tbuckley/cabot-search huggingface dataset:
Perioperative Statin Use in Noncardiac Surgery
Authors: Richard L. Weinberg, Kim A. Eagle
Journal: JAMA Internal Medicine (2016)

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 Internal Medicine 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 Internal Medicine journal
Abstract 1754: BPR2P001S0, a Coumarin derivative, induced cell cycle arrest in A549 through inhibiting PDPK1 activity
Authors: Pi-Han Lin, Tzu-Ming Jao, Yu-Lin Hung, Hsing-Pang Hsieh, Ya-Chien Yang, Sui-Yuan Chang
Journal: Cancer Research (2015)

Abstract Lung cancer is one of the most common causes of cancer deaths in the world, and the emergence of resistant lung cancer cells can lead to treatment failure. The development of new drugs to treat lung cancer, especially those resistant lung cancer cells, is urgent. Previously we identified that coumarin could inhibit replication of human lung cancer A549 cells. The efficacy of 284 coumarin derivatives on human lung cancer A549 cells was examined, and BPR2P001S0 was the most potent compound. BPR2P001S0 exhibited growth inhibition and apoptotic activity on A549 cells with an IC50 of 10 nM. A similar level of inhibitory effects was also observed in cisplatin-resistant A549 cells (IC50 = 12.5 nM). The ability of colony formation and migration capability of A549 cells decreased significantly in the presence of BPR2P001S0. In cell cycle analysis, BPR2P001S0 induced cell cycle arrest at the G0/G1 phase through down-regulation of cyclin D1 and Cdk4 protein expression. The expression of cyclinD1/Cdk4 regulatory protein, Akt, was also decreased. Subsequently, we found that the expression level of Ser241 phosphorated PDPK1 protein, an Akt activator in Akt pathway, was also reduced. By molecular docking analysis, we found that the reduced PDPK1 phosphorylation is likely resulted from the allosteric effect of interactions between BPRHIV001 and PDPK1. In conclusion, our results suggest that the anti-tumor activity of BPR2P001S0 is likely resulting from its ability to interfere with PDPK1 autophosphorylation at Ser241, which leads to reduced Akt protein and subsequent cyclin D1 degradation. Citation Format: Pi-Han Lin, Tzu-Ming Jao, Yu-Lin Hung, Hsing-Pang Hsieh, Ya-Chien Yang, Sui-Yuan Chang. BPR2P001S0, a Coumarin derivative, induced cell cycle arrest in A549 through inhibiting PDPK1 activity. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1754. doi:10.1158/1538-7445.AM2015-1754
Novel Role of the CXC Chemokine Receptor 3 in Inflammatory Response to Arterial Injury: Involvement of mTORC1: Retraction
Journal: Circulation Research (2011)

The authors of the following article have requested that it be retracted from publication in Circulation Research :

Schwarz JB, Langwieser N, Langwieser NN, Bek MJ, Seidl S, Eckstein HH, …
Quantitative Monitoring of Lineage-Specific Chimerism after Dual Hematopoietic Stem Cell Transplantation (Umbilical Cord Blood with Co-Infusion of Third Party Donor CD34+ Cells).
Authors: Noemi Sanchez-Hernandez, Cintia Manzano, Diana Barroso, Gustavo Iglesias, Pascual Balsalobre, David Serrano, Rafael Carrion, Alfonso Gomez-Pineda, Jose L. Diez-Martin, Ismael Buño
Journal: Blood (2006)
Air Leak Syndrome (ALS) Following Allogeneic Stem Cell Transplantation (SCT): A Report of 22 Patients from Kanto Study Group for Cell Therapy (KSGCT) in Japan.
Authors: Rika Sakai, Heiwa Kanamori, Shinichiro Okamoto, Fumiaki Yoshiba, Katsumichi Fujimaki, Tohru Sakura, Shin Fujisawa, Nobutaka Kawai, Chiaki Nakaseko, Masahiro Onoda, Takafumi Matsushima, Atsuo Maruta, Hisashi Sakamaki
Journal: Blood (2007)
Valproic Acid as Adjunct to Induction Therapy in Patients with Acute Myeloid Leukemia: First Results of Two Randomized Studies of the AMLSG.
Authors: Richard F. Schlenk, Martin Bommer, Mathias Schmid, Stefan Fröhling, Katrin Lehmann, Silja Groner, Rainer Hann, Jürgen Krauter, Konstanze Döhner, Arnold Ganser, Martin Göttlicher, Hartmut Döhner
Journal: Blood (2005)
Treatment with Nutlin-3, a Small-Molecule Antagonist of MDM2, in Combination with Low Doses of Pegylated Interferon Alpha 2a Targets Hematopoietic Progenitor Cells From Polycythemia Vera (PV) Patients
Authors: Min Lu, Joseph Tripodi, Yan Li, Xiaoli Wang, Vesna Najfeld, John Mascarenhas, Ronald Hoffman
Journal: Blood (2011)
Artificial Antigen-Presenting Cells Permit Selective In Vitro Generation of CMV-Specific T-Cells of Desired HLA Allelic Restriction for Adoptive Immunotherapy in Recipients of HLA Disparate Allografts.
Authors: Deepa Trivedi, Wouter J.W. Kollen, Lorna Barnett, Michel Sadelain, Richard J. O’Reilly
Journal: Blood (2005)
Abstract 4968: microRNA-mediated silencing of COP1 and altered ubiquitination of key oncogenic transcription factors promote cancer stem cell (CSC) phenotype and prostate cancer progression
Authors: Cecilia Dallavalle, Domenico Albino, Gianluca Civenni, Laura Curti, Paola Ostano, Maurizia Mello-Grand, Ramon Garcia-Escudero, Giovanna Chiorino, Carlo V. Catapano, Giuseppina M. R. Carbone
Journal: Cancer Research (2015)

Abstract Mutations and deletions of ubiquitin ligase complex proteins are emerging as important mechanisms driving tumorigenesis. In this study we report an alternative mechanism, depending on microRNA-mediated post-transcriptional silencing, leading to altered ubiquitination of key oncogenic proteins and induction of tumorigenic and CSC properties in prostate epithelial cells (PrECs). We found that increased expression of miR-424 promotes malignant transformation of normal PrECs by targeting the E3 ubiquitin ligase COP1. miR-424 was upregulated in primary prostate cancers and prevalently in ERG negative tumors. Bioinformatics and functional analysis demonstrated that miR-424 targeted COP1 mRNA in PrECs drastically reducing its protein level. Moreover, miR-424 and COP1 expression were inversely correlated in prostate tumors and associated with enrichment of CSC features. Functionally, over-expression of miR-424 or knockdown of COP1 in PrECs increased anchorage-independent growth, cell migration and prostatosphere formation under CSC selective conditions. Consistently, inhibition of miR-424 or over-expression of COP1 prevented these phenotypic changes in normal PrECs and prostate cancer cell lines. Moreover, COP1 knockdown reproduced closely the effects of miR-424 upregulation in PrECs. Mechanistically, we found that silencing of COP1 by miR-424 resulted in reduced turnover and increased level of several oncogenic transcription factors, including known COP1 substrates like c-JUN and ETV1. Furthermore, we identified STAT3 as a novel substrate of the miR-424/COP1 axis. Consistently, miR-424 upregulation and COP1 silencing increased STAT3 protein level and enhanced basal and cytokine induced STAT3 activity in PrECs and prostate cancer cells. These effects were blocked by miR-424 inhibition and COP1 overexpression. These results establish the miR-424/COP1 axis as a relevant oncogenic pathway acting through deregulation of key transcription factors and with important prognostic and therapeutic implications. Citation Format: Cecilia Dallavalle, Domenico Albino, Gianluca Civenni, Laura Curti, Paola Ostano, Maurizia Mello-Grand, Ramon Garcia-Escudero, Giovanna Chiorino, Carlo V. Catapano, Giuseppina M. R. Carbone. microRNA-mediated silencing of COP1 and altered ubiquitination of key oncogenic transcription factors promote cancer stem cell (CSC) phenotype and prostate cancer progression. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4968. doi:10.1158/1538-7445.AM2015-4968
Physical Activity or Rest After Concussion in Youth
Authors: Sara P. D. Chrisman, Frederick P. Rivara
Journal: JAMA (2016)

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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
599. Microfluidic Based Synthesis of Folate-Targeted Monomolecular siRNA-Lipid Particles
Authors: Rafał Krzysztoń, Bässem Salem, Gerlinde Schwake, Joachim O. Rädler
Journal: Molecular Therapy (2016)

The limiting factors of the effective therapies based on RNA interference are the design and synthesis of efficient transfection agent. Optimal extra- and intracellular transport demands particle to be small, stable and functional in terms of selective cell uptake and triggered release of encapsulated cargo. Strong relation between structure and function of non-viral transfection nanoagents leads to approaches based on tailored design where control over composition and molecular order of nanoparticle is needed. In this context, control over the particle synthesis and its efficiency are the bottlenecks on the way to successful pharmaceutical performance. Here the characterization of small (~30nm) mono-nucleic acid / lipid particles (mNALP) based on rational design of particle structure is made. mNALP particle consists of single 21bp double-stranded oligonucleotide covered by asymmetric lipid bilayer and PEG shielding layer. Bilayer composition of DOTAP:DOPE:DOPC:DSPE-PEG(2000) in molar ratio of 1:5:6:1,2 is an effect of considerations, aiming on a tight coverage of single oligonucleotide in order to minimize the size of whole particle structure. We emphasize the controlled formation of particles by solvent exchange method performed in hydrodynamic focusing microchip. This micromixing method shows significant improvement in physicochemical parameters e.g. reduced polydispersity, negligible aggregate formation and 20% increase in encapsulation efficiency when compared with standard bulk mixing approaches. Furthermore, mNALPs show high stability in blood plasma and serum due to the shielding PEG layer on the particle surface. Also addition of small amounts of folic-acid-conjugated PEG-lipid to the mNALP structure results in specific binding and uptake by epithelial carcinoma KB cells overexpressing folate receptor. Small size, high stability and receptor-specific cell uptake makes the mNALP a highly promising system for systemic delivery of short double stranded oligonucleotides like siRNA.
Position statement on the need for improved training for treatment of patients with combined substance use and other psychiatric disorders
Journal: American Journal of Psychiatry (1994)

The diagnosis and management of patients with combined psychiatric and substance use disorders is an important aspect of modern psychiatry, and psychiatrists should be strongly encouraged to become involved in this area. These efforts should be supported by training and educational programs involving a wide range of institutions, including local treatment facilities, hospital centers, universities, and government. Restructuring or adding improvements to existing psychiatric treatment facilities and maintaining good working relationships with existing substance abuse treatment programs are desirable goals for improving care of dually diagnosed patients.
Pre-Clinical Evaluation of a Small Molecule Inhibitor of CDK1 as Potential Therapy for MYC Expressing Mutiple Myeloma Tumors
Authors: Seda Zeng, Zhi Hua Li, Marta Chesi, Chungyee Leung-Hagesteijn, Sheng-ben Liang, P. Leif Bergsagel, Suzanne Trudel
Journal: Blood (2008)
Abstract 156: LncRNA BC200 is induced by estradiol and regulates apoptosis in MCF-7 breast cancer cells
Authors: Ramesh Singh, Yin-yuan Mo
Journal: Cancer Research (2015)

Abstract LncRNA BC200 is a small functional RNA which has been implicated in the regulation of protein synthesis in neurons. It is dysregulated in invasive carcinomas of the breast. In this study, we reported that BC200 is upregulated in breast cancer, as detected by RT-PCR analysis of breast cancer tissue scan, suggesting its possible role as an oncogene. We then demonstrated that BC200 is transcriptionally induced by estradiol (E2) treatment in ER positive breast cancer cell lines through multiple functional estrogen response elements (EREs), including the full ERE sequence ∼800bp from transcriptional start site. Luciferase reporter assay combined with mutation analysis indicated that the full ERE region is critical to the estradiol-induced promoter activity. Furthermore, BC200 is crucial for cell growth and viability; its knockdown induces apoptosis in MCF-7 cells. This may explain in part why estrogen can promote cell proliferation in ER positive breast cancer cells. To better study its role in breast cancer development and progression, we generated BC200 knockout MCF-7 cell cells using CRISPR/Cas9 technique. BC200 knockout leads to the release of cytochrome c from mitochondria and promotes the cleavage of PARP-1, both of which are an indicator of cell apoptosis. This was further confirmed by TUNEL assay. It has been reported that hnRNP A2/B1 alters the bcl-X pre-mRNA splicing in favor of anti-apoptotic bcl-XL. Of great interest, BC200 knockout enhances expression of pro-apoptotic bcl-XS form at both mRNA and protein level. RNA pulldown assays using biotin-labeled BC200 probe suggested that BC200 can bind to hnRNP Q and hnRNP A2/B1. On the other hand, RNA immunoprecipitation using hnRNP A2/B1 antibody in BC200 knockout MCF-7 cells showed a significant reduction in enrichment of bcl-X mRNA as compared to control cells. We propose that the regulation of bcl-X alternative splicing depends upon endogenous expression of BC200 that would help hnRNP A2/B1 to position itself on bcl-X mRNA and modulate splicing in favor of bcl-XL. Thus, loss of BC200 leads to generation of bcl-XS protein synthesis and to apoptosis. Together, these results suggest that BC200 functions as a negative regulator of apoptosis in breast cancer and thus, it may serve as a potential target for cancer therapies. Citation Format: Ramesh Singh, Yin-yuan Mo. LncRNA BC200 is induced by estradiol and regulates apoptosis in MCF-7 breast cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 156. doi:10.1158/1538-7445.AM2015-156
Abstract 14692: Evaluation of Subaortic Right Ventricular Function in ccTGA: How Do Echocardiography Parameters Compare to CMR?
Authors: Zakariya Albinmousa, Lan-Chau Kha, Alessia D Carlo, Alton Wong, Andrew Crean, Rachel Wald, William Wilson, Lucy S Roche
Journal: Circulation (2015)

Background: Subaortic right ventricular (RV) functional assessment in patients with congenitally corrected transposition of the great arteries (ccTGA) is important for both long-term outcome and as an indication for tricuspid valve replacement. Cardiac magnetic resonance (CMR) imaging is considered the reference standard for assessment of subaortic RV systolic function. However, two-dimensional echocardiography (2DE) remains the most frequently used imaging modality in clinical practice. Objective: To compare 2DE and CMR parameters of RV function in patients with ccTGA. Methods: We identified adults (≥18) with the diagnosis of ccTGA who underwent consecutive CMR and 2DE imaging within 6 months between 2005 and 2015. Patients with tricuspid valve replacement or pacemaker were excluded. 2DE images were reviewed and the following RV parameters re-measured by a single observer: fractional area shortening (FAC), tricuspid annular plane systolic excursion (TAPSE), tricuspid annular systolic velocity (Ts’), the rate of systolic RV pressure increase (dp/dt) and myocardial acceleration during isovolumic contraction (IVA). RVEF as measured by CMR was recorded. Results: There were 82 matched 2DE and CMR studies in 42 ccTGA patients (50% male). Median age at 2DE was 33.1 years (IQR = 22.7- 48.2 year). Pearson correlation analysis demonstrated a weak correlation between FAC and RVEF (r 2 =0.143, p=0.0005). Other 2DE parameters failed to show any correlation with RVEF (Figure 1). Conclusion: In general, 2DE parameters for the assessment of subaortic RV systolic function correlate poorly with CMR measured RVEF in patients with ccTGA. This is important information for selection and interpretation of various modalities in the long-term follow-up of this patient population.
Abstract 487: Whole genome screen to identify genes targeting MYCN-driven embryonal tumors
Authors: Carol J. Thiele, Zhihui Liu, Veronica Veschi, Eugene Buehler, Scott Martin
Journal: Cancer Research (2015)

Abstract MYCN is a driver of neuroblastoma (NB) tumorigenesis and is over-expressed in a number of tumors of embryonal origin, including rhabdomyosarcoma, medulloblastoma and diffuse intrinsic pontine gliomas. We sought to identify regulators of MYCN transcription by performing a whole genome screen (WGS) for regulators of MYCN promoter activity using a NB cell model. A plasmid containing the MYCN promoter (1.3kb upstream of MYCN TSS) fused to luciferase and stably integrated into the genome of NGP NB cells was the readout system. NGP-MYCNpluc, was selected based on MYCN luciferase activity inhibition by ATRA and HDAC inhibitors to a similar extent as endogenous MYCN mRNA levels. After assay optimization, siRNAs targeting 11,000 genes using 3 siRNAs/gene were evaluated. The siRNA library encompassed the druggable genome and the majority of human transcription factors. Using a 384-well format, siRNAs were reverse transfected in duplicate into NGP-MYCNpluc cells, cultured for 3 days at 37oC and analyzed for luciferase activity and cell viability using a ONE-Glo and Cell Titer-Glo assays (Promega), respectively. A robust statistical measure of median absolute deviation (MAD) was used to standardize siRNA activities in the screen. This identified 36 “high-confidence” genes in which all 3 siRNAs significantly decreased NGP-MYCNpluc luciferase activity, and 49 genes which significantly decrease cell viability. Most drugs associated with the essential viability genes have shown activity in NB cells (bortizamab, gemcitabine/paclitaxel, erlotinib/gemcitabine, UCN-01 and BI 2536). A number of MYCN reporter hits also decreased a CMV luciferase promoter in HEK293 cells, suggesting these hits did not specifically regulate the MYCN promoter. However, several hits did not affect CMV reporter activity, suggesting specificity to the MYCN reporter system. Low-throughput secondary screens are being utilized for assay confirmation and mechanistic evaluation. A 23,000 unique gene set is currently under evaluation and more elegant informatics tools are being used to further illuminate actives within the data Citation Format: Carol J. Thiele, Zhihui Liu, Veronica Veschi, Eugene Buehler, Scott Martin. Whole genome screen to identify genes targeting MYCN-driven embryonal tumors. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 487. doi:10.1158/1538-7445.AM2015-487
Whole Body Magnetic Resonance Imaging with Diffusion Weighted Imaging Is a Valuable Alternative to Contrast-Enhanced Computed Tomography for the Initial Staging in Hodgkin’s and Non-Hodgkin’s Lymphoma
Authors: Annalisa Balbo-Musetto, Riccardo Bruna, Angela Gueli, Chiara Saviolo, Massimo Petracchini, Daniela Gottardi, Alberto De Crescenzo, Stefano Cirillo, Corrado Tarella
Journal: Blood (2014)
NAD(P)H oxidase genetic polymorphisms and anthracyclines-induced cardiac lesions in patients with cancer.
Authors: A. Cascales, F. Pastor, B. Sanchez-Vega, J. Corral, A. Vicente, T. Garcia, V. Vicente, F. Ayala
Journal: Journal of Clinical Oncology (2011)

2596 Background: Anthracyclines (ANT)-induced cardiotoxicity is a growing problem in cancer survivors. Polymorphisms of NAD(P)H oxidase, involved in cardiac oxidative stress and remodeling, have been associated to cardiac dysfunction in ANT-treated individuals. Although no clear correlation has been found between pathologic findings and clinical events related to ANT, both cardiac fibrosis and myocytolisis are observed in these patients. So far, no reports are available that address the influence of inter-individual genetic variations on heart lesions related to ANT. Methods: Cardiac lesions were evaluated in a series of 97 consecutive autopsies from patients with solid and hematologic tumors. An unmatched comparison was performed between 48 decedents treated with ANT and 49 without ANT. H-E and Masson trichrome staining of random samples from the ventricular wall of all cases were examined. DNA was extracted from FFPE tissue and we genotyped single nucleotide polymorphisms (SNP) of NAD(P)H oxidase (212A-G of NCF4 subunit: rs1883112; C242T of p22phox subunit: rs4673; 7508T-A of RAC2 subunit: rs13058338) using Taqman probes. Association of SNPs with cardiac histological lesions, clinical events and cardiovascular risk factors was evaluated in the two groups. Results: Cardiac interstitial fibrosis (diffuse or patched) (p=0.019 and p=0.045), myocytolisis (p<0.001) and patched myocardial necrosis (0.001) were associated to ANT treatment. In the ANT group, cardiac interstitial fibrosis was strongly associated to rs1883112 (OR: 5.11; p=0.006), and was observed in all A/A homozygotes (n=7). Patched myocardial necrosis was also associated to rs4673 (OR: 4.01; p=0.036). No association was found for rs13058338. In this group, the presence of these lesions was not related to dose, previous cardiac disease nor cardiovascular risk factors, and we only observed a trend for association of patched fibrosis to heart failure (p=0.08). In the group without ANT, no relationship of cardiac lesions nor clinical events with any of the NAD(P)H SNPs was found. Conclusions: Our results support the modulation of anthracyclines-induced myocardial damage and heart fibrosis by genetic variability on NAD(H)P oxidase.