tbuckley/cabot-search huggingface dataset:
Incremental Dental Expenditures Associated With Diabetes Among Noninstitutionalized U.S. Adults Aged ≥18 Years Old in 2016–2017
Authors: Yu Chen, Ping Zhang, Elizabeth T. Luman, Susan O. Griffin, Deborah B. Rolka
Journal: Diabetes Care (2021)

Diabetes is associated with poor oral health, but incremental expenditures for dental care associated with diabetes in the U.S. are unknown. We aimed to quantify these incremental expenditures per person and for the nation.We analyzed data from 46,633 noninstitutionalized adults aged ≥18 years old who participated in the 2016-2017 Medical Expenditure Panel Survey. We used two-part models to estimate dental expenditures per person in total, by payment source, and by dental service type, controlling for sociodemographic characteristics, health status, and geographic variables. Incremental expenditure was the difference in predicted expenditure for dental care between adults with and without diabetes. The total expenditure for the U.S. was the expenditure per person multiplied by the estimated number of people with diabetes. Expenditures were adjusted to 2017 USD.The mean adjusted annual diabetes-associated incremental dental expenditure was $77 per person and $1.9 billion for the nation. Of this incremental expenditure, 51% ($40) and 39% ($30) were paid out of pocket and by private insurance, 69% ($53) of the incremental expenditure was for restorative/prosthetic/surgical services, and adults with diabetes had lower expenditure for preventive services than those without (incremental, -$7). Incremental expenditures were higher in older adults, non-Hispanic Whites, and people with higher levels of income and education.Diabetes is associated with higher dental expenditures. These results fill a gap in the estimates of total medical expenditures associated with diabetes in the U.S. and highlight the importance of preventive dental care among people with diabetes.
ACETYLCHOLINESTERASE INHIBITOR AMELIORATES CARDIAC DYSFUNCTION THROUGH REDUCING NECROPTOSIS IN DOXORUBICIN-INDUCED CARDIOTOXICITY IN RATS
Authors: Thawatchai Khuanjing, Benjamin Ongnok, Nanthip Prathumsap, Apiwan Arinno, Chayodom Maneechote, Titikorn Chunchai, Krekwit Shinlapawittayatorn, Busarin Arunsak, Thidarat Jaiwongkam, Sasiwan Kerdphoo, Siriporn Chattipakorn, Nipon Chattipakorn
Journal: Journal of the American College of Cardiology (2021)
N<sup>6</sup>‐methyladenosine Steers RNA Metabolism and Regulation in Cancer
Authors: Shenghua Dong, Yutong Wu, Yadi Liu, Hengyou Weng, Huilin Huang
Journal: Cancer Communications (2021)

Abstract As one of the most studied ribonucleic acid (RNA) modifications in eukaryotes, N 6 ‐methyladenosine (m 6 A) has been shown to play a predominant role in controlling gene expression and influence physiological and pathological processes such as oncogenesis and tumor progression. Writer and eraser proteins, acting opposite to deposit and remove m 6 A epigenetic marks, respectively, shape the cellular m 6 A landscape, while reader proteins preferentially recognize m 6 A modifications and mediate fate decision of the methylated RNAs, including RNA synthesis, splicing, exportation, translation, and stability. Therefore, RNA metabolism in cells is greatly influenced by these three classes of m 6 A regulators. Aberrant expression of m 6 A regulators has been widely reported in various types of cancer, leading to cancer initiation, progression, and drug resistance. The close links between m 6 A and cancer shed light on the potential use of m 6 A methylation and its regulators as prognostic biomarkers and drug targets for cancer therapy. Given the notable effects of m 6 A in reversing chemoresistance and enhancing immune therapy, it is a promising target for combined therapy. Herein, we summarize the recent discoveries on m 6 A and its regulators, emphasizing their influences on RNA metabolism, their dysregulation and impacts in diverse malignancies, and discuss the clinical implications of m 6 A modification in cancer.
Illuminating RNA trafficking and functional delivery by extracellular vesicles
Authors: Willemijn S de Voogt, Marvin E Tanenbaum, Pieter Vader
Journal: Advanced Drug Delivery Reviews (2021)

RNA-based therapeutics are highly promising for the treatment of numerous diseases, by their ability to tackle the genetic origin in multiple possible ways. RNA molecules are, however, incapable of crossing cell membranes, hence a safe and efficient delivery vehicle is pivotal. Extracellular vesicles (EVs) are endogenously derived nano-sized particles and possess several characteristics which make them excellent candidates as therapeutic RNA delivery agent. This includes the inherent capability to functionally transfer RNAs in a selective manner and an enhanced safety profile compared to synthetic particles. Nonetheless, the fundamental mechanisms underlying this selective inter- and intracellular trafficking and functional transfer of RNAs by EVs are poorly understood. Improving our understanding of these systems is a key element of working towards an EV-based or EV-mimicking system for the functional delivery of therapeutic RNA. In this review, state-of-the-art approaches to detect and visualize RNA in situ and in live cells are discussed, as well as strategies to assess functional RNA transfer, highlighting their potential in studying EV-RNA trafficking mechanisms.
Refining genotype–phenotype correlations in 304 patients with autosomal recessive polycystic kidney disease and PKHD1 gene variants
Authors: Kathrin Burgmaier, Leonie Brinker, Florian Erger, Bodo B. Beck, Marcus R. Benz, Carsten Bergmann, Olivia Boyer, Laure Collard, Claudia Dafinger, Marc Fila, Claudia Kowalewska, Bärbel Lange-Sperandio, Laura Massella, Antonio Mastrangelo, Djalila Mekahli, Monika Miklaszewska, Nadina Ortiz-Bruechle, Ludwig Patzer, Larisa Prikhodina, Bruno Ranchin, Nadejda Ranguelov, Raphael Schild, Tomas Seeman, Lale Sever, Przemyslaw Sikora, Maria Szczepanska, Ana Teixeira, Julia Thumfart, Barbara Uetz, Lutz Thorsten Weber, Elke Wühl, Klaus Zerres, Jörg Dötsch, Franz Schaefer, Max Christoph Liebau, Loai Akram Eid, Klaus Arbeiter, Nathalie Godefroid, Jacques Lombet, Aurélie De Mul, Markus Feldkoetter, Jakub Zieg, Franziska Grundmann, Matthias Galiano, Björn Buchholz, Anja Buescher, Karsten Häffner, Oliver Gross, Ludwig Patzer, Jun Oh, Dieter Haffner, Wanja Bernhardt, Susanne Schaefer, Simone Wygoda, Jan Halbritter, Ute Derichs, Günter Klaus, Felix Lechner, Sabine Ponsel, Jens König, Hagen Staude, Donald Wurm, Martin Bald, Michaela Gessner, Neveen A. Soliman, Gema Ariceta, Juan David Gonzalez Rodriguez, Francisco de la Cerda Ojeda, Jerome Harambat, Denis Morin, Claire Dossier, Guillaume Dorval, Rukshana Shroff, Stella Stabouli, Nakysa Hooman, Francesca Mencarelli, William Morello, Germana Longo, Francesco Emma, Augustina Jankauskiene, Katarzyna Taranta-Janusz, Ilona Zagozdzon, Katarzyna Zachwieja, Malgorzata Stanczyk, Beata Bienias, Mieczyslaw Litwin, Aurelia Morawiec-Knysak, Alberto Caldas Afonso, Oliver Dunand, Andreea Rachisan, Gordana Miloševski-Lomić, Svetlana Papizh, Rina Rus, Houweyda Jilani, Bahriye Atmis, Ali Duzova, Alper Soylu, Cengiz Candan, Salim Caliskan, Alev Yilmaz, İbrahim Gökce, Nurver Akinci, Sevgi Mir, Ismail Dursun, Yilmaz Tabel, Hulya Nalcacioglu
Journal: Kidney International (2021)
CARDIOVASCULAR ADMISSIONS ACCOUNT FOR THE MAJORITY OF U.S. HOSPITALIZATIONS IN PATIENTS WITH SARCOIDOSIS: INSIGHTS FROM THE NATIONAL INPATIENT SAMPLE 2016-2017
Authors: Aditya Mantha, Kristin Mathias, Lauren M. Mathias, Glenn R. Ehresmann, Parveen Garg
Journal: Journal of the American College of Cardiology (2021)
OUTCOMES OF ELDERLY PATIENTS WITH PULMONARY EMBOLISM UNDERGOING PERCUTANEOUS MECHANICAL THROMBECTOMY WITH INARI FLOWTRIEVER SYSTEM COMPARED WITH SYSTEMIC THROMBOLYSIS
Authors: Nour Albast, Yasser Al-Khadra, Basma Al-bast, Venkata Missula, Radhika Deshpande, Prashanth Singanallur, Raad Al Tamimi, Manasik Abdu, Abdul Moiz Hafiz
Journal: Journal of the American College of Cardiology (2021)
ANATOMY VERSUS ISCHEMIA IN THE ISCHEMIA-CKD TRIAL: DOES EITHER PREDICT OUTCOME?
Authors: Kevin Bainey, Jerome Fleg, Judith Hochman, Philip Jones, Dennis Kunichoff, Alexander Chernyavskiy, Marcin Demkow, Juan Lopez Quijano, Jorge Escobedo, Kian Keong Poh, Ruben Ramos, Eduardo Lima, Herwig Schuchlenz, David Maron, Sean O'Brien, John Spertus, Sripal Bangalore
Journal: Journal of the American College of Cardiology (2021)
ORTNER SYNDROME DUE TO SACCULAR AORTIC ARCH ANEURYSM IN A MAN WITH CORONARY ARTERY DISEASE: OPTIONS FOR DIAGNOSIS AND MANAGEMENT USING HYBRID INTERVENTIONS
Authors: Nicole Girlyn T. Pang, Gwen R. Marcellana, Maria Janelle M. Fajardo, Terence M. Cuezon, Ferdinand V. Alzate, Marvin D. Martinez, Ramiro Thadeus P. Pablo, Fabio Enrique B. Posas
Journal: Journal of the American College of Cardiology (2021)
Abstract 16976: Derangements in Cardiac Oxidative Metabolism in Humans With Dilated Cardiomyopathy
Authors: Daniel Clark, Giovanni E Davogustto, Susan P Bell, RAVINDER MALLUGARI, William S Bradham, Mark Lawson, Deepak K Gupta, Marvin W Kronenberg
Journal: Circulation (2020)

Introduction: Dilated cardiomyopathy (DCM) is associated with impaired myocardial perfusion reserve and impaired myocardial oxidative metabolism. However, the association between myocardial perfusion reserve and oxidative metabolism, is not fully understood. Hypothesis: Reduced myocardial perfusion reserve is associated with reduced myocardial oxidative metabolism. Methods: Using non-invasive cardiac imaging, we studied 8 DCM patients and 14 normal subjects. Myocardial perfusion reserve index (MPRI) was calculated using cardiac magnetic resonance as the normalized rate of myocardial signal augmentation following gadolinium contrast injection between rest and regadenoson induced stress. Resting oxidative metabolism was calculated as the myocardial mono-exponential decay rate (Kmono) of [ 11 C]acetate by positron emission tomography normalized per unit demand (rate-pressure product, RPP) (Kmono/RPP). Results: MPRI was lower in DCM compared to controls (1.25 ± 0.22 vs 1.59 ± 0.49, p=0.038). Similarly, Kmono/RPP was lower in DCM compared with normal subjects (0.6x10e-3 ± 0.15 x10e-3 vs 1.2x10e-3 ± 0.9x10e-3, p&lt;0.0001). There was a linear relation between Kmono and RPP in normal subjects. However, DCM patients showed no increase in Kmono regardless of RPP (Figure 1A). Kmono/RPP was not significantly related to MPRI in either group (Figure 1B). Conclusions: Patients with DCM exhibit markedly impaired myocardial oxidative metabolism compared to normal subjects. However, this impairment was not quantitatively related to impaired myocardial perfusion reserve. Of the various mechanisms that could explain decrease in oxidative metabolism in DCM, these data suggest that reduced myocardial perfusion is not the principal driver of impaired oxidative metabolism.
PROPENSITY SCORE MATCHED OUTCOMES OF HEART FAILURE WITH PRESERVED EJECTION FRACTION PATIENTS WITH PULMONARY HYPERTENSION
Authors: Krunalkumar Patel, Kirtenkumar Patel, Muhammad Zubair Khan, Harsh Patel, Amitkumar Patel, Samarthkumar Thakkar, Devina Adalja, Umang Patel, Vincent Figueredo
Journal: Journal of the American College of Cardiology (2021)
METABOLIC RISK FACTORS AND THE EFFECT OF ALIROCUMAB ON CARDIOVASCULAR EVENTS IN PATIENTS AFTER ACUTE CORONARY SYNDROME: AN ANALYSIS OF THE ODYSSEY OUTCOMES RANDOMIZED CONTROLLED TRIAL
Authors: Petr Ostadal, Philippe Gabriel Steg, Yan Poulouin, Deepak Bhatt, Vera Bittner, Terrence Chua, Rafael Diaz, Shaun Goodman, Robert Harrington, Johan Wouter Jukema, Yuri Karpov, Robert Pordy, Michel Scemama, Michael Szarek, Harvey D. White, Andreas Zeiher, Gregory Schwartz
Journal: Journal of the American College of Cardiology (2021)
Mitochondrial Metabolism Regulation of T Cell–Mediated Immunity
Authors: Elizabeth M. Steinert, Karthik Vasan, Navdeep S. Chandel
Journal: Annual Review of Immunology (2021)

Recent evidence supports the notion that mitochondrial metabolism is necessary for T cell activation, proliferation, and function. Mitochondrial metabolism supports T cell anabolism by providing key metabolites for macromolecule synthesis and generating metabolites for T cell function. In this review, we focus on how mitochondrial metabolism controls conventional and regulatory T cell fates and function.
Recent insights in the PI3K/Akt pathway as a promising therapeutic target in combination with EGFR‐targeting agents to treat head and neck squamous cell carcinoma
Authors: Hannah Zaryouh, Ines De Pauw, Hasan Baysal, Marc Peeters, Jan Baptist Vermorken, Filip Lardon, An Wouters
Journal: Medicinal Research Reviews (2021)

Abstract Resistance to therapies targeting the epidermal growth factor receptor (EGFR), such as cetuximab, remains a major roadblock in the search for effective therapeutic strategies in head and neck squamous cell carcinoma (HNSCC). Due to its close interaction with the EGFR pathway, redundant or compensatory activation of the phosphatidylinositol 3‐kinase (PI3K)/Akt pathway has been proposed as a major driver of resistance to EGFR inhibitors. Understanding the role of each of the main proteins involved in this pathway is utterly important to develop rational combination strategies able to circumvent resistance. Therefore, the current work reviewed the role of PI3K/Akt pathway proteins, including Ras, PI3K, tumor suppressor phosphatase and tensing homolog, Akt and mammalian target of rapamycin in resistance to anti‐EGFR treatment in HNSCC. In addition, we summarize PI3K/Akt pathway inhibitors that are currently under (pre)clinical investigation with focus on overcoming resistance to EGFR inhibitors. In conclusion, genomic alterations in and/or overexpression of one or more of these proteins are common in both human papillomavirus (HPV)‐positive and HPV‐negative HNSCC tumors. Therefore, downstream effectors of the PI3K/Akt pathway serve as promising drug targets in the search for novel therapeutic strategies that are able to overcome resistance to anti‐EGFR treatment. Co‐targeting EGFR and the PI3K/Akt pathway can lead to synergistic drug interactions, possibly restoring sensitivity to EGFR inhibitors and hereby improving clinical efficacy. Better understanding of the predictive value of PI3K/Akt pathway alterations is needed to allow the identification of patient populations that might benefit most from these combination strategies.
Longitudinal proteomic analysis of severe COVID-19 reveals survival-associated signatures, tissue-specific cell death, and cell-cell interactions
Authors: Michael R. Filbin, Arnav Mehta, Alexis M. Schneider, Kyle R. Kays, Jamey R. Guess, Matteo Gentili, Bánk G. Fenyves, Nicole C. Charland, Anna L.K. Gonye, Irena Gushterova, Hargun K. Khanna, Thomas J. LaSalle, Kendall M. Lavin-Parsons, Brendan M. Lilley, Carl L. Lodenstein, Kasidet Manakongtreecheep, Justin D. Margolin, Brenna N. McKaig, Maricarmen Rojas-Lopez, Brian C. Russo, Nihaarika Sharma, Jessica Tantivit, Molly F. Thomas, Robert E. Gerszten, Graham S. Heimberg, Paul J. Hoover, David J. Lieb, Brian Lin, Debby Ngo, Karin Pelka, Miguel Reyes, Christopher S. Smillie, Avinash Waghray, Thomas E. Wood, Amanda S. Zajac, Lori L. Jennings, Ida Grundberg, Roby P. Bhattacharyya, Blair Alden Parry, Alexandra-Chloé Villani, Moshe Sade-Feldman, Nir Hacohen, Marcia B. Goldberg
Journal: Cell Reports Medicine (2021)

Mechanisms underlying severe coronavirus disease 2019 (COVID-19) disease remain poorly understood. We analyze several thousand plasma proteins longitudinally in 306 COVID-19 patients and 78 symptomatic controls, uncovering immune and non-immune proteins linked to COVID-19. Deconvolution of our plasma proteome data using published scRNA-seq datasets reveals contributions from circulating immune and tissue cells. Sixteen percent of patients display reduced inflammation yet comparably poor outcomes. Comparison of patients who died to severely ill survivors identifies dynamic immune-cell-derived and tissue-associated proteins associated with survival, including exocrine pancreatic proteases. Using derived tissue-specific and cell-type-specific intracellular death signatures, cellular angiotensin-converting enzyme 2 (ACE2) expression, and our data, we infer whether organ damage resulted from direct or indirect effects of infection. We propose a model in which interactions among myeloid, epithelial, and T cells drive tissue damage. These datasets provide important insights and a rich resource for analysis of mechanisms of severe COVID-19 disease.
A Revisitation of “Doc, How Much Time Do I Have?”
Authors: Lidia Schapira, Peter D. Eisenberg, Neil MacDonald, Matthew P. Mumber, Charles Loprinzi
Journal: Journal of Clinical Oncology (2000)

Article Tools THE ART OF ONCOLOGY: WHEN THE TUMOR IS NOT THE TARGET Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2000.18.13.2640 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 10893300 A Revisitation of “Doc, How Much Time Do I Have?” Lidia SchapiraxLidia SchapiraSearch for articles by this author , Peter D. EisenbergxPeter D. EisenbergSearch for articles by this author , Neil MacDonaldxNeil MacDonaldSearch for articles by this author , Matthew P. MumberxMatthew P. MumberSearch for articles by this author , Charles LoprinzixCharles LoprinziSearch for articles by this author Show More From the Beth Israel Deaconess Medical CenterHarvard Medical School, Brookline, MA; Marin Oncology, Greenbrae, CA; Cancer Ethics Programme, Centre for Bioethics, Clinical Research Institute of Montreal, Montreal, Canada; InterCommunity Cancer Center, Rome, GA; and Mayo Clinic, Rochester, MN. https://doi.org/10.1200/JCO.2000.18.13.2640 First Page Full Text PDF Figures and Tables © 2000 by American Society of Clinical Oncology
Effect of Adjuvant Metronomic Capecitabine on Disease-Free Survival Among Patients With Early-Stage Triple-Negative Breast Cancer
Authors: Deep Chakrabarti, Naseem Akhtar, Vijay Kumar
Journal: JAMA (2021)

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
Therapeutic effects of dihydroartemisinin in multiple stages of colitis-associated colorectal cancer
Authors: Bingjun Bai, Fei Wu, Kangkang Ying, Yuzi Xu, Lina Shan, Yiming Lv, Xing Gao, Dengyong Xu, Jun Lu, Binbin Xie
Journal: Theranostics (2021)

Colitis-associated colorectal cancer (CAC) develops from chronic intestinal inflammation. Dihydroartemisinin (DHA) is an antimalarial drug exhibiting anti-inflammatory and anti-tumor effects. Nonetheless, the therapeutic effects of DHA on CAC remain unestablished. Methods: Mice were challenged with azoxymethane (AOM) and dextran sulfate sodium (DSS) to establish CAC models. DHA was administered via oral gavage in different stages of CAC models. Colon and tumor tissues were obtained from the AOM/DSS models to investigate inflammatory responses and tumor development. Inflammatory cytokines in the murine models were detected through qRT-PCR and ELISA. Toll-like receptor 4 (TLR4) signaling-related proteins were detected by western blot. Macrophage infiltration was measured using immunostaining analysis, and apoptosis in the colon cancer cells was detected by flow cytometry and western blot. Results: DHA inhibited inflammatory responses in the early stage of the AOM/DSS model and subsequent tumor formation. In the early stage, DHA reversed macrophage infiltration in colon mucosa and decreased the expression of pro-inflammatory cytokines. DHA inhibited the activation of macrophage by suppressing the TLR4 signal pathway. In the late stage of CAC, DHA inhibited tumor growth by enhancing cell cycle arrest and apoptosis in tumor cells. Administration of DHA during the whole period of the AOM/DSS model generated an addictive effect based on the inhibition of inflammation and tumor growth, thereby improving the therapeutic effect of DHA on CAC. Conclusion: Our study indicated that DHA could be a potent agent in managing the initiation and development of CAC without obvious side effects, warranting further clinical translation of DHA for CAC treatment.
Abstract 14159: Alternative Autophagy is the Predominant Form of Autophagy in Estrogen-Mediated Mitochondrial Quality Control in Artery
Authors: Yuichi Sasaki, Yoshiyuki Ikeda, Yuichi Akasaki, Yoshihiro Uchikado, Mitsuru Ohishi
Journal: Circulation (2019)

Introduction: Mitochondria plays a crucial role to regulate cellular senescence, which undergo mitophagy to maintain mitochondrial quality. This study aims to examine whether estrogen modulates mit...
Neural Correlates of Affective Benefit From Real-life Social Contact and Implications for Psychiatric Resilience
Authors: Gabriela Gan, Ren Ma, Markus Reichert, Marco Giurgiu, Ulrich W. Ebner-Priemer, Andreas Meyer-Lindenberg, Heike Tost
Journal: JAMA Psychiatry (2021)

This cohort study examines the association of daily-life social affective benefit with brain structure and psychiatric risk and resilience measures in 2 independent community-based samples.
Bone physiological microenvironment and healing mechanism: Basis for future bone-tissue engineering scaffolds
Authors: Guanyin Zhu, Tianxu Zhang, Miao Chen, Ke Yao, Xinqi Huang, Bo Zhang, Yazhen Li, Jun Liu, Yunbing Wang, Zhihe Zhao
Journal: Bioactive Materials (2021)

Bone-tissue defects affect millions of people worldwide. Despite being common treatment approaches, autologous and allogeneic bone grafting have not achieved the ideal therapeutic effect. This has prompted researchers to explore novel bone-regeneration methods. In recent decades, the development of bone tissue engineering (BTE) scaffolds has been leading the forefront of this field. As researchers have provided deep insights into bone physiology and the bone-healing mechanism, various biomimicking and bioinspired BTE scaffolds have been reported. Now it is necessary to review the progress of natural bone physiology and bone healing mechanism, which will provide more valuable enlightenments for researchers in this field. This work details the physiological microenvironment of the natural bone tissue, bone-healing process, and various biomolecules involved therein. Next, according to the bone physiological microenvironment and the delivery of bioactive factors based on the bone-healing mechanism, it elaborates the biomimetic design of a scaffold, highlighting the designing of BTE scaffolds according to bone biology and providing the rationale for designing next-generation BTE scaffolds that conform to natural bone healing and regeneration.
Abstract 3517: Long-Term Prognosis of Vascular Surgery Patients Using Perioperative Troponin T Release: Is there a Threshold?
Authors: Harm H Feringa, Radosav Vidakovic, Stefanos Karagiannis, Martin Dunkelgrun, Olaf Schouten, Ron van Domburg, Sanne Hoeks, Don Poldermans
Journal: Circulation (2006)

Background: Debate surrounds the impact of renal function on the prognostic value of minor troponin T release in vascular surgery patients. Objective of this study was to assess the long-term progn...