tbuckley/cabot-search huggingface dataset:
Use of hematopoietic colony-stimulating factors: the American Society of Clinical Oncology survey. The Health Services Research Committee of the American Society of Clinical Oncology.
Authors: C L Bennett, T J Smith, J C Weeks, A B Bredt, J Feinglass, J H Fetting, B E Hillner, M R Somerfield, R J Winn
Journal: Journal of Clinical Oncology (1996)

PURPOSE Dissemination of use of the hematopoietic colony-stimulating factors (CSFs) is unprecedented in oncology, with almost all physicians having experience with granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) shortly after the drugs received Food and Drug Administration (FDA) approval in 1991. The American Society of Clinical Oncology (ASCO) Health Services Research Committee sought to assess patterns of use of CSFs before dissemination of its first-ever publication of ASCO guidelines. METHODS A questionnaire describing clinical scenarios was mailed to American oncologists and hematologists who practice medical oncology. In each scenario, the physician was asked whether he would prefer to use a CSF to prevent or treat neutropenia. RESULTS The response rate to the mailed survey was 49% (N = 475). Most physicians preferred to use CSFs for secondary prophylaxis in patients receiving chemotherapy at rates of 44% to 85%, rather than reduce doses. Patterns of use did not differ for palliative, curative, or adjuvant chemotherapy. While the majority of CSF patterns of care were similar to those recommended in the ASCO guidelines, more than half of the physicians chose to use CSFs in the treatment of febrile neutropenia, an area not supported in the subsequent guidelines. In general, physicians at academic medical centers and in Health Maintenance Organization (HMO) practices were more likely to prefer dose-reduction strategies over addition of CSFs, while fee-for-service physicians preferred the opposite strategies. CONCLUSION Variations in CSF preferences for use were related to differences in clinical characteristics (history of afebrile v febrile neutropenia), drug characteristics (G-CSF or GM-CSF), and physician practice characteristics (HMO or fee-for-service setting). However, before dissemination of the guidelines, the majority of American oncologists preferred strategies that were subsequently included in the ASCO CSF guidelines. CSF guidelines would be most likely to reduce CSF use for treatment of afebrile and uncomplicated febrile neutropenia.
Bipolar II: the most common bipolar phenotype?
Authors: S G Simpson, S E Folstein, D A Meyers, F J McMahon, D M Brusco, J R DePaulo
Journal: American Journal of Psychiatry (1993)

The purpose of this study was to compare the pattern of affective psychopathology in families ascertained for genetic linkage studies through bipolar I probands to that in families ascertained through bipolar II probands.All available first-degree relatives (N = 266) of 48 bipolar I and eight bipolar II probands were interviewed with the Schedule for Affective Disorders and Schizophrenia--Lifetime Version by one of two psychiatrists who had attained high interrater reliability for bipolar II disorder and other diagnoses.Bipolar II disorder was the most common affective disorder in both family sets. Forty percent of the 47 first-degree relatives of the bipolar II probands and 22% of the 219 first-degree relatives of the bipolar I probands were diagnosed with bipolar II disorder. On the other hand, only one bipolar I relative was found in the bipolar II families.Bipolar II disorder was the most prevalent affected phenotype in both bipolar I and bipolar II families and was the only expressed phenotype in half of the bipolar II families. This suggests that bipolar II disorder is genetically related to but less complex than bipolar I disorder. Accurate diagnosis of bipolar II disorder may be crucial in finding the genetic loci underlying bipolar disorders generally.
Effectiveness of indacaterol with or without tiotropium in patients with moderate or severe chronic obstructive pulmonary disease (COPD) - the GOLDEN II study
Authors: Mihail Toumbis, Eirini Mitsiki, Dimosthenis Papapetrou, Konstantinos Marosis, Vasileios Gkoumas, Dionysis Spyratos, Konstantinos Kallergis, Panagiotis Demertzis, Despoina Zorpidou, Stylianos Michaelidis, Konstantinos Gourgoulianis
Journal: European Respiratory Journal (2014)

Introduction: Lung function decline (FEV1) in COPD patients has been associated with increased mortality. According to GOLD 2013 bronchodilators are the recommended foundation treatment for COPD.

Aim: To evaluate the effectiveness of indacaterol monotherapy and free combination with tiotropium in patients with COPD on FEV1, dyspnea (mMRC) and health status (EQ5D-VAS).

Methods: GOLDEN II was a multicenter, non-interventional, observational study. Patients with moderate or severe COPD >40 years, available medical history on treatment with indacaterol, tiotropium or both no longer than 10 days prior to enrolment, could be recruited. Study duration was 3 months. Treatment effectiveness was recorded in two visits (Day 1; month 3).

Results: Of 333 patients recruited, 299 completed the study; (84% male), mean age 68±10 years. Most patients had moderate and severe COPD (mean post-bronchodilator FEV1 55.9±14.7%, 61%GOLDΙΙ, 33%GOLDΙΙΙ) and dyspnea (mean mMRC 1.7±1.0); 41% were treated with indacaterol, 59% were under a free combination of indacaterol + tiotropium. On study completion, post-bronchodilation FEV1 improved from baseline (from 62±14% to 66±15% for the indacaterol group; from 52±14% to 55±14% for the indacaterol + tiotropium group, p<0.001) as did dyspnea (-0.2±0.7 and -0.3±0.8; p<0.001 respectively in mMRC) and health status (EQ5D-VAS from 68±19mm to 76±14mm; from 66±17mm to 71±16mm respectively, p<0.001).

Conclusions: In these patients with moderate to severe COPD, both indacaterol and the free combination of indacaterol + tiotropium improved FEV1, reduced dyspnea and improved the health status after 3 months of treatment.
Salvage surgery for chemorefractory gestational trophoblastic disease.
Authors: E Lehman, D M Gershenson, T W Burke, C Levenback, E G Silva, M Morris
Journal: Journal of Clinical Oncology (1994)

To investigate and define better the role of salvage surgery for patients with chemorefractory gestational trophoblastic disease (GTD).A retrospective review of medical records at The University of Texas M.D. Anderson Cancer Center identified 33 patients with chemorefractory GTD who underwent salvage surgery between 1962 and 1991. The end points selected for analysis were serologic response and survival.Initial salvage procedures consisted of 29 hysterectomies, four thoracotomies, and one nephrectomy (in conjunction with a hysterectomy). Fourteen patients (42%) had a serologic complete response (CR) to surgery (normalization of human chorionic gonadotropin [hCG]), 10 (30%) had a partial response (> 50% decrease in hCG level), and nine had no response (< or = 50% decrease in hCG level). Of 19 patients who received further chemotherapy, eight (42%) attained a CR. Four patients underwent a second salvage surgery: two thoracotomies, one craniotomy, and one partial hepatectomy. All achieved a CR. The probability of achieving a CR was influenced by the time from diagnosis to surgery, number of preoperative disease sites, preoperative World Health Organization (WHO) score, and histologic type. Survival was influenced by the type of antecedent pregnancy, number of preoperative regimens, number of preoperative disease sites, time from diagnosis to surgery, and preoperative WHO score.Based on the findings of this study, it appears that a select subset of patients with chemorefractory GTD who have a limited number of clinically detectable tumor foci may benefit from salvage surgery.
Conversion of interferon-induced, long-term cytogenetic remissions in chronic myelogenous leukemia to polymerase chain reaction negativity.
Authors: R Kurzrock, Z Estrov, H Kantarjian, M Talpaz
Journal: Journal of Clinical Oncology (1998)

PURPOSE Interferon alfa (IFN-alpha) induces complete cytogenetic remission in a significant minority of patients with chronic myelogenous leukemia (CML). To date, use of the polymerase chain reaction (PCR) has suggested that residual disease is present in virtually all these individuals at median follow-up intervals of approximately 1 year after initial achievement of cytogenetic remission. We sought to determine the PCR status of CML patients with very long continuous complete cytogenetic remissions on IFN-alpha. PATIENTS AND METHODS Blood and/or bone marrow samples from 18 CML patients maintained in continuous cytogenetic remission by IFN-alpha for at least 1 year were studied for residual BCR-ABL mRNA by single-step reverse-transcriptase (RT)-PCR methodology, followed by detection of the amplification product by the hybridization protection assay (HPA). RESULTS Ten of 18 patients showed RT-PCR negativity for BCR-ABL. The median duration of continuous complete cytogenetic remission at the time of sample collection for the negative patients was 42 months versus 21 months for the patients whose tests remained positive (P = .05). CONCLUSION Very long-term follow-up of IFN-alpha-treated CML patients in continuous complete cytogenetic remission is associated with a decrease in the number of BCR-ABL transcripts to a level below that detectable by the RT-PCR assay used in this study.
Abstract 15334: Association Between Angiographic Restenosis Patterns and Morphologic Characteristics Evaluated by Optical Coherence Tomography in In-Stent Restenosis Lesions
Authors: Takeshi Tada, Kazushige Kadota, Shunsuke Kubo, Masatomo Ozaki, Yusuke Hyoudou, Koshi Miyake, Yuki Hayakawa, Naoki Saito, Hideaki Otsuji, Suguru Otsuru, Daiji Hasegawa, Yoshikazu Shigemoto, Seiji Habara, Hiroyuki Tanaka, Yasushi Fuku, Naoki Oka, Harumi Kato, Hiroyuki Yamamoto, Tsuyoshi Goto, Kazuaki Mitsudo
Journal: Circulation (2012)

Background: The morphological assessment of neointimal tissue using optical coherence tomography (OCT) is highly significant to clarify the pathophysiology of in-stent restenosis (ISR). Little is k...
Bias in Peripheral Depression Biomarkers
Authors: André F. Carvalho, Cristiano A. Köhler, André R. Brunoni, Kamilla W. Miskowiak, Nathan Herrmann, Krista L. Lanctôt, Thomas N. Hyphantis, João Quevedo, Brisa S. Fernandes, Michael Berk
Journal: Psychotherapy and Psychosomatics (2016)

To aid in the differentiation of individuals with major depressive disorder (MDD) from healthy controls, numerous peripheral biomarkers have been proposed. To date, no comprehensive evaluation of the existence of bias favoring the publication of significant results or inflating effect sizes has been conducted.Here, we performed a comprehensive review of meta-analyses of peripheral nongenetic biomarkers that could discriminate individuals with MDD from nondepressed controls. PubMed/MEDLINE, EMBASE, and PsycINFO databases were searched through April 10, 2015.From 15 references, we obtained 31 eligible meta-analyses evaluating biomarkers in MDD (21,201 cases and 78,363 controls). Twenty meta-analyses reported statistically significant effect size estimates. Heterogeneity was high (I2 ≥ 50%) in 29 meta-analyses. We plausibly assumed that the true effect size for a meta-analysis would equal the one of its largest study. A significant summary effect size estimate was observed for 20 biomarkers. We observed an excess of statistically significant studies in 21 meta-analyses. The summary effect size of the meta-analysis was higher than the effect of its largest study in 25 meta-analyses, while 11 meta-analyses had evidence of small-study effects.Our findings suggest that there is an excess of studies with statistically significant results in the literature of peripheral biomarkers for MDD. The selective publication of 'positive studies' and the selective reporting of outcomes are possible mechanisms. Effect size estimates of meta-analyses may be inflated in this literature.
Metastasis of Ocular and Flank Implants of the 13762NF Mammary Adenocarcinoma in Syngeneic Rats&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: J Szalay, H Sabzevari
Journal: JNCI Journal of the National Cancer Institute (1987)

Solid fragments of a syngeneic tumor of low immunogenicity were implanted on the anterior surface of the iris or posterior surface of the cornea in young Fischer 344 rats. Growth and metastasis of these implants were examined and compared with those occurring following sc tumor implantation in the flank. Corneal implants did not grow well or metastasize. Iridial implants grew well, and tumor typically filled the eye within a few weeks. If tumor-filled eyes were left intact, all rats died or became moribund 7–9 weeks later. Metastasis was seen in the lungs (11/11), cervical lymph nodes (7/11), body wall (5/11), heart (4/11), kidney (4/11), and liver (3/11). Removal (enucleation) of tumor-filled eyes prior to spread to the orbit prevented the development of overt metastatic disease for 1–2 years (11/11). When healthy enucleated rats were necropsied 0 days to 26 weeks post enucleation, small nodules were seen in the lung (9/13), liver (3/13), or spleen (1/13). Nodules were not seen in rats that had been housed in our animal facility for 1–2 years (16/16), had eye surgery with tumor implanted on the posterior surface of the cornea (6/6), or had been subjected to the surgical procedures of corneal implantation and enucleation (3/3). When tumors were implanted sc, rats died after 6–7 weeks. Metastasis was seen in the lung (12/12), lymph nodes (12/12), spleen (1/12), and liver (1/12). Removal of very small flank tumors failed to prevent animals from dying 7–8 weeks later with pulmonary and lymph node metastasis (10/10). In summary, iridial implantation resulted in an altered pattern of metastasis. Animals that had iridial implants and enucleation failed to develop overt metastatic disease and had small nodules in the lung, liver, or spleen.
Murine Models Demonstrate Distinct Vasculogenic and Cardiomyogenic cKit <sup>+</sup> Lineages in the Heart
Authors: Konstantinos E. Hatzistergos, Joshua M. Hare
Journal: Circulation Research (2016)

After 2 recent genetic studies in mice addressing the developmental origins and regenerative activity of cardiac cKit+ cells, 2 additional reports by Sultana et al and Liu et al provide further information on the expression of cKit in the embryonic and adult hearts. Here, we synthesize the findings from the 4 distinct cKit models to gain insights into the biology of this important cell type.
The 5-factor ORBIT bleeding score predicted major bleeding at 2 years in patients with atrial fibrillation
Authors: Gregory Y. H. Lip, Deirdre A. Lane
Journal: Annals of Internal Medicine (2016)

Source Citation O’Brien EC, Simon DN, Thomas LE, et al. The ORBIT bleeding score: a simple bedside score to assess bleeding risk in atrial fibrillation. Eur Heart J. 2015 Sep 29. [Epub ahead of print] 26424865
Butyrate-Induced Cytoarchitectural Reorganization of Mallory Body-Containing Rat Hepatic Tumor Cells&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: M P Ryan, E Borenfreund, P J Higgins
Journal: JNCI Journal of the National Cancer Institute (1987)

Journal Article Butyrate-Induced Cytoarchitectural Reorganization of Mallory Body-Containing Rat Hepatic Tumor Cells Get access Michael P. Ryan, Michael P. Ryan Search for other works by this author on: Oxford Academic PubMed Google Scholar Ellen Borenfreund, Ellen Borenfreund Search for other works by this author on: Oxford Academic PubMed Google Scholar Paul J. Higgins Paul J. Higgins Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 79, Issue 3, September 1987, Pages 555–567, https://doi.org/10.1093/jnci/79.3.555 Published: 01 September 1987 Article history Received: 10 October 1986 Accepted: 02 April 1987 Published: 01 September 1987
Abstract 19005: PGC1α Play a Critical Role in TWEAK Mediating Cardiac Dysfunction
Authors: Jianru Shi, Bingbing Jiang, Yiling Qiu, Jian Guan, Xin Cao, Lihe Su, Linda C Burkly, Daniel P Kelly, Ronglih Liao
Journal: Circulation (2012)

Inflammatory cytokines contribute to the pathogenesis of cardiac dysfunction and symptomatic heart failure (HF). We recently identified that a novel TNF superfamily member, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), was increased in patients with HF. Genetic overexpression of TWEAK in mice results in dilated cardiomyopathy and HF. This study was performed to investigate the molecular mechanisms underlying TWEAK-induced cardiomyocyte dysfunction. Methods and Results. Circulating levels of TWEAK were increased in mice through IV injection of recombinant TWEAK (r-TWEAK). r-TWEAK resulted in cardiac dysfunction and deleterious remodeling in a dose dependent manner. Histologic examination of r-TWEAK hearts revealed severe mitochondrial damage. In conjunction with mitochondrial pathology, genes required for mitochondrial oxidative phosphorylation were downregulated with r-TWEAK treatment. Importantly, PGC1α, a key regulator of mitochondrial gene transcription was downregulated in r-TWEAK hearts prior to the onset of cardiac dysfunction, suggesting a potential causal relationship. In isolated adult rat cardiomyocytes, r-TWEAK recapitulated contractile dysfunction, suggesting a cell autonomous mechanism. Adenoviral-mediated overexpression of PGC1α maintained mitochondrial levels in r-TWEAK-treated cardiomyocytes and protected against r-TWEAK induced contractile dysfunction, as revealed by percent cell fraction shortening experiments (control 4.23±0.22%; r-TWEAK 2.73±0.31%, p&lt;0.05 vs. control; PGC1α+r-TWEAK 4.23±0.25%, p&lt;0.05 vs. r-TWEAK). Using shRNA mediated genetic silencing and adenoviral-mediated overexpression, we further implicate the upstream signaling molecule TRAF2, and the downstream regulator NFκB in TWEAK regulation of PGC1α, mitochondrial levels, and cardiomyocyte dysfunction. Conclusion. Our data identify TRAF2-NFκB-PCG1 axis as a critical molecular mechanism to the development of TWEAK-induced cardiomyocyte dysfunction and the development of HF. Modulation of mitochondrial levels or antagonism of TRAF2-NFκB may serve as candidate therapeutic targets for the treatment of heart failure.
Timing of Initiation of Maintenance Dialysis
Authors: Susan P. Y. Wong, Elizabeth K. Vig, Janelle S. Taylor, Nilka R. Burrows, Chuan-Fen Liu, Desmond E. Williams, Paul L. Hebert, Ann M. O’Hare
Journal: JAMA Internal Medicine (2016)

There is often considerable uncertainty about the optimal time to initiate maintenance dialysis in individual patients and little medical evidence to guide this decision.To gain a better understanding of the factors influencing the timing of initiation of dialysis in clinical practice.A qualitative analysis was conducted using the electronic medical records from the Department of Veterans Affairs (VA) of a national random sample of 1691 patients for whom the decision to initiate maintenance dialysis occurred in the VA between January 1, 2000, and December 31, 2009. Data analysis took place from June 1 to November 30, 2014.Central themes related to the timing of initiation of dialysis as documented in patients' electronic medical records.Of the 1691 patients, 1264 (74.7%) initiated dialysis as inpatients and 1228 (72.6%) initiated dialysis with a hemodialysis catheter. Cohort members met with a nephrologist during an outpatient clinic visit a median of 3 times (interquartile range, 0-6) in the year prior to initiation of dialysis. The mean (SD) estimated glomerular filtration rate at the time of initiation for cohort members was 10.4 (5.7) mL/min/1.73 m(2). The timing of initiation of dialysis reflected the complex interplay of at least 3 interrelated and dynamic processes. The first was physician practices, which ranged from practices intended to prepare patients for dialysis to those intended to forestall the need for dialysis by managing the signs and symptoms of uremia with medical interventions. The second process was sources of momentum. Initiation of dialysis was often precipitated by clinical events involving acute illness or medical procedures. In these settings, the imperative to treat often seemed to override patient choice. The third process was patient-physician dynamics. Interactions between patients and physicians were sometimes adversarial, and physician recommendations to initiate dialysis sometimes seemed to conflict with patient priorities.The initiation of maintenance dialysis reflects the care practices of individual physicians, sources of momentum for initiation of dialysis, interactions between patients and physicians, and the complex interplay of these dynamic processes over time. Our findings suggest opportunities to improve communication between patients and physicians and to better align these processes with patients' values, goals, and preferences.
Leukocyte Migration Inhibition by Soluble Extracts of MCF-7 Tissue Culture Cell Line Derived From Breast Carcinoma2
Authors: J. L. McCoy, L. F. Jerome, C. Anderson, G. B. Cannon, T. C. Alford, R. J. Connor, R. K. Oldham, R. B. Herberman
Journal: JNCI Journal of the National Cancer Institute (1976)

Studies were conducted to determine whether MCF-7, a tissue culture cell line derived from a pleural effusion of a patient with breast carcinoma, could be used as a source of tumor-associated antigen for direct leukocyte migration-inhibition (LMI) assays. Of 32 patients with breast carcinoma, 27 (84.4%) gave positive migration-inhibition results on their initial tests with a 25-µg protein/ml concentration of a 3 m KCI extract of MCF-7; 1 of 24 (4.5%) normal donors reacted with MCF-7. An intermediate incidence of reactivity (7/16) was observed with the extract when leukocytes of patients with melanoma, lung carcinoma, and Ewing's sarcoma were used. In further specificity studies, leukocytes of patients with breast carcinoma gave a lower incidence of LMI reactivity than did those of patients with Ewing's sarcoma and lung carcinoma with KCI extracts of the appropriate histologic type of tumor. The results indicated that the MCF-7 cells possessed a tumor-associated antigen to which many patients with breast carcinoma are sensitized.