tbuckley/cabot-search huggingface dataset:
A Case of Acute Tubular Necrosis With Intestinal Visualization of Tc-99m DMSA
Authors: M Yüksel, F Ustün, A Salan, S Sen, S Berkarda
Journal: Clinical Nuclear Medicine (2000)

A 36-year-old woman who had an upper respiratory tract infection 3 weeks previously was seen in the nephrology clinic because of edema of the lower extremities, nausea, vomiting, and oliguria. Urinalysis showed abundant erythrocytes and leukocytes, granular sediment, 15 to 20 epithelial cells, 4+ protein, and a specific gravity of 1.010. Her creatinine clearance was 35 ml/minute. She was referred for static and dynamic renal scintigraphy. Tc-99m DTPA imaging showed reduced excretion. Tc-99m DMSA imaging showed intestinal activity secondary to radionuclide retention in the liver associated with renal dysfunction from acute tubular necrosis.
FDG PET/CT Can Assess the Response of Locally Advanced Rectal Cancer to Neoadjuvant Chemoradiotherapy
Authors: Ben Rymer, Nathan J. Curtis, Muhammed R.S. Siddiqui, Manish Chand
Journal: Clinical Nuclear Medicine (2016)

Introduction Neoadjuvant chemoradiotherapy (CRT) is indicated in locally advanced rectal adenocarcinoma where there is a high risk of local recurrence based on preoperative imaging. Optimal radiological assessment of CRT response is unknown, and metabolic assessment of the tumor has been suggested to gauge response before surgical resection. Patients and Methods A systematic search of the MEDLINE database was performed using the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement to identify papers comparing pre- and post-CRT PET/CT in patients with locally advanced rectal adenocarcinoma with histopathological assessment of tumor regression. Papers were assessed with the QUADAS (Quality Assessment of Diagnostic Accuracy Studies) tool. Meta-analysis was performed for response index (RI) and SUVmax post-CRT. Results Ten of 69 studies met inclusion criteria containing a total of 538 patients. Methodological quality was high with low heterogeneity. In all studies, post-CRT PET/CT showed a reduction in SUVmax and the RI irrespective of histological findings. Tumors confirmed to have regressed after CRT had a mean difference of 12.21% higher RI (95% confidence interval, 6.51–17.91; P < 0.00001) compared with nonresponders. Mean difference between pre- and post-CRT SUVmax groups was −2.48 (95% confidence interval, −3.06 to −1.89; P < 0.00001) with histopathological responders having a lower post-CRT SUVmax. Conclusions The available evidence suggests that PET/CT may be a useful addition to the current imaging modalities in the assessment of treatment response.
P631Heterozygous deletion of pitx2 function selectively promotes spontaneous action potentials in mouse right atrial myocytes
Authors: S Serra, A Herraiz, C Tarifa, R Benitez, E Lozano-Velasco, A Aranega, D Franco, L Hove-Madsen
Journal: Cardiovascular Research (2014)

Purpose: Atrial fibrillation has been associated with risk variants at chromosome 4q25 that presumably modulate the expression or activity of the transcription factor pitx2. Moreover, pitx2 expression is much higher in left than right atrium, and we here tested the hypothesis that pitx2 modulates cardiomyocyte features associated to atrial fibrillation such altered cell size and spontaneous calcium release differentially in right and left atrial myocytes.
Abstract 4095: Decreased caspase 8 protein expression and incomplete caspase 3 activation in TRAIL-resistant normal human fibroblasts and epithelial cells
Authors: Roslyn N. Crowder, David T. Dicker, Wafik S. El-Deiry
Journal: Cancer Research (2011)

Abstract TNF-related apoptosis-inducing ligand (TRAIL)-mediated cell death is currently being utilized in newly developed cancer therapies. The molecular basis of normal cell resistance to TRAIL-mediated apoptosis, and thus therapeutic index, remains largely unexplored. We investigated TRAIL sensitivity in normal fibroblasts (HFF, WI-38, MRC-5) and epithelial cells (FHs 74 Int). We found that MRC-5 cells were moderately sensitive to TRAIL after 18 hours of treatment while WI-38, HFF, and FHs 74 Int cells were not. Normal fibroblasts and epithelial cells expressed both pro-apoptotic TRAIL receptors DR4 and DR5, although normal cell DR4 and DR5 expression was slightly lower when compared to human lung and colon cancer cells. While normal and cancer cells showed comparable DcR2 expression, normal fibroblasts and epithelial cells expressed little DcR1. c-Myc, a major determinant of TRAIL sensitivity in cancer cells, was found to be decreased in all normal cells compared to cancer cells. Expression of initiator caspase 8, required for complete TRAIL signaling, was assessed. Markedly reduced caspase 8 protein expression was detected in WI-38, HFF and FHs 74 Int cells compared to tumor cells that generally show robust caspase 8 expression. MRC-5 caspase 8 protein expression was found to be noticeably increased compared to TRAIL-resistant normal fibroblasts and epithelial cells and may be a contributing factor in MRC-5 TRAIL sensitivity. Expression and activation of effector caspase 3 was also examined. After 4 hours of TRAIL exposure, expression of full length caspase 3 declined in normal fibroblasts, epithelial cells and tumor cells. Yet, appearance of the mature active caspase 3 subunit p17 was only seen in MRC-5 fibroblasts and cancer cells. Interestingly, cleavage of caspase 3 substrate, PARP, was only seen in cancer cells after 4 hours of TRAIL exposure suggesting that MRC-5 fibroblasts have a delayed cytotoxic response to TRAIL. TRAIL-insensitive normal cells were treated with TRAIL and a proteasome inhibitor to increase susceptibility to TRAIL-mediated cell death. TRAIL-induced cell death was observed in WI-38, HFF and FHs 74 Int cells after combined treatment of TRAIL and MG132. Our current studies are focused on further analysis of caspase 3 activation and stabilization after TRAIL treatment in TRAIL-resistant normal cells. Additionally, we are investigating whether treatment of normal fibroblasts and epithelial cells with histone deacetylase inhibitors, and/or DNA methylation inhibitors might result in increased caspase 8 protein expression and susceptibility to TRAIL-mediated apoptosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4095. doi:10.1158/1538-7445.AM2011-4095
Abstract P6-08-02: Comparative Analysis between Primary and Secondary in Breast Tumors by Polymorphysim of Androgen Receptor Gene and Mitochondria D-Loop Somatic Mutation
Authors: SM Umemura, T Kadowaki, N Kumaki, X Tang, S Takekoshi, S Yoshimura, Y Suzuki, Y Tokuda, RY. Osamura
Journal: Cancer Research (2010)

Abstract Background: It has not been fully understood how we can differentiate a new primary breast cancer from a recurrent tumor, when second tumor arises in ipsilateral breast after the surgery for primary breast cancer. To address this research question, we estimate the usefulness of a method analyzing polymorphism of androgen receptor gene and mitochondrial D-loop somatic mutation. Materials and methods: 1) Select patients: Among the 558 patients who received the breast conservative surgery in Tokai University Hospital (1991∼2004), 9 ipsilateral breast tumors and 11 contralateral breast tumors were submitted for the analysis. 2) Formalin-fixed paraffin-embedded (FFPE) sections of non-neoplastic lymph node were examined whether polymorphism of AR gene present or not. 3) When polymorphism of AR gene in non-neoplastic lymphoid tissue were demonstrated, ipsilateral and contralateral breast cancers were further examined. 4) When AR gene in breast cancers on same allele in primary and secondary tumors, FFPE sections were further analyzed by mutaion analysis of mitochondrial D-loop region. Results: 1) Polymorphism of AR was demonstrated in 8/9 (88.9%) and 9/11 (81.8%) non-neoplastic lymph nodes obtained from the patients who had ipsilateral and contralateral breast tumor, respectively. 2) Only 2 of 8 ipsilateral breast cancers demonstrated AR polymorphism different from primary cancer. In contrast, 6 of 9 contralateral breast cancers had different polymorphism for AR from primary breast cancers. 3) Analysis of mitochondrial D-loop mutation showed that 8 seconary ipsilateral cancers had different mutation in 3/8 (37.5%), identical mutation in 3/8 (37.5%), and no mutation in 2/8 (25.0%). Results of analysis for ipsilateral secondary breast cancers Conclusion: Half of the ipsilateral in breast secondary tumors were estimated as new primary lesions by molecular estimation. Combination analyses of AR gene polymorphism and mitochondrial D-loop somatic mutation unable us to distinguish between true recurrent or new primary cancers. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-08-02.
Abstract 3469: The expression and prognostic significance of neutrophil gelatinase-asssociated lipocalin (NGAL) in primary breast cancer.
Authors: Lee-Su Kim, Hae Sung Kim
Journal: Cancer Research (2013)

Abstract Introduction: Neutrophil gelatinase-associated lipocalin (NGAL; also known as lipocalin 2), a member of the lipocalin family that transports small lipophilic ligands, has gained recent attention as both a potential biomarker and a modulator of human cancers including breast cancer. In this study, we examined the expression of NAGL in breast carcinoma and evaluated the prognostic value of its expression. Methods: Tissue microarray (TMA) blocks were made with formalin-fixed paraffin-embedded tissues from 207 breast cancer patients and the immunohistochemical staining was done using an anti-NGAL antibody. The correlation between NGAL expression and the clinicopathologic parameters such as age, tumor size, lymph node status, Ki-67 labeling index, histologic grade, hormone receptors and HER2/neu expression as well as clinical outcome was evaluated. Results: NGAL was expressed in 60 breast carcinomas (21.9%). A higher NGAL expression was noted in the younger (p=0.018) and premenopausal women (p=0.036). NGAL expression correlated with a high Ki-67 labeling index (p=0.001) and poor histologic grade (p=0.002). No significant association between NGAL expression and hormone receptor status and HER2/neu overexpression. With a median follow-up of 63 months, NGAL expression was associated with decreased disease-free survival, especially for patients with estrogen receptor negative group (p=0.013) and lymph node positive group (p=0.005), but not associated with overall survival. Conclusion: NGAL is expressed in approximately one-fifth of the breast carcinomas and its expression is correlated with several poor prognostic markers and decreased disease-free survival. This results show that NGAL expression may be a predictor of poor prognosis in primary human breast cancer, especially with more aggressive clinical features Citation Format: Lee-Su Kim, Hae Sung Kim. The expression and prognostic significance of neutrophil gelatinase-asssociated lipocalin (NGAL) in primary breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3469. doi:10.1158/1538-7445.AM2013-3469
Graft-versus-Host Disease and Survival in Patients with Aplastic Anemia Treated by Marrow Grafts from HLA-Identical Siblings
Authors: Rainer Storb, Ross L. Prentice, C. Dean Buckner, R. A. Clift, Fred Appelbaum, Joachim Deeg, Kristine Doney, John A. Hansen, Mark Mason, Jean E. Sanders, Jack Singer, Keith M. Sullivan, Robert P. Witherspoon, E. Donnall Thomas
Journal: New England Journal of Medicine (1983)

One hundred thirty patients with severe aplastic anemia were conditioned with cyclophosphamide for transplantation of marrow from HLA-identical siblings. The patients were selected for the present analysis according to the criterion of sustained marrow engraftment. Of the 130 patients, 97 are now alive between 1.4 and 11 years (median, 5) after transplantation. Twenty-nine of the thirty-three who died had either acute or chronic graft-versus-host disease (GVHD). Our analysis was directed at identifying factors predicting GVHD and survival after transplantation in patients. Our key findings were that moderately severe to severe acute GVHD had a strong adverse influence on survival; that a protective environment significantly reduced mortality, which corresponded in part to a reduction in and delayed onset of acute GVHD; that refractoriness to random-donor platelet infusions at transplantation adversely influenced survival, particularly among patients with acute GVHD; and that increasing age was associated with increased mortality. (N Engl J Med. 1983; 308:302–7.)
Abstract 1339: The role of TNF-α in PGE2-induced tumorigenesis in gastric cancer mouse model
Authors: Hiroko Oshima, Tomo-o Ishikawa, Masanobu Oshima
Journal: Cancer Research (2012)

Abstract Accumulating evidence has indicated that chronic inflammation is associated with cancer development. Mouse genetic studies have shown that the proinflammatory mediator, PGE2, plays an essential role in gastrointestinal tumorigenesis. Moreover, the proinflammatory cytokine TNF-α also plays a key role in tumorigenesis, including colitis-associated colon cancer. However, the relationship between PGE2 and TNF-α in tumorigenesis has not yet been fully investigated. We previously constructed a gastric tumor mouse model, Gan mice, that recapitulates human intestinal-type gastric cancer, in which both the PGE2 pathway and Wnt signaling are activated simultaneously in the stomach by transgenic expression of the COX-2, mPGES-1, and Wnt1 genes. The induction of the PGE2 pathway triggers an inflammatory response in the Gan mouse stomach, and the expression of proinflammatory cytokines and chemokines is induced in gastric tumor tissues. We herein examined the role of TNF-α in the PGE2-induced inflammation-associated gastric tumorigenesis by crossing Gan mice with TNF-α knockout mice. Importantly, the gastric tumorigenesis in the Gan TNF-α (-/-) compound mice was significantly suppressed in comparison to the control Gan mice. Moreover, the β-catenin level decreased significantly in the gastric tumors of Gan TNF-α (-/-) mice, suggesting a role for TNF-α in the promotion of Wnt signaling. Interestingly, inflammatory cells, including macrophages and CD4+ T cells, still infiltrated into the Gan TNF-α (-/-) mouse tumors, and the expression levels of IL-1α and IL-6 were almost the same as those in the control Gan mouse tumors. Accordingly, it is possible that TNF-α is an important tumor-promoting factor for gastric tumorigenesis, although TNF-α is not essential for PGE2-induced inflammation in the stomach. Notably, macrophages in the Gan TNF-α (-/-) mouse tumors lost their expression of the M2 marker CD206. It has been suggested that macrophages polarized to the M2(-like) type are important for tissue remodeling and tumorigenesis. It is therefore possible that TNF-α is required for macrophage polarization to a pro-tumorigenic status, which may be important for Wnt activation and gastric tumor promotion. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1339. doi:1538-7445.AM2012-1339
P1292 EVIDENCE OF CONTINUED INJECTING DRUG USE AFTER ATTAINING SUSTAINED TREATMENT-INDUCED CLEARANCE OF THE HEPATITIS C VIRUS: IMPLICATIONS FOR RE-INFECTION
Authors: H.M. Valerio, S.J. Hutchinson, D.J. Goldberg, J. Lewsey, A. Weir, H. Innes
Journal: Journal of Hepatology (2014)
Efficacy of Implantable Cardioverter–Defibrillators for the Prevention of Sudden Death in Patients with Hypertrophic Cardiomyopathy
Authors: Barry J. Maron, Win-Kuang Shen, Mark S. Link, Andrew E. Epstein, Adrian K. Almquist, James P. Daubert, Gust H. Bardy, Stefano Favale, Robert F. Rea, Giuseppe Boriani, N.A. Mark Estes, Paolo Spirito, Susan A. Casey, Marshall S. Stanton, Sandro Betocchi
Journal: New England Journal of Medicine (2000)

Hypertrophic cardiomyopathy is a genetic disease associated with a risk of ventricular tachyarrhythmias and sudden death, especially in young patients.
Granulocyte Colony-Stimulating Factor
Authors: GUNDLAPALLI SAI, M. P.H. OJHA, M.D. BUDDHIWARDHAN, M. P.H. MOUNTZ, M. JAMES
Journal: Clinical Nuclear Medicine (2002)

SAI, GUNDLAPALLI M.D.; OJHA, M. P.H.; BUDDHIWARDHAN, M.D.; MOUNTZ, M. P.H.; JAMES, M. M.D. P h.D. Author Information
EFFECT OF PERCUTANEOUS REVASCULARIZATION ADDED TO OPTIMAL MEDICAL THERAPY ON CLINICAL OUTCOMES IN PATIENTS WITH PRIOR MYOCARDIAL INFARCTION, HEART FAILURE, OR REDUCED SYSTOLIC FUNCTION: A POST HOC ANALYSIS OF THE COURAGE TRIAL
Authors: Dmitri Belov, Mandeep Sidhu, Pamela Hartigan, David Maron, G.B. John Mancini, John Spertus, Koon Teo, Steven Sedlis, Bernard Chaitman, William Weintraub, David Brown, William Boden
Journal: Journal of the American College of Cardiology (2016)
On "I": the conceptual foundations of responsibility
Authors: G G Globus
Journal: American Journal of Psychiatry (1980)

In clinical practice, great emphasis is placed on the patient's being responsible, yet the conceptual bases of this therapeutic posture are obscure. The author examines the conceptual foundations of responsibility by focusing on the subjective "I". Although "I" is widely considered to be an empty term, signifying only an illusory "ghost in the machine," the author argues that our acquaintance with "I" is acceptable at face value. "I" is strictly identified with the tacit, rule-governed, grammatical actions of distinguishing (or meaning) that constitute the experienced personal world. The author discusses the clinically important distinction between "having" and "assuming" responsibility.
Abstract 1950: The effects of combination treatment of NO-donor and MEK inhibitor on proliferation and invasion of cancer cell lines
Authors: Satoshi Furuhashi, Hiroki Sugita, Hiroshi Takamori, Kei Horino, Osamu Nakahara, Hirohisa Okabe, Shinya Abe, Hiroshi Tanala, Toru Beppu, Hideo Baba
Journal: Cancer Research (2011)

Abstract [Background] Nitric oxide (NO) possesses cytostatic and cytotoxic actions on cancer cells. MAPK and PI3K/Akt signaling pathways, those exist downstream of IGF-IR and EGFR, are two major pathways of oncogenic transformation and tumor maintenance in many kinds of cancer cells. Several studies demonstrated that NO inhibits PI3K/Akt pathway, on the other hand, NO enhances activates MAPK pathway by means of activation of H- and N-Ras. MEK inhibitor blocks MAPK pathway. Hence, we hypothesized that combination of NO-donor and MEK inhibitor inhibits proliferation and invasion of cancer cells in comparison with NO-donor or MEK inhibitor alone. [Methods and Results] We assessed effects of combination of GSNO (NO-donor) and U0126 (MEK inhibitor) on phosphorylation of Akt, and Erk1/2 after stimulation of IGF-I and EGF using Western blotting analyses. Combination of GSNO (500 μM) and U0126 (10 μM) down-regulates phosphorylation of Akt, and Erk1/2 after stimulation of IGF-I (25 nM) and EGF (100 ng/ml) more strongly in comparison with GSNO or U0126 alone in MIAPaCa-2 cells and HCT-116 cells. Combination of GSNO (200, 500 μM) and U0126 (10 μM) also inhibited cell proliferation of MIAPaCa-2 cells and HCT-116 cells more strongly in comparison with NO-donor or MEK inhibitor alone. Furthermore, combination of these compounds inhibited invasion of MIAPaCa-2 cells and HCT-116 cells more strongly in comparison with NO-donor or MEK inhibitor alone in vitro. [Discussion] Recent reports revealed that inhibition of PI3K/Akt or MAPK pathway alone was insufficient to robustly induce tumor shrinkage. It indicated that a feedback pathway between intracellular signalings might be up-regulated, if one main signaling pathway was inhibited. Concomitant inhibition of both PI3K/Akt and MAPK pathway by means of NO-donor and MEK inhibitor could inhibit not only cell growth but also invasion to suppress feedback loops. These results suggest that the combination treatment of NO-donor and MEK inhibitor may be useful for cancer therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1950. doi:10.1158/1538-7445.AM2011-1950
THU0315 Long-term outcome of juvenile idiopathic arthritis (JIA): A french multicenter study based on 353 patients
Authors: I. Melki, C. Garcin, P. Quartier, C. Job Deslandre, I. Lemelle, P. Landais, B. Bader-Meunier, A.-M. Prieur
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Studies about JIA outcome in adulthood are still limited. <h3>Objectives</h3> To describe medical outcome in adulthood of a cohort of JIA patients followed in 3 French paediatric rheumatology centers since the disease onset. <h3>Methods</h3> Data were collected through an auto-questionnaire completed by JIA patients. <h3>Results</h3> Three hundred fifty three patients were included. Median age at the time of evaluation was 26 years [range 20 50]. Fifty-six patients out of 353 had no more medical follow-up. The other patients were followed either by a general practitioner (79.4%), and or a rheumatologist (64.5%) and/or an ophtalmologist (47,6%). Twenty-eight percent patients had never seen a rheumatologist after the end of the paediatric care. At the time of the study, JIA activity was still present as follows: 1) 240 patients were complaining of joint pain during the last weeks, and 228 had at least one arthritis 2) Sixty three patients were affected by uveitis, which was still active in 26. Disease sequelae were 1) Growth retardation with height &lt; -2SD in 28 females and in 5 males. Among them, three patients received growth hormone therapy. 2) At least one fracture occurred in 30% of the patients and 3 or more fractures in 20%. Auto-immune diseases in adulthood were reported in 20 patients out of 353: Crohn's disease (n=5), ulcerative colitis (n=3), celiac disease (n=1), pulmonary interstitial syndrome (n=2), multiple sclerosis (n=1), myasthenia (n=1), diabetes (n=1), hypo- and hyper- thyroidism (n=5) and vitiligo (n=1). One hundred ninety six patients out of 348 still received medical treatment for their disease: 47% non-steroid anti-inflammatory drugs (NSAIDs), 31% steroids, 37.2% DMARDs, and 39% biologics. <h3>Conclusions</h3> In this series, disease's activity and/or damage including eye involvement and growth retardation were observed in a large number of patients, reflecting probably in part the difficulty of JIA management before the era of "modern" therapies. Surprisingly, the high rate (6%) of auto-immune diseases in these patients, never been reported previously, deserves further investigations. <h3>Acknowledgements</h3> Work supported by the Foundation Wyeth-Pfizer pour l'enfant et l'adolescent. <h3>Disclosure of Interest</h3> None Declared
BODY MASS INDEX AND THE DEVELOPMENT OF ATRIAL FIBRILLATION IN HISPANICS, BLACKS AND NON-HISPANIC WHITES
Authors: Eric H. Shulman, Faraj Kargoli, Ethan Hoch, Ephraim Leiderman, Scott Schafler, Joseph Donnelly, Lynn Zaremski, Cecilia Berardi, Andrea Natale, Luigi Di Biase, John Fisher, Andrew Krumerman, Kevin Ferrick
Journal: Journal of the American College of Cardiology (2016)