tbuckley/cabot-search huggingface dataset:
Case 6-1993
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, Robert B. Greer, Andrew E. Rosenberg
Journal: New England Journal of Medicine (1993)

Presentation of CaseA 69-year-old woman was admitted to the hospital because of pain in the right thigh and fever.The patient was in good health until approximately one week earlier, when urinary frequency developed and a potential urinary tract infection was treated with cefoperazone; a urine culture yielded Escherichia coli. Five days before admission continuous pain developed in the distal right thigh and knee. Three days later x-ray films of the right thigh (Figure 1) showed a sclerotic lesion in the middle third of the femur, with periosteal bone formation and cortical thickening. A radionuclide bone scan revealed a . . .
Feds Move to Strengthen Tobacco Control
Authors: E. DeVita
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Feds Move to Strengthen Tobacco Control Get access Elizabeth DeVita Elizabeth DeVita Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 7, April 1992, Page 473, https://doi.org/10.1093/jnci/84.7.473 Published: 01 April 1992
P237 The utility of the Nottingham Health Profile in exacerbations of non-cystic fibrosis bronchiectasis
Authors: M. P. Murray, J. Twiss, S. P. McKenna, A. T. Hill
Journal: Thorax (2010)

<h3>Aim</h3> The aim of this study was to assess the utility of a generic health status questionnaire, the Nottingham Health Profile (NHP) in non-cystic fibrosis bronchiectasis. <h3>Methods</h3> The NHP is a generic health status measure that contains 6 scales: energy (3 items), pain (8 items), emotional reactions (9 items), sleep (5 items), social isolation (5 items) and physical mobility (8 items). In addition the NHP also has a total score including 24 items called the NHP-D. High scores on the questionnaire indicate worse health status. Patients with an exacerbation of bronchiectasis requiring 2 weeks9 intravenous antibiotic therapy completed the NHP at the start of the exacerbation and then 1 week following completion of treatment. In addition, they completed the Leicester Cough Questionnaire, a cough severity score, previously validated for use in bronchiectasis. The LCQ assesses three components: physical, psychological and social. The total score ranges from 3 to 21 with a lower score indicating a more severe cough. The change scores and effect size (ES) of the NHP and LCQ were measured. The ES is based on the ratio of difference between the mean measure at baseline and at follow-up (related to the SD for baseline scores) and the thresholds are: 0.2 for a small group change, 0.5 for a moderate group change, and 0.8 for a large group change. <h3>Results</h3> 44 patients completed the study. Abstract P237 Table 1 shows the change in the components of the NHP and the LCQ at the start and end treatment of the exacerbation. The change score and effect size in the NHP included: Energy Level: −18.18 and −0.56; Pain Scale: −4.26 and −0.14; Emotional Reaction:−7.58 and −0.29; Sleep Scale:−18.2 and −0.56; Social Isolation: −5.45 and −0.21; Physical Mobility: −9.94 and −0.34; NHP-D: −2.27 and −0.43. The change score and effect size for the LCQ included: Physical: 1.28 and 1.32; Psychological: 1.61 and 1.11; Social: 1.62 and 1.09; Total: 4.51 and 1.25. <h3>Conclusion</h3> The NHP was responsive to change in acute exacerbations of bronchiectasis but further validation studies are needed.
Use of dual-color interphase FISH for the detection of inv(16) in acute myeloid leukemia at diagnosis, relapse and during follow-up: a study of 23 patients
Authors: M Mancini, M Cedrone, D Diverio, B Emanuel, M Stul, H Vranckx, M Brama, MR De Cuia, M Nanni, F Fazi, C Mecucci, G Alimena, A Hagemeijer
Journal: Leukemia (2000)
Repeated Aerosol Exposure to Small Doses of Allergen
Authors: S. HASAN ARSHAD, ROBERT G. HAMILTON, N. FRANKLIN ADKINSON
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

To improve our understanding of the pathophysiology of chronic allergic asthma, we mimicked natural allergen exposure by giving tiny doses of dust-mite extract (equivalent to estimated daily exposure in a typical bedroom) in three weekly sessions for 4 wk. Nine mild asthmatic adults who were highly sensitive to dust-mite allergen participated in the study. Serial assessments of bronchial reactivity by methacholine challenge, pulmonary function, symptoms, and bronchodilator requirements were obtained. Seven of nine subjects had a twofold or more (median: 6, range: 2.7 to 25) reduction (p = 0.008) in PC20, after which saline inhalations were substituted for dust-mite extract. Bronchial reactivity returned to normal within 2 to 3 wk after cessation of dust-mite inhalations in all but one subject. Predosing FEV1 dropped 10% over 4 wk of provocation (p = 0.001) and 7 of 9 returned to prestudy level within 2 wk after dosing was stopped. Late-phase responses were seen in 6 of 9 subjects. We conclude that repeated aerosol exposure to dust-mite allergen in doses comparable to natural bedroom exposure is sufficient to adversely affect pulmonary function and bronchial hyperractivity in sensitized individuals. These changes are rapidly reversible. This low-dose provocational strategy provides an attractive model for the experimental study of allergic asthma. Arshad SH, Hamilton RG, Adkinson NF, Jr. Repeated aerosol exposure to small doses of allergen: a model for chronic allergic asthma.
Standardized Uptake Value as an Unreliable Index of Renal Disease on Fluorodeoxyglucose PET Imaging
Authors: HONGMING ZHUANG, PAULO S. DUARTE, MICHAEL POURDEHNAD, PEIYONG LI, ABASS ALAVI
Journal: Clinical Nuclear Medicine (2000)

Fluorine-18 2-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography has been used extensively in the diagnosis of malignant conditions with high rates of sensitivity and specificity. However, increased FDG uptake is not limited to malignant tissue. In general, lesions with a mild degree of FDG uptake as measured by standardized uptake values less than 2.0 are considered benign, whereas those with values greater than 2.5 are usually regarded as malignant. Standardized uptake values in the kidney can be as high as 22 as a result of excretion of FDG through urine. Two cases are reported in which renal abnormalities could not be distinguished from urine based on standard uptake values alone.
1094 URI GENERATES METABOLIC ALTERATIONS-DEPENDENT DNA DAMAGE INDUCING HETEROGENEOUS LIVER TUMOURS
Authors: K.S. Tummala, A.L. Gomes, I.M. Ruppen, L. Bakiri, R.C. Olivas, O. Graña, M.P. Ximénez de Embún, M. Cañamero, D.G. Pisano, E. Wagner, M. Rodriguez-Justo, N. Djouder
Journal: Journal of Hepatology (2013)
Abstract LB-308: Hypoxia affects gene expression and proteome of prostate cancer cells
Authors: Christian R. Gomez, Gaylord J. Knutson, Claire A. Schreiber, Farhad Kosari, George Vasmatzis, Stanimir Vuk-Pavlovic
Journal: Cancer Research (2011)

Abstract Tumor-associated hypoxia facilitates malignant progression, metastasis and poor prognosis in prostate cancer (CaP); however, effects of oxygen tension (pO2) in CaP are just beginning to be investigated. To establish mechanisms whereby hypoxia enhances malignant properties and survival of CaP and to identify pO2-regulated tumor-associated macromolecules, we propagated CaP cell lines LnCaP, VCaP and DU145 in hypoxia (pO2=2 kPa) and compared them with normoxically grown cells (pO2=20 kPa); hypoxic cells proliferated faster and secreted more vascular endothelial growth factor (p&amp;lt;0.05). Transcriptome studies revealed different gene expression in cells grown in hypoxia relative to those in normoxia. Interestingly, in hypoxic cells transcripts associated with cancer and urologic disease were overexpressed in comparison to normoxic cells (p&amp;lt;0.001) suggesting an association of low pO2 and aggressive features of CaP. Further, we analyzed the transcriptome in primary CaP cells isolated by laser-capture microdissection (LCM) and whole CaP tissue. We compared the data to those from CaP cells cultured at pO2=20 kPa or pO2=2 kPa. Notably, hypoxia increased transcript levels for pyruvate dehydrogenase kinase isozyme 1, nuclear prelamin A recognition factor, glucose phosphate isomerase, and glyceraldehyde-3-phosphate dehydrogenase in all three cell lines (p&amp;lt;0.05) to levels comparable to those found in primary bulk tissue and LCM isolated cells (p&amp;lt;0.005). This finding suggests that gene expression in hypoxically cultured cells is more akin to that in tumor cells in situ than are cells grown normoxically. By 2D-gel electrophoresis, we found that change in pO2 affected the proteome mostly quantitatively (i.e., by change in spot intensity). Our results suggest that hypoxia affects transcriptome and proteome in CaP cells. In addition, we screened 20 patient sera and 20 healthy control sera for spontaneous antibodies cross-reactive with VCaP cells and found that the sera reacted with numerous proteins, some previously reported to elicit an immune response in CaP patients (e.g., nucleoporin 62 and transitional endoplasmic reticulum ATPase). By this method we detected numerous novel autoantigens (under validation). Currently we are clarifying the pO2 effects on the relationship of transcriptome, proteome and tumor-associated antigens in CaP cells. Support: DOD PC094680 (CRG), Minnesota Partnership for Biotechnology and Medical Genomics, Mayo Clinic Prostate SPORE 5P50CA091956 (FK); Mrs. Adelyn L. Luther, Singer Island, Florida and Mayo Clinic Cancer Center (SV-P). 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 LB-308. doi:10.1158/1538-7445.AM2011-LB-308
Influence of Cigarette Smoking on the Efficacy of Radiation Therapy in Head and Neck Cancer
Authors: George P. Browman, Gene Wong, Ian Hodson, Jinka Sathya, Rosemary Russell, Lisa McAlpine, Peter Skingley, Mark N. Levine
Journal: New England Journal of Medicine (1993)

Smoking is a risk factor for several cancers and may also limit the efficacy of treatment. In this study, we evaluated the influence of cigarette smoking during radiation therapy on the efficacy of treatment in patients with head and neck cancer.Using a questionnaire, we obtained information on smoking behavior at base line and weekly during therapy in 115 patients with head and neck cancer who were treated with radiation therapy with or without fluorouracil. The side effects of therapy were evaluated weekly, and response was assessed 13 weeks after treatment was completed. The main outcomes measured were treatment response and survival.The prognostic variables were similar among the patients who smoked and those who did not smoke during treatment. The 53 patients who continued to smoke during radiation therapy had a lower rate of complete response (45 percent vs. 74 percent, P = 0.008) and poorer two-year survival (39 percent vs. 66 percent, P = 0.005) than the 62 patients who did not smoke or who had quit before treatment. Among the nonsmoking patients, mortality was influenced by the length of time between quitting and treatment, with a risk reduction (relative to that for patients who continued to smoke) of 40 percent for patients who had quit less than 12 weeks before diagnosis and of 70 percent for patients who had quit more than 1 year before diagnosis. After adjustment for other variables with proportional-hazards regression analysis, smoking remained an independent prognostic factor (P = 0.002), with a relative risk of 2.5 (95 percent confidence interval, 1.4 to 4.4) favoring the patients who abstained from smoking. The results could not be explained by the type of chemotherapy received, the presence of coexisting morbid conditions, differences in the side effects of radiation, or the number of interruptions of treatment.Patients with head and neck cancer who continue to smoke during radiation therapy have lower rates of response and survival than patients who do not smoke during radiation therapy.
AB1038 Metabolic Syndrome in Patients with Newly Diagnosed Inflammatory Joint Diseases
Authors: A. Kononoff, L. Arstila, H. Kautiainen, P. Elfving, E. Savolainen, J. Rutanen, O. Marjoniemi, H. Niinisalo, O. Kaipiainen-Seppänen
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Inflammatory joint diseases are systemic processes conveying an increased risk for cardiovascular (CV) diseases. The traditional risk factor profile does not explain the augmented risk in inflammatory joint diseases. Most work on CV risk evaluation has been done on established disease. We aimed to evaluate the occurrence of metabolic syndrome (MetS), a cardiovascular risk constellation, by using a simple and clinically applicable method, the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATPIII) definition of MetS, at diagnosis of and before any disease modifying treatment for, rheumatoid arthritis (RA), spondyloarthritis (SpA) and undifferentiated arthritis (UA), in a population based inception cohort. <h3>Objectives</h3> To investigate the occurrence of MetS among patients with newly diagnosed RA, SpA and UA. <h3>Methods</h3> Patients with inflammatory joint diseases participating in Northern Savo 2010 Study were evaluated for components of MetS according to the definition by NCEP-ATPIII. <h3>Results</h3> Two-hundred and two patients, 58 with RA, 69 with SpA and 75 with UA, were classified according to their metabolic condition. MetS was detected in half of the patients with RA and UA and in one third of patients with SpA. There were no differences between the sexes. Disease activity increased along with the number of MetS components in RA and UA, but the association was significant only in UA, p=0.021. <h3>Conclusions</h3> Metabolic syndrome is common already at diagnosis of inflammatory joint diseases. If this is a consequence of the insiduously progressing rheumatoid inflammation, or a risk factor in itself for rheumatic diseases, is an intriguing question. Nevertheless, metabolic syndrome contributes to the inflammatory activity of arthritis and efforts to influence the metabolic burden should be undertaken right from the beginning of treating early arthritis. <h3>References</h3> Chung CP, Oeser A, Solus JF, Avalos I, et al. Prevalence of the metabolic syndrome is increased in rheumatoid arthritis and is associated with coronary atherosclerosis. Atherosclerosis 2008;196:756-63 Karvounaris SA, Sidiropoulos PI, Papadakis JA, et al. Metabolic syndrome is common among middle- to older-aged Mediterranean patients with rheumatoid arthritis and correlates with disease activity: a retrospective, cross-sectional, controlled study. Ann Rheum Dis 2007;66:28-33 doi:10.1136/ard.2006.053488 Sidiropoulos PI, Karvounaris SA, Boumpas DT. Metabolic syndrome in rheumatic diseases: epidemiology, pathophysiology, and clinical implications. Arthr Res Ther 2008;10:207. doi:10.1186/ar2397 <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3112
Abstract 2647: <i>In vitro</i> niche created by cancer stem-like cells derived from mouse induced pluripotent stem cell.
Authors: Akifumi Mizutani, Shuichi Matsuda, Tin Yan, Tatsuyuki Sota, Tomonari Kasai, Takayuki Kudoh, Hiroshi Murakami, Masaharu Seno
Journal: Cancer Research (2013)

Abstract Cancer stem cell (CSC) is a cell within tumor, which is considered to possess the capacity of self-renewal and differentiation for providing heterogeneous lineages of cancer cells in the tumor. Previously, we converted mouse iPS (miPS) cells into CSCs by treatment with conditioned medium prepared from Lewis Lung Carcinoma culture (miPS-LLCcm)1. RT-PCR and FACS analysis revealed that miPS-LLCcm could give rise to endothelial cells. When miPS-LLCcm were cultured on MatrigelTM, they exhibited the tubular structure containing CD31 positive cells. In contrast, undifferentiated cells enriched population, which were resistant to puromycin (puro) as parental miPS cell2, failed to form tubes. After puro was removed to allow the differentiate cells to survive, the tube formation was observed again, indicating that the differentiated cells were likely to contribute to tube formation. To confirm the stability of this tube formation capacity, we repeated further two cycles of puro selection and releasing differentiation. As the result, the tube formation ability of the differentiated cells decreased. In parallel, we added the conditioned medium of miPS-LLCcm culture into sphere-forming assay, observed the increase of size and number of spheroids. This effect was partly depended on Notch signaling pathway. These results raise the possibility that the differentiated cells from miPS-LLCcm including endothelial cells or their progenitor cells should be required for the maintenance of miPS-LLCcm to differentiate towards vascular endothelial linage. Collectively, we concluded that the differentiated cells from miPS-LLCcm create a niche in vitro for the self-renewal of CSC in the aspect of not only proliferation but also differentiation lineage. 1. Chen, L., et al. PLoS ONE 7, e33544 (2012). 2. Okita, K., et al. Nature 448, 313-317 (2007). Citation Format: Akifumi Mizutani, Shuichi Matsuda, Tin Yan, Tatsuyuki Sota, Tomonari Kasai, Takayuki Kudoh, Hiroshi Murakami, Masaharu Seno. In vitro niche created by cancer stem-like cells derived from mouse induced pluripotent stem cell. [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 2647. doi:10.1158/1538-7445.AM2013-2647
Abstract 1107: Transforming growth factor-beta (TGF-β) increases Par-4 expression via activation of Smad and NF-κB in endometrial cancer cells
Authors: Mohan Singh, Parvesh Chaudhry, Eric Asselin
Journal: Cancer Research (2011)

Abstract Prostate apoptosis response-4 (Par-4) gene was originally identified in prostate cancer cells undergoing apoptosis. Further studies have shown that Par-4 selectively induces apoptosis in cancer cells without effecting normal cells. Recently it has been evidenced that Par-4 has a tumor suppressor role in endometrial cancer. We have previously demonstrated that TGF-β isoforms are expressed in endometrial tumors and determined cellular fate by regulating apoptosis through the activation of NF-κB. In the present study, we have investigated the mechanisms through which TGF-β isoforms regulate Par-4 expression in endometrial cancer cells. KLE and Hec-1-A endometrial cancer cell lines were used as model in this study. Transcript and protein levels were assessed by reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting, respectively. The results revealed that both cell lines express TGF-β receptor I and receptor II. Blocking TGF-β signalling by neutralizing TGF-β antibody reduced endogenous Par-4 mRNA and protein levels. Exogenous treatment with all the TGF-β isoforms (10ng/ml) upregulated Par-4 mRNA and protein levels. Furthermore, there was increase in the levels of phosphorylated Smad2 and Smad3 in response to TGF-β treatment, thus indicating that Smad pathway was activated by TGF-β isoforms in these cells. However, there was no change in the protein levels of total Smad2/3. TGF-β treatment resulted in rapid phosphorylation of IκB-α with no effect on total IκB-α levels thus suggesting an activation, nuclear translocation and increase in transcriptional activity of NF-κB. Collectively, these results suggest that each TGF-β isoform induces Par-4 levels via the activation of Smad and NF-κB pathway in endometrial cancer cells. Since downregulation of Par-4 is a common event in different types of cancers, we suggest in these cases that TGF-β could be an interesting therapy and strategy to induce Par-4 and apoptosis in endometrial cancer cells. 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 1107. doi:10.1158/1538-7445.AM2011-1107
Resistance to Activated Protein C as a Basis for Venous Thrombosis
Authors: Peter J. Svensson, Bjorn Dahlback
Journal: New England Journal of Medicine (1994)

In three families with various forms of venous thrombosis, we observed an apparently inherited poor response to the anticoagulant activated protein C (APC). The condition was due to a deficiency in a previously unrecognized anticoagulant factor that functioned as a cofactor to activated protein C.We conducted the present study to determine the prevalence of resistance to APC in patients with venous thrombosis. We compared 104 consecutive patients with venous thrombosis confirmed by objective tests with 130 controls. In addition, 211 members of 34 families of persons with resistance to APC were studied. The anticoagulant response to APC was measured with a modified version of the activated partial-thromboplastin time test; the results were expressed as APC ratios.Forty-five percent of patients had a family history of thrombosis. A significant (P < 0.001) difference in APC ratios was observed between the controls and the patients with thrombosis. For 33 percent of patients, the APC ratio was below the 5th percentile of the control values, although the results of the family studies suggested that the prevalence of APC resistance may be even higher (approximately 40 percent) in the patients with thrombosis. The inherited nature of the defect was confirmed in a majority of cases, and the family studies suggested the mode of inheritance to be autosomal dominant. The thrombosis-free survival of APC-resistant family members was significantly less than that of non-APC-resistant family members.There was a high prevalence of APC resistance among young persons with a history of venous thrombosis, and this resistance appeared to be inherited as an autosomal dominant trait.