tbuckley/cabot-search huggingface dataset:
Predictive and prognostic factors in patients with blood-culture-positive community-acquired pneumococcal pneumonia
Authors: Rosanel Amaro, Adamantia Liapikou, Catia Cilloniz, Albert Gabarrus, Francesc Marco, Jacobo Sellares, Eva Polverino, Javier Garau, Miquel Ferrer, Daniel M. Musher, Antoni Torres
Journal: European Respiratory Journal (2016)

In patients with pneumococcal community-acquired pneumonia (CAP), the risk factors for bacteraemia and its impact on outcomes are not fully elucidated. We aimed to compare characteristics of patients with blood-culture-positive versus blood-culture-negative pneumococcal CAP, and to characterise bacteraemic serotypes.We describe a prospective, observational study on nonimmunocompromised patients with pneumococcal CAP, from 1996 to 2013. We define severe pneumonia according to American Thoracic Society/Infectious Diseases Society of America guidelines.Of a total of 917 patients with pneumococcal CAP, 362 had blood-culture-positive pneumococcal pneumonia (BCPPP; 39%). High C-reactive protein (CRP) (≥20 mg·dL(-1)) (odds ratio (OR) 2.36, 95% CI 1.45-3.85), pleural effusion (OR 2.03, 95% CI 1.13-3.65) and multilobar involvement (OR 1.69, 95% CI 1.02-2.79) were independently associated with bacteraemic CAP, while nursing home resident (OR 0.12, 95% CI 0.01-1.00) was found as a protective factor. Despite the clinical differences, BCPPP showed similar outcomes to blood-culture-negative pneumococcal pneumonia (BCNPP). 14% of the serotypes (period 2006-2013) causing bacteraemia are included in pneumococcal conjugate vaccine PVC7, 74% in pneumococcal conjugate vaccine PVC13 and 83% in pneumococcal polysaccharide vaccine PPSV23.Pleural effusion, a high level of CRP and multilobar involvement predicted an increased risk of BCPPP. Although BCPPP patients were more severely ill at admission, mortality was not significantly greater than in BCNPP patients.
Total Plasma Protein Values in Premature and Mature Newborn Infants: A Preliminary Report
Authors: M FELBO, K H KRISTENSEN, J C MELCHIOR
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
PIK3CA mutations are associated with reduced pathological complete response rates in primary HER2-positive breast cancer: pooled analysis of 967 patients from five prospective trials investigating lapatinib and trastuzumab
Authors: S. Loibl, I. Majewski, V. Guarneri, V. Nekljudova, E. Holmes, E. Bria, C. Denkert, C. Schem, C. Sotiriou, S. Loi, M. Untch, P. Conte, R. Bernards, M. Piccart, G. von Minckwitz, J. Baselga
Journal: Annals of Oncology (2016)
The role of ADAMTS13 in acute myocardial infarction: cause or consequence?
Authors: Elise S. Eerenberg, Paul F.A. Teunissen, Bert-Jan van den Born, Joost C.M. Meijers, Maurits R. Hollander, Matthijs Jansen, Ruben Tijssen, Jeroen A.M. Beliën, Peter M. van de Ven, Mohamed F. Aly, Otto Kamp, Hans W. Niessen, Pieter Willem Kamphuisen, Marcel Levi, Niels van Royen
Journal: Cardiovascular Research (2016)

ADAMTS13, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13, is a metalloprotease that cleaves von Willebrand factor (VWF). There is considerable evidence that VWF levels increase and ADAMTS13 levels decrease in ST-elevation myocardial infarction (STEMI) patients. It is unclear whether this contributes to no reflow, infarct size, and intramyocardial haemorrhage (IMH). We aimed to determine the role of ADAMTS13 in STEMI patients and to investigate the benefits of recombinant ADAMTS13 (rADAMTS13) in a porcine model of myocardial ischaemia-reperfusion. In 49 consecutive percutaneous coronary intervention (PCI)-treated STEMI patients, blood samples were collected directly after through 7 days following PCI. Cardiac magnetic resonance was performed 4–6 days after PCI to determine infarct size and IMH. In 23 Yorkshire swine, the circumflex coronary artery was occluded for 75 min. rADAMTS13 or vehicle was administered intracoronary following reperfusion. Myocardial injury and infarct characteristics were assessed using cardiac enzymes, ECG, and histopathology. In patients with IMH, VWF activity and VWF antigen were significantly elevated directly after PCI and for all subsequent measurements, and ADAMTS13 activity significantly decreased at 4 and 7 days following PCI, in comparison with patients without IMH. VWF activity and ADAMTS13 activity were not related to infarct size. In rADAMTS13-treated animals, no differences in infarct size, IMH, or formation of microthrombi were witnessed compared with controls. No correlation was found between VWF/ADAMTS13 and infarct size in patients. However, patients suffering from IMH had significantly higher VWF activity and lower ADAMTS13 activity. Intracoronary administration of rADAMTS13 did not decrease infarct size or IMH in a porcine model of myocardial ischaemia-reperfusion. These data dispute the imbalance in ADAMTS13 and VWF as the cause of no reflow.
Newer drugs for refractory and relapsed multiple myeloma are effective but costly, review finds
Authors: Michael McCarthy
Journal: BMJ (2016)

Several newer generation drugs used to treat relapsed and refractory multiple myeloma offer slightly improved health outcomes but would need to be substantially discounted to be cost effective, a review by an independent non-profit US institute has concluded.1

The Institute for Clinical and Economic Review conducts clinical and cost effectiveness analyses of treatments, tests, and procedures to guide health policy. It reviewed treatments used as second line or later in adults with multiple myeloma who were relapsing after or not responding to treatment and were not currently on maintenance treatment or being considered for a stem cell transplant.

The reviewers noted that the introduction of proteasome inhibitor and immunomodulatory drug therapy has led to an increase in survival of patients with newly diagnosed multiple myeloma …
Prognostic Impact of Adverse Karyotype and Treatment in Patients with Myelodysplastic Syndrome and Acute Myeloid Leukemia
Authors: Virginia Escamilla, Jose Falantes, Cristina Calderon, Jose Gonzalez Campos, Rosario Morales Camacho, Isabel Montero, Rocio Parody, Ricardo Bernal, Ildefonso Espigado, Jose A Perez-Simón
Journal: Blood (2015)
Frequent mutations in acetylation and ubiquitination sites suggest novel driver mechanisms of cancer
Authors: Soumil Narayan, Gary D. Bader, Jüri Reimand
Journal: Genome Medicine (2016)

Discovery of cancer drivers is a major goal of cancer research. Driver genes and pathways are often predicted using mutation frequency, assuming that statistically significant recurrence of specific somatic mutations across independent samples indicates their importance in cancer. However, many mutations, including known cancer drivers, are not observed at high frequency. Fortunately, abundant information is available about functional "active sites" in proteins that can be integrated with mutations to predict cancer driver genes, even based on low frequency mutations. Further, considering active site information predicts detailed biochemical mechanisms impacted by the mutations. Post-translational modifications (PTMs) are active sites that are regulatory switches in proteins and pathways. We analyzed acetylation and ubiquitination, two important PTM types often involved in chromatin organization and protein degradation, to find proteins that are significantly affected by tumor somatic mutations.We performed computational analyses of acetylation and ubiquitination sites in a pan-cancer dataset of 3200 tumor samples from The Cancer Genome Atlas (TCGA). These analyses were targeted at different levels of biological organization including individual genes, pathway annotated gene sets, and protein-protein interaction networks.Acetylation and ubiquitination site mutations are enriched in cancer with significantly stronger evolutionary conservation and accumulation in protein domains. Gene-focused analysis with the ActiveDriver method reveals significant co-occurrences of acetylation and ubiquitination PTMs and mutation hotspots in known oncoproteins (TP53, AKT1, IDH1) and highlights candidate cancer driver genes with PTM-related mechanisms (e.g. several histone proteins and the splicing factor SF3B1). Pathway analysis shows that PTM mutations in acetylation and ubiquitination sites accumulate in cancer-related processes such as cell cycle, apoptosis, chromatin regulation, and metabolism. Integrated mutation analysis of clinical information and protein interaction networks suggests that many PTM-specific mutations associate with decreased patient survival.Mutation analysis of acetylation and ubiquitination PTM sites reveals their importance in cancer. As PTM networks are increasingly mapped and related enzymes are often druggable, deeper investigation of specific associated mutations may lead to the discovery of treatment-relevant cellular mechanisms.
Wireless Capsule Endoscopy in the Evaluation of Patients with Suspected or Known Crohn’s Disease
Authors: K. A. Papadakis, S. K. Lo, Z. Fireman, S. Hollerbach
Journal: Endoscopy (2005)

Wireless capsule endoscopy (WCE) is a novel, noninvasive technique that can detect obscure mucosal lesions along the entire length of the small bowel. Early systematic studies of WCE in patients with Crohn's disease suggest that this technique is a very effective diagnostic tool in patients with a high clinical probability of having the disease, but whose classic endoscopic and radiographic studies have been negative. It is likely that WCE will replace radiographic studies in this setting in the near future. A careful clinical history must be taken and imaging studies of the small bowel are mandatory prior to WCE in patients with inflammatory bowel disease, in order to avoid the rare complication of capsule retention in intestinal strictures, although the use of the "patency capsule" will probably greatly facilitate the exclusion of relevant strictures in the near future.
Gene Therapy Using a Self-Inactivating Lentiviral Vector Improves Clinical and Laboratory Manifestations of Wiskott-Aldrich Syndrome
Authors: Julia I Chu, Lauren A Henderson, Myriam Armant, Frances Male, Colleen H Dansereau, Brenda MacKinnon, Christopher J Burke, Matthew E Cavanaugh, Wendy B. London, Isil B Barlan, Ahmet Özen, Safa Baris, Elif Karakoc-Aydiner, Ayça Kiykim, Imelda Celine Hanson, Jenny M. Despotovic, Akihiko Saitoh, Takayuki Takachi, Kohsuke Imai, Alejandra King, Silvia Arredondo, Jerome Ritz, Frederic D Bushman, Anne Galy, Luigi Daniele Notarangelo, David A. Williams, Sung-Yun Pai
Journal: Blood (2015)
Medical-School Education, 1975–1979
Authors: Ludwig W. Eichna
Journal: New England Journal of Medicine (1980)

FOR a number of years before retirement in July 1974 from the chairmanship of the Department of Medicine, State University of New York, Downstate Medical Center, Brooklyn, I was increasingly dissatisfied with the course and results of medical-school education. Where lay the problems? It seemed reasonable that a medical educator who was aware of the end-product of medical-school education and who had long had contact with patients might contribute useful information by personally undergoing the medical-school process. The dean, faculty, and students were apprised of this intent. All agreed to let me give it a try. Accordingly, in September 1975, . . .
PAK1 Is a Novel Therapeutic Target in Tyrosine Kinase Inhibitor–Resistant Lung Adenocarcinoma Activated by the PI3K/AKT Signaling Regardless of <i>EGFR</i> Mutation
Authors: De-Wei Wu, Tzu-Chin Wu, Chih-Yi Chen, Huei Lee
Journal: Clinical Cancer Research (2016)

EGFR mutation as a biomarker has documented that EGFR-mutant patients will derive clinical benefit from tyrosine kinase inhibitor (TKI) treatment. Unfortunately, most patients show TKI resistance and tumor recurrence after therapy. Therefore, we expected that an adjuvant biomarker other than EGFR mutation is needed for predicting TKI resistance.Molecular manipulations were performed to verify whether TKI resistance mediated by p21-activated kinase (PAK1) could be through increasing Mcl-1 protein stability via the PI3K/AKT/C/EBP-β/miR-145 cascade. Xenograft mouse models were used to confirm the mechanistic action of PAK1 on TKI resistance. Forty-six tumor tissues from patients with lung adenocarcinoma who received TKI therapy were collected to evaluate PAK1 and E-cadherin mRNA expressions by real-time PCR. The association of PAK1 and E-cadherin mRNA expressions with tumor response to TKI treatment and outcomes was evaluated.We demonstrate that PAK1 confers TKI resistance in EGFR-mutant cells as well as in EGFR-wild-type cells. Mechanistically, the positive feedback loop of PAK1/PI3K/AKT/C/EBP-β/miR-145 cascades persistently activates the PI3K/AKT signaling pathway to protect Mcl-1 degradation by Fbw7, which results, in turn, in TKI resistance and cell invasion via epithelial-to-mesenchymal transition due to a decrease in E-cadherin expression. The mechanism underlying the cell model is further confirmed in xenograft tumors. Among patients, high-PAK1 or low-E-cadherin tumors more commonly exhibited an unfavorable response to TKI and poorer outcome compared with low-PAK1 or low-E-cadherin tumors.The combination of TKI with AKT inhibitor might confer TKI sensitivity and in turn improve outcomes in patients with lung adenocarcinoma who harbored high PAK1 mRNA-expressing tumors. Clin Cancer Res; 22(21); 5370-82. ©2016 AACR.
Hepatocellular carcinoma repression by TNFα‐mediated synergistic lethal effect of mitosis defect‐induced senescence and cell death sensitization
Authors: Dan Li, Jing Fu, Min Du, Haibin Zhang, Lu Li, Jin Cen, Weiyun Li, Xiaotao Chen, Yunfei Lin, Edward M. Conway, Eli Pikarsky, Hongyan Wang, Guoyu Pan, Yuan Ji, Hong‐Yang Wang, Lijian Hui
Journal: Hepatology (2016)

Hepatocellular carcinoma (HCC) is a cancer lacking effective therapies. Several measures have been proposed to treat HCCs, such as senescence induction, mitotic inhibition, and cell death promotion. However, data from other cancers suggest that single use of these approaches may not be effective. Here, by genetic targeting of Survivin, an inhibitor of apoptosis protein (IAP) that plays dual roles in mitosis and cell survival, we identified a tumor necrosis factor alpha (TNFα)-mediated synergistic lethal effect between senescence and apoptosis sensitization in malignant HCCs. Survivin deficiency results in mitosis defect-associated senescence in HCC cells, which triggers local inflammation and increased TNFα. Survivin inactivation also sensitizes HCC cells to TNFα-triggered cell death, which leads to marked HCC regression. Based on these findings, we designed a combination treatment using mitosis inhibitor and proapoptosis compounds. This treatment recapitulates the therapeutic effect of Survivin deletion and effectively eliminates HCCs, thus representing a potential strategy for HCC therapy.Survivin ablation dramatically suppresses human and mouse HCCs by triggering senescence-associated TNFα and sensitizing HCC cells to TNFα-induced cell death. Combined use of mitotic inhibitor and second mitochondrial-derived activator of caspases mimetic can induce senescence-associated TNFα and enhance TNFα-induced cell death and synergistically eliminate HCC. (Hepatology 2016;64:1105-1120).
Identical point mutations of PMP–22 in Trembler–J mouse and Charcot–Marie–Tooth disease type 1A
Authors: Linda J. Valentijn, Frank Baas, Ruud A. Wolterman, Jessica E. Hoogendijk, Norbert H.A. van den Bosch, Ina Zorn, Anneke A.W.M. Gabreëls-Festen, Marianne de Visser, Pieter A. Bolhuis
Journal: Nature Genetics (1992)
Abstract 1562: Endothelial Progenitor Cell Dysfunction in Morbid Obese is Reversible After Rapid and Intense Weight Loss Despite Maintenance of Increased Body Mass Index
Authors: Paulo F Leite, Claudia R Andrade, Luis A Cesar, Protasio L Da Luz, Santa Poppe, Silmara R Coimbra, Victor Debbas, Francisco R Laurindo
Journal: Circulation (2009)
An Address on EUGENICS--AND THE DOCTOR
Authors: L. Horder
Journal: BMJ (1933)

rMETIL BJOUsR 157 aims first of all at improving upon natural selection An Address by introducing control over the reproduction of unfit types, such as the mentally deficient, and by' encou ON raginog fertility among types possessed of qualities EUGENICS-AND THE DOCTOR* that are above the average.There is therefore a dua' -BY purpose in eugenics: it is negative in its attitude towards the unfit, it is positive in its attitude towards the fit.LORD HORDER, K.C.V.O., M.D., F.R.C.P
The disunity of cultural group selection
Authors: Olivier Morin
Journal: Behavioral and Brain Sciences (2016)

Abstract I argue that demographic selection, migration, and cultural diffusion, three mechanisms of institutional change, have little in common. Two of these lack the key features associated with group selection: they do not present us with group-level selection pressures counteracting individual-level ones, need not produce behavioral altruism, and do not require competition between groups whose members cooperate preferentially with one another. Cultural norms vary, change, and influence cooperation; but that is not group selection.
Networking Our Way to Better Ecosystem Service Provision
Authors: David Bohan, Dries Landuyt, Athen Ma, Sarina Macfadyen, Vincent V. Martinet, Francois Massol, Greg Mcinerny, Jose M. Montoya, Christian Mulder, Unai Pascual, Michael J O Pocock, Piran White, Sandrine Blanchemanche, Michael Bonkowski, Vincent V. Bretagnolle, Christer Bronmark, Lynn Dicks, Alex Dumbrell, Nico Eisenhauer, Nikolai Friberg, Mark O Gessner, Richard Gill, Clare Gray, Alison Haughton, Sébastien Ibanez, John Jensen, Erik Jeppesen, Jukka Jokela, Gerard Lacroix, Christian Lannou, Sandra Lavorel, Jean-François Le Galliard, Francoise Lescourret, Shanlin Liu, Nicolas Loeuille, Orla Mclaughlin, Stephen H. Muggleton, Josep Penuelas, Theodora Petanidou, Sandrine Petit, Francesco Pomati, Dave Raffaelli, Jes Rasmussen, Alan Raybould, Xavier Reboud, Guy Richard, Christoph Scherber, Stefan Scheu, William J Sutherland, Alireza Tamaddoni-Nezhad, J.F. ter Braak Cajo, Mette M. Termansen, Murray  S. A. Thompson, Teja Tscharntke, Corinne C. Vacher, Harm van Der Geest, Winfried Voigt, J Arie Vonk, Xin Zhou, Guy Woodward
Journal: Trends in Ecology & Evolution (2016)
Work of the Clinical Psychologist in General Practice: Preliminary Communication
Authors: Richard France, Meredith Robson
Journal: Journal of the Royal Society of Medicine (1982)

A randomized, controlled trial to assess the value of a health centre-based clinical psychology service is described. Outcome is measured by means of (1) psychosocial rating scales; (2) drug costs; and (3) the costs of relevant hospital referrals. At the end of the first year, the six general practitioners had admitted 239 patients to the trial and of these 81 had been followed up for 34 weeks after entry. This preliminary report reviews the data obtained from these patients. The main finding is a tendency, which reaches statistical significance at some points, for those patients with access to a clinical psychologist to improve more rapidly on the psychosocial measures than the controls.
Sprouty 2: a novel attenuator of B-cell receptor and MAPK-Erk signaling in CLL
Authors: Ashima Shukla, Karan Rai, Vipul Shukla, Nagendra K. Chaturvedi, R. Gregory Bociek, Samuel J. Pirruccello, Hamid Band, Runqing Lu, Shantaram S. Joshi
Journal: Blood (2016)
Antibodies for Rous Sarcoma Virus (Bryan) in Fowl, Animal, and Human Populations of East Africa. II. Antibodies in Domestic Chickens, Wildfowl, Primates, and Man in Kenya, and Antibodies for Burkitt Lymphoma Cells in Man&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Herbert R. Morgan, M.D.
Journal: JNCI Journal of the National Cancer Institute (1967)

Antibodies for Bryan Rous sarcoma virus indicating infection with a member or members of group A avian sarcoma leukosis viruses were found in sera of game fowl, including wild ducks, francolins, guinea fowl, bustards, and ostriches, in three areas of Kenya (Lake Naivasha, Makindu, and Selengai). Antibodies For group A viruses were also common in sera of domestic chickens, whether maintained ona large, commercial farm or in small flocks in native villages. Infection with these agents could apparently maintain itself in game fowl with different social habits (guinea fowl vs. bustards) and contact between game fowl and, domestic chickens did not seem essential to the persistence of infection in either group. Sera obtained from domesticated game fowl raised in the United States were all negative for antibodies to the group A viruses. Two of seventy-seven persons examined from the three areas of Kenya showed antibodies for RSV-B,whereas the sera from primates, including baboons, chimpanzees, and green monkeys living in Kenya and Tanganyika, were negative as were those from baboons born in the United States. Antibodies binding to the EB3 strain of cells derived from a Burkitt lymphoma tumor were found commonly in the sera of Africans living in the three areas of Kenya studied.
Cancer and Occupation in Denmark 1935-1939
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal