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Structured Scientific Abstract Guide

 Please name your file as:
LastName_FirstName_SchoolName_Abstract (word file format only)
Example: Smith_John_DawsonHS_Abstract.docx
Use underscores (_) instead of spaces.”

A scientific abstract is a self-contained summary of a research article, up to 300 words.
A structured abstract includes labeled sections: Introduction, Methods, Results, and Conclusion.

Title
Authors
Affiliation for all authors

Introduction: Background and purpose of the study.
Methods: What was done.
Results: What was found.
Conclusion: Interpretation and broader impact.

Write clearly, accurately, and concisely. Use present tense for general statements,
past tense for methods/results, and future tense if applicable.

Each student should also include:
- Profile description with your name, grade, your school, about yourself, and your hobby.
- Your profile photo to be included in the abstract book

References:

1.     Harbourt AM, Knecht LS, Humphreys BL. Structured abstracts in MEDLINE, 1989-1991. Bull Med Libr Assoc. 1995 Apr;83(2):190-5. PMID: 7599584; PMCID: PMC226026. https://pubmed.ncbi.nlm.nih.gov/7599584/

2.     Structured Abstracts by National Library of Medicine Pubmed Resources: https://www.nlm.nih.gov/bsd/policy/structured_abstracts.html

3.     Effective Writing by Nature Education: https://www.nature.com/scitable/topicpage/effective-writing-13815989/

4.     Examples: 

Example 1:

Huang S, Li Y, Chen Y, Podsypanina K, Chamorro M, Olshen AB, Desai KV, Tann A, Petersen D, Green JE, Varmus HE. Changes in gene expression during the development of mammary tumors in MMTV-Wnt-1 transgenic mice. Genome Biol. 2005;6(10):R84. doi: 10.1186/gb-2005-6-10-r84. Epub 2005 Sep 30. PMID: 16207355; PMCID: PMC1257467. https://pubmed.ncbi.nlm.nih.gov/16207355/ 

Changes in gene expression during the development of mammary tumors in MMTV-Wnt-1 transgenic mice

Shixia Huang, Yi Li, Yidong Chen, Katrina Podsypanina, Mario Chamorro, Adam B Olshen, Kartiki V Desai, Anne Tann, David Petersen, Jeffrey E Green, Harold E Varmus

Program in Cancer Biology and Genetics, Sloan-Kettering Institute, New York, NY 10021, USA; Breast Center, Baylor College of Medicine, Houston, TX 77030, USA

Abstract

Introduction: In human breast cancer normal mammary cells typically develop into hyperplasia, ductal carcinoma in situ, invasive cancer, and metastasis. The changes in gene expression associated with this stepwise progression are unclear. Mice transgenic for mouse mammary tumor virus (MMTV)-Wnt-1 exhibit discrete steps of mammary tumorigenesis, including hyperplasia, invasive ductal carcinoma, and distant metastasis. These mice might therefore be useful models for discovering changes in gene expression during cancer development.

Methods: We used cDNA microarrays to determine the expression profiles of five normal mammary glands, seven hyperplastic mammary glands and 23 mammary tumors from MMTV-Wnt-1 transgenic mice, and 12 mammary tumors from MMTV-Neu transgenic mice. Adipose tissues were used to control for fat cells in the vicinity of the mammary glands.

Results:  In these analyses, we found that the progression of normal virgin mammary glands to hyperplastic tissues and to mammary tumors is accompanied by differences in the expression of several hundred genes at each step. Some of these differences appear to be unique to the effects of Wnt signaling; others seem to be common to tumors induced by both Neu and Wnt-1 oncogenes.

Conclusion: We described gene-expression patterns associated with breast-cancer development in mice, and identified genes that may be significant targets for oncogenic events. The expression data developed provide a resource for illuminating the molecular mechanisms involved in breast cancer development, especially through the identification of genes that are critical in cancer initiation and progression.

Example 2:

Mohorn PL, Vakkalanka JP, Rushton W, Hardison L, Woloszyn A, Holstege C, Corbett SM. Evaluation of dexmedetomidine therapy for sedation in patients with toxicological events at an academic medical center. Clin Toxicol (Phila). 2014 Jun;52(5):525-30. doi: 10.3109/15563650.2014.913175. Epub 2014 May 5. PMID: 24792780. https://pubmed.ncbi.nlm.nih.gov/24792780/ 

Evaluation of dexmedetomidine therapy for sedation in patients with toxicological events at an academic medical center

P L Mohorn 1, J P Vakkalanka, W Rushton, L Hardison, A Woloszyn, C Holstege, S M Corbett

1Department of Clinical Pharmacy and Outcomes Sciences, South Carolina College of Pharmacy, University of South Carolina , Columbia, SC , USA.

Abstract

Introduction: Although clinical use of dexmedetomidine (DEX), an alpha2-adrenergic receptor agonist, has increased, its role in patients admitted to intensive care units secondary to toxicological sequelae has not been well established.

Objectives: The primary objective of this study was to describe clinical and adverse effects observed in poisoned patients receiving DEX for sedation.

Methods: This was an observational case series with retrospective chart review of poisoned patients who received DEX for sedation at an academic medical center. The primary endpoint was incidence of adverse effects of DEX therapy including bradycardia, hypotension, seizures, and arrhythmias. For comparison, vital signs were collected hourly for the 5 h preceding the DEX therapy and every hour during DEX therapy until the therapy ended. Additional endpoints included therapy duration; time within target Richmond Agitation Sedation Score (RASS); and concomitant sedation, analgesia, and vasopressor requirements.

Results: Twenty-two patients were included. Median initial and median DEX infusion rates were similar to the commonly used rates for sedation. Median heart rate was lower during the therapy (82 vs. 93 beats/minute, p < 0.05). Median systolic blood pressure before and during therapy was similar (111 vs. 109 mmHg, p = 0.745). Five patients experienced an adverse effect per study definitions during therapy. No additional adverse effects were noted. Median time within target RASS and duration of therapy was 6.5 and 44.5 h, respectively. Seventeen patients (77%) had concomitant use of other sedation and/or analgesia with four (23%) of these patients requiring additional agents after DEX initiation. Seven patients (32%) had concomitant vasopressor support with four (57%) of these patients requiring vasopressor support after DEX initiation.

Conclusion: Common adverse effects of DEX were noted in this study. The requirement for vasopressor support during therapy warrants further investigation into the safety of DEX in poisoned patients. Larger, comparative studies need to be performed before the use of DEX can be routinely recommended in poisoned patients.

Example 3:

Zhang W, Bado IL, Hu J, Wan YW, Wu L, Wang H, Gao Y, Jeong HH, Xu Z, Hao X, Lege BM, Al-Ouran R, Li L, Li J, Yu L, Singh S, Lo HC, Niu M, Liu J, Jiang W, Li Y, Wong STC, Cheng C, Liu Z, Zhang XH. The bone microenvironment invigorates metastatic seeds for further dissemination. Cell. 2021 Apr 29;184(9):2471-2486.e20. doi: 10.1016/j.cell.2021.03.011. Epub 2021 Apr 19. PMID: 33878291; PMCID: PMC8087656. 

The bone microenvironment invigorates metastatic seeds for further dissemination

Weijie Zhang 1, Igor L Bado 1, Jingyuan Hu 2, Ying-Wooi Wan 3, Ling Wu 1, Hai Wang 1, Yang Gao 1, Hyun-Hwan Jeong 3, Zhan Xu 1, Xiaoxin Hao 1, Bree M Lege 4, Rami Al-Ouran 5, Lucian Li 5, Jiasong Li 6, Liqun Yu 1, Swarnima Singh 1, Hin Ching Lo 1, Muchun Niu 7, Jun Liu 1, Weiyu Jiang 1, Yi Li 1, Stephen T C Wong 8, Chonghui Cheng 4, Zhandong Liu 3, Xiang H-F Zhang 9

Affiliation and note see link and text end of the abstract: https://pubmed.ncbi.nlm.nih.gov/33878291/

Abstract

Introduction: Metastasis has been considered as the terminal step of tumor progression. However, recent genomic studies suggest that many metastases are initiated by further spread of other metastases. Nevertheless, the corresponding pre-clinical models are lacking, and underlying mechanisms are elusive.

Methods: Using several approaches, including parabiosis and an evolving barcode system, we demonstrated that the bone microenvironment facilitates breast and prostate cancer cells to further metastasize and establish multi-organ secondary metastases.

Results: We uncovered that this metastasis-promoting effect is driven by epigenetic reprogramming that confers stem cell-like properties on cancer cells disseminated from bone lesions. Furthermore, we discovered that enhanced EZH2 activity mediates the increased stemness and metastasis capacity. The same findings also apply to single cell-derived populations, indicating mechanisms distinct from clonal selection.

Conclusion: Taken together, our work revealed an unappreciated role of the bone microenvironment in metastasis evolution and elucidated an epigenomic reprogramming process driving terminal-stage, multi-organ metastases.

1

Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030, USA

2

Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA

3

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA

4

Jan and Dan Duncan Neurological Research Institute, Texas Children’s Hospital, Houston, TX 77030, USA

5

Quantitative and Computational Biosciences Program, Baylor College of Medicine, Houston, TX 77030, USA

6

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA

7

Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA

8

Department of Systems Medicine and Bioengineering and Translational Biophotonics Laboratory, Houston Methodist Cancer Center, Houston, TX 77030, USA

9

Integrative Molecular and Biomedical Sciences Graduate Program, Baylor College of Medicine, Houston, TX 77030, USA

10

McNair Medical Institute, Baylor College of Medicine, Houston, TX 77030, USA

11

These authors contributed equally

12

Lead contact