tbuckley/cabot-search huggingface dataset:
Placing a Lumbar Epidural Catheter
Authors: Alexander Kim, Garrett Sendlewski, Erica Zador, Mandip Kalsi, Lara Zador, Viji Kurup
Journal: New England Journal of Medicine (2018)

A lumbar epidural catheter may be used to induce anesthesia and analgesia. This video presents the indications for and contraindications to the placement of a lumbar epidural catheter, the necessary equipment, the relevant anatomy, and placement technique.
Apport de l'endoscopie digestive haute chez les insuffisants rénaux chroniques: prévalence et étude comparative
Authors: F Aissaoui, A Guediche, A Sabbek, R Baklouti, W Bouhlel, W Ben Mansour, MH Loghmari, L Safer
Journal: Endoscopy (2018)

Les complications digestives au cours de l'insuffisance rénale chronique sont dominées par les lésions de la muqueuse gastroduodénale. Ces anomalies sont classiquement décrites comme de plus en plus fréquentes au fur et à mesure que l'insuffisance rénale évolue.
A Fully Integrated High-Speed Intravascular OFDI-NIRF Structural-Molecular Imaging in vivo With a FDA-Approved Indocyanine Green to Detect Inflamed, Lipid-Rich Atheromata in Coronary Sized Vessels
Authors: Sunki Lee, Min Woo Lee, Han Saem Jo, Sunwon Kim, Jinho Choi, Young-Duk Kim, Sunju Jang, Hyunjin Chung, Dong Joo Oh, Kyeongsoon Park, Wang-Yuhl Oh, Hongki Yoo, Jin Won Kim
Journal: Circulation (2013)

Background: Lipid-rich, inflamed coronary plaques are prone to rupture. The purpose of this study is to in vivo assess lipid-rich, inflamed plaque via a fully integrated, high-speed OFDI (optical f...
High Baseline Levels of Tumor Necrosis Factor Receptor 1 Are Associated With Progression of Kidney Disease in Indigenous Australians With Diabetes: The eGFR Follow-up Study
Authors: Elizabeth L.M. Barr, Federica Barzi, Jaquelyne T. Hughes, George Jerums, Wendy E. Hoy, Kerin O’Dea, Graham R.D. Jones, Paul D. Lawton, Alex D.H. Brown, Mark Thomas, Elif I. Ekinci, Ashim Sinha, Alan Cass, Richard J. MacIsaac, Louise J. Maple-Brown
Journal: Diabetes Care (2018)

OBJECTIVE To examine the association between soluble tumor necrosis factor receptor 1 (sTNFR1) levels and kidney disease progression in Indigenous Australians at high risk of kidney disease. RESEARCH DESIGN AND METHODS This longitudinal observational study examined participants aged ≥18 years recruited from &amp;gt;20 sites across diabetes and/or kidney function strata. Baseline measures included sTNFR1, serum creatinine, urine albumin-to-creatinine ratio (uACR), HbA1c, C-reactive protein (CRP), waist-to-hip ratio, systolic blood pressure, and medical history. Linear regression was used to estimate annual change in estimated glomerular filtration rate (eGFR) for increasing sTNFR1, and Cox proportional hazards were used to estimate the hazard ratio (HR) and 95% CI for developing a combined renal outcome (first of a ≥30% decline in eGFR with a follow-up eGFR &amp;lt;60 mL/min/1.73 m2, progression to renal replacement therapy, or renal death) for increasing sTNFR1. RESULTS Over a median of 3 years, participants with diabetes (n = 194) in the highest compared with the lowest quartile of sTNFR1 experienced significantly greater eGFR decline (−4.22 mL/min/1.73 m2/year [95% CI −7.06 to −1.38]; P = 0.004), independent of baseline age, sex, eGFR, and uACR. The adjusted HR (95% CI) for participants with diabetes per doubling of sTNFR1 for the combined renal outcome (n = 32) was 3.8 (1.1–12.8; P = 0.03). No association between sTNFR1 and either renal outcome was observed for those without diabetes (n = 259). CONCLUSIONS sTNFR1 is associated with greater kidney disease progression independent of albuminuria and eGFR in Indigenous Australians with diabetes. Further research is required to assess whether TNFR1 operates independently of other metabolic factors associated with kidney disease progression.
Abstract 13819: Cancer After Heart Transplantation: Incidence, Risk Factors and Prognosis
Authors: Jan Van Keer, Walter Droogne, Johan Van Cleemput, Gábor Vörös, Filip Rega, Bart Meyns, Stefan Janssens, Johan Vanhaecke
Journal: Circulation (2015)

Introduction: Malignancy is a major cause of morbidity and mortality after heart transplantation. We determined incidence, risk factors and prognosis of cancer after heart transplantation in a large single center cohort with long-term follow-up. Methods: We retrospectively analyzed all patients undergoing heart transplantation at our institution between January 1987 and December 2013. Patients who died within the first month of transplantation were excluded. All remaining patients were followed up until death or December 2014 for development of cancer. Results: Five hundred and forty-one patients were followed up for a mean of 10.7 ± 6.7 years. Cancer was diagnosed in 181 patients, at a mean of 7.7 ± 5.0 years after transplantation. Cumulative incidence of any cancer at 1, 5 and 10 years was 2 %, 14 % and 29 %, respectively. Almost half of all cancers were skin tumors (83 patients), squamous-cell carcinoma (57 patients) being more frequent than basal-cell carcinoma (51 patients). The most frequent non-skin cancer was lung cancer (41 patients), followed by lymphoma (30 patients) and prostate cancer (25 patients). Several patients had more than one cancer. Age at transplantation older than 50 years (HR 3.3, p &lt; 0.001), male gender (HR 2.1, p = 0.001), ischemic etiology for transplantation (HR 1.4, p = 0.02), transplantation era before 2000 (HR 1.4, p=0.04), azathioprine versus mycophenolate (HR 1.4, p= 0.04) and cyclosporine versus tacrolimus as initial immunosuppression (HR 1.7, p = 0.005) were significant risk factors for post-transplant malignancy in a univariate Cox proportional hazards model. Of these, age at transplantation and male gender were independent risk factors in multivariate analysis. Median patient survival after diagnosis of cancer was 2.9 years for patients with non-skin cancer, versus 13.1 years for patients with only skin cancer (p &lt; 0.001). Conclusions: This study highlights the importance of cancer after heart transplantation. Older recipient age at transplantation and male gender were independent risk factors in multivariate analysis. Strategies to individualize immunosuppression according to the patient’s needs could potentially help reduce this important cause of morbidity and mortality after heart transplantation.
High-grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements with diffuse large B-cell lymphoma morphology
Authors: David W. Scott, Rebecca L. King, Annette M. Staiger, Susana Ben-Neriah, Aixiang Jiang, Heike Horn, Anja Mottok, Pedro Farinha, Graham W. Slack, Daisuke Ennishi, Norbert Schmitz, Michael Pfreundschuh, Grzegorz S. Nowakowski, Brad S. Kahl, Joseph M. Connors, Randy D. Gascoyne, German Ott, William R. Macon, Andreas Rosenwald
Journal: Blood (2018)
Abstract 9218: Troponin Elevation, Ischemic Electrocardiographic Changes and Prognosis after a Postoperative Myocardial Infarction
Authors: Santiago Garcia, Nicholas Marston, Jorge Brenes, Selcuk Adabag, Demetris Yannopoulos, Michael Kuskowski, Edward O McFalls
Journal: Circulation (2011)

Background: In the postoperative period the majority of myocardial infarctions are clinically silent and its diagnosis relies heavily on a biomarker elevation. Although an elevated troponin level following vascular surgery is associated with a poor long-term outcome, the utility of abnormal EKG changes as additional prognostic information is unclear. Methods: Single center registry of 435 patients undergoing high-risk vascular surgery at the Minneapolis VA Medical Center between January 2005 and December 2009. Blood was obtained in all patients in the first two days following vascular surgery and the troponin I levels were measured by the Dade Behring Dimension Analyzer. Those values that exceeded the URL were categorized as either LOW (+) (≥ the URL but &lt; 3 times the URL) or HIGH (+) (≥ 3 times the URL). Electrocardiograms obtained before the operation and within the first 3 postoperative days were reviewed by 2 independent cardiologists and classified as ischemic (ST-segment depression, ≥ 2 mm T-wave inversion) or non-ischemic. Long-term survival was retrieved using BIRLS. Results: The mean age of the population was 68±8 and the most common vascular problem was an expanding abdominal aneurysm (49%). Eighty-one (18.6%) patients were classified as HIGH (+) and 104 (24%) as LOW (+) with regard to troponin values. Thirty-one (7%) patients had evidence of myocardial ischemia on electrocardiography. An increase in mortality was seen with incremental troponin values (p &lt;0.001). However, the presence of electrocardiographic changes did not provide additional prognostic information to that conveyed by troponins in any category (p: 0.91, Figure). Conclusions: The requirement for an electrocardiographic correlate of myocardial ischemia to define a myocardial infarction appears to be insensitive in the post-operative period. Further, in the presence of a troponin elevation the incremental prognostic value of an ischemic ECG is minimal.
Biomarker-Guided Versus Guideline-Based Treatment of Patients With Heart Failure
Authors: Wouter Ouwerkerk, Aeilko H. Zwinderman, Leong L. Ng, Biniyam Demissei, Hans L. Hillege, Faiez Zannad, Dirk J. van Veldhuisen, Nilesh J. Samani, Piotr Ponikowski, Marco Metra, Jozine M. ter Maaten, Chim C. Lang, Pim van der Harst, Gerasimos Filippatos, Kenneth Dickstein, John G. Cleland, Stefan D. Anker, Adriaan A. Voors
Journal: Journal of the American College of Cardiology (2018)
Facteurs prédictifs d'échec et complications de la polypectomie colique endoscopique: Expérience d'un centre tunisien
Authors: K Agar, M Medhioub, S Jardak, L Hamzaoui, K Amal, MM Azouz
Journal: Endoscopy (2018)

Les polypes coliques présentent une pathologie bénigne fréquente. La polypectomieendoscopique est une technique simple et efficace qui peut se solder de complicationsparfois graves pouvant nécessiter la chirurgie. Le but de ce travail est de décrire l'incidence de polypes coliques, les facteurs d'échec de lapolypectomie et ses complications.
Eosinophil-Derived Exosomes Contribute to Asthma Remodeling by Activating Structural Lung Cells
Authors: Beatriz Sastre, Jose A. Cañas, Jose M. Rodrigo-Muñoz, Mar Fernandez-Nieto, Pilar Barranco, Santiago Quirce, Joaquin Sastre, Victoria Del Pozo
Journal: Journal of Allergy and Clinical Immunology (2018)
Early Resuscitation for Adults With Sepsis in a Low-income Country—Reply
Authors: Matthew W. Semler, Ben Andrews, Gordon R. Bernard
Journal: JAMA (2018)

In Reply Drs Nedel and Deutschendorf highlight 2 key considerations for the interpretation of our trial and the management of patients with sepsis across settings: (1) timing of antibiotic administration and (2) volume of intravenous fluid.
Oncogenic JAK2 <sup>V617F</sup> causes PD-L1 expression, mediating immune escape in myeloproliferative neoplasms
Authors: Alessandro Prestipino, Alica J. Emhardt, Konrad Aumann, David O’Sullivan, Sivahari P. Gorantla, Sandra Duquesne, Wolfgang Melchinger, Lukas Braun, Slavica Vuckovic, Melanie Boerries, Hauke Busch, Sebastian Halbach, Sandra Pennisi, Teresa Poggio, Petya Apostolova, Pia Veratti, Michael Hettich, Gabriele Niedermann, Mark Bartholomä, Khalid Shoumariyeh, Jonas S. Jutzi, Julius Wehrle, Christine Dierks, Heiko Becker, Annette Schmitt-Graeff, Marie Follo, Dietmar Pfeifer, Jan Rohr, Sebastian Fuchs, Stephan Ehl, Frederike A. Hartl, Susana Minguet, Cornelius Miething, Florian H. Heidel, Nicolaus Kröger, Ioanna Triviai, Tilman Brummer, Jürgen Finke, Anna L. Illert, Eliana Ruggiero, Chiara Bonini, Justus Duyster, Heike L. Pahl, Steven W. Lane, Geoffrey R. Hill, Bruce R. Blazar, Nikolas von Bubnoff, Erika L. Pearce, Robert Zeiser
Journal: Science Translational Medicine (2018)

Oncogenic JAK mutation sensitizes myeloproliferative neoplasms to immune checkpoint inhibition.
The expression of TRPV1 and innate Th2-cytokines in patients with chronic rhinosinusitis and asthma
Authors: Joo-Hee Kim, Joong-Seob Lee, Young-Suk Jang, Ji Young Park, Yong Il Hwang, Sunghoon Park, Seung-Hun Jang, Ki-Suck Jung
Journal: Journal of Allergy and Clinical Immunology (2018)
Single-cell RNAseq reveals seven classes of colonic sensory neuron
Authors: James R F Hockley, Toni S Taylor, Gerard Callejo, Anna L Wilbrey, Alex Gutteridge, Karsten Bach, Wendy J Winchester, David C Bulmer, Gordon McMurray, Ewan St John Smith
Journal: Gut (2018)

Objective Integration of nutritional, microbial and inflammatory events along the gut-brain axis can alter bowel physiology and organism behaviour. Colonic sensory neurons activate reflex pathways and give rise to conscious sensation, but the diversity and division of function within these neurons is poorly understood. The identification of signalling pathways contributing to visceral sensation is constrained by a paucity of molecular markers. Here we address this by comprehensive transcriptomic profiling and unsupervised clustering of individual mouse colonic sensory neurons. Design Unbiased single-cell RNA-sequencing was performed on retrogradely traced mouse colonic sensory neurons isolated from both thoracolumbar (TL) and lumbosacral (LS) dorsal root ganglia associated with lumbar splanchnic and pelvic spinal pathways, respectively. Identified neuronal subtypes were validated by single-cell qRT-PCR, immunohistochemistry (IHC) and Ca 2+ -imaging. Results Transcriptomic profiling and unsupervised clustering of 314 colonic sensory neurons revealed seven neuronal subtypes. Of these, five neuronal subtypes accounted for 99% of TL neurons, with LS neurons almost exclusively populating the remaining two subtypes. We identify and classify neurons based on novel subtype-specific marker genes using single-cell qRT-PCR and IHC to validate subtypes derived from RNA-sequencing. Lastly, functional Ca 2+ -imaging was conducted on colonic sensory neurons to demonstrate subtype-selective differential agonist activation. Conclusions We identify seven subtypes of colonic sensory neurons using unbiased single-cell RNA-sequencing and confirm translation of patterning to protein expression, describing sensory diversity encompassing all modalities of colonic neuronal sensitivity. These results provide a pathway to molecular interrogation of colonic sensory innervation in health and disease, together with identifying novel targets for drug development.
The Immune Response to<i>Mycobacterium tuberculosis</i>in HIV-1-Coinfected Persons
Authors: Hanif Esmail, Catherine Riou, Elsa du Bruyn, Rachel Pei-Jen Lai, Yolande X.R. Harley, Graeme Meintjes, Katalin A. Wilkinson, Robert J. Wilkinson
Journal: Annual Review of Immunology (2018)

Globally, about 36.7 million people were living with HIV infection at the end of 2015. The most frequent infection co-occurring with HIV-1 is Mycobacterium tuberculosis—374,000 deaths per annum are attributable to HIV-tuberculosis, 75% of those occurring in Africa. HIV-1 infection increases the risk of tuberculosis by a factor of up to 26 and alters its clinical presentation, complicates diagnosis and treatment, and worsens outcome. Although HIV-1-induced depletion of CD4 + T cells underlies all these effects, more widespread immune deficits also contribute to susceptibility and pathogenesis. These defects present a challenge to understand and ameliorate, but also an opportunity to learn and optimize mechanisms that normally protect people against tuberculosis. The most effective means to prevent and ameliorate tuberculosis in HIV-1-infected people is antiretroviral therapy, but this may be complicated by pathological immune deterioration that in turn requires more effective host-directed anti-inflammatory therapies to be derived.
OBSERVATOIRE FRANCAIS DE LA RESECTION TRANSPARIETALE PER ENDOSCOPIQUE PAR LE SYSTEME «FTRD» (Full Thickness Resection Device)
Authors: Y Le Baleur, S Leblanc, M Pioche, J Jacques, JB Chevaux, G Vanbiervliet, V Lepilliez, E Coron, S Koch, K Aziz, J Privat, E Kull, G Rahmi
Journal: Endoscopy (2018)

La resection transparietale per endoscopique par le systeme «FTRD OVESCO» est une technique recente inovante permettant la prise en charge de lésions coliques en echec des techniques de résection muqueuse ou sous muqueuse traitées auparavant par resection colique segmentaire.
Respiratory syncytial virus prevention and asthma in healthy preterm infants: a randomised controlled trial
Authors: Nienke M Scheltema, Elisabeth E Nibbelke, Juliëtte Pouw, Maarten O Blanken, Maroeska M Rovers, Christiana A Naaktgeboren, Natalie I Mazur, Joanne G Wildenbeest, Cornelis K van der Ent, Louis J Bont
Journal: The Lancet Respiratory Medicine (2018)
Effect of lung deflation with indacaterol plus glycopyrronium on ventricular filling in patients with hyperinflation and COPD (CLAIM): a double-blind, randomised, crossover, placebo-controlled, single-centre trial
Authors: Jens M Hohlfeld, Jens Vogel-Claussen, Heike Biller, Dominik Berliner, Korbinian Berschneider, Hanns-Christian Tillmann, Simone Hiltl, Johann Bauersachs, Tobias Welte
Journal: The Lancet Respiratory Medicine (2018)
Rapamycin, mTOR inhibitor, a potent inhibitor for the cell growth and proliferation by p21- dependent mitotic arrest in human gastric cancers
Authors: Ji-Young Shin, Teak-Chin Cheong, Seok-Jun Kim, Kyung-Hee Chun
Journal: Cancer Research (2008)

1467   Although the mortality decreased by early diagnosis, the only available treatment in gastric cancer is surgical resection. Therefore, improvement of curable treatment is needed in gastric cancer patients. One of the promising approaches is the development of novel therapeutic drugs that specifically target molecular regulators of cancer growth and proliferation. Interestingly, the mammalian target of rapamycin (mTOR), a downstream effecter of the PI3K/Akt signaling pathway plays the important roles to mediate cell survival and proliferation, and one of potent mTOR inhibitor, rapamycin has been undergoing clinical trials. However, the exact role of rapamycin in mediating growth inhibitory effects in gastric cancers is not yet clear.In this study, it was demonstrated mTOR inhibition by rapamycin on gastric cancer proliferation with focus on its cell cycle arrest activity. After treatment with rapamycin in 6 gastric cancer cell lines, AGS, SNU216, and SNU638 cells were most sensitive by dose- and time- dependent manner. To elucidate the mechanism by rapamycin in gastric cancers, cell cycle arrest was detected by PI staining. AGS cells showed G2/M arrest after 1 to 3 day treatment with rapamycin. Rapamycin also changed the expression levels of cell cycle related proteins. Interestingly, p21 expression increased and sustained until 48 hr after treatment in AGS. The protein expression of p27 and p53 was not detected in change. Cdc2 and cyclin B1 increased and cdc25c decreased after treatment. Increasing levels of polo like kinase 1 (PLK1) and aurora A, and phosphorylated histone H3, which was known mitotic arrest index, also were detected after rapamycin treatment. It supposed that rapamycin arrests cell cycle in late G2 and/or in mitotic phase. We confirmed that mitotic arrest by rapamycin in AGS cells, mitotic arresting shaped cells increased almost 25% compared to control, and phosphorylated histone H3 staining cells were found in rapamycin treated or in nocodazole treated gastric cancer cells, but not in control cells. Finally, it was detected by confocal microscope that rapamycin treatment prevented centrosome maturation and mitotic spindle bypolarity, and resulted in accumulation of aberrant prometaphase cells. In conclusion, it was demonstrated that rapamycin inhibits gastric cancer cell growth by mitotic arrest to accumulate abnormal prometaphase cells. Our results suggest that rapamycin, clinically useful mTOR inhibitor is promising in the treatment of gastric cancer and further clinical studies are needed to validate the therapeutic potential of rapamycin in gastric cancer patients.
Drug resistance in a sarcoma xenograft model is overcome by schedule-dependent proteasome inhibition using Velcade™ (Bortezomib, formerly PS-341).
Authors: David Ljungman, John Flannery, Rong Liu, Lijun Xia, Julian Adams, Peter Elliott, Margaret Read, Oscar Kashala, James C. Cusack
Journal: Cancer Research (2004)

2135  Doxorubicin is an effective anti-breast cancer drug currently used as a first-line drug for patients with metastatic breast cancer. We have shown previously that the activity of PI3-K/Akt conferred an increased resistance on breast cancer cells to doxorubicin-induced toxicity. We furthered this study on modulation of doxorubicin toxicity by PI3-K/Akt in a panel of 9 breast cancer cell lines. Within 24-48 hours after exposure of the cells to doxorubicin, there was a transient drug dose-dependent (up to 1 μM) increase in the levels of phosphorylated Akt in MCF7, MDA468, MDA361 and T47D cells. In contrast, no such change was found in MDA157 and BT474 cells; and a drug dose-dependent decrease in the levels of phosphorylated Akt was found in SKBR3, MDA453 and MDA231 cells. This doxorubicin-mediated phosphorylation of Akt is correlated with increased Akt kinase activity, shown by in vitro kinase assays on two well-documented Akt substrates, Bad and GSK3, and by an increased nuclear translocation of Akt following the treatment. The doxorubicin-mediated Akt activation is mediated by the PI3-K because it was prevented in the presence of LY294002 (a PI3-K-specific inhibitor). Forced overexpression of HER2 or FAK in MCF7 cells, each of which elevated basal activity of PI3-K/Akt, led to an increased potential of Akt phosphorylation by doxorubicin. Treatment of MCF7HE2 cells with Herceptin (an anti-HER2 mAb) or expression of FRNK (a FAK dominant-negative vector) in MCF7 cells reduced the potential of doxorubicin-mediated Akt phosphorylation. Compared with regular culture medium, there was no change in the level of doxorubicin-mediated Akt phosphorylation of MCF7 cells cultured in estrogen-depleted medium or in medium supplemented with an estrogen antagonist (ICI 182,780), indicating a lack of hormone-mediated signaling in the event. Further study was conducted in SKBR3 cells, which in contrast showed a reduced phosphorylation of Akt following doxorubicin treatment. SKBR3 cells express high level of HER2 but have no detectable level of HER3. Forced expression of HER3 in SKBR3 cells prevented doxorubicin-mediated reduction in the level of phosphorylated Akt, indicating an important role of HER2/HER3 heterodimerization in determining cellular responses to doxorubicin treatment. Our data suggest that breast cancer cells may utilize HER (or FAK)/PI3-K/Akt pathways as a mechanism of resistance to doxorubicin-induced toxicity, and thus justify targeting PI3-K/Akt for enhancing the efficacy of doxorubicin.
Similar survival of patients with multiple versus single primary melanomas based on Utah Surveillance, Epidemiology, and End Results data (1973-2011)
Authors: Douglas Grossman, James M. Farnham, John Hyngstrom, Marki E. Klapperich, Aaron M. Secrest, Sarah Empey, Glen M. Bowen, David Wada, Robert H.I. Andtbacka, Kenneth Grossmann, Tawnya L. Bowles, Lisa A. Cannon-Albright
Journal: Journal of the American Academy of Dermatology (2018)
Novel Adapter Chimeric Antigen Receptor (aCAR) T Cells for Temporally Controllable Targeting of Single and Multiple Tumor Antigens
Authors: Christian M. Seitz, Patrick Schlegel, Jana Hau, Ann-Christin Krahl, Sarah Schroeder, Giulia Bender, Selina Reiter, Sabine Schleicher, Karin Schilbach, Martin Ebinger, Philipp Knopf, Manfred Kneilling, Bernd J. Pichler, Joerg Mittelstaet, Dominik Lock, Andrew Kaiser, Peter J. Lang, Rupert Handgretinger
Journal: Blood (2017)