tbuckley/cabot-search huggingface dataset:
Recalling breast cancer presentation and therapy: Associations between patient inaccuracy and demographic characteristics.
Authors: W. C. Mertens, C. Loke, D. Katz, R. Barham, G. Makari-Judson
Journal: Journal of Clinical Oncology (2011)

9067 Background: Uncertainty over the knowledge base of breast cancer survivors has led to a call for increased survivorship research and for the use of survivorship care plans. Purpose: To evaluate patient recall surrounding breast cancer presentation and treatment. Methods: A questionnaire was administered to 300 Stage I–III breast cancer patients diagnosed from 1997-2007 to assess their knowledge of tumor stage, key tumor characteristics, and past treatments, with verification performed by chart review. Descriptive analyses of recall accuracy as well as comparisons with patient demographic data were undertaken; stepwise logistic multivariable regression analyses were conducted to evaluate univariate associations. Results: Tumor stage was correctly recalled by 53.1% of patients; younger participants (p<.0001), pre-menopausal status (p=.019), white race (p=.024), and higher income (p=.0003) and educational attainment (p=.0017) were univariate associations; multivariate analysis retained age (p=.002), income (p=.009) and education (p=.035) as independent variables. Patients reporting no recollection of stage were older (p<.0001) and had less education (p=.0009) in multivariate analysis. Most (74%) accurately recalled hormone receptor status with older patients and those with less education and income having less accuracy. The majority (98.2%) recalled receiving chemotherapy but 40% could not accurately identify the regimen; inaccuracy was associated with older age (p<.0001), non-white race (p=.0004), and lower income (p=.008) and education (p=.025) as univariate variables; multivariate analysis retained age and non-white race (both p<.0001) as significant. Patients treated with tamoxifen exhibited accurate recall (95.7%) compared with those receiving anastrazole (84.0%) or no hormonal therapy (76%). Conclusions: Patients seemed to recall the general treatment plan but finer details often were recalled imprecisely; generally, increased age, non-white race, and lower education and income levels were associated with inaccuracies. Future studies should assess whether survivorship care plans overcome these disparities.
Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma
Authors: B A van der Kolk, D Pelcovitz, S Roth, F S Mandel, A McFarlane, J L Herman
Journal: American Journal of Psychiatry (1996)

A century of clinical research has noted a range of trauma-related psychological problems that are not captured in the DSM-IV framework of posttraumatic stress disorder (PTSD). This study investigated the relationships between exposure to extreme stress, the emergence of PTSD, and symptoms traditionally associated with "hysteria," which can be understood as problems with stimulus discrimination, self-regulation, and cognitive integration of experience.The DSM-IV field trial for PTSD studied 395 traumatized treatment-seeking subjects and 125 non-treatment-seeking subjects who had also been exposed to traumatic experiences. Data on age at onset, the nature of the trauma, PTSD, dissociation, somatization, and affect dysregulation were collected.PTSD, dissociation, somatization, and affect dysregulation were highly interrelated. The subjects meeting the criteria for lifetime (but not current) PTSD scored significantly lower on these disorders than those with current PTSD, but significantly higher than those who never had PTSD. Subjects who developed PTSD after interpersonal trauma as adults had significantly fewer symptoms than those with childhood trauma, but significantly more than victims of disasters.PTSD, dissociation, somatization, and affect dysregulation represent a spectrum of adaptations to trauma. They often occur together, but traumatized individuals may suffer from various combinations of symptoms over time. In treating these patients, it is critical to attend to the relative contributions of loss of stimulus discrimination, self-regulation, and cognitive integration of experience to overall impairment and provide systematic treatment that addresses both unbidden intrusive recollections and these other symptoms associated with having been overwhelmed by exposure to traumatic experiences.
Soft tissue sarcoma (STS): Challenges in identification, treatment patterns, and costs of disease management in the U.S.
Authors: J. E. Butrynski, M. S. Duh, A. Fournier, E. Moyneur, E. Dial, M. P. Neary, G. D. Demetri
Journal: Journal of Clinical Oncology (2008)

10573 Background: The absence of large centralized medical data systems in the US and the wide range of ICD-9 codes associated with STS make it challenging to identify accurately its patterns of care. To understand current practice patterns, we have chosen to identify STS patients (pts) from claims data, and examine their real-world treatment patterns and associated medical costs. Methods: By mining a large US health insurance claims database consisting of > 30 commercial health plans covering over 39 million people from Jan 2002 to Dec 2006, 9,382 pts were identified with ≥ 2 claims of STS (ICD-9: 171). Systemic therapies, including chemotherapies, biological agents and angiogenesis inhibitors, were captured and analyzed from the first STS claim until the end of pt enrollment. Costs reported were actual payments made by insurers. Average cost per-pt per-month was calculated for all STS pts. Results: 18% of identified STS pts received a pharmacological treatment. Among STS pts, doxorubicin (4.2%) was the most frequent single-agent regimen. Docetaxel/gemcitabine (2.6%) and doxorubicin/ifosfamide (2.1%) were the most common combination regimens. 35% of pts underwent surgery related to the STS claim, 28% radiotherapy, and 13% both. The average monthly medical cost incurred across all STS pts was $3,168, with 18%, 6%, and 3% for surgeries, radiotherapies, and systemic medications, respectively. Conclusions: The costs of care for STS pts is high at $38,016 per-pt per-year. This analysis suggests the use of systemic therapies in pts with STS may be surprisingly low, potentially due to several factors including STS stage, regional disparities, and perception of limited response to conventional drugs. More effective treatments are needed to meet the substantial unmet need in STS. Further refinements of the STS case-finding algorithms are being developed and will be presented to better delineate the STS population so that practice patterns and outcomes can be tracked and understood with accuracy. Costs Type Mean cost ($) per pt per month Share of total cost Total $3,168 100% Surgeries 572 18.1% Radiotherapies 177 5.6% STS systemic pharmacotherapies 82 2.6% Other hospitalizations 980 30.9% Other outpatient services 1033 32.6% Other Rx drugs 324 10.2% Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration GlaxoSmithKline Amgen, Ariad, Bayer, Genentech, GlaxoSmithKline, Infinity, Johnson & Johnson, Novartis, Pfizer, PharmaMar GlaxoSmithKline Novartis, Pfizer, PharmaMar Amgen, Ariad, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Infinity, Johnson & Johnson, Novartis, OSI, Pfizer, PharmaMar Ariad, GlaxoSmithKline, Infinity, Johnson & Johnson, Novartis, Pfizer, PharmaMar
Update: Ongoing Zika Virus Transmission — Puerto Rico, November 1, 2015–July 7, 2016
Authors: Laura Adams, Melissa Bello-Pagan, Matthew Lozier, Kyle R. Ryff, Carla Espinet, Jomil Torres, Janice Perez-Padilla, Mitchelle Flores Febo, Emilio Dirlikov, Alma Martinez, Jorge Munoz-Jordan, Myriam Garcia, Marangely Olivero Segarra, Graciela Malave, Aidsa Rivera, Carrie Shapiro-Mendoza, Asher Rosinger, Matthew J. Kuehnert, Koo-Whang Chung, Lisa L. Pate, Angela Harris, Ryan R. Hemme, Audrey Lenhart, Gustavo Aquino, Sherif Zaki, Jennifer S. Read, Stephen H. Waterman, Luisa I. Alvarado, Francisco Alvarado-Ramy, Miguel Valencia-Prado, Dana Thomas, Tyler M. Sharp, Brenda Rivera-Garcia
Journal: MMWR Morbidity and Mortality Weekly Report (2016)

Zika virus is a flavivirus transmitted primarily by Aedes aegypti and Aedes albopictus mosquitoes, and infection can be asymptomatic or result in an acute febrile illness with rash (1). Zika virus infection during pregnancy is a cause of microcephaly and other severe birth defects (2). Infection has also been associated with Guillain-Barré syndrome (GBS) (3) and severe thrombocytopenia (4,5). In December 2015, the Puerto Rico Department of Health (PRDH) reported the first locally acquired case of Zika virus infection. This report provides an update to the epidemiology of and public health response to ongoing Zika virus transmission in Puerto Rico (6,7). A confirmed case of Zika virus infection is defined as a positive result for Zika virus testing by reverse transcription-polymerase chain reaction (RT-PCR) for Zika virus in a blood or urine specimen. A presumptive case is defined as a positive result by Zika virus immunoglobulin M (IgM) enzyme-linked immunosorbent assay (MAC-ELISA)* and a negative result by dengue virus IgM ELISA, or a positive test result by Zika IgM MAC-ELISA in a pregnant woman. An unspecified flavivirus case is defined as positive or equivocal results for both Zika and dengue virus by IgM ELISA. During November 1, 2015-July 7, 2016, a total of 23,487 persons were evaluated by PRDH and CDC Dengue Branch for Zika virus infection, including asymptomatic pregnant women and persons with signs or symptoms consistent with Zika virus disease or suspected GBS; 5,582 (24%) confirmed and presumptive Zika virus cases were identified. Persons with Zika virus infection were residents of 77 (99%) of Puerto Rico's 78 municipalities. During 2016, the percentage of positive Zika virus infection cases among symptomatic males and nonpregnant females who were tested increased from 14% in February to 64% in June. Among 9,343 pregnant women tested, 672 had confirmed or presumptive Zika virus infection, including 441 (66%) symptomatic women and 231 (34%) asymptomatic women. One patient died after developing severe thrombocytopenia (4). Evidence of Zika virus infection or recent unspecified flavivirus infection was detected in 21 patients with confirmed GBS. The widespread outbreak and accelerating increase in the number of cases in Puerto Rico warrants intensified vector control and personal protective behaviors to prevent new infections, particularly among pregnant women.
Royal college told to stop taking money from infant formula milk firms
Authors: Anne Gulland
Journal: BMJ (2016)

Paediatricians have told their college to stop taking money from infant formula milk manufacturers in a vote at the college’s annual general meeting (AGM).

Some 66 delegates at the AGM of the Royal College of Paediatrics and Child Health (RCPCH) voted in favour of a motion that urged it to “decline any commercial transactions or any other kind of funding or support” from all companies that market breast milk substitutes. Some 53 delegates voted against the motion.1

The motion is not binding, however, and in a statement college president Neena Modi said that the “implications of the vote” would be considered at the next …
Is There Any Effect of Killer Cell Immunoglobulin-like Receptor (KIR) on Outcomes after Single Unrelated Cord Blood Transplantation?
Authors: Vanderson Rocha, Annalisa Ruggeri, Stephen R. Spellman, Tao Wang, Medhat Askar, Ron Sobecks, Eliane Gluckman, Mary Eapen
Journal: Blood (2014)
A Synthetic Cell-Penetrating Dominant-Negative ATF5 Peptide Exerts Anticancer Activity against a Broad Spectrum of Treatment-Resistant Cancers
Authors: Georg Karpel-Massler, Basil A. Horst, Chang Shu, Lily Chau, Takashi Tsujiuchi, Jeffrey N. Bruce, Peter Canoll, Lloyd A. Greene, James M. Angelastro, Markus D. Siegelin
Journal: Clinical Cancer Research (2016)

Abstract Purpose: Despite significant progress in cancer research, many tumor entities still have an unfavorable prognosis. Activating transcription factor 5 (ATF5) is upregulated in various malignancies and promotes apoptotic resistance. We evaluated the efficacy and mechanisms of the first described synthetic cell-penetrating inhibitor of ATF5 function, CP-d/n-ATF5-S1. Experimental Design: Preclinical drug testing was performed in various treatment-resistant cancer cells and in vivo xenograft models. Results: CP-d/n-ATF5-S1 reduced the transcript levels of several known direct ATF5 targets. It depleted endogenous ATF5 and induced apoptosis across a broad panel of treatment-refractory cancer cell lines, sparing non-neoplastic cells. CP-d/n-ATF5-S1 promoted tumor cell apoptotic susceptibility in part by reducing expression of the deubiquitinase Usp9X and led to diminished levels of antiapoptotic Bcl-2 family members Mcl-1 and Bcl-2. In line with this, CP-d/n-ATF5-S1 synergistically enhanced tumor cell apoptosis induced by the BH3-mimetic ABT263 and the death ligand TRAIL. In vivo, CP-d/n-ATF5-S1 attenuated tumor growth as a single compound in glioblastoma, melanoma, prostate cancer, and triple receptor–negative breast cancer xenograft models. Finally, the combination treatment of CP-d/n-ATF5-S1 and ABT263 significantly reduced tumor growth in vivo more efficiently than each reagent on its own. Conclusions: Our data support the idea that CP-d/n-ATF5-S1, administered as a single reagent or in combination with other drugs, holds promise as an innovative, safe, and efficient antineoplastic agent against treatment-resistant cancers. Clin Cancer Res; 22(18); 4698–711. ©2016 AACR.
Neuro-immune interactions in chemical-induced airway hyperreactivity
Authors: Fien C. Devos, Brett Boonen, Yeranddy A. Alpizar, Tania Maes, Valérie Hox, Sven Seys, Lore Pollaris, Adrian Liston, Benoit Nemery, Karel Talavera, Peter H.M. Hoet, Jeroen A.J. Vanoirbeek
Journal: European Respiratory Journal (2016)

Asthma may be induced by chemical sensitisers, via mechanisms that are still poorly understood. This type of asthma is characterised by airway hyperreactivity (AHR) and little airway inflammation. Since potent chemical sensitisers, such as toluene-2,4-diisocyanate (TDI), are also sensory irritants, it is suggested that chemical-induced asthma relies on neuro-immune mechanisms.We investigated the involvement of transient receptor potential channels (TRP) A1 and V1, major chemosensors in the airways, and mast cells, known for their ability to communicate with sensory nerves, in chemical-induced AHR.In vitro intracellular calcium imaging and patch-clamp recordings in TRPA1- and TRPV1-expressing Chinese hamster ovarian cells showed that TDI activates murine TRPA1, but not TRPV1. Using an in vivo model, in which an airway challenge with TDI induces AHR in TDI-sensitised C57Bl/6 mice, we demonstrated that AHR does not develop, despite successful sensitisation, in Trpa1 and Trpv1 knockout mice, and wild-type mice pretreated with a TRPA1 blocker or a substance P receptor antagonist. TDI-induced AHR was also abolished in mast cell deficient Kit(Wsh) (/Wsh) mice, and in wild-type mice pretreated with the mast cell stabiliser ketotifen, without changes in immunological parameters.These data demonstrate that TRPA1, TRPV1 and mast cells play an indispensable role in the development of TDI-elicited AHR.
Inotropic Therapy for Heart Failure
Authors: Jay N. Cohn
Journal: New England Journal of Medicine (1989)

For those who have believed that the primary defect in chronic heart failure is a reduction in myocardial contractile force, the search for a potent, oral positive inotropic agent has been one of the most important efforts in cardiology. In recent years the search has focused on drugs that inhibit cardiac phosphodiesterase activity, since these drugs can increase myocardial levels of cyclic AMP and enhance the contractility of the failing ventricle. Early optimism about these drugs was based on their favorable and apparently sustained hemodynamic effects and on early reports of dramatic clinical improvement in patients with advanced heart failure. . . .
Loss of the cyclin-dependent kinase 4-inhibitor (p16; MTS1) gene is frequent in and highly specific to lymphoid tumors in primary human hematopoietic malignancies
Authors: S Ogawa, A Hangaishi, S Miyawaki, S Hirosawa, Y Miura, K Takeyama, N Kamada, S Ohtake, N Uike, C Shimazaki
Journal: Blood (1995)
High incidence of the t(2;5)(p23;q35) translocation in anaplastic large cell lymphoma and its lack of detection in Hodgkin's disease. Comparison of cytogenetic analysis, reverse transcriptase-polymerase chain reaction, and P-80 immunostaining
Authors: L Lamant, F Meggetto, T al Saati, L Brugieres, BB de Paillerets, N Dastugue, A Bernheim, H Rubie, MJ Terrier-Lacombe, A Robert, F Rigal, D Schlaifer, M Shiuta, S Mori, G Delsol
Journal: Blood (1996)
TCTAP A-026 Association Between Anemia and Acute Coronary Syndrome Among 10,875 Chinese Patients Hospitalized from 2004 to 2013: A Retrospective Case-Control Study
Authors: Harry Hao-Xiang Wang, Xiao Rong Chen, Jia Ji Wang, Pei Xi Wang, Jian Guang Wen, Jin Ming Wang, Ruo Ling Chen, Sian M. Griffiths, Martin C.S. Wong
Journal: Journal of the American College of Cardiology (2016)
Hypertrophic Cardiomyopathy—One Case per Year?
Authors: Steve R. Ommen, Rick A. Nishimura
Journal: JAMA Cardiology (2016)

Luke K. Kim, MD; Rajesh V. Swaminathan, MD; Patrick Looser, MD; Robert M. Minutello, MD; S. Chiu Wong, MD; Geoffrey Bergman, MD; Srihari S. Naidu, MD; Christopher L. F. Gade, MD; Konstantinos Charitakis, MD; Harsimran S. Singh, MD; Dmitriy N. Feldman, MD
Evaluation of epidermal growth factor receptor (EGFR) as a prognostic factor for survival in non-small-cell lung cancer (NSCLC) patients treated with platinum-based chemotherapy as first-line treatment
Authors: M. Janas, L. R. Bailey, K. Schmidt, N. Bindslev, M. Wolf, A. Fandi, J. Askaa, R. Herbst, G. Giaccone, D. H. Johnson
Journal: Journal of Clinical Oncology (2004)

7024 Background: Two double-blind placebo-controlled randomized multicenter trials (INTACT 1 & 2) in NSCLC failed to show survival benefit for gefitinib (‘Iressa’, ZD1839) in combination with first-line platinum-based chemotherapy. However, these large studies provide an opportunity to evaluate if EGFR staining is prognostic for survival. Methods: Tumor biopsies (n=516) taken between diagnosis and start of therapy were assessed by immunohistochemistry for EGFR using the DakoCytomation EGFR pharmDx assay™. The analysis was stratified by trial and performed independently for patients randomized to placebo and gefitinib. A restricted backwards elimination Cox regression analysis was conducted to identify independent EGFR factors that were statistically significant (p<0.10) and these were also tested for treatment interaction to assess if they served as predictive factors. Results: The analysis found 2 statistically significant EGFR-based prognostic factors representing the growth pattern and percent membrane staining in patients treated with gefitinib (p=0.0023, df=2) and placebo (p=0.0128, df=2). A further analysis including interaction terms of the EGFR variables with treatment confirmed these as highly significant (p<0.0001, df=2) but not the interaction. The EGFR factors remained independently prognostic when conditioning for previously found factors (PS2; stage IV; bone, brain, liver metastasis; sex; histology; weight loss) and were comparably significant (p=0.0011 and p=0.0158). Results will also be presented for secondary endpoints (time to progression, objective response). Conclusion: While the majority of previous studies indicate higher EGFR expression correlates with poor survival, the analysis from 2 large Phase III trials provides statistically significant evidence that the combination of EGFR expression and growth pattern is a strong prognostic indicator for improved survival within this setting. ‘Iressa’ is a trademark of the AstraZeneca group of companies ‘PharmDx assay’ is a trademark of DakoCytomation Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration AstraZeneca Pharmaceuticals; DakoCytomation DakoCytomation; Genentech AstraZeneca AstraZeneca
Distinct Functions of Autoantibodies Against Interferon in Systemic Lupus Erythematosus: A Comprehensive Analysis of Anticytokine Autoantibodies in Common Rheumatic Diseases
Authors: Sarthak Gupta, Ioanna P. Tatouli, Lindsey B. Rosen, Sarfaraz Hasni, Ilias Alevizos, Zerai G. Manna, Juan Rivera, Chao Jiang, Richard M. Siegel, Steven M. Holland, Haralampos M. Moutsopoulos, Sarah K. Browne
Journal: Arthritis & Rheumatology (2016)

Anticytokine autoantibodies occur across a range of hematologic, pulmonary, and infectious diseases. However, systematic investigation of their presence and significance in autoimmune diseases is lacking. This study was undertaken to examine the distinct functions of anticytokine autoantibodies in patients with systemic lupus erythematosus (SLE) compared to patients with other rheumatic diseases and healthy controls.Serum samples from patients with SLE (n = 199), patients with primary Sjögren's syndrome (SS) (n = 150), patients with rheumatoid arthritis (RA) (n = 149), and healthy controls (n = 200) were screened for 24 anticytokine autoantibodies using a multiplex bead-based assay. To evaluate the biologic activity of anticytokine autoantibodies, their ability to block cytokine-induced signal transduction or protein expression was measured. RNA sequencing was performed on whole blood in a subset of healthy controls and patients with SLE.Patients with SLE and those with SS had a striking excess of autoantibodies against interferons and the interferon-responsive chemokine interferon-inducible protein 10 (IP-10). Only autoantibodies against type I interferon, interleukin-12 (IL-12), and IL-22 exhibited neutralizing activity. In SLE, the presence of anti-interferon-γ autoantibodies was correlated with more severe disease activity, higher levels of anti-double-stranded DNA antibodies, and elevated expression of interferon-α/β-inducible genes. Conversely, in SLE patients with blocking anti-interferon-α autoantibodies, the type I interferon gene expression signature was normalized. Anti-type III interferon autoantibodies (λ2, λ3) and anti-IP-10 autoantibodies were newly recognized in SLE patient serum, and autoantibodies against macrophage-colony stimulating factor, IL-4, IL-7, IL-17, and IL-22, none of which have been previously identified in rheumatic conditions, were discovered.Anticytokine autoantibodies are associated with distinct patterns of disease in SLE, SS, and RA. Anti-interferon autoantibodies are overrepresented in patients with SLE and those with SS, and fall into distinct functional classes, with only a subset of anti-type I interferon antibodies exhibiting neutralizing activity. Anti-interferon-γ autoantibodies are correlated with increased disease activity and interferon-related gene expression, suggesting that such autoantibodies may contribute to the pathogenesis of SLE.