a mystery. Insight into the mechanisms that regulate CRG might be gained by identifying genetic factors that influence this complex phenotype. In a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown Norway rat, a genome scan for quantitative trait loci (QTL) that regulate CRG was performed. The CRG score was expressed as a ratio of the weight of the remnant right kidney at 8 wk of age to the weight of the left kidney at 5 wk of age, both adjusted for body weight. QTL mapping was performed using Map Manager QT and the strain distribution patterns of more than 600 genetic markers. It was found that CRG after unilateral nephrectomy is a multifactorially determined trait with a substantial genetic component. The heritability of CRG approached 40%. Genome wide scan analysis revealed significant evidence of linkage to a region of rat chromosome 4 designated Crg 1 that accounted for more than 50% of the additive genetic variance of CRG in the recombinant inbred strains. The detection of a major QTL influencing CRG in the rat should provide new opportunities for identifying mechanisms that regulate this historically enigmatic phenomenon and may also have implications for research on the pathogenesis of end-stage kidney disease.
Acquired Hyperoxaluria with Regional Enteritis After Ileal Resection
Authors: JOHN Q. STAUFFER
Journal: Annals of Internal Medicine (1973)

Urinary oxalate excretion was measured in 11 patients with inflammatory bowel disease involving the terminal ileum. Group A consisted of six patients with minimal or no resection of terminal ileum and group B of six patients with resections greater than 30 cm. Basal urinary oxalate excretion was normal in group A but was significantly elevated in group B. After treatment with oral cholestyramine, a drug known to bind bile salts, urinary oxalate excretion fell promptly in group B to within the normal range but remained unchanged in group A. Five of six patients in group B had severe, explosive, watery diarrhea, which was dramatically reversed by cholestyramine. Hyperoxaluria in two patients was reversed when oxalate was removed from the diet, and in-vitro studies showed that cholestyramine binds oxalic acid. These data suggest that the mechanism of acquired hyperoxaluria in patients with ileal resection is related to enhanced absorption of dietary oxalate.
Feasibility and Cardiac Safety of Trastuzumab Emtansine After Anthracycline-Based Chemotherapy As (neo)Adjuvant Therapy for Human Epidermal Growth Factor Receptor 2–Positive Early-Stage Breast Cancer
Authors: Ian E. Krop, Thomas M. Suter, Chau T. Dang, Luc Dirix, Gilles Romieu, Claudio Zamagni, Marc L. Citron, Mario Campone, Na Xu, Melanie Smitt, Luca Gianni
Journal: Journal of Clinical Oncology (2015)

Trastuzumab emtansine (T-DM1), an antibody-drug conjugate comprising the cytotoxic agent DM1, a stable linker, and trastuzumab, has demonstrated substantial activity in human epidermal growth factor receptor 2 (HER2) -positive metastatic breast cancer, raising interest in evaluating the feasibility and cardiac safety of T-DM1 in early-stage breast cancer (EBC).Patients (N = 153) with HER2-positive EBC and prechemotherapy left ventricular ejection fraction (LVEF) ≥ 55% received (neo)adjuvant doxorubicin plus cyclophosphamide or fluorouracil plus epirubicin plus cyclophosphamide followed by T-DM1 for four cycles. Patients could then receive three to four cycles of optional docetaxel with or without trastuzumab. T-DM1 was then resumed with optional radiotherapy (sequential or concurrent) for 1 year (planned) of HER2-directed therapy. The coprimary end points were rate of prespecified cardiac events and safety.Median follow-up was 24.6 months. No prespecified cardiac events or symptomatic congestive heart failures were reported. Four patients (2.7%) had asymptomatic LVEF declines (≥ 10 percentage points from baseline to LVEF < 50%), leading to T-DM1 discontinuation in one patient. Of 148 patients who received ≥ one cycle of T-DM1, 82.4% completed the planned 1-year duration of HER2-directed therapy. During T-DM1 treatment, 38.5% and 2.7% of patients experienced grade 3 and 4 adverse events, respectively. Approximately 95% of patients receiving T-DM1 plus radiotherapy completed ≥ 95% of the planned radiation dose with delay ≤ 5 days.Use of T-DM1 for approximately 1 year after anthracycline-based chemotherapy was feasible and generally well tolerated by patients with HER2-positive EBC, providing support for phase III trials of T-DM1 in this setting.
BIOCHEMICAL BASIS FOR ALTERATIONS IN STRUCTURE AND FUNCTION OF H<scp>E</scp>L<scp>A</scp> CELLS INFECTED WITH NEWCASTLE DISEASE VIRUS
Authors: E. Frederick Wheelock, Igor Tamm
Journal: The Journal of Experimental Medicine (1961)

The ability of NDV-infected HeLa cells to synthesize DNA, protein, and RNA was investigated by measuring the incorporation of tritiated precursors into these substances at intervals after infection of cells with a virus/cell multiplicity of 500:1. A significant decrease in incorporation of precursors into DNA and protein was first observed at 3(1/4) hours after infection. By 4(1/2) hours, an 80 to 90 per cent decrease had occurred, and by 5(1/4) hours, incorporation of precursors into DNA and protein was almost completely inhibited. Incorporation of precursor into RNA decreased gradually following infection; by the 10th hour, a 40 per cent decrease had occurred. These results, integrated with earlier observations on biological aspects of infection, suggest the following causal relationships among events in NDV-infected cells: (a) The cessation of virus production is probably caused by inhibition of protein or RNA synthesis, and is not due to inhibition of DNA synthesis or to interferon. (b) The production of infective virus does not per se interfere with the ability of an infected cell to divide, nor is inhibition of mitosis caused by either inhibition of DNA synthesis or development of marked degenerative changes in infected cells. Inhibition of mitosis may be the result of inhibition of protein or RNA synthesis, (c) Marked cell damage could have been caused by inhibition of protein, DNA, or RNA synthesis, (d) Interference by NDV with the multiplication of influenza virus was probably due to the inhibitory effects of NDV on cellular biosynthetic activities.
Experience with mediastinoscopy
Authors: T. L. Otto, J. Zaslonka, M. Lukianski
Journal: Thorax (1972)

Six hundred and eighty diagnostic mediastinoscopies are presented. Of these, 552 were classical, 114 anterior mediastinal, 12 posterior mediastinal, and 2 from below the sternum. In addition, 20 therapeutic mediastinoscopies were performed for the insertion of a pacemaker electrode or evacuation of a mediastinal cyst. Of 125 mediastinoscopies performed on patients with an initial diagnosis of sarcoidosis, in most the diagnosis was confirmed, the rate of false negative results being 2·4%. Extremely encouraging were the results in patients with an initial diagnosis of Hodgkin9s disease. Out of 60 patients, a different diagnosis was established in 30 and further follow-up proved this to be correct. In mediastinal tumours the results were discouraging, the rate of false results being as high as 43%. Four hundred and ten patients were mediastinoscoped for lung cancer. In 52, mediastinoscopy was the first successful biopsy. Metastases to lymph nodes were found in 139 (33·9%). The percentage of exploratory thoracotomies following the introduction of mediastinoscopy fell from 22% to 14%. Mediastinoscopy was also used to investigate the spread of oesophageal cancer and enabled us to exclude patients who were obviously inoperable.
Experimental pneumococcal and staphylococcal sepsis: effects of hydrocortisone and phenoxybenzamine upon mortality rates.
Authors: H G Robson, L E Cluff
Journal: Journal of Clinical Investigation (1966)

resistance, and terminal hypotension (16). These findings suggest that the effects of adrenal corticosteroid or adrenergic blocking agents upon the outcome of these infections might not be the same. Accordingly, studies were undertaken to investigate the effects of these forms of adjunctive therapy upon the mortality rates of experimental staphylococcal and pneumococcal infections in rabbits. They show that in pneumococcal infection hydrocortisone administered with penicillin prevents death not prevented by penicillin alone, whereas phenoxybenzamine is ineffective in preventing death. In staphylococcal infection, phenoxybenzamine plus methicillin prevents death not prevented by methicillin alone, whereas hydrocortisone is ineffective.
The cytoskeletal protein ezrin regulates EC proliferation and angiogenesis via TNF-α–induced transcriptional repression of cyclin A
Authors: Raj Kishore, Gangjian Qin, Corinne Luedemann, Evelyn Bord, Allison Hanley, Marcy Silver, Mary Gavin, David Goukassain, Douglas W. Losordo
Journal: Journal of Clinical Investigation (2005)

TNF-α modulates EC proliferation and thereby plays a central role in new blood vessel formation in physiologic and pathologic circumstances. TNF-α is known to downregulate cyclin A, a key cell cycle regulatory protein, but little else is known about how TNF-α modulates EC cell cycle and angiogenesis. Using primary ECs, we show that ezrin, previously considered to act primarily as a cytoskeletal protein and in cytoplasmic signaling, is a TNF-α–induced transcriptional repressor. TNF-α exposure leads to Rho kinase–mediated phosphorylation of ezrin, which translocates to the nucleus and binds to cell cycle homology region repressor elements within the cyclin A promoter. Overexpression of dominant-negative ezrin blocks TNF-α–induced modulation of ezrin function and rescues cyclin A expression and EC proliferation. In vivo, blockade of ezrin leads to enhanced transplanted EC proliferation and angiogenesis in a mouse hind limb ischemia model. These observations suggest that TNF-α regulates angiogenesis via Rho kinase induction of a transcriptional repressor function of the cytoskeletal protein ezrin and that ezrin may represent a suitable therapeutic target for processes dependent on EC proliferation.