7th Annual Leaders in Medicine Research Symposium

October 30th, 20151:00 – 6:30 pm

Abstract Submission deadline: Friday, October 2, 2015

Presenter’s Name:

Title of Presentation:

Supervisor and Department:

Program (MD, MD/MSc, MD/PhD, MD/MBA, MD/MA, etc.) and year:

Description of Previous Research Experience (e.g. MSc degree, undergraduate thesis):

Preferred Presentation Format (poster, oral, or either):

Category of Project ([1] Basic/Translational Science; [2]Epidemiology/Health Services;

[3] Imaging; [4] Case Report; [5] Emerging medical/social program):

I am aware that my abstract will be published: ☐Yes

* By selecting YES, you confirm that you have received permission from your supervisor and / or other co-authors to publish the submitted abstract.

Please submit to:

Abstracts must be in 12 pt. Times New Roman font, single-spaced, maximum 1 page in length as a Microsoft Word Document attachment. The abstract must include a title, contributing authors, affiliations, introduction / background, methods (if appropriate), results and a conclusion.

Please note the following:

The title should appear at the top of the page in bolded font.

All author names should appear under the title with the presenting author’s name in bold, and author affiliations should appear thereafter.

Avoid the use of jargon, and define abbreviations the first time the word/phrase is used (eg. Computed axial tomographic scan [CT scan]).

If you do not follow the guidelines, we will send your abstract submission back to have you make the appropriate changes.

Examples of abstracts are provided below.

Please send the abstract to:


with the subject line: Last Name, First Name, Program
(MD, MD/MSc, MD/PhD, MD/MBA, MD/MA, etc.)

byFriday, October 2nd, 2015

Example: (from Muhl et al. BMC Neurology2014,14:163)

Mobilization after thrombolysis (rtPA) within 24hours of acute stroke: what factors influence inclusion of patients in A Very Early Rehabilitation Trial (AVERT)?

Linnéa Muhl1, Jenny Kulin1, Marie Dagonnier2,3, Leonid Churilov2,3, Helen Dewey2,3,4, Thomas Lindén5, and Julie Bernhardt2,3

1Linköpings University, Linköping, Sweden; 2AVERT, Early Intervention Research Program, The Florey Institute of Neurosciences and Mental Health, Austin Campus, 245 Burgundy St, Heidelberg 3084, VIC, Australia; 3The University of Melbourne, Melbourne, Australia; 4Department of Neurology, Austin Health, Heidelberg, Australia; 5The Centre of Brain Research and Rehabilitation, Gothenburg University, Gothenburg, Sweden.

Introduction: A key treatment for acute ischaemic stroke is thrombolysis (rtPA). However, treatment is not devoid of side effects and patients are carefully selected. AVERT (A Very Early Rehabilitation Trial), a large, ongoing international phase III trial, tests whether starting out of bed activity within 24hours of stroke onset improves outcome. Patients treated with rtPA can be recruited if the physician allows (447 included to date). This study aimed to identify factors that might influence the inclusion of rtPA treated patients in AVERT.

Methods: Data from all patients thrombolysed at Austin Health, Australia, between September 2007 and December 2011 were retrospectively extracted from medical records. Factors of interest included: demographic and stroke characteristics, 24hour clinical response to rtPA treatment, cerebral imaging and process factors (day and time of admission).

Results: 211 patients received rtPA at Austin Health and 50 (24%) were recruited to AVERT (AVERT). Of the 161 patients not recruited, 105 (65%) were eligible, and could potentially have been included (pot-AVERT). There were no significant differences in demographics, Oxfordshire classification or stroke severity (NIHSS) on admission between groups. Size and localization of stroke on imaging and symptomatic intracerebral heamorrhage rate did not differ. Patients included in AVERT showed less change in NIHSS 24hours post rtPA (median change = 1, IQR (−1,4)) than those in the pot-AVERT group (median change = 3, IQR (0,6)) by the median difference of 2 points (95%CI:0.3; p = 0.03). A higher proportion of rtPA treated AVERT patients were admitted on weekdays (p = 0.04).

Conclusion: Excluding a possible clinical instability, no significant clinical differences were identified between thrombolysed patients included in AVERT and those who were not. Over 500 AVERT patients will be treated with rtPA at trial end. These results suggest we may be able to generalize findings to other rtPA treated patients beyond the trial population.

Example: (from Hirohata et al. BMC Neurology2014,14:150)

Subarachnoid hemorrhage secondary to a ruptured middle cerebral aneurysm in a patient with osteogenesisimperfecta: a case report

Toshio Hirohata1,2,Satoru Miyawaki1,2, Akiko Mizutani3, Takayuki Iwakami1, So Yamada1, Hajime Nishido1, Yasutaka Suzuki1, Shinya Miyamoto1, Katsumi Hoya1, Mineko Murakami1, and Akira Matsuno1,2

1Department of Neurosurgery, Teikyo University Chiba Medical Center, 3426-3 Anesaki, Ichihara City, Chiba 299-0111, Japan; 2Department of Neurosurgery, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan;3Teikyo Heisei University, 2-51-4 Higashi-Ikebukuro, Toshima-ku, Tokyo 170-8445, Japan.

Background: Osteogenesisimperfecta (OI) is a heterogeneous group of inherited disorders that occur owing to the abnormalities in type 1 collagen, and is characterized by increased bone fragility and other extraskeletal manifestations. We report the case of a patient who was diagnosed with OI following subarachnoid hemorrhage (SAH) secondary to a ruptured saccular intracranial aneurysm (IA).

Case Presentation: A 37-year-old woman was referred to our hospital because of sudden headache and vomiting. She was diagnosed with SAH (World Federation of Neurosurgical Society grade 2) owing to an aneurysm of the middle cerebral artery. She then underwent surgical clipping of the aneurysm successfully. She had blue sclerae, a history of several fractures of the extremities, and a family history of bone fragility and blue sclerae in her son. According to these findings, she was diagnosed with OI type 1. We performed genetic analysis for a single nucleotide G/C polymorphism (SNP) of exon 28 of the gene encoding for alpha-2 polypeptide of collagen 1, which is a potential risk factor for IA. However, this SNP was not detected in this patient or in five normal control subjects. Other genetic analyses did not reveal any mutations of the COL1A1 or COL1A2 gene. The cerebrovascular system is less frequently involved in OI. OI is associated with increased vascular weakness owing to collagen deficiency in and around the blood vessels. SAH secondary to a ruptured IA with OI has been reported in only six cases.

Conclusion: The patient followed a good clinical course after surgery. It remains controversial whether IAs are caused by OI or IAs are coincidentally complicated with OI.

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