tbuckley/cabot-search huggingface dataset:
Commentary: Ingestion of Asbestos
Authors: S. H. Zaidi
Journal: Environmental Health Perspectives (1974)

Several papers at this conference have dealt with studies of ingestion of asbestos in one form or the other. In one experiment, following asbestos ingestion, a gastric ulcer with an asbestos fiber perforating it was observed. One investigator did not find any significant pathology in the gastrointestinal tract with ingestion of asbestos, and some other workers found few particles here and there. I suggest that one of our most urgent needs is a proper and suitable choice of an experimental animal. In my opinion, the rat is one of the animals that should not be used. The simple reason is that half of the rat's stomach is lined by squamous epithelium and therefore does not simulate the human stomach. Dr. Shay from the United States (1) has been using rats to produce gastric ulcers which are not at all similar to those found in humans. The ulcers developed in rumenal mucosa which is lined by squamous epithelium. A second difficulty is collection of gastric juice. I do not know of much work that has been done with small intestine-or for that matter, with cecum and colon. I think that the monkey is a difficult animal to deal with. The fact that it is vegetarian also presents difficulties. You always find some food particles in the stomach-there is always some roughage left over. Therefore, if we have to do work on stomach or for that matter on intestine, we should not use monkeys. Now let us take the rabbit. Twenty years ago, I did some experiments on rabbits. I kept them without food for 4 days, put them on water and after 3 or 4
Abstract 5382: Etoposide enhances TRAIL cytotoxicity by increase of TRAIL-R2 expression via a NF-κB pathway in neuroblastoma cells
Authors: Myoung Woo Lee, Hye Ryung Kim, Dae Seong Kim, Yoo Hun Noh, Hye Jin Kim, Soo Hyun Lee, Hee Won Cheuh, Keon Hee Yoo, Ki Woong Sung, Hong Hoe Koo, Hye Lim Jung
Journal: Cancer Research (2010)

Abstract Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which induces apoptosis in tumor cells while not in normal cells. TRAIL binds with two types of receptors which are apoptosis-inducing death receptors (TRAIL-R1 and TRAIL-R2) and non-apoptosis-inducing decoy receptors (TRAIL-R3 and TRAIL-R4). TRAIL has been considered as a promising agent for selective cancer therapy, although some cancer cells show resistance to apoptosis induction by this ligand. In this study, we examined whether combination treatment of chemotherapeutic drugs with TRAIL induces synergistic cell death in neuroblastoma cells. We showed that pre-treatment with sublethal concentrations of etoposide followed by exposure to TRAIL synergistically enhanced apoptotic cell death compared to treatment with etoposide or TRAIL alone in SK-N-MC cells (28 ± 2% versus 12 ± 3% or 2 ± 2% apoptotic cell death in 48 h), while not in IMR-32 cells (26 ± 4% versus 26 ± 7% or 0.5 ± 0.6% apoptotic cell death in 48 h). These synergistic cell death was inhibited by addition of fusion chimera protein (recombinant human TRAIL-R2: Fc), which can block TRAIL binding to TRAIL-R1 or TRAIL-R2. In addition, pre-treatment with sublethal concentrations of etoposide in SK-N-MC cells induced degradation of IκBα, resulting in NF-κB activation and up-regulation of TRAIL-R2 expression. The increase of TRAIL-R2 expression resulted in TRAIL-induced synergistic cell deaths, which were effectively inhibited by exposure to NF-κB inhibitor. Moreover, we showed that combination treatment significantly decreased the Mcl-1 expression and increased caspase-3 activation compared to treatment with etoposide or TRAIL alone. Our data suggest that pre-treated etoposide activates NF-κB by down-regulation of IκBα, and then NF-κB up-regulates TRAIL-R2 expression enhancing TRAIL-induced apoptosis in neuroblastoma cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5382.
BILIRUBIN AS AN INDEPENDENT PREDICTOR FOR INOTROPE REQUIREMENT IN PATIENTS POST LEFT VENTRICULAR ASSIST DEVICE IMPLANTATION
Authors: Enrique Orellana, Ajay Sundara Raman, Swathy Subramany, Bindu Akkanti, Biswajit Kar, Pranav Loyalka, Sriram Nathan, Farshad Raissi, Indranee Rajapreyar, Igor Gregoric
Journal: Journal of the American College of Cardiology (2015)
Missed Diagnoses of Acute Cardiac Ischemia in the Emergency Department
Authors: J. Hector Pope, Tom P. Aufderheide, Robin Ruthazer, Robert H. Woolard, James A. Feldman, Joni R. Beshansky, John L. Griffith, Harry P. Selker
Journal: New England Journal of Medicine (2000)

Discharging patients with acute myocardial infarction or unstable angina from the emergency department because of missed diagnoses can have dire consequences. We studied the incidence of, factors related to, and clinical outcomes of failure to hospitalize patients with acute cardiac ischemia.
Hypertrophic Pulmonary Osteoarthropathy and Tripe Palms
Authors: Hayder Saeed, Suleiman Massarweh
Journal: New England Journal of Medicine (2012)

A 56-year-old female smoker presented with cough, a weight loss of 27 kg, and diffuse bone pain. There was digital clubbing, and the palms had a raised, velvety texture. There was a fixed, tender lump (4 cm in diameter) on the right lower leg and one over the lower lumbar spine.
Abstract 4760: A novel immune potentiating strategy for cancer vaccine
Authors: Hong Qin, Soung-chul Cha, Xiao-feng Qin, Yong-Jun Liu, Larry W. Kwak
Journal: Cancer Research (2010)

Abstract A major obstacle for translational research of cancer vaccine is the weak immunogenicity of tumor antigens. Thus, the development of new, more potent strategy that aims at breaking such an immune tolerance is a prerequisite of vaccine therapy. Here we show that the unexpected effect of inducing sterile inflammation at vaccination sites by myotoxins potentiated induction of tumor-specific immunity by genetic vaccines and converted a non-immunogenic lymphoma idiotype antigen into a tumor rejection vaccine. This potent immunostimulatory effect was immune-mediated, requiring recruitment of dendritic cells (DC). Sterile inflammation induced by myotoxins was associated with upregulation of chemokines, proinflammatory cytokines, Toll-like receptors and their endogenous ligands, and activation of innate immunity. Mechanistic experiments in vivo also elucidated the requirement for genes triggering DC maturation including TLR signaling and CD40. These studies suggest that inducing sterile inflammation at vaccination sites generates a favorable microenvironment that promotes adaptive immunity. This novel mechanism of immune potentiation may be exploited for development of adjuvants for vaccines against cancer. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4760.
Comparison of the Thrombotest with the One-Stage Prothrombin Time
Authors: Armand J. Quick, Clara V. Hussey
Journal: New England Journal of Medicine (1961)

THE one-stage prothrombin time was developed to serve as a diagnostic tool and was initially employed to study the bleeding state that was frequently encountered postoperatively in the jaundiced patient.1 A sequence to this investigation was the finding that the prothrombin time was increased in vitamin K deficiency and in poisoning from spoiled sweet-clover hay.2 As a result of these observations, as well as because of the simplicity of the procedure, the test was immediately employed to control dosage when bishydroxycoumarin was introduced into therapy.3 , 4 Before this new use the test had been perfected by the preparation of a thromboplastin . . .
Metastatic Inguinal Lymphadenopathy
Authors: Enes Hajdarbegovic, Deepak Balak
Journal: New England Journal of Medicine (2012)

A 59-year-old man presented with a weeping mole on his back that had been growing for 8 years. On examination, a 10-cm ulcerated lesion was found on his lower back, and multiple subcutaneous areas of swelling were found in both inguinal regions.
Abstract LB-333: A CREBZF/Zhangfei isoform activates CHOP and promotes apoptosis during prolonged endoplasmic reticulum stress
Authors: Yu Li, Yani Zhang, Timothy E. Audas, Amanda C. Martyn, Ray Lu
Journal: Cancer Research (2010)

Abstract The basic leucine zipper transcription factor CREBZF (Zhangfei or ZF) was identified through its interaction with Herpes Simplex Virus-1 related cellular protein HCF-1, and has been implicated in cellular stress responses through its interaction with other proteins, such as CREB3/Luman and ATF4. Here we investigated the production of four CREBZF isoforms, which arise from translational initiation of a downstream AUG at codon 83 and mRNA alternative splicing that adds an IFFFR pentapeptidyl tail to the C-terminus. We found that in addition to transcriptional induction, the short-tailed CREBZF (stZF) isoform was specifically induced by prolonged ER stress treatment and amino acid deprivation. This stZF isoform is a potent transcriptional activator of the pro-apoptotic protein CHOP. Overexpression of stZF activates transcription of CHOP through a CCAAT enhancer binding protein (C/EBP)-ATF site, and promotes apoptosis. We propose that 1) CREBZF is a key component of the integrated stress response; 2) stZF is tightly regulated and induced primarily under prolonged cellular stress, and is essential for the role of CREBZF in inducing CHOP and promoting cell death. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-333.
Ovarian Cancer and Older Women: Is Treatment Less Aggressive?
Authors: Susan Jenks
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Ovarian Cancer and Older Women: Is Treatment Less Aggressive? Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 1, 1 January 1992, Pages 6–7, https://doi.org/10.1093/jnci/84.1.6 Published: 01 January 1992
Abstract 956: Targeting prostate cancer chemoprevention via the androgen receptor in a preclinical mouse model
Authors: Hiroyuki Koike, Marco A. De Velasco, Yuka Miyazaki, Chiori Asahi, Hiroshi Ushida, Keiji Shimada, Kazuhiro Yoshikawa, Kazuto Nishio, Noboru Konishi, Hirotsugu Uemura
Journal: Cancer Research (2010)

Abstract Prostate cancer is strongly associated with increasing age, with about 96 % of the cases occurring in men over 60 years of age. The high incidence and late age of onset make prostate cancer an ideal target for chemoprevention strategies as even a modest delay in carcinogenesis would significantly reduce the incidence of the disease. Chlormadinone acetate (CA) is one of the steroidal anti-androgen agents used in combined androgen blockade therapy as well as monotherapy for prostate cancer in Japan. However, no reports have been published for the chemopreventive potential of CA. We evaluated the efficacy of low-dose administration of CA to prevent or suppress prostate cancer using our PTEN conditional gene targeting mouse model. Six-week-old mice were injected subcutaneously with CA (50 mg/kg 3X/week) until the age of 15 or 20 weeks. The genitourinary tracts (GUTs), consisting of the prostate, urethra, bladder, seminal vesicles and coagulating gland, were collected, weighed, fixed in formalin and imaged. GUT weights were significantly lower in CA-treated mice compared to untreated controls in a time dependent manner (P&amp;lt;0.01). Morphometric image analysis performed on the GUT to measure the prostate area revealed significant shrinkage of the prostate gland in CA-treated mice vs. the corresponding controls (P&amp;lt;0.001). Histopathological distribution analysis of normal, prostatic intraepithelial neoplasia (PIN) and tumor glands showed a decrease in the PIN but not normal or cancer glands in 15-week-old CA-treated mice compared to controls. However, similar analysis showed a dramatic decrease of cancer gland shrinkage in 20-week-old CA-treated mice with only marginal decreases of PIN compared to untreated controls. Immunohistochemical analysis of androgen receptor (AR) expression showed a significant decrease in nuclear localization and intensity CA-treated mice (P&amp;lt;0.001). Proliferation analysis of tumors by PCNA immunostaining showed a 30% reduction in 20-week-old mice treated with CA compared to untreated control mice (P&amp;lt;0.001). The apoptotic index in tumors if mice treated with CA increased three-fold to 3.16% compared to 1.12% on the corresponding control mice (P&amp;lt;0.004). Our data suggests that chemopreventive treatment with CA does not prevent the incidence of prostate cancer, however, it does inhibit the growth and progression of prostate cancer. Our findings may reveal a promising prophylactic strategy for the chemopreventive treatment of prostate cancer in high-risk individuals. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 956.
Gastroesophageal Reflux and Myocardial Imaging
Authors: LIOE-FEE de GEUS-OEI, JAN-WILLEM ARNDT, MARCEL STOKKEL
Journal: Clinical Nuclear Medicine (2000)

A 74-year-old woman who previously underwent a Billroth II procedure was examined before abdominal surgery. She reported typical angina pectoris, grade III–IV, and dyspnea. Consequently, she was referred to the nuclear medicine department for a myocardial perfusion study. The 2-day pharmacologic stress and rest study using adenosine revealed T-wave inversions in V2-V5 on an electrocardiogram but no ischemia. In addition, scintigraphy showed neither persistent defects nor ischemia. During SPECT acquisition, however, severe gastroesophageal reflux was observed. Excretion of tetrofosmin in the intestines is often regarded as a disadvantage. Nevertheless, in this patient, this feature helped to establish the diagnosis.
THE MECHANISM OF SYMPTOMS IN AORTIC STENOSIS: NOVEL INSIGHTS FROM INTRACORONARY MEASUREMENTS DURING EXERCISE
Authors: Matthew Lumley, Rupert Williams, Satpal Arri, Kaleab Asrress, Brian Clapp, Simon Redwood, Jan Piek, Michael Marber, John Chambers, Maria Siebes, Divaka Perera
Journal: Journal of the American College of Cardiology (2015)
A Clinical and Experimental Study of Isuprel in Spontaneous and Induced Asthma
Authors: Francis C. Lowell, John J. Curry, Irving W. Schiller
Journal: New England Journal of Medicine (1949)

ONE of the synthetic analogues of epinephrine — l-(3, 4 -dihydroxyphenyl)-2-isopropylaminoethanol — has been studied under the name of aleudrin for a number of years in Europe. The experimental and clinical use of this drug in bronchial asthma and emphysema has been reviewed by Dautrebande,1 and a report has been published in this country by Charlier.2 The drug, administered as an aerosol, has been described as being especially effective in relieving attacks of bronchial asthma and significantly more active than epinephrine.In this country Segal3 has reported excellent results in the treatment of bronchial asthma with the same preparation, also . . .
Abstract 4092: Alteration of caspase-mediated events following DNA damage due to the absence of poly(ADP-ribose) glycohydrolase
Authors: Yiran Zhou, Xiaoxing Feng, David W. Koh
Journal: Cancer Research (2011)

Abstract The synthesis of poly(ADP-ribose) (PAR) is an immediate cellular response to DNA damaging stresses. We reported previously that the absence of PAR glycohydrolase (PARG) led to increased cell death following DNA-damaging treatments. OBJECTIVE: To investigate the possible mechanism underlying the ability of PARG inhibition to produce cell hypersensitivity of DNA-damaging stresses. METHODS: Utilizing PARG null trophoblast stem (TS) cells, DNA damage following treatment with N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) or UV radiation were examined by immunocytochemistry. Cell viability was measured by DAPI staining and caspase 3/7 activity was measured by activity assay and the immunoblotting detection of procaspase-3 and PARP-1 cleavage. RESULTS: Increased amounts of DNA alkylation and UV-induced DNA damage were observed in PARG null TS cells. In addition, elevated amounts of cell death were detected following those treatments. However, both procaspase-3 and PARP-1 cleavage were detected at decreased levels and in a delayed fashion after UV treatment in PARG null TS cells. Caspase-3/7 activity assay confirmed the decreased activation of caspase-3/7 in PARG null-TS cells. Furthermore, PARG null-TS cells exhibited less caspase-3/7 activity after UV radiation than wild type TS cells. CONCLUSION: The results show that the functionality of caspase-3 following DNA damage is decreased and delayed due to the absence of PARG. This suggests that PAR or PARG itself may play a role in modulating caspase-mediated apoptosis after UV-induced DNA damage and cell death. 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 4092. doi:10.1158/1538-7445.AM2011-4092
Hyaluronic acid injection for sustained control of bleeding from a sclerotic ulcer base
Authors: H. Kim, S. Park, M. Park, W. Moon
Journal: Endoscopy (2012)

A 55-year-old man with recurrent duodenal ulcers presented to our institution with massive hematemesis. Emergent endoscopy revealed a duodenal ulcer scar and pulsatile bleeding at the base of the ulcer ([Fig. 1]).
Abstract 1911: Dietary intake of riboflavin and risk of lung cancer among non-smokers: A prospective cohort study among Chinese women
Authors: Qiuyin Cai, Alicia Beeghly-Fadiel, Martha J. Shrubsole, Xiao-Ou Shu, Gong Yang, Bu-Tian Ji, Honglan Li, Wong-Ho Chow, Yu-Tang Gao, Wei Zheng
Journal: Cancer Research (2011)

Abstract Lung cancer is the leading cause of cancer death in the United States and many other countries. A significant subset of lung cancers is not associated with smoking, and risk factors for these cancers remain unclear. Riboflavin (vitamin B2), a water-soluble vitamin, is involved in vital metabolic processes and is necessary for normal cell function, growth, and energy production. Riboflavin is the central component of the flavin mononucleotide (FMN) and flavin dinucleotide (FAD), coenzymes for a wide variety of oxidative enzymes. We prospectively examined the association of dietary intake of riboflavin with lung cancer risk in the Shanghai Women's Health Study cohort. A total of 73,237 women aged 40-70 years and free of cancer at enrollment were included in this analysis. Usual dietary intake was assessed at baseline (1997-2000) through in-person interviews by using a validated food-frequency questionnaire. We used Cox proportional hazards regression to estimate the relative risks (RR) and 95% confidence intervals (CI) for the association of lung cancer risk with dietary riboflavin consumption. In 665,554 person-years of follow-up, we identified 328 lung cancer cases, of which 303 were non-smokers. Dietary intake of riboflavin was inversely associated with lung cancer risk. The RRs (95% CI) of developing lung cancer among non-smokers decreased with increasing quintiles of riboflavin intake (P for trend = 0.007) from 1.0 to 1.01 (0.73-1.42), 0.77 (0.53-1.13), 0.81 (0.55-1.20), and 0.51 (0.31-0.83) for the lowest to highest quintiles. Exclusion of 51 cases diagnosed within two years of follow-up did not change the HR estimations appreciably. Further, adjusting for dietary intakes of other B vitamins (B1, B6, B12, niacin, and folate) and methionine did not meaningfully affect the HR estimates. No statistically significant associations were found for other B vitamins. In summary, our findings among non-smoking Chinese women suggest that dietary intake of riboflavin may reduce the risk of lung cancer. 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 1911. doi:10.1158/1538-7445.AM2011-1911
Abstract P6-04-07: Pathway Activation Probability Score Analysis Reveals Patterns of Pathway Deregulation in Inflammatory Breast Cancer
Authors: S Van Laere, I Van der Auwera, P van Dam, P Vermeulen, L. Dirix
Journal: Cancer Research (2010)

Abstract Background: Inflammatory breast cancer (IBC) is the most aggressive manifestation of primary epithelial breast cancer and differs from non-IBC both from a clinical and a biological perspective. The high metastatic potential of IBC is highlighted by the low 5-year survival rate of 50%. In the past, we demonstrated that IBC is characterized by a specific molecular profile, partly mediated by increased NFkB-activation. In the current study we aim to identify additional molecular alterations responsible for the altered gene expression profile. Methods: We profiled 46 IBC samples and 56 non-stage matched nIBC samples using the Affymetrix HGU133plus2 platform. Using a set of recently published gene signatures (Gatza et al, PNAS, 2010) we calculated the activation probability scores for 18 distinct pathways (ER, PR, HER2, P53, P63, EGFR, RAS, SRC, TNFa, INFa, INFg, TGFb, STAT3, E2F1, PI3K, AKT, CTNNB and MYC). Unsupervised cluster analysis was performed on the IBC samples only to identify IBC-specific transcriptional heterogeneity. The silhouette-algorithm was used to test the robustness of clustering. Supervised analysis was performed to compare IBC to nIBC. All P-values were FDR-corrected. Results: Using only IBC samples, unsupervised hierarchical cluster analysis identified four robust sample clusters (Average silhouette width = 0.345; P&amp;lt;0.0001). Interestingly, the primary bifurcation of the resulting dendrogram is determined by INFa-, INFg-and TNFa-signalling. In addition to ER-, PR-, HER2- and P53-signalling, the transcriptional heterogeneity in IBC is also determined by AKT-, RAS-, STAT3- and TGFb-signalling. When comparing IBC to nIBC we identified 12 pathways that are differentially regulated (P&amp;lt;0.05). Out of these 12 pathways, 4 (CTNNB, PI3K, E2F1 and P63) did not reveal any IBC-specific heterogeneity and all of these were hyperactivated in IBC. Interestingly, the PI3K-, E2F1- and P63-pathways form a tightly correlated signaling nodule (Spearman correlation coefficients &amp;gt; 0.65, P&amp;lt;0.001). Conclusions: In this study we demonstrated that IBC is transcriptionally heterogeneous and this heterogeneity is mainly determined INFa-, INFg-and TNFa-signalling. Also, we identified four pathways (CTNNB, PI3K, E2F1 and P63) which are differentially regulated in IBC as compared to nIBC but which do not contribute to the establishment of transcriptional heterogeneity within IBC. Therefore, we reason that these pathways can be added to the molecular repertoire of IBC. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-04-07.