tbuckley/cabot-search huggingface dataset:
Abstract 1873: Effect of intermittent calorie restriction on cancer stem cells.
Authors: Yi Luo, Yasuhiko Kitadai, Yoshitomo Chihara, Rina Fujiwara, Kiyohide Fujimoto, Hiroki Kuniyasu
Journal: Cancer Research (2013)

Abstract Effect of intermittent calorie restriction (ICR) on cancer is controversial. We then examined the effect of ICR and food contents on cancer using mouse model. CT26 mouse colon cancer cells were inoculated into the back of syngeneic BALB/c mouse. A 24 hours-fasting was performed once a week for 4 weeks. A control diet and a high calorie diet were used for feeding. The body weight at week 4 of mice was not different among control diet (Group C), control diet+ICR (Group CI) and high fat diet+ICR (Group FI). The tumor weight, nodal metastasis and CD133-positive cancer stem cells (CSC) in the tumor were more pronounced in Group CI and FI than those in Group C and F. Blood CD133 mRNA levels after fasting breakage were increased in Group CI and FI. We have reported the prometastatic effect of trans fatty acids in colorectal cancer. Here effect of oral intake of trans fatty acids on tumor stem cells with ICR was examined using the same model. Mice fed with 10% elaidic acid diet with ICR- (Group E) or ICR+ (Group EI) were compared with Group C and CI. The tumor weight and tumor MIB1 index was Group EI, Group E, Group CI and Group C in high order. In Group EI, nucleostemin (NS)-positive tumor cells were transiently increased on the next day of ICR. During 12 ICR cycle, NS-positive CSCs were gradually increased in Group EI. These findings suggest that ICR might enhance cancer stem cell-activating factors. Citation Format: Yi Luo, Yasuhiko Kitadai, Yoshitomo Chihara, Rina Fujiwara, Kiyohide Fujimoto, Hiroki Kuniyasu. Effect of intermittent calorie restriction on cancer stem cells. [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 1873. doi:10.1158/1538-7445.AM2013-1873
Tissue inhibitor of metalloproteinases-1 protects the human breast carcinoma cell line MCF-7 S1 against anthracycline-induced cell death by activation of the akt survival pathway.
Authors: S[ Würtz, A Schrohl, N Brünner, U Lademann
Journal: Cancer Research (2009)

Abstract Abstract #2019 Würtz S and Schrohl A contributed equally.&amp;#x2028; Background. A large proportion of breast cancer patients are offered chemotherapy following primary surgery, however, many of these patients do not benefit from the treatment. Currently, only few markers exist to predict whether a breast cancer patient will respond to chemotherapy in general or to specific types of chemotherapy. Thus, additional predictive markers need to be identified to ensure a more effective treatment of the patients. In this regard, recent clinical studies performed in our laboratory have demonstrated that high tumor tissue levels of TIMP-1 are associated with a poor response to the most frequently used chemotherapeutic drugs (CMF or anthracyclines) (Schrohl et al., Clin. Cancer Res. 2006 and Klintman et al. manus. in prep.). The purpose of the present study was to investigate the molecular explanation for the clinical findings concerning the predictive value of TIMP-1 using an in vitro approach.&amp;#x2028; Methods. We stably transfected the human breast carcinoma cell line MCF-7 S1 with the human TIMP-1 gene and established single cell clones expressing different levels of TIMP-1. We then compared the sensitivity of these cells to epirubicin and taxol using cell death and apoptosis assay. In addition, we investigated the signalling pathway that could be involved in the TIMP-1 mediated protection against treatment using western blotting of key molecules.&amp;#x2028; Results. We found that clones expressing high levels of TIMP-1 were significantly less sensitive to epirubicin. In contrast, no difference in sensitivity to taxol was demonstrated between high and low TIMP-1 clones. When investigating the signalling pathway involved in the difference in sensitivity we found that phosphorylated Akt was highly up-regulated in the high TIMP-1 clones compared to the low TIMP-1 clones following chemotherapeutic treatment.&amp;#x2028; Conclusion. TIMP-1 protects the MCF-7 S1 cells against anthracycline-induced cell death but not against taxol. Thus, TIMP-1 may be used to discriminate between patients likely to benefit from anthracyclines and patients who should be offered an alternative drug. Furthermore, we found that this protection is probably executed through counteraction of the apoptotic signal by activation of the Akt survival pathway. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2019.
Glucostatic Mechanism of Regulation of Food Intake
Authors: Jean Mayer
Journal: New England Journal of Medicine (1953)

THE regulation of energy intake is fundamental to all homeostatic mechanisms. Yet this basic process has received less attention than many of the physiologic regulations that it makes possible.Before this century, three theories were advanced to account for the phenomenon of hunger. The theories of peripheral origin (Haller, Erasmus Darwin, Johannes Müller and Weber) held that the taking of food resulted from the stimulation either of all afferent nerves by some change in the tissues or of a strictly local group of sensory nerves, mainly in the stomach. The theory of central origin (Magendie, Tidewald and Milne-Edwards) postulated that . . .
Abstract 4410: Initiative for Molecular Profile and Advanced Cancer Therapy (IMPACT): A personalized medicine Phase I clinical trials program at MD Anderson Cancer Center
Authors: Apostolia M. Tsimberidou, David S. Hong, Jennifer Wheler, Siqing Fu, Sarina Piha-Paul, Aung Naing, Gerald Falchook, Raja Luthra, Nancy G. Iskander, Sijin Wen, Razelle Kurzrock
Journal: Cancer Research (2011)

Abstract Introduction: Ongoing clinical trials are based on targeting specific pathways in addition to the tumor histology. We examined the results of mutational analyses performed in patients with advanced cancer seen in the Phase I clinic at The University of Texas MD Anderson Cancer Center. Methods: Mutational analysis was mostly performed in the Clinical Laboratory Improvement Amendments (CLIA)-certified pathology laboratory of MD Anderson. DNA was extracted from microdissected paraffin-embedded tumor samples, and analysis was performed on specific exons, depending on the test ordered, for the following genes: PIK3CA (exon 9: codons 532-554; exon 20: codons 1011-1062); BRAF (exon 15: codons 595 to 600); KRAS and NRAS (codons 12, 13, and 61); EGFR (exons 18 to 21 of the kinase domain); KIT (exons 9, 11, 13, and 17); and RET (exon 10: codons 609, 611, 618, and 620; codon 634 of exon 11; codon 918 of exon 16). The loss of the tumor suppressor nuclear protein, PTEN, was determined using immunohistochemical staining. Results. Tumor mutational analysis was ordered for 952 patients. Overall, 103 patients did not have adequate tissue. Of the remaining 849 patients, 354 (41.69%) had ≥ 1 mutation and 495 did not have a mutation. More women (45%) than men (38%) had a mutation (p = 0.02), but age was not associated with the presence of mutations (p=0.76). Of the patients with mutations, 313 had 1 mutation, 38 had 2 mutations, and 3 had 3 mutations. The distribution of mutations by diagnosis is shown in the Table. The total distribution of mutations in our patient population was as follows: BRAF, 19.01%; KRAS, 18.74%; PIK3CA, 9.85%; NRAS, 8.17%; EGFR, 3.38%; KIT, 2.13%; and PTEN loss, 21.20%. Conclusion: Testing for PIK3CA, KRAS, NRAS, BRAF, EGFR, KIT, and RET mutations and PTEN loss in 849 patients with available tissue demonstrated that molecular driver aberrations are common in advanced 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 4410. doi:10.1158/1538-7445.AM2011-4410
Alcohol in the Treatment of Angina Pectoris
Authors: Samuel Stearns, Joseph E. F. Riseman, William Gray
Journal: New England Journal of Medicine (1946)

THE earliest description of angina pectoris, that of Heberden1 in 1786, refers to "the relief afforded by wine and spirituous cordials." Since then alcoholic beverages have frequently been recommended or at least permitted in the treatment of angina pectoris, but few efforts to evaluate such therapy have appeared in the literature. The present study was carried out to obtain an objective evaluation of the use of alcohol in the treatment of angina pectoris.Summary of the LiteratureThe comparative value of brandy, carminatives and nitroglycerin in the treatment of attacks of angina pectoris was studied in 1934 by Evans and . . .
AB0439 Contribution of anti-ferritin antibodies to the diagnosis of giant cell arteritis
Authors: A. Regent, K. H. Ly, A. Blet, C. Agard, X. Puéchal, N. Tamas, C. Le-Jeunne, E. Vidal, L. Guillevin, L. Mouthon
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The diagnosis of giant cell arteritis (GCA) can only be ascertained by performing temporal artery biopsy (TAB), and there is no validated biomarker valuable for the diagnosis and/or characterization of the prognosis in this condition. Recently, Baerlecken et al. reported on the detection of antibodies directed at the human ferritin heavy chain (FTH1)in 92% of patients with GCA vs 1% of healthy controls. <h3>Objectives</h3> We decided to evaluate the diagnostic value of anti-ferritin antibodies in patients undergoing TAB for a suspicion of GCA. <h3>Methods</h3> We included 122 consecutive patients suspected of GCA. Blood sampling was performed at the time of TAB. Among these, 40 had biopsy proven GCA (TAB+ GCA), 29 had biopsy-negative GCA (TAB- GCA), 6 had polymyalgia rheumatica (PMR) and another diagnosis that GCA (GCA controls) and/or PMR was retained in 47 patients. Sera from 40 healthy individuals served as negative controls. We investigated for the presence of IgG directed against 19-45 FTH1 amino-acids by using an ELISA test. Correlations between FTH1 antibodies and clinical manifestations were investigated using non parametrical tests. <h3>Results</h3> Anti-FTH1 antibodies were identified in 72.5%, 41.3.9%, 31.9% and 2.5% of patients with TAB+ GCA, TAB- GCA, GCA controls and healthy individuals, respectively, with a threshold at the mean of healthy controls + 2 standard deviations (SD). With a threshold at the mean of healthy controls + 3 SD, anti-FTH1 antibodies were identified in 60%, 34.5%, 21.2% and 0% of the patients with TAB+ GCA, TAB- GCA, GCA controls and healthy individuals, respectively. By grouping TAB+ GCA, TAB- GCA patients with a threshold at 2 SD, the positive and negative predictive value were of 71.9 and 56.9%, respectively. Positive and negative likely ratio were at 1.96 and 0.58, respectively. In addition, in our population, anti-FTH1 antibody titer as measured by OD level correlated significantly with CRP and no correlation was found with aortic and/or visual impairment. <h3>Conclusions</h3> We therefore confirm the presence of anti-FTH1 in 72.5% of patients with histologically proven GCA. However, the detection of anti-FTH1 is not contributory to the diagnosis of GCA in a cohort of patients with suspected ACG. The ability to identify a specific sub-group of patients by ELISA should be evaluated by testing a larger cohort of patients with GCA. <h3>References</h3> Baerlecken et al. Ann Rheum Dis. 2012 Jun;71(6):943-7. <h3>Disclosure of Interest</h3> None Declared
VALORACION DEL GRADO DE SATISFACCIÓN DE LOS PACIENTES SOMETIDOS A ENDOSCOPIAS DIGESTIVAS EN EL SERVICIO DE ENDOSCOPIAS DEL HOSPITAL INFANTA CRISTINA(PARLA)
Authors: B Botella, C Esteban, D Domingo, S Sánchez Prudencio, F De la Morena, B De Cuenca
Journal: Endoscopy (2011)

Introducción: La valoración del grado de satisfacción de los pacientes es fundamental ya que puede influir en la conducta que este adopte a la hora de seguir las indicaciones médicas.
THU0240 Rosuvastatin improves impaired endothelial function and lowers high sensitivity CRP in patients with systemic sclerosis – a prospective case-series study
Authors: O. Timár, Z. Szekanecz, G. Kerekes, J. Végh, A.V. Oláh, Z. Csiki, K. Dankό, S. Szamosi, Ά. Németh, P. Soltész, G. Szücs
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic sclerosis (SSc) has been associated with vasculopathy and increased cardiovascular morbidity and mortality. Both microvascular and macrovascular diseases are characteristic for SSc. There is an immense need for proper vasculoprotective prevention and treatment. <h3>Objectives</h3> We wished to study the effect of rosuvastatin on endothelial and macrovascular function and laboratory cardiovascular risk factors in patients with SSc. <h3>Methods</h3> Altogether 28 patients with SSc underwent laboratory and complex vascular assessments before and after 6 months of 20mg rosuvastatin treatment. Flow-mediated dilation (FMD) of the brachial artery and carotid artery intima-media thickness (ccIMT) were analyzed by ultrasound. Carotid-femoral and aorto-femoral pulse wave-velocity (PWV) were measured by ECG-synchronized pulsed wave Doppler ultrasound. Ankle-brachial index (ABI) was determined by Doppler, forearm skin microcirculation was assessed by Laser Doppler perfusion monitoring. <h3>Results</h3> Brachial artery FMD significantly improved upon rosuvastatin therapy (2.2±3.3% before vs. 5.7±3.9% after treatment, p=0.0002), while changes in PWV, ccIMT and ABI were not significant. Deceleration slope of Laser Doppler flowmetry also significantly improved (-1.13±0.92 U/s vs. -0.64±1.09 U/s, p=0.021). Mean triglyceride (1.7±0.97 vs. 1.3±0.46 mmol/l, p=0.0004), total cholesterol (5.3±1.6 mmol/l vs. 4.2±1.3 mmol/l, p=0.0003), LDL-C (3.0±1.3 vs. 2.2±1.0 mmol/l, p=0.005) and CRP levels (5.1±5.2 vs. 3.4±2.7, p=0.01) significantly decreased after rosuvastatin treatment. <h3>Conclusions</h3> Six-month rosuvastatin therapy improves endothelial function and lowers CRP levels indicating possible favourable effects of this statin on the cardiovascular system in SSc. <h3>Disclosure of Interest</h3> None Declared
Abstract 4734: Validation of genome-wide colorectal cancer genetic risk factors in African- and European-Americans
Authors: Sonia Kupfer, Jeffrey Anderson, Stanley Hooker, Cory Henderson, Rick Kittles, Karen Kim, Temitope Keku, Robert S. Sandler, Nathan A. Ellis
Journal: Cancer Research (2010)

Abstract Background: Genome-wide association studies have identified several colorectal cancer (CRC) genetic risk factors. However, these studies have been performed primarily in individuals of European descent and none include African Americans (AAs). Determining CRC genetic risk factors in AAs is important because CRC incidence and mortality rates are highest of all US populations. Aim: To validate genome-wide CRC genetic risk factors, we tested single nucleotide polymorphism (SNP) associations in ten chromosome (chr) regions in AAs and European-Americans (EAs). Methods: We genotyped 22 SNPs in 1725 AA and 883 EA CRC cases and controls using Sequenom iPLEX. Ancestry estimates were obtained using STRUCTURE 2.1. We tested for allelic association and calculated odds ratios and confidence intervals using logistic regression adjusting for ancestry, age and gender. Results: Association results are shown in the Table. In AAs, rs10795668 (chr 10) and rs10318 (chr 15) were significantly associated with CRC. rs7014346 (chr 8) and rs355527 (chr 20) trended toward significant associations. In EAs, three SNPs on chr 8 were significantly associated with CRC. In addition, two chr 11 SNPs (rs3802842 &amp; rs1074997) and rs1862748 (chr 16) were significantly associated with disease in EAs. SNPs on chr 15 and chr 16 are located in or near genes GREM1 and CDH1 respectively. SNPs on chr 8, 10, 11 and 20 are in gene deserts. Conclusion: This is the first study to validate genome-wide SNP associations in AAs. We also confirm several associations in EAs. SNPs on chr 15 &amp; 16 are located in genes involved in TGFβ signaling (GREM1 &amp; CDH1) which has been implicated in CRC pathogenesis, while those on chr 8, 10, 11 and 20 are in gene deserts. Future fine-mapping in these regions is warranted to identify functional variants.Genome-wide SNP associations in African- and European-AmericansChr (gene)SNPReference alleleAllele frequency casesAllele frequency controlsOR [95% CI]p*African Americans 8rs7014346A0.420.391.14 [0.99-1.31]0.0710rs10795668A0.080.061.41 [1.07-1.87]0.0415 (GREM1)rs10318T0.050.031.45 [1.02-2.05]0.0520rs355527A0.180.200.87 [0.73-1.04]0.09European Americans 8rs6983626T0.120.091.38 [1.00-1.91]0.058rs6983267G0.520.471.24 [1.01-1.51]0.048rs7837328A0.430.371.30 [1.06-1.60]0.0111rs3802842C0.330.281.26 [1.02-1.57]0.0211rs10749971G0.410.331.42 [1.15-1.74]0.000216 (CDH1)rs1862748T0.280.320.80 [0.64-0.99]0.04 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 4734.
PTU-139 Outcomes Of Patients With Liver Cirrhosis In A Non Liver-specialist Intensive Care Unit: Do Admission Lactate And Apache 2 Score Help Predict Successful Discharge?
Authors: W Waddingham, M Cepkova
Journal: Gut (2014)

<h3>Introduction</h3> Hospitalised patients with cirrhosis often require admission to intensive care (ITU), usually for management of secondary complications such as GI bleeding, sepsis, or organ failure. Prognosis of these patients is poor. Despite demonstration of modest improvements in recent years, overall in-hospital mortality in this group remained 54.6% in a recent study.<sup>1</sup> Our study aimed to explore the characteristics and outcomes of cirrhotic patients admitted to ITU, and whether this was comparable to published data. We also aimed to explore whether parameters such as APACHE 2 score and admission blood lactate differ between those who survived their ITU stay and those that did not, and if this may help predict discharge. <h3>Methods</h3> A retrospective analysis was performed of patients admitted to the Whittington hospital ITU from January 2011-June 2013. Information regarding patients with a diagnosis of cirrhosis was gathered from the Intensive Care National Audit and Research unit (ICNARC) database, and discharge summaries. <h3>Results</h3> We identified 60 patients with cirrhosis, 3.07% of total ITU admissions, mean age 54.8 years (range 19–78). 49/60 patients had alcoholic cirrhosis, 5/60 had non-alcoholic steatohepatitis related cirrhosis. Primary reason for admission included GI bleed (24/60, 40%), pneumonia (16/60, 26.7%), other sepsis (10/60, 16.7%), encephalopathy (8/60, 13.3%). Overall mortality figures were 41.7% in-ITU, 48.3% at 30 days, and 70% at 1 year. In-ITU mortality for patients requiring only ventilatory support was 48.9%, those requiring inotropic support was 61.2% and those requiring renal support 64.2%. 24/60 patients required all 3 methods of support, 66.7% of those died in ITU and 75% at 30 days. 23 patients were admitted with sepsis and decompensated liver disease, 65% died in ITU and 73.9% at 30 days. Mean APACHE 2 scores for patients that died in ITU vs. those discharged from ITU were 23 (range 9–30) and 20 (range 8–36) respectively, with a statistically significant difference between the two groups (p = 0.036). Mean admission serum lactate for patients who died in ITU vs. those discharged from ITU was 7.6 (range 1–23) and 4.6 (range 1–17) respectively, demonstrating a statistically significant difference (p = 0.015). <h3>Conclusion</h3> As expected for a non liver-specialist unit, most patients had alcohol related cirrhosis. Mortality was high but comparable to other published data. The worst outcomes were seen in patients with sepsis and decompensated liver disease, and those requiring organ support. Admission lactate levels and APACHE 2 scores were significantly lower in patients successfully discharged from ITU; admission lactate could potentially aid prediction of successful discharge. Further study is needed. <h3>Reference</h3> Intensive Care Med. Jun;2012;38(6):991–1000 <h3>Disclosure of Interest</h3> None Declared.
QL-15 * A RETROSPECTIVE ANALYSIS OF INTRACRANIAL HEMORRHAGE IN PATIENTS RECEIVING ANTICOAGULATION FOR VENOUS THROMBOEMBOLISM IN THE SETTING OF GLIOBLASTOMA
Authors: M. N. Khoury, S. Missios, N. Edwin, S. Sakruti, A. Khorana, G. Stevens, D. Peereboom, M. Ahluwalia
Journal: Neuro-Oncology (2014)

BACKGROUND: Venous thromboembolism (VTE) is a complication of glioblastoma. Anticoagulating patients with glioblastoma carries a theoretical risk of intracranial hemorrhage (ICH). METHODS: We performed a retrospective review of consecutive glioblastoma patients (2007-2013) diagnosed with VTE, with documentation of historical, clinical, and radiologic findings. RESULTS: 173 (33%) of 523 glioblastoma patients had VTE events. Seventeen (9.8%) had ICH: 6 (35%) subdural hematomas and 11 (65%) intratumoral hemorrhage. Enhancement in the area of subsequent intratumoral hemorrhage was noted in 9 of 10 with available pre-ICH scans. Multivariable regression did not show associations between ICH and tumor enhancement diameter or VEGF-inhibitor use. Fifteen (16%) patients receiving anticoagulation had ICH compared to 2 (2.6%) not receiving anticoagulation (p = 0.005). The type of anticoagulant used was not associated with development of ICH. Median survival from VTE diagnosis to death was 7.2 months in ICH group, compared to 6.2 months in non-ICH individuals (p = 0.4). Median survival from VTE diagnosis to death were 7.9 and 4.7 months (p = 0.07) in patients receiving anticoagulation and those not on anticoagulation, respectively; percentage of patients with KPS scores ≥ 70 was not statistically significant between the groups (p = 0.14). Of fifty-one patients with perioperative VTEs, 38 (74%) were not treated with anticoagulation, while 13 (26%) did receive anticoagulation post-VTE diagnosis (p < 0.0001). CONCLUSION: Patients with glioblastoma and VTE on anticoagulation have increased incidence of ICH. However, ICH was not associated with lower median survival from time of VTE. Additionally, patients receiving anticoagulation trended towards longer survival from time of VTE. Intratumoral hemorrhage typically occurs within the enhancing portion of tumor; however, no relationship was identified between the development of ICH and (i)the diameter of enhancement or (ii)type of anticoagulant used. It is appropriate to initiate anticoagulation in glioblastoma patients with VTEs and, in the case of peri-operative VTEs, start anticoagulation during post-operative outpatient visits.
IMPACT OF PLASMA LP-PLA2 ACTIVITY LEVEL ON THE PROGRESSION OF AORTIC STENOSIS: THE PROGRESSA STUDY
Authors: Romain Capoulade, Ablajan Mahmut, Lionel Tastet, Marie Arsenault, Élisabeth Bédard, Jean Dumesnil, Jean-Pierre Despres, Patrick Mathieu, Philippe Pibarot
Journal: Journal of the American College of Cardiology (2014)
Bilateral Symmetric Photon Defects in the Parietal Bones on Tc-99m MDP Bone Scintigraphy
Authors: SEOK TAE LIM, MYUNG-HEE SOHN
Journal: Clinical Nuclear Medicine (2001)

Supported by Korea Research Foundation grant KRF-99-041-F00273. From the Department of Nuclear Medicine* and Institute for Medical Sciences,† Chonbuk National University Medical School, Chonju, Korea Received for publication March 6, 2000. Accepted September 25, 2000. Reprint requests: Myung-Hee Sohn, M.D., Department of Nuclear Medicine, Chonbuk National University Medical School, 2-20 Keumam-dong Duckjin-gu, Chonju, Chonbuk 561-182, Korea. E-mail: [email protected]