tbuckley/cabot-search huggingface dataset:
Abstract 12992: Management of Valvular Atrial Fibrillation in Real-Life Practice: Insights from the RealiseAF Survey
Authors: Habib Gamra, Lisa Naditch-Brule, Chern-En Chiang, Thorsten Lewalter, Jan Murin, Marten Rosenqvist, Samir Alam, Gabriel Steg
Journal: Circulation (2011)

Background: There is a paucity of data regarding the risk profile and real life management of valvular atrial fibrillation (AF) that is often excluded from large trials, compared to nonvalvular AF....
Abstract 2680: Tight Heart Rate Control Reduces Secondary Adverse Events in Patients with Type B Acute Aortic Dissection
Authors: Kazuhisa Kodama, Kazuhiro Nishigami, Tadashi Sawamura, Koichi Nakao, Takashi Honda
Journal: Circulation (2007)

Background : Although type B aortic dissection (AD) has been treated with beta-blocker to lower the arterial blood pressure (BP), there has been little evidences about reduction in heart rate (HR). We assessed whether tight HR control improved the outcome of medical treatment in patients with AD. Methods and Results : From 1997 to 2005, consecutive 223 patients with AD medically treated and controlled to lower BP under 120 mmHg were enrolled. Based on the average HR at 3, 5, and 7 days after the onset, patients were divided to tight HR (&lt;60 bpm) control group (39 patients; mean HR of 56 .8bpm) and conventional HR (equal or more than 60 bpm) control group (184 patients; mean HR of 71.6 bpm). We compared the frequency of aortic events including aortic rupture, recurrent dissection, and aortic expansion of more than 5mm, and surgical requirement between two groups. During a median follow-up of 33.3 months, aortic rupture, recurrent dissection, pathological aortic expansion, and aortic surgery occurred in 3, 14, 43, and 30 patients respectively. Reductions in aortic events and surgical requirement were observed in tight HR control group (10.3% and 2.6%) compared to conventional HR control group (28.3% and 15.8%) (Odds ratio: 0.29 and 0.14. C.I.:0.10 to 0.90 and 0.02 to 1.07, p&lt;0.01.). Kaplan-Meier curves of aortic event and surgical requirement free rates were shown in figure 1 and 2 . Conclusions : The present study demonstrated that tight heart rate control improved the outcome of medical treatment in patients with AD.
Abstract 290: Sex Disparities in Chest Compression Quality
Authors: Elizabeth Retzer, Trevor C Yuen, Jefferson L Cua, Dana P Edelson
Journal: Circulation (2011)

BACKGROUND: Multiple studies have documented improved outcomes from cardiac arrest for women compared to men, but the etiology of this disparity is unknown. Prior out-of-hospital work has suggested that men have stiffer chests than women, requiring more force to compress the same depth. We hypothesized that this would result in women receiving deeper chest compressions during CPR. METHODS: We conducted a prospective study of consecutive, adult, index in-hospital cardiac arrests within a single academic institution between April 2006 and March 2011. CPR quality measures were recorded using a CPR-recording defibrillator (MRX/QCPR, Philips Healthcare). Force data were available for only a subset (n=69). Paired t-tests and chi-squared analyses were used to compare patient demographics, CPR quality parameters and outcomes by sex. RESULTS: A total of 503 patients were included in the analysis, of which 53% were women. Results are shown in the table below. Women received deeper chest compressions (48±8mm vs 46±8mm, p=0.005) with higher duty cycles (0.39±0.03 vs 0.38±0.03, p=0.001) and a trend toward decreased leaning compared to men. This was associated with a trend toward improved return of spontaneous circulation (ROSC) and survival to discharge in women. In the subset for whom force data were available, women required less elastic force to reach 5 cm of compression depth (24.5 ± 5.7 kg vs 30.5 ± 8.8 kg, p&lt;0.001), even after adjusting for body mass index (BMI), age, and arrest location (p=0.004). CONCLUSION: Men have stiffer chest and receive shallower chest compressions than their female counterparts. This may be a contributor to the differences in survival noted in prior studies. Rescuers should be aware of the need to push harder for male victims of cardiac arrest.
Abstract P6-08-39: Influence of lifestyle factors and tumor cell dissemination in 632 early breast cancer patients
Authors: Bahriye Aktas, Anna Frackenpohl, Siegfried Hauch, Johann Kraus, Hans Armin Kestler, Rainer Klaus Kimmig, Sabine Kasimir-Bauer
Journal: Cancer Research (2015)

Abstract Introduction: Influence of lifestyle behaviour in risk of developing breast cancer is supported by several lines. Data from 632 early breast cancer (EBC) patients were collected to evaluate the influence of lifestyle factors in progression free survival (PFS) and overall survival (OS). Results of disseminated tumor cell (DTC) in bone marrow and circulating tumor cells (CTC) in blood were available as well. A complete pathological data set and medical history were obtained. It was the purpose of the present study to correlate these data to compare the findings. Methods: We evaluated 629 bone marrow samples and 606 blood samples from EBC patients treatet between 2004 to 2010 at the time of first diagnosis. All samples underwent immunomagnetic enrichment using the AdnaTest BreastCancerSelect (AdnaGen AG, Germany) within 4 hours after blood withdrawal followed by RNA isolation and subsequent gene expression analysis by reverse transcription and Multiplex-PCR in separated tumor cells using the AdnaTest BreastCancerDetect. CTCs were analyzed for the three breast cancer associated markers: GA733-2, Muc-1, Her-2 and actin as an internal PCR control. BM aspirates were analyzed for DTCs by immunocytochemistry using the pan-cytokeratin antibody A45-B/B3. Lifestyle data icluding menopausal status, BMI, usage of Metformin, hormone replacement drugs, beta blockers and Bisphosphonates were collected by accessing the patient files. Histological data of the primary tumor were available for each patient. Results: The overall detection rate for CTCs was 15.41% (88/571 patients) and for DTC was 38.5% (242/628 patients), respectively. The mean BMI of 428 patients was 26.4 in 81/574 premenopausal, 426/574 postmenopausal and 67/574 perimenopausal patients. Medical history of smoking (128/394 patients), using hormone replacement therapy (92/354 patients), alcohol consumption (68/378 patients), having allergies (188/419), using Metformin (22/389 patients), taking beta blockers (83/392 patients) and Bisphosphonates (201/526 patients) were compared to PFS and OS as well as the histological data of the primary tumor. Conclusion: Lifestyle factors seems to influence the outcome in our cohort of EBC patients as shown in previous studies. Final data and results regarding to tumor cell dissemination compared to lifestyle behaviour will be available for the SABCS 2014. Citation Format: Bahriye Aktas, Anna Frackenpohl, Siegfried Hauch, Johann Kraus, Hans Armin Kestler, Rainer Klaus Kimmig, Sabine Kasimir-Bauer. Influence of lifestyle factors and tumor cell dissemination in 632 early breast cancer patients [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P6-08-39.
Abstract P185: TV Campaign for Automated External Defibrillator Promotion in Hyogo Prefecture, Japan
Authors: Takuro Hayashi, Kohei Adachi, Atsunori Hashimoto, Haruhiko Hiramatsu, Seishiro Marukawa, Tetsuya Miyamoto, Hiroyuki Nakao, Kazutoshi Kuboyama
Journal: Circulation (2008)
The Pim Kinase Inhibitor AZD1208 Enhances Apoptosis Induction By Clinically Active FLT3 Inhibitors in FLT3-ITD Acute Myeloid Leukemia Cells in Vitro and in Vivo through Synergistic Downregulation of Mcl-1 and of Bcl-xL
Authors: Karthika Natarajan, Trevor J Mathias, Kshama A Doshi, Adriana E Tron, Manfred Kraus, Rossana Trotta, Danilo Perrotti, Dennis Huszar, Maria R Baer
Journal: Blood (2014)
Genetic linkage of UGT1A7 and UGT1A9 polymorphisms to UGT1A1*6 is associated with low glucuronidase activity for irinotecan metabolite SN-38 in Japanese cancer patients
Authors: Ken-Ichi Fujita, Yuichi Ando, Fumio Nagashima, Wataru Yamamoto, Hisashi Endo, Kazuhiro Araki, Keiji Kodama, Toshimichi Miya, Masaru Narabayashi, Yasutsuna Sasaki
Journal: Cancer Research (2006)

1314    Purpose:  Irinotecan is metabolized to its active metabolite SN-38, which is further conjugated predominantly by UDP-glucuronosyltransferase (UGT) 1A1. In vitro studies have revealed that UGT1A7 and UGT1A9, in addition to UGT1A1, were also responsible for the metabolism of SN-38 to yield SN-38 glucuronide (SN-38G). In the present study, the phenotypic effects of  UGT1A7  and  UGT1A9  genetic polymorphisms related to lower catalytic or transcriptional activity on the in vivo pharmacokinetics (PK) of irinotecan were examined.  Methods:  Sixty-five Japanese cancer patients who received various regimens of irinotecan-containing chemotherapy were enrolled. Genetic polymorphisms present in  UGT1A7  (T to G transversion at -57 and  UGT1A7*3 ) and  UGT1A9  (9 repeat of T at -118) as well as  UGT1A1  ( UGT1A1*6 ,  UGT1A1*27  and  UGT1A1*28 ) were analyzed for all patients. Haplotype analysis was performed with an expectation-maximization-based program using SNPAlyze 5.0 (Dynacom, Yokohama, Japan). Irinotecan PK was examined with 34 patients.  Results:  The most frequent haplotype (55.6%, 95%CI 51.2 to 60.0) consisted of polymorphisms related to normal catalytic or transcriptional activity, T allele at -57 of  UGT1A7 ,  UGT1A7*1 , 10 repeat of T allele at -118 of  UGT1A9  and  UGT1A1*1 . The second frequent haplotype consisted of those related to lower catalytic or transcriptional activity in which G allele at -57 of  UGT1A7 ,  UGT1A7*3  and 9 repeat of T allele at -118 of  UGT1A9  linked to  UGT1A1*6  (14.5%, 95%CI 11.0 to 17.9) (haplotype 2). The PK analyses revealed that seven of patients showed the apparently lower glucuronidase activity than the others, as judged by AUC ratios of SN-38 to SN-38G higher than the mean value plus 1 standard deviation (SD) (0.61+0.4). Among them, 2 patients were homozygous for the haplotype 2 related to the low catalytic and transcriptional activities of UGTs. They did not have  UGT1A1*28 . Another patient was heterozugous for the haplotype 2 and the opposite allele contained  UGT1A1*28 , although  UGT1A7  and  UGT1A9  were normal. These configurations of diplotypes were not found in other patients showing the AUC ratios lower than the mean value plus 1 SD. These results indicate that the homozygous combination of the haplotype 2 and its combination with  UGT1A1*28  allele may be important to predict lower SN-38 glucuronidation capacity in Japanese cancer patients.  Conclusion:  Genetic linkage of  UGT1A7  and  UGT1A9  polymorphisms to  UGT1A1*6  related to low catalytic and transcriptional activities of UGTs is associated with the irinotecan PK with the lower glucuronidase activity for SN-38.
Safety Profile and Clinical Response To MEDI-551, a Humanized Monoclonal Anti-CD19, In a Phase 1/2 Study In Adults With Relapsed Or Refractory Advanced B-Cell Malignancies
Authors: Andres Forero-Torres, Mehdi Hamadani, Michelle A. Fanale, Celeste M. Bello, Thomas J. Kipps, Fritz Offner, Gregor Verhoef, Massimo Federico, Stephanie A. Gregory, Anne Sonet, Sarit Assouline, Jaime Pérez de Oteyza, Jose Francisco Tomas, Antonio Cuneo, Nairouz Elgeioushi, Trishna Goswami, Ramy Ibrahim, Ronald Herbst, Bruce D. Cheson
Journal: Blood (2013)
Quality of life was ignored in meta-analysis
Authors: I. Higginson
Journal: BMJ (1996)

cycles of either mitomycin, ifosfamide, and cisplatin or mitomycin, vinblastine, and cisplatin.Nine thousand patients will be required for the trial to give a reliable and clinically relevant result.Potentially all patients with non-small cell lung cancer will be eligible.Similar large trials have been conducted in breast and ovarian cancer, with considerable success.The "big lung trial" will be the first large scale randomised trial to ask this basic but important question about the treatment of this major disease.
The protein tyrosine phosphatase PTPL1 modulates Ewing’s sarcoma tumorigenesis.
Authors: Ogan D. Abaan, Amy Levenson, Aykut Uren, Jeffrey A. Toretsky
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

2398 

Ewing’s Sarcoma Family Tumors (ESFT) are characterized by a translocation t(11:22) forming an aberrant transcription factor EWS/FLI1. This fusion protein acts as a potential oncogene. Although few targets of EWS/FLI1 are identified, the exact mechanism of how EWS/FLI1 causes ESFT is not well understood. In this sense, identification of EWS/FLI1 targets that are important for tumorigenesis is crucial. Microarray data suggested a protein tyrosine phosphatase PTPL1 as a gene upregulated in EWS/FLI1 transfected cells. We have hypothesized that PTPL1 could be a target for EWS/FLI1, and modulate ESFT tumorigenesis. ESFT cells, mouse embryo fibroblasts (MEF) expressing EWS/FLI1 and COS7 cells were used in PTPL1 promoter activation studies. PTPL1 protein levels were reduced by stably expressing an RNA antisense in ESFT cells. We found that PTPL1 protein is highly expressed in all eight ESFT cell lines we tested and expressed very low in nontransformed cells (n=3). In addition, PTPL1 expression was investigated in ESFT samples using immunohistochemsitry. Patients with both localized (n=20) and metastatic tumors (n=21) showed strong staining, where metastatic tumors had a trend toward higher PTPL1 staining (p<0.1). Chromatin immunoprecipitation experiments showed an association between the native PTPL1 promoter and EWS/FLI1, and promoter activation experiments demonstrated that this association causes the upregulation of PTPL1. ESFT cells stably expressing an antisense RNA against PTPL1 showed both reduced anchorage-dependent and -independent growth. Moreover, ESFT cells with reduced PTPL1 levels were more sensitive to chemotherapy-induced apoptosis. These results suggest that PTPL1 is a direct transcriptional target of EWS/FLI1 and appears to be a modulator of ESFT tumorigenesis.
Characterization of transport properties of breast cancer resistance protein
Authors: Vishal S. Narang, Clinton F. Stewart, Christopher M. Waters
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

607 

Breast cancer resistance protein (BCRP), a member of the ATP-binding cassette family of protein transports a large variety of structurally unrelated chemotherapeutic drugs. To characterize the efflux properties of BCRP, we transiently transfected U2-OS cells (an osteosarcoma cell line that is BCRP-null) with increasing concentrations (1 μg to 8 μg) of pcDNA3.2-BCRP vector. Increasing concentrations of cDNA led to a corresponding increase in efflux function and protein expression (confirmed by western blotting). By comparing the amount of Hoechst 33342 (Ho342, an established BCRP substrate) accumulated in BCRP-null cells with the amount accumulated in BCRP-expressing cells at steady-state, we measured the efflux transport capacity of cells expressing different levels of BCRP. The efflux transport capacity was evaluated 24-48 hours after transfection, and ranged from 0.132 ± 0.086 x 109 to 1.18 ± 0.18 x 109 (molecules/cell)/(μM Ho342) with increasing levels of vector applied. To investigate whether BCRP efflux is mediated from the inner plasma membrane leaflet or outer leaflet, we utilized a lipid analogue, 1-[4-(trimethylamino) phenyl]-6-phenylhexa-1, 3,5-triene (TMA-DPH), that is fluorescent only in the plasma membrane and that diffuses very slowly from the outer leaflet to the inner leaflet. Using on-line spectrofluormetric measurements in U2-OS, we demonstrated that BCRP-expressing cells accumulate significantly lower levels of TMA-DPH in comparison to the parent cell line, suggesting that TMA-DPH is a substrate for BCRP. The unique properties of this dye are being currently utilized to investigate whether efflux mediated by BCRP is initiated at the inner or outer leaflet of the plasma membrane. Quantitative information about efflux transport capacities of BCRP and delineation of molecular mechanisms of BCRP-mediated efflux may help in designing improved therapeutic agents for cancer treatment.
Phase 1b Study Of The MDM2 Antagonist RG7112 In Combination With 2 Doses/Schedules Of Cytarabine
Authors: Karen Yee, Giovanni Martinelli, Sarit Assouline, Margaret Kasner, Norbert Vey, Kevin R. Kelly, Mark W. Drummond, Michael Dennis, Karen Seiter, Steven Blotner, Lori Jukofsky, Steven Middleton, Jianguo Zhi, Gong Chen, Hua Zhong, Gwen Nichols
Journal: Blood (2013)
Medical Insurance Coverage and Alzheimer Disease
Authors: Carol F. Lippa
Journal: JAMA Neurology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Abstract 2755: Insulin Resistance and Coronary Artery Calcification measured by Electron Beam Tomography
Authors: Robert Lee, Fereshteh Hajsadeghi, Jessica Ramirez, Behnaz Sarlak, Ambarish gopal, Naser Ahmadi, Matthew J Budoff
Journal: Circulation (2007)

Background: Elevation in the ratio of triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) has been suggested as a marker of insulin resistance (IR), conferring an increased risk of atherosclerosis in these patients. The association between TG/HDL-C and coronary artery calcification (CAC) measured by computed tomography has yet to be established. The goal of this study was to examine the relationship between IR, as determined by TG/HDL-C ≥ 3.5, and significant CAC (absolute score ≥ 100). Methods: Fasting lipid levels, homocysteine, C reactive protein and lipoprotein (a) levels of 336 asymptomatic individuals, who also underwent electron beam tomography (EBT), were measured. Results: The mean age of participants was 55 ±10 years. 71.7% were male. 37.4% had hypertension, 52.5% had hypercholesterolemia, 12.4% had diabetes mellitus (DM) and 52.5% had family history of premature CHD. Individuals with IR had higher significant CAC (≥100) than those without IR (70% vs. 27%, P=0.0001). After adjustment for age, gender, hypertension, hypercholesterolemia and DM, multivariate regression analysis demonstrated that individuals with IR had more significant CAC (odds ratio 2.1, 95% CI=1.1–3.9, p=0.01). Further sub-analysis revealed that individuals with IR had significantly higher lipoprotein (a) (Lp(a)) than those without IR (odds ratio 1.31, 95% CI=1.09-.16, p=0.03). No significant differences in C-reactive protein (CRP) and homocysteine were found between the two groups. Conclusion: Insulin resistance, as measured by TG/HDL-C ≥ 3.5, was associated with a significantly higher incidence of accelerated atherosclerosis on EBT (absolute CAC score ≥ 100), independent of age, gender and conventional risk factors. IR was also significantly associated with elevated levels of Lp(a). Further studies regarding the clinical significance of insulin resistance and elevated CAC score, as well as its association with Lp(a), may be warranted.
Remote Magnetic Navigation
Authors: Luigi Di Biase, Tamer S. Fahmy, Dimpi Patel, Rong Bai, Kenneth Civello, Oussama M. Wazni, Mohamed Kanj, Claude S. Elayi, Chi Keong Ching, Mohamed Khan, Lucie Popova, Robert A. Schweikert, Jennifer E. Cummings, J. David Burkhardt, David O. Martin, Mandeep Bhargava, Thomas Dresing, Walid Saliba, Mauricio Arruda, Andrea Natale
Journal: Journal of the American College of Cardiology (2007)
Abstract 8939: Mild And Moderate Pre-dialysis Chronic Kidney Disease Is Associated With Increased Coronary Artery Calcium
Authors: Sion K Roy, Albert Cespedes, Dong Li, Tae-young Choi, Matthew J Budoff
Journal: Circulation (2011)

BACKGROUND It is increasingly evident that patients with chronic kidney disease (CKD) are more likely to die from heart disease than kidney failure. We evaluated whether pre-dialysis CKD is an independent risk factor for coronary artery calcium (CAC) in patients undergoing multi-detector computed tomography (MDCT) for CAC scoring. METHODS We analyzed 544 consecutive patients who underwent MDCT at our center. Eleven patients requiring regular hemodialysis were excluded. Patients were divided into three groups: normal GFR (GFR&gt;90 ml/min/1.73 m 2 ), mild CKD (90≥GFR&gt;60 ml/min/1.73m 2 ) and moderate CKD (60≥GFR&gt;30 ml/min/1.73m 2 ). Continuous and categorical variables were compared using ANOVA and the χ 2 statistic. A multiple logistic regression model was used for detecting the association between total CAC score and GFR. An unadjusted model was used, followed by a second model adjusted for covariates known to be related to CAC. Another multivariable binary logistic model predicting presence of CAC (&gt;10) was performed and odds of incidence of CAC (&gt;10) were calculated among the three GFR sub-groups respectively. RESULTS In the unadjusted analysis, patients with mild CKD had mean CAC scores 174 points higher than those with the referent normal GFR (p=0.03), while patients with moderate CKD had mean CAC scores 575 points higher than the referent (p&lt;0.001). After adjustment for the proper covariates, patients with mild CKD had mean CAC scores 175 points higher than those with normal GFR (p=0.048), while those with moderate CKD had mean CAC scores 693 points higher than the referent (p&lt;0.001). Without adjustment, in the full population, patients with mild CKD were 1.9 times more likely to have incident CAC (defined as CAC score&gt;10) (95p%CI 1.3-2.9, p=0.002), while patients with moderate CKD were 4.1 times more likely to have incident CAC when compared to the group with normal GFR (95p% CI 2.3-7.8, p&lt;0.001). After adjustment for covariates, patients with mild CKD were found to be 2.2 times more likely (95p%CI 1.3-3.7, p=0.004) and patients with moderate CKD were 6.4 times more likely (95p% CI 2.9-14.3, p&lt;0.001) to have incident CAC compared to the referent group. CONCLUSION Mild and moderate pre-dialysis CKD are independent risk factors for increased mean and incident CAC.
Predicting Chronic Pain in Children with Juvenile Idiopathic Arthritis: Results from the Childhood Arthritis Prospective Study
Authors: A Rashid, K Holliday, L Cordingley, R Carrasco, B Fu, HE Foster, E Baildam, A Chieng, J Davidson, L Wedderburn, K Hyrich, W Thomson
Journal: Arthritis & Rheumatology (2014)
Comparative Study of Obinutuzumab (GA101) Vs. Rituximab Against CD20+ rituximab-Sensitive and -Resistant Burkitt (BL) and Acute Lymphoblastic Leukemia (B-ALL): Potential Targeted Therapy in Patients with High Risk BL and Pre-B-ALL
Authors: Aradhana Awasthi, Janet Ayello, Carmella van de Ven, Mona Elmacken, Christopher Reggio, Matthew J. Barth, Mitchell S. Cairo
Journal: Blood (2014)