Abstract fees are:
Regular Abstract Submission* $50
Student Abstract Submission $25
*Post doc and Research Technician abstracts are submitted at the Regular Abstract Submission rate.
Abstracts will be accepted in both electronic and paper formats, though electronic abstract submission is preferred. SIVB’s online electronic abstract system includes online payment capabilities with immediate submission and confirmations. The Regular Abstract Deadline to have your abstract considered for an oral presentation is February 20, 2017.
Below are directions for formatting your heading and abstract plus a sample for reference to assist you in preparing your submission.
Format your abstract heading into a single paragraph. Formatting instructions for each sentence and a sample are below:
- First sentence is the title of the abstract and in title case. Hyphenated words should have the second word in lower case.
- Second sentence is the list of authors
A. Presenting author should be listed first and in all capital letters.
B. Other authors are not capitalized.
C. If there are 2 or more authors, please place the word “and” before the last author’s name.
D. Author’s affiliations are noted by superscript numbers at the end of their name. Please use numbers 1,2,3,4). Do NOT use letters (a,b,c) or other punctuation (*) to delineate affiliations.
- Third sentence is affiliations:
A. Please list complete address of affiliation starting with the affiliation.
B. If one affiliation, no superscript is necessary; if 2 or more affiliations are listed, please use numerical superscript to delineate each. Superscript should be listed at the beginning of the address.
C. Countries should be capitalized. Do not list country if affiliation is in USA.
D. If more than two affiliations are listed, please place a semicolon (;) between affiliations and place the word “and” before the last affiliation
- Fourth sentence is the presenting author’s email address.
A. Please begin the sentence with “Email: ”
B. Do not put a period after the email address.
C. If the corresponding author is different than the presenting author, both email addresses can be listed.
- The body of the abstract will be limited to 1,800 characters
- Cited references should be included in the body of the abstract text, and NOT listed at the end.
- There will be no tables, figures, end references or keywords in the body of the abstract. If submitted with these items, they will be removed from the abstract.
A Human in Vitro Model to Study Epigenetic Dysregulations in Non-Communicable Diseases. MAGNOLIA ARIZA-NIETO1, Joshua B Alley2, Laura Fitzgerald2, Sanjay Samy2, Peggy Stock3, Thomas J. VanderMeer2, and Michael L. Shuler1. 1Department of Biomedical Engineering, Cornell University, Ithaca NY; 2Guthrie Clinic, Sayre, PA; and 3University of Leipzig. Leipzig, GERMANY. Email: email@example.com
Obesity is a chronic disease with complex origins. The outcomes of weight loss interventions are highly variable despite diet and physical activity. Furthermore the link between obesity and cancer is not fully understood and the state of the epigenome appears to be a common complication. Our group is working in the development of a human in vitro model to study epigenetic dysregulatory states in a personalized matter by isolating, expanding and differentiating mesenchymal stem cells (MSCs) from each patient donors. The aim of this research was to identify secretory biomarkers in human plasma that would indicate dysregulatory states of the epigenome (episensors) and that could be used both in clinical studies as well as with the human in vitro model. This research is part of the IRB approved clinical trial GHS # 1207-27. The personalized human in vitro model uses cells from patient donors, those cells carry the individual’s complete genome including polymorphisms and epigenetic signatures. MSCs from 3 different sources (circulating in blood, from bone marrow and from visceral adipose tissue) were isolated, expanded and differentiated into hepatocyte-like cells. The model will serve as a tool to test the influence of dietary and pharmacological compounds in the inhibition or activation of target genes in regulatory signaling pathways. In fasting plasma we identified a series of episensors (adiponectin, irisin, CD14 and mature microRNAs), they are still to be assayed in MSCs. We also developed a qPCR based eleven target regulatory signaling panel (ETRSP) that includes the expression of liver DNMT1 known to preserved the patterns of DNA methylation and its function is controlled via SIRT1/PGC1/FNDC5, insulin/PI3K/PTEN/AKT, MAT1/MAT2, the activation of the TLR/CD14 superfamily and the bioavailability of methyl donors. Preliminary results using the episensors together with the ETRSP profiles suggest changes in signaling pathways can be detected and could be used both in vivo and in vitro, as a tool to understand the personalized etiology of non-communicable diseases.