tbuckley/cabot-search huggingface dataset:
Linking combat and physical health: the legacy of World War II in men's lives
Authors: Glen H. Elder, Michael J. Shanahan, Elizabeth Colerick Clipp
Journal: American Journal of Psychiatry (1997)

This longitudinal study investigated the health effects of experiences during World War II among veterans by examining how well-being changed across the postwar years and varied by prewar individual attributes.The subjects were men from the Stanford-Terman data archives who served in World War II and were born before 1925 (N = 328). Of these veterans, 236 were known to have been overseas during the war, and 64 had remained in the United States; 204 of the men who had been sent overseas experienced combat. Life history records were used to construct measures that described physical and emotional health over a range of time points and intervals in the postwar years.Exposure to combat predicted that a subject would experience physical decline or death during the postwar interval from 1945 to 1960, after the effects of self-reported physical health in 1945 and birth cohort were controlled. Rank and theater of engagement, however, were of little consequence, either additively or in interaction with combat. Self-worth before the war did not moderate the risk of physical decline or death that was associated with combat.Combat in World War II predicted that in the 15 years after the war, a subject would experience physical decline or death. There was no evidence that the effect of combat was more pronounced among men of different ranks, theaters of engagement, or levels of self-worth in 1940.
Bone Metastases from Rcc are not Always Associated with a Poor Prognosis
Authors: D. Santini, M. Santoni, A. Conti, G. Procopio, C. Porta, T. Ibrahim, S. Barni, A. Fontana, A. Berruti, B. Vincenzi, C. Ortega, G. Carteni, S.L. Fedeli, V. Adamo, E. Maiello, R. Sabbatini, A. Felici, G. Tonini, S. Bracarda, S. Cascinu
Journal: Annals of Oncology (2014)
Case 22-2000
Authors: James S. Allen, Eric C. Sheffer
Journal: New England Journal of Medicine (2000)

Presentation of CaseA 74-year-old man was referred to the hospital because of worsening dysphagia.The patient had been in good health until seven months earlier, when dysphagia developed and subsequently worsened, with epigastric and subxiphoid pain. The results of a cardiac stress test were normal. Six and a half months before admission, a double-contrast upper gastrointestinal series (Figure 1) showed a 12-mm stricture at the gastroesophageal junction, with slight spontaneous reflux; the stomach and duodenum appeared normal. An esophagogastroduodenoscopic examination showed a benign-appearing stricture without evidence of a mass. Microscopical examination of biopsy specimens from the esophagus showed squamous . . .
Spontaneous DNA Damage and Aberrant Epigenome In Multiple Myeloma Constitute The Path To Disease Genomic Instability
Authors: Maria Gkotzamanidou, Masood A. Shammas, Vassilis L. Souliotis, Jagannath Pal, Jun Qi, Andrew Brown, James E Bradner, Kenneth C. Anderson, Nikhil C. Munshi
Journal: Blood (2013)
Hiatal hernia on thoracic computed tomography in pulmonary fibrosis
Authors: Céline Tossier, Clairelyne Dupin, Laurent Plantier, Julie Leger, Thomas Flament, Olivier Favelle, Thierry Lecomte, Patrice Diot, Sylvain Marchand-Adam
Journal: European Respiratory Journal (2016)

Gastro-oesophageal reflux has long been suspected of implication in the genesis and progression of idiopathic pulmonary fibrosis (IPF). We hypothesised that hiatal hernia may be more frequent in IPF than in other interstitial lung disease (ILD), and that hiatal hernia may be associated with more severe clinical characteristics in IPF.We retrospectively compared the prevalence of hiatal hernia on computed tomographic (CT) scans in 79 patients with IPF and 103 patients with other ILD (17 scleroderma, 54 other connective tissue diseases and 32 chronic hypersensitivity pneumonitis). In the IPF group, we compared the clinical, biological, functional, CT scan characteristics and mortality of patients with hiatal hernia (n=42) and without hiatal hernia (n=37).The prevalence of hiatal hernia on CT scan at IPF diagnosis was 53%, similar to ILD associated with scleroderma, but significantly higher than in the two other ILD groups. The size of the hiatal hernia was not linked to either fibrosis CT scan scores, or reduction in lung function in any group. Mortality from respiratory causes was significantly higher among IPF patients with hiatal hernia than among those without hiatal hernia (p=0.009).Hiatal hernia might have a specific role in IPF genesis, possibly due to pathological gastro-oesophageal reflux.
N-Glycosylation Of Human ITP Autoantibodies Affects Complement Activation, Platelet Phagocytosis, and Platelet Survival In a Murine Model
Authors: Ulrich J. Sachs, Kathrin Walek, Annika Krautwurst, Mathias J. Rummel, Gregor Bein, Sentot Santoso, Tamam Bakchoul
Journal: Blood (2013)
Ranitidine and Duodenal Ulceration: A Short-Term and Maintenance Study
Authors: Roger Sheers, John S McKay, Stephen Hughes
Journal: Journal of the Royal Society of Medicine (1982)

Forty-eight patients successfully completed a six-week, double blind, placebo controlled trial of ranitidine hydrochloride 200 mg twice daily for active duodenal ulceration. Following endoscopy 68% of the patients taking ranitidine had healed, compared to 35% of those who were taking placebo. Nineteen of the patients who had not healed then took a further six weeks of open active treatment; of these, 14 were successfully treated. Thirty-one of the patients who had healed duodenal ulcers then took ranitidine hydrochloride 100 mg at night as a maintenance treatment for one year: 71% remained endoscopically and symptomatically in remission. No serious side effects were encountered.
Identification of lesion images from gastrointestinal endoscope based on feature extraction of combinational methods with and without learning process
Authors: Ding-Yun Liu, Tao Gan, Ni-Ni Rao, Yao-Wen Xing, Jie Zheng, Sang Li, Cheng-Si Luo, Zhong-Jun Zhou, Yong-Li Wan
Journal: Medical Image Analysis (2016)
P0915 : Clinical relevance of baseline/early detection and persistence of resistant associated variants in HCV-1 patients treated with protease-inhibitors assessed by ultra-deep sequencing
Authors: V.C. Di Maio, D. Armenia, M.C. Bellocchi, D. Di Paolo, V. Cento, M. Tontodonati, V. Micheli, L. Carioti, F. De Leonardis, M. Aragri, E. Polilli, A. Manunta, C. Magni, F.P. Antonucci, F. De Luca, C. Sarrecchia, A. Bertoli, I. Lenci, S. Francioso, M.M. Santoro, J. Vecchiet, A. De Maria, A. Picciotto, L. Nosotti, F. Morisco, S. Bruno, M. Puoti, S. Babudieri, M.S. Mura, G. Taliani, M. Andreoni, G. Rizzardini, G. Parruti, M. Angelico, C.F. Perno, F. Ceccherini-Silberstein
Journal: Journal of Hepatology (2015)
Immune activation and response to pembrolizumab in POLE-mutant endometrial cancer
Authors: Janice M. Mehnert, Anshuman Panda, Hua Zhong, Kim Hirshfield, Sherri Damare, Katherine Lane, Levi Sokol, Mark N. Stein, Lorna Rodriguez-Rodriquez, Howard L. Kaufman, Siraj Ali, Jeffrey S. Ross, Dean C. Pavlick, Gyan Bhanot, Eileen P. White, Robert S. DiPaola, Ann Lovell, Jonathan Cheng, Shridar Ganesan
Journal: Journal of Clinical Investigation (2016)

Antibodies that target the immune checkpoint receptor programmed cell death protein 1 (PD-1) have resulted in prolonged and beneficial responses toward a variety of human cancers. However, anti-PD-1 therapy in some patients provides no benefit and/or results in adverse side effects. The factors that determine whether patients will be drug sensitive or resistant are not fully understood; therefore, genomic assessment of exceptional responders can provide important insight into patient response. Here, we identified a patient with endometrial cancer who had an exceptional response to the anti-PD-1 antibody pembrolizumab. Clinical grade targeted genomic profiling of a pretreatment tumor sample from this individual identified a mutation in DNA polymerase epsilon (POLE) that associated with an ultramutator phenotype. Analysis of The Cancer Genome Atlas (TCGA) revealed that the presence of POLE mutation associates with high mutational burden and elevated expression of several immune checkpoint genes. Together, these data suggest that cancers harboring POLE mutations are good candidates for immune checkpoint inhibitor therapy.
Acute Leukemias of Ambiguous Lineage; Study on 247 Pediatric Patients
Authors: Ondrej Hrusak, Ales Luks, Iveta Janotova, Ester Mejstrikova, Martina Vaskova, Kirsten Bleckmann, Benigna Konatkowska, Julie Irving, Kamila Polgarova, Hiroto Inaba, Kjeld Schmiegelow, Jorge Gabriel Rossi, Maria Sara Felice, Luciano Dalla-Pozza, Jessa Morales, Mary Sartor, Michael Dworzak, Anja Moricke, Myriam Campbell, Maria Elena Cabrera, Neda Marinov, Sarah Elitzur, Shai Izraeli, Valerie De Haas, Alexandra Kolenova, Peter Svec, Elena Kreminska, Simone Stokley, Sophia Polychronopoulou, Elaine da Costa, Hanne Vibeke Marquart, Antonis Kattamis, Richard Ratei, Dirk Reinhardt, Kathy Jackson, Anthony V Moorman, Martin Schrappe, Jan Stary
Journal: Blood (2015)
C-Group Chromosome Marker in Long-Term Leukocyte Cultures<xref ref-type="fn" rid="FN2">2</xref>
Authors: Gertrude Kohn, Volker Diehl, William J. Mellman, Werner Henle, Gertrude Henle
Journal: JNCI Journal of the National Cancer Institute (1968)

A characteristic chromosomal marker in what we have called the #10 chromosome has previously been described in several Burkitt lymphoma cell lines. It is reported here in high frequency in cell lines established from peripheral leukocytes of 3 patients with acute infectious mononucleosis, and in very low frequency in lines from 4 healthy donors. The cause for this marker chromosome and its possible relationship to the EB virus observed in many of these cultures are discussed.
Targeting super-enhancer-associated oncogenes in oesophageal squamous cell carcinoma
Authors: Yan-Yi Jiang, De-Chen Lin, Anand Mayakonda, Masaharu Hazawa, Ling-Wen Ding, Wen-Wen Chien, Liang Xu, Ye Chen, Jin-Fen Xiao, William Senapedis, Erkan Baloglu, Deepika Kanojia, Li Shang, Xin Xu, Henry Yang, Jeffrey W Tyner, Ming-Rong Wang, H Phillip Koeffler
Journal: Gut (2016)

<h3>Objectives</h3> Oesophageal squamous cell carcinoma (OSCC) is an aggressive malignancy and the major histological subtype of oesophageal cancer. Although recent large-scale genomic analysis has improved the description of the genetic abnormalities of OSCC, few targetable genomic lesions have been identified, and no molecular therapy is available. This study aims to identify druggable candidates in this tumour. <h3>Design</h3> High-throughput small-molecule inhibitor screening was performed to identify potent anti-OSCC compounds. Whole-transcriptome sequencing (RNA-Seq) and chromatin immunoprecipitation sequencing (ChIP-Seq) were conducted to decipher the mechanisms of action of CDK7 inhibition in OSCC. A variety of in vitro and in vivo cellular assays were performed to determine the effects of candidate genes on OSCC malignant phenotypes. <h3>Results</h3> The unbiased high-throughput small-molecule inhibitor screening led us to discover a highly potent anti-OSCC compound, THZ1, a specific CDK7 inhibitor. RNA-Seq revealed that low-dose THZ1 treatment caused selective inhibition of a number of oncogenic transcripts. Notably, further characterisation of the genomic features of these THZ1-sensitive transcripts demonstrated that they were frequently associated with super-enhancer (SE). Moreover, SE analysis alone uncovered many OSCC lineage-specific master regulators. Finally, integrative analysis of both THZ1-sensitive and SE-associated transcripts identified a number of novel OSCC oncogenes, including PAK4, RUNX1, DNAJB1, SREBF2 and YAP1, with PAK4 being a potential druggable kinase. <h3>Conclusions</h3> Our integrative approaches led to a catalogue of SE-associated master regulators and oncogenic transcripts, which may significantly promote both the understanding of OSCC biology and the development of more innovative therapies.
An international, multicenter, prospective, observational study of neutropenia in patients being treated with lenalidomide + dexamethasone for relapsed or relapsed/refractory multiple myeloma (RR‐MM)
Authors: Xavier Leleu, Evangelos Terpos, Ramón García Sanz, Julian Cooney, Peter O'Gorman, Jiri Minarik, Richard Greil, Catherine Williams, Diep Gray, Zsolt Szabo
Journal: American Journal of Hematology (2016)

Neutropenia is a well‐known dose‐limiting toxicity associated with lenalidomide plus dexamethasone treatment in patients with multiple myeloma; however, little is known about its management and associated outcomes in the real world setting. The present prospective, multicenter, observational study evaluated the incidence, management, and outcomes of grade 3/4 neutropenia in patients with relapsed or relapsed/refractory multiple myeloma who initiated treatment with lenalidomide plus dexamethasone. Of 198 patients, 62 (31%, 95% CI: 25, 38) experienced grade 3/4 neutropenia, and half of these patients experienced 3 or more events during the 12‐month observational period. Grade 3/4 neutropenia occurred throughout lenalidomide treatment, with a median time to first event of 8.8 weeks (Q1, Q3: 5.9, 17.3). In a multivariate analysis, diagnosis of relapsed and refractory disease was associated with grade 3/4 neutropenia. Lenalidomide exposure reduction, use of G‐CSF, unplanned hospitalization, and outpatient clinic visits were more common in patients who experienced grade 3/4 neutropenia than in those who did not. In conclusion, grade 3/4 neutropenia is a common toxicity and patients are at continued risk throughout treatment with lenalidomide and dexamethasone. Further efforts should be made to improve the recommendations for neutropenia management in this population. Am. J. Hematol. 91:806–811, 2016. © 2016 Wiley Periodicals, Inc.
Constitutive Intracellular Na <sup>+</sup> Excess in Purkinje Cells Promotes Arrhythmogenesis at Lower Levels of Stress Than Ventricular Myocytes From Mice With Catecholaminergic Polymorphic Ventricular Tachycardia
Authors: B. Cicero Willis, Sandeep V. Pandit, Daniela Ponce-Balbuena, Manuel Zarzoso, Guadalupe Guerrero-Serna, Bijay Limbu, Makarand Deo, Emmanuel Camors, Rafael J. Ramirez, Sergey Mironov, Todd J. Herron, Héctor H. Valdivia, José Jalife
Journal: Circulation (2016)

In catecholaminergic polymorphic ventricular tachycardia (CPVT), cardiac Purkinje cells (PCs) appear more susceptible to Ca(2+) dysfunction than ventricular myocytes (VMs). The underlying mechanisms remain unknown. Using a CPVT mouse (RyR2(R4496C+/Cx40eGFP)), we tested whether PC intracellular Ca(2+) ([Ca(2+)]i) dysregulation results from a constitutive [Na(+)]i surplus relative to VMs.Simultaneous optical mapping of voltage and [Ca(2+)]i in CPVT hearts showed that spontaneous Ca(2+) release preceded pacing-induced triggered activity at subendocardial PCs. On simultaneous current-clamp and Ca(2+) imaging, early and delayed afterdepolarizations trailed spontaneous Ca(2+) release and were more frequent in CPVT PCs than CPVT VMs. As a result of increased activity of mutant ryanodine receptor type 2 channels, sarcoplasmic reticulum Ca(2+) load, measured by caffeine-induced Ca(2+) transients, was lower in CPVT VMs and PCs than respective controls, and sarcoplasmic reticulum fractional release was greater in both CPVT PCs and VMs than respective controls. [Na(+)]i was higher in both control and CPVT PCs than VMs, whereas the density of the Na(+)/Ca(2+) exchanger current was not different between PCs and VMs. Computer simulations using a PC model predicted that the elevated [Na(+)]i of PCs promoted delayed afterdepolarizations, which were always preceded by spontaneous Ca(2+) release events from hyperactive ryanodine receptor type 2 channels. Increasing [Na(+)]i monotonically increased delayed afterdepolarization frequency. Confocal imaging experiments showed that postpacing Ca(2+) spark frequency was highest in intact CPVT PCs, but such differences were reversed on saponin-induced membrane permeabilization, indicating that differences in [Na(+)]i played a central role.In CPVT mice, the constitutive [Na(+)]i excess of PCs promotes triggered activity and arrhythmogenesis at lower levels of stress than VMs.
Mitochondrial Transfer by Photothermal Nanoblade Restores Metabolite Profile in Mammalian Cells
Authors: Ting-Hsiang Wu, Enrico Sagullo, Dana Case, Xin Zheng, Yanjing Li, Jason S. Hong, Tara TeSlaa, Alexander N. Patananan, J. Michael McCaffery, Kayvan Niazi, Daniel Braas, Carla M. Koehler, Thomas G. Graeber, Pei-Yu Chiou, Michael A. Teitell
Journal: Cell Metabolism (2016)
The Tuberous Sclerosis Complex
Authors: Peter B. Crino, Katherine L. Nathanson, Elizabeth Petri Henske
Journal: New England Journal of Medicine (2006)

The tuberous sclerosis complex (TSC), a multisystem, autosomal dominant disorder affecting children and adults, results from mutations in one of two genes, TSC1 (encoding hamartin) or TSC2 (encoding tuberin). In this article, the current knowledge of the pathogenesis of the disease and its management are discussed.
Unrestrictive Aortopulmonary Window
Authors: Patrick O. Myers, Frédéric Lador, Anne-Lise Hachulla, Judith Bouchardy, Stéphane Noble, Marc Licker, Jean-Claude Pache, Dimitra Kalimanovaska-Ostric, Milan Djukic, Afksendiyos Kalangos, Maurice Beghetti
Journal: Circulation (2016)
Impact of study participation on survival of early-stage breast cancer patients: Results from the BRENDA study, a multicenter clinical cohort on quality of breast cancer care
Authors: C. Kurzeder, J. König, A. Woeckel, G. Sauer, M. Wischnewsky, M. Blettner, R. Kreienberg
Journal: Journal of Clinical Oncology (2009)

521 Background: Over the past two decades significant progress in treatment of early breast cancer has been accomplished through well designed, clinical trials (CTs). It has been hypothesized that trial participation could also be beneficial for the individual breast cancer patient. The BRENDA study group has been analysing quality of care provided by one university based and 16 regional breast cancer centers in south germany. In this study we investigated the impact of study participation on survival in an unselected clinical cohort of early stage breast cancer patients. Methods: The study population includes 5,966 patients who received primary therapy for early breast cancer between 1992 and 2005. Influence on survival by study participation was calculated by Cox proportional hazard analyses. Model adjustments include prognostic factors, type of treatment, age, risk group and time period. Guideline compliant treatment was assessed based on the St Gallen expert consensus recommendations and the German national S3 Guidelines. Results: A total of 738 patients (12%) received adjuvant (n = 552) or neoadjuvant (n = 186) systemic therapy within one out of 42 registered prospective multicenter phase II or III clinical trials. For patients not receiving neoadjuvant systemic therapy trial participation was associated with improved overall and disease free survival (hazard ratio [HR] = 0.75, 95% confidence interval [CI] 0.57–0.99, HR = 0.78, CI 0.63 - 0.97, respectively). The calculated effect was of similar magnitude after additional adjustment for co-existing morbidity of patients. Descriptional analysis revealed that guideline violations for locoregional or systemic treatment were more frequently found in patients receiving adjuvant treatment outside CTs. No significant effect on survival was calculated for 183 patients receiving neoadjuvant systemic therapy within CT protocols. Conclusions: In our study population participation in prospective clinical trials for adjuvant systemic therapy was associated with improved survival irrespective of treatment actually given. Intrinsic mechanisms within the framework of clinical trials can improve quality of breast cancer patient care. No significant financial relationships to disclose.
AHCCCS
Authors: Ronald J. Vogel
Journal: New England Journal of Medicine (1983)

Cost containment in the health-care sector has increasingly been seen as a predominant public-policy goal.1 Because Medicare and Medicaid pay for some 27 per cent of all health care in the nation,2 they have the potential for exerting a considerable amount of leverage on changes in the manner in which health care is provided and used. Yet, since their inception, these two programs have not done so, except in minor ways. The creators of Medicare and Medicaid made them structurally similar to the health insurance offered at that time by Blue Cross–Blue Shield and the commercial companies.3 However, Medicare and . . .
Abstract 16694: Transplantation of Bone Marrow Cells From miR150 Knockout Mice Attenuates Arterial Stiffness and Hypertension in Senescence-accelerated Mice P1 (SAMP1)
Authors: Jun Fan, Shirley Wang, Zhongjie Sun
Journal: Circulation (2015)

Background &amp; Objective. Aging is associated with increased prevalence of arterial stiffness and hypertension. The senescence-accelerated mouse P1 (SAMP1) demonstrates early and spontaneous aging phenotypes around 6-8 months of age. In contrast, microRNA-150 knockout (miR15-KO) slows down the aging process and extends lifespan in mice by 20-30%. The objective of this study is to investigate if arterial stiffness and hypertension occur in SAMP1 mice and if transplantation of bone marrow cells (BMCs) from miR-150 KO mice affects arterial stiffening and hypertension in SAMP1 mice. Method &amp; Results. The results showed that blood pressure (BP) and pulse wave velocity (PWV) were increased significantly in the SAMP1 mice vs. the age-matched control (AKR/J) mice (10 months). Therefore, SAMP1 mice developed arterial stiffening and hypertension. Western blot analysis showed that collagen 1 and TGFβ1 expression were increased but the elastin expression was decreased in aortas of SAMP1 mice, indicating arterial remodeling. Klotho is a recently-discovered aging-suppressor gene. Plasma levels klotho protein and renal expression of klotho protein were decreased in SAMP1 mice. Interestingly, transplantation of BMCs from miR150-KO mice decreased PWV and BP in SAMP1 mice to nearly control levels within 3 months, suggesting that BMC transplantation attenuates senescence-related arterial stiffening and hypertension. BMC transplantation from miR150-KO mice increased plasma levels of klotho and renal expression of klotho and abolished T cell and macrophage infiltration in aortas and kidneys in SAMP1 mice. BMC transplantation decreased expression of collagen 1 and TGFβ1 but increased expression of elastin in aortas in SAMP1 mice. Conclusion. Accelerated aging led to arterial stiffness and hypertension in SAMP1 mice. BMC transplantation from miR150-KO mice reversed arterial stiffness and hypertension in SAMP1 mice. This study demonstrates, for the first time, that BMC transplantation may be an effective therapeutic approach for aging-related arterial stiffness and hypertension. (supported by NIH R01 HL105302 &amp; HL102074).
Meeting the challenge of COPD care delivery in the USA: a multiprovider perspective
Authors: MeiLan K Han, Carlos H Martinez, David H Au, Jean Bourbeau, Cynthia M Boyd, Richard Branson, Gerard J Criner, Ravi Kalhan, Thomas J Kallstrom, Angela King, Jerry A Krishnan, Suzanne C Lareau, Todd A Lee, Kathleen Lindell, David M Mannino, Fernando J Martinez, Catherine Meldrum, Valerie G Press, Byron Thomashow, Laura Tycon, Jamie Lamson Sullivan, John Walsh, Kevin C Wilson, Jean Wright, Barbara Yawn, Patrick M Zueger, Surya P Bhatt, Mark T Dransfield
Journal: The Lancet Respiratory Medicine (2016)