tbuckley/cabot-search huggingface dataset:
Predictive Value for Future Arrhythmic Events of Fractal Dimension, a Measure of Time Clustering of Ventricular Premature Complexes, After Myocardial Infarction fn1fn1This study was supported in part by a substudy grant from the Cardiac Arrhythmia Suppression Trial and by contracts from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
Authors: Jeffrey L. Anderson, Labros A. Karagounis, Kenneth M. Stein, Fidela L. Moreno, Robert Ledingham, Alfred Hallstrom
Journal: Journal of the American College of Cardiology (1997)
100. An Evaluation of the Use of Adeno-Associated Virus Serotypes AAV1 and AAV8 To obtain Stable Therapeutic Levels of Apolipoprotein A-I in Mouse Plasma
Authors: Karen F. Kozarsky, Deborah A. Welham, Mary H. Donahee
Journal: Molecular Therapy (2004)

Apolipoprotein A-I (ApoA-I) is the major protein component of HDL cholesterol. Numerous studies have demonstrated that high circulating plasma levels of ApoA-I protects against atherosclerosis. Previous studies have used adenovirus encoding the ApoA-I gene in mice and have achieved therapeutic plasma levels. However, the maximum expression is measured between 7 and 14 days and is usually transient. We used an adeno-associated virus serotype 8 (hybrid AAV2/8) to deliver the human ApoA-I gene. AAV2/8 transduces hepatic cells with a high efficiency and provides longer sustained expression of the transgene than adenovirus. Normal male C57Bl/6 mice were injected intravenously with AAV2/8-ApoA-I, AAV2/8-ApoE, or PBS. Therapeutic levels of ApoA-I and ApoE were measured at 6 weeks post injection and were sustained for at least 6 months. AAV2/8 DNA in the liver was subjected to Southern blot analysis to evaluate the molecular state of the AAV genome as well as persistence. Furthermore, expression levels of AAV2/8 delivered to the liver were compared to the most efficient AAV serotype for intramuscular delivery, AAV1. Levels of ApoA-I from hepatic delivery of AAV2/8 were significantly higher than those from intramuscular delivery of AAV2/1, indicating that hepatic delivery may be needed to achieve therapeutic levels of transgene expression.
Abstract 3633: Combination of innate immune activators stimulates leukocyte populations in the tumor microenvironment
Authors: Ehud Shahar, Raphael Gorodetsky, Elina Aizenshtein, Jacob Pitcovski
Journal: Cancer Research (2014)

Abstract Tumor microenvironment (TME) harbors a multitude of immune cells which can comprise up to 50% of the tumor. The most abundant cells in the TME often are tumor associated macrophages (TAM) and tumor associated neutrophils (TAN). These cells potentially possess anti-tumoral cytotoxic effects, and have the potential to induce a broad range of cellular immune responses. However, in the developing tumor, due to elements secreted by the tumor cells, TAM and TAN are altered to act in a pro-tumor manner. The purpose of our study was the optimization and characterization of a treatment aimed at inducing an anti-tumoral response of innate immune cells in the TME. In a melanoma B16 mice model, micro-particles carrying targeting and induction components were injected intra-tumorally and the responses of the tumors, including immune cells populations were monitored. Without treatment the CD45+ cells ratio of total TME decreased as tumor progressed. Particles carrying Toll-like receptor ligands inhibited tumor growth, inducing significant elevation of CD45+ cells in the TME. Using different inducing molecules (inducers) or simultaneous use of several inducers enabled the stimulation of specific immune cell populations within the tumor. The current study suggests that by using tumor targeted particles with adequate inducers, one could change the tumor microenvironment innate immune cells toward an anti-tumor response. Citation Format: Ehud Shahar, Raphael Gorodetsky, Elina Aizenshtein, Jacob Pitcovski. Combination of innate immune activators stimulates leukocyte populations in the tumor microenvironment. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3633. doi:10.1158/1538-7445.AM2014-3633
Studies Probe US Traffic Injuries, Deaths
Authors: Mike Mitka
Journal: JAMA (2009)

This article will discuss accident statistics reported by the National Highway Traffic Safety Administration (NHTSA) and released in July. There has been substantial progress in reducing motor vehicle accidents and fatalities in the United States and recent research has found that additional deaths and injuries can be prevented by lowering speed limits and banning drivers from engaging in potentially fatal distractions, such as dialing or text messaging on cellular phones. In addition to the curtailment of impaired driving, increased seat belt use, improved roadways, and safety related vehicle features are also factors that can contribute to the reductions in motor vehicle accidents.
Angiogenesis markers in sunitinib-treated clear-cell renal carcinoma patients.
Authors: Loukas Kontovinis, Konstantinos Papazisis, Panagiota Touplikioti, Despoina Mouratidou, Lazaros Boutis, Alexandros Kortsaris
Journal: Cancer Research (2008)

235   Introduction: Sunitinib is a protein tyrosine kinase-inhibitor targeting VEGFR, c-kit and PDGFR. It has been approved for the treatment of metastatic renal-cell carcinoma and gastrointestinal stromal tumors (GISTs). Although it has been shown to prolong disease-free and overall survival in renal-cell carcinoma patients, only 70% of the treated population receive a clinical benefit (CB) form the treatment. Currently there are no clear data to correlate response to sunitinib with any changes in angiogenetic factors in those patients. Surrogate markers that could predict clinical benefit to sunitinib would be an important aid in monitoring and following their treatment.  Patients and methods: We have examined 32 patients with metastatic clear-cell renal carcinoma that received sunitinib, 50 mg daily for 30 out of 45 days per cycle. Blood samples were collected after informed consent in several time-points during their treatment and angiogenesis factors were estimated in the plasma with ELISA.  Results: From the 27 evaluable for response patients (that received at least three months of therapy), twenty patients (74%) had a clinical benefit (CB), with 14 patients (52%) having a partial response and 6 (22%) disease stabilization. Seven patients (26%) experienced a disease progression (PD) and the treatment was discontinued. Side-effects included fatigue, mucositis, hypertension, skin discoloration, peripheral oedema and hypothyroidism (two patients). In three patients the dose was reduced to 37.5 mg per day due to adverse events; however there was no treatment discontinuation due to intolerance. Two patients experienced disease flare-up in the off-treatment periods and continued treatment with no-stop, 37.5 mg sunitinib daily.  Soluble VEGF receptors (sVEGFR) were decreased during sunitinib treatment both in CB and in PD patients. During the off-treatment periods sVEGFR plasma levels were increased (buy a factor of 2) only in CB patients, having no difference in the non-responders9 group. Plasma PDGF levels were significantly lower in the CB group throughout the treatment period. Treatment with sunitinib resulted in lower PDGF levels in all patient group. On the contrary VEGF was increased, especially in patients that did not responded as well as in responders just before the subsequent disease progression.  Conclusions: Sunitinib treatment offers a significant clinical benefit in the majority of patients with an acceptable and manageable toxicity profile. Monitoring plasma levels of angiogenetic factors may prove to be an important tool in predicting response to treatment or disease progression. The study is ongoing.
Oral complications of cancer and cancer therapy
Authors: Joel B. Epstein, Juliette Thariat, Rene‐Jean Bensadoun, Andrei Barasch, Barbara A. Murphy, Leanne Kolnick, Leslie Popplewell, Ellie Maghami
Journal: CA A Cancer Journal for Clinicians (2012)

Abstract Answer questions and earn CME/CNE Oral complications resulting from cancer and cancer therapies cause acute and late toxicities that may be underreported, underrecognized, and undertreated. Recent advances in cancer treatment have led to changes in the incidence, nature, and severity of oral complications. As the number of survivors increases, it is becoming increasingly recognized that the aggressive management of oral toxicities is needed to ensure optimal long‐term oral health and general well‐being. Advances in care have had an impact on previously recognized oral complications and are leading to newly recognized adverse effects. Here, the authors briefly review advances in cancer therapy, including recent advances in surgery, oral care, radiation therapy, hematopoietic cell transplantation, and medical oncology; describe how these advances affect oral health; and discuss the frequent and/or severe oral health complications associated with cancer and cancer treatment and their effect upon long‐term health. Although some of the acute oral toxicities of cancer therapies may be reduced, they remain essentially unavoidable. The significant impact of long‐term complications requires increased awareness and recognition to promote prevention and appropriate intervention. It is therefore important for the primary oncologist to be aware of these complications so that appropriate measures can be implemented in a timely manner. Prevention and management is best provided via multidisciplinary health care teams, which must be integrated and communicate effectively in order to provide the best patient care in a coordinated manner at the appropriate time. CA Cancer J Clin 2012. © 2012 American Cancer Society.
Responsibility in Health Care.
Authors: George J. Agich
Journal: Annals of Internal Medicine (1984)

Section I / Health Care Teams and the Physician-Patient Relationship.- An Historical View of Health Care Teams.- Once On Top, Now On Tap: American Physicians View Their Relationships With Patients, 1920-1970.- Section II / Authority and Responsibility in the Practice of   Concept of Responsibility in  Comments on The Concept of Responsibility in Medicine.- Authority and the Profession of  Power, Authority, and Rights in the Practice of  Medical Authority and Professional Medical Authority:  Nature of Authority in Medicine for Decisions by Lay Persons and Professionals.- Section III / Ethics of Consultation and Interprofessional Relationships.- Medical Consultations in the Context of the Physician-Patient Relationship.- Integrity in Interprofessional Relationships.- Consulting With Integrity: Some Reflections on Team Health Care and Professional Responsibility.- Logical Confusions and Moral Dilemmas in Health Care Teams and Team Talk.- Responsibility and Health Care Teams: A Health Professional's Perspective.- Section IV / Legal and Political Responsibility in Health Care Matters.- Legal Responsibility in Health Care: Whose Fault is It Anyway?.- Reaching Closure on Health-Related Controversies.- Responsibility and Public Policy in Health Care: Commentary on Essays by Williams and Rich.- Notes on Contributors.
Radiation Compensation Rules
Authors: Brian Vastag
Journal: JAMA (2002)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Abstract 14029: Microrna-27a Regulates Beta-Myosin Heavy Chain Gene Expression by Targeting Thyroid Hormone Receptor Beta 1 in Neonatal Rat Ventricular Myocytes
Authors: Hitoo Nishi, Koh Ono, Takahiro Horie, Minao Kinoshita, Shin Watanabe, Yasuhide Kuwabara, Osamu Baba, Yasuhiro Nakashima, Kazuya Nagao, Rieko Takanabe-Mori, Koji Hasegawa, Toru Kita, Takeshi Kimura
Journal: Circulation (2010)

MicroRNAs (miRNAs), small non-coding RNAs, are negative regulators of gene expression and play important roles in gene regulation in the heart. To examine the role of miRNAs in the expression of two isoforms of the cardiac myosin heavy chain (MHC) gene, α- and β-MHC, which regulate cardiac contractility, endogenous miRNAs were down-regulated in neonatal rat ventricular myocytes (NRVMs) using lentivirus-mediated siRNA against Dicer, an essential enzyme for miRNA biosynthesis, and MHC expression levels were examined. As a result, Dicer siRNA could down-regulate endogenous miRNAs simultaneously, including ubiquitous miR-16 and muscle-specific miR-133b and the β-MHC gene but not α-MHC, suggesting that specific miRNAs could up-regulate the β-MHC gene. After screening for β-MHC mRNA expression in NRVMs over-expressing 21 randomly selected miRNAs, miR-27a was found to up-regulate the β-MHC gene but not α-MHC. Moreover, β-MHC protein was down-regulated by silencing endogenous miR-27a. These results suggest that m...
Abstract 17412: Vital Exhaustion and Incident Cardiovascular Disease: a Meta-Analysis
Authors: Jincy Thankachen, Chirag Bavishi, Randy Cohen, Alan Rozanski
Journal: Circulation (2014)

Background: A number of psychosocial conditions are associated with cardiovascular disease (CVD) events. One such condition is vital exhaustion (VE), defined as a combination of fatigue, increased irritability and feelings of demoralization. To date, a number of studies have examined the association between VE, fatigue (as a stand-alone entity) and subsequent cardiovascular events with varying results. In order to evaluate the potency of VE/fatigue as a CVD risk factor, we conducted a meta-analysis of existing studies concerning these factors in the literature. Methods: A systematic search of PubMed, EMBASE and PsychINFO (1972-May, 2014) was performed to identify all prospective studies involving subjects without baseline CVD, investigating the relationship between VE/fatigue and incident CVD. Unadjusted and adjusted effect estimates were extracted from individual studies. Pooled effect estimates were calculated with DerSimonian and Laird random effects models. Results: Eleven prospective studies with a total of 60, 610 participants and a mean follow-up period of 6.5 years were included in the analysis. A significant association was observed between VE/fatigue and incident CVD, using both unadjusted estimates [Pooled Relative Risk: 1.69 (CI: 1.31-2.18), p&lt;0.001] and adjusted estimates from individual studies [Pooled RR: 1.36 (CI: 1.14-1.63), p=0.001]. Subgroup analysis by years of follow-up and type of VE/fatigue questionnaire yielded similar increased risk of incident CVD. Conclusions: VE/fatigue is a significant risk factor for incident CVD in healthy subjects, comparable in potency to some of the other common psychosocial risk factors for cardiac disease.
Abstract 18084: MiR-30e Targets IGF2-Regulated Osteogenesis in Bone Marrow Derived Mesenchymal Stem Cells, Aortic Smooth Muscle Cells, and APOE-/- Mice
Authors: Wen Ding, Jihe Li, Jayanti Singh, Razan Alif, Roberto I Vazquez-Padron, Samirah A Gomes, Joshua M Hare, Lina A Shehadeh
Journal: Circulation (2014)

Objective:  In atherosclerosis, activation of an osteogenic transcriptional program in de-differentiated mesenchymal-like smooth muscle cells (SMCs) contributes substantially to the initiation of aortic calcification. We found that aortic miR-30e is downregulated with age and atherosclerosis and inversely proportional to osteogenic markers. To assess the effect of miR-30e downregulation, we tested the hypothesis that miR-30e regulates osteogenic program in bone marrow derived mesenchymal stem cells (MSCs), aortic SMCs, and APOE-/- mice.   Method and Results:  In aortas of old (13.5 mo) and young (6 mo) wild type and APOE-/- mice (n=4-15), we found that NFYC gene and hosted miR-30e transcripts are downregulated with age and atherosclerosis while the osteogenic markers Runx2, Opn, and Igf2 are upregulated - p   Conclusion:  MiR-30e represses the osteogenic program in MSCs and SMCs by targeting IGF2 and drives their differentiation into different lineages. Downregulation of miR-30e in aortas with age and atherosclerosis may trigger vascular calcification.
Abstract 1925: CK2 phosphorylates and inhibits tumor suppressor TAp73 function to promote cancer stem cell gene expression and phenotype in head and neck cancer
Authors: Hai Lu, Carol H. Yan, Yansong Bian, Zhong Chen, Carter Van Waes
Journal: Cancer Research (2014)

Abstract Cancer development, cell survival, and therapeutic resistance have recently been linked to a small sub-population of cells expressing stem cell genes, and capable of reproducing the cancer cell population, called cancer stem cells (CSC). CK2 (formerly casein kinase II) has emerged as a key signal serine/threonine kinase that modulates diverse signal cascades that regulate cell fate and growth. We previously showed that CK2 is aberrantly expressed and activated in head and neck squamous cell carcinomas (HNSCC). Concomitant inactivation of tumor suppressor TAp73, along with mutation of related family member TP53, is also often observed, but the relationship between CK2, TAp73 inactivation, and CSC is unknown. Here, we observed that classical stem cell genes NANOG, SOX2, and OCT4, are overexpressed in HNSCC with inactivated TAp73 and mtTP53. Inhibition of CK2 by pharmacologic inhibitors or siRNA increased TAp73 mRNA and protein expression, while inhibiting CSC gene expression and the SP. Conversely, knockdown of TAp73 increased CSC gene expression and the SP. Bioinformatic analysis identified a single predicted CK2 threonine phosphorylation site (T27) within the N-terminal transactivation domain of TAp73. Nuclear CK2 and TAp73 interaction, confirmed by co-immunoprecipitation, was attenuated by CK2 inhibitor, or a T27A point-mutation of the predicted CK2 threonine phospho-acceptor site of TAp73. Furthermore, T27A mutation attenuated TAp73 phosphorylation, while enhancing its function in repressing CSC gene expression, and SP cells. Novel CK2 inhibitor CX-4945 inhibited CSC related SP cells, clonogenic survival, and spheroid formation, identifying CK2 modulation of tumor suppressor TAp73 as a potential target for inhibition of CSCs. Our study reveals a novel regulatory mechanism whereby aberrant CK2-mediated inactivation of TAp73 tumor suppressor function promotes key CSC genes and phenotype. Supported by NIDCD intramural project ZIA-DC-00073 Citation Format: Hai Lu, Carol H. Yan, Yansong Bian, Zhong Chen, Carter Van Waes. CK2 phosphorylates and inhibits tumor suppressor TAp73 function to promote cancer stem cell gene expression and phenotype in head and neck cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1925. doi:10.1158/1538-7445.AM2014-1925
Abstract 2781: Elimination of PanIn2/3 in a GEMM for pancreatic cancer with disrupted p16 and activated Kras
Authors: Richard D. Dinnen, Wanglong Qiu, Gloria H. Su, Daniel P. Petrylak, Robert L. Fine
Journal: Cancer Research (2014)

Abstract When treated with clinically achievable concentrations of arsenic trioxide, ascorbic acid and antabuse (disulfiram) (AAA), we found that four human pancreatic cancer cell lines underwent robust cell death associated with ATP decline and ROS accumulation. In these cells, early apoptosis shifted to aponecrosis, and was dependent on VDAC since shRNA antagonistic to VDAC-1 abrogated the ROS accumulation and blocked cell death. In this study, assessment of AAA was performed in Pdx1-Cre transgenic mice with a conditional p16 knockout (p16flox/flox), and oncogenic KrasG12D. The KrasG12D, p16flox/flox; LSL-KrasG12D; Pdx1-Cre mice develop a full spectrum of pancreatic intraepithelial neoplasia (PanIN) lesions, pancreatic ductal adenocarcinoma (PDA), and frequent metastases. Eight week old mice were treated for 8 weeks, 3 times/week with AAA, sacrificed, and assessed for the development of pancreatic cancer. Little or no toxicity was observed in the AAA-treated mice. The development of frank pancreatic tumors was decreased from 37% in controls to 0% in AAA-treated mice. The mean number of PanIN 3 lesions/mouse declined from 14.2 in controls to 1.6 in AAA-treated mice (p=0.004); the mean number of PanIN 2 lesions declined from 5.8 in controls to 1.7 in AAA-treated mice (p=0.029), and the mean number of PanIN 1 lesions in control mice was 14.2 and in AAA-treated mice was 16.0 (p=0.82), indicating no difference in PanIN 1 occurrence between control and AAA-treated mice. The data also suggests that PanIN 2 and PanIN 3 lesions are killed after exposure to AAA, since mice prior to treatment had high levels of PanIN 2 (8.1 lesions/mouse) and PanIN 3 (11.4 lesions/mouse), similar to controls at 4 months of age. Therefore, AAA may have eliminated pre-existing PanINs rather than blocking their development. Results from immunohistochemical staining of the PanIN lesions for VDAC, indicated that PanIN 1 lesions have low, and PanIN 2 and 3 lesions have high, VDAC expression. This result parallels the in vitro human cell line data showing VDAC expression is critical to AAA sensitivity, and suggests a similar mechanism of action in the murine model, as we see in vitro. This is the first treatment that has shown potential to kill existing PanIN lesions and arrest the development of tumors in this pancreatic cancer murine model. Citation Format: Richard D. Dinnen, Wanglong Qiu, Gloria H. Su, Daniel P. Petrylak, Robert L. Fine. Elimination of PanIn2/3 in a GEMM for pancreatic cancer with disrupted p16 and activated Kras. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2781. doi:10.1158/1538-7445.AM2014-2781
Essentials of Human Physiology.
Authors: Gordon Ross
Journal: JAMA (1907)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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