Education & Certifications


  • Bachelor of Health Sciences, McMaster University (2013)

All Publications


  • The Impact of Post-Operative Therapy on Primary Cardiac Sarcoma The Journal of Thoracic and Cardiovascular Surgery Wu, Y., Million, L., Moding, E. J., Scott, G., Berry, M., Ganjoo, K. N. 2018
  • Patient-Centered Care Challenges and Surprises: Through the Clerkship Students' Eyes. Family medicine Boggiano, V. L., Wu, Y., Bruce, J. S., Merrell, S. B., Schillinger, E. 2017; 49 (1): 57-61

    Abstract

    The patient-centered care model for health care delivery encourages medical providers to respect patients' preferences and give patients more autonomy over their health care decisions. This approach has gained importance within US medical school curricula. Yet, little is known about student perspectives on both patient-centered care and the benefits and challenges that lie therein. This manuscript explores the greatest impediments to, as well as the benefits from, student engagement in patient-centered care from the perspectives of students participating in their family medicine outpatient clerkship.Clerkship students on their core family medicine clerkship at Stanford University School of Medicine were provided the following open-ended prompt: "Describe a patient-centered care challenge or surprise in the family medicine core clerkship." Free-text responses were collected and analyzed using content and thematic analysis.A total of 326 responses from 216 students were analyzed for frequency and patient-centered themes. Nine final themes emerged and were grouped into three domains: student definitions of patient-centered care, patient-centered care impact on patients, and patient-centered care impact on medical professionals.Our study suggests that students find the patient-centered care model for health care delivery to be challenging but worthwhile. We highlight that students find communication with patients in a patient-centered manner challenging and discuss the need for improved medical education about patient-centered care in order to better prepare students to implement the model in a variety of psychosocial and medical contexts.

    View details for PubMedID 28166582

  • Patient-Centered Care Challenges and Surprises FAMILY MEDICINE Boggiano, V. L., Wu, Y., Bruce, J. S., Merrell, S. B., Schillinger, E. 2017; 49 (1): 57-61
  • Predictors of Toxicity Associated With Stereotactic Body Radiation Therapy to the Central Hepatobiliary Tract INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS Osmundson, E. C., Wu, Y., Luxton, G., Bazan, J. G., Koong, A. C., Chang, D. T. 2015; 91 (5): 986-994

    Abstract

    To identify dosimetric predictors of hepatobiliary (HB) toxicity associated with stereotactic body radiation therapy (SBRT) for liver tumors.We retrospectively reviewed 96 patients treated with SBRT for primary (53%) or metastatic (47%) liver tumors between March 2006 and November 2013. The central HB tract (cHBT) was defined by a 15-mm expansion of the portal vein from the splenic confluence to the first bifurcation of left and right portal veins. Patients were censored for toxicity upon local progression or additional liver-directed therapy. HB toxicities were graded according to Common Terminology Criteria for Adverse Events version 4.0. To compare different SBRT fractionations, doses were converted to biologically effective doses (BED) by using the standard linear quadratic model α/β = 10 (BED10).Median follow-up was 12.7 months after SBRT. Median BED10 was 85.5 Gy (range: 37.5-151.2). The median number of fractions was 5 (range: 1-5), with 51 patients (53.1%) receiving 5 fractions and 29 patients (30.2%) receiving 3 fractions. In total, there were 23 (24.0%) grade 2+ and 18 (18.8%) grade 3+ HB toxicities. Nondosimetric factors predictive of grade 3+ HB toxicity included cholangiocarcinoma (CCA) histology (P<.0001), primary liver tumor (P=.0087), and biliary stent (P<.0001). Dosimetric parameters most predictive of grade 3+ HB toxicity were volume receiving above BED10 of 72 Gy (VBED1072) ≥ 21 cm(3) (relative risk [RR]: 11.6, P<.0001), VBED1066 ≥ 24 cm(3) (RR: 10.5, P<.0001), and mean BED10 (DmeanBED10) cHBT ≥14 Gy (RR: 9.2, P<.0001), with VBED1072 and VBED1066 corresponding to V40 and V37.7 for 5 fractions and V33.8 and V32.0 for 3 fractions, respectively. VBED1072 ≥ 21 cm(3), VBED1066 ≥ 24 cm(3), and DmeanBED10 cHBT ≥14 Gy were consistently predictive of grade 3+ toxicity on multivariate analysis.VBED1072, VBED1066, and DmeanBED10 to cHBT are associated with HB toxicity. We suggest VBED1072 < 21 cm(3) (5-fraction: V40 < 21 cm(3); 3-fraction: V33.8 < 21 cm(3)), VBED1066 < 24 cm(3) (5-fraction: V37.7 < 24 cm(3); 3-fraction: V32 < 24 cm(3)) as potential dose constraints for the cHBT when clinically indicated.

    View details for DOI 10.1016/j.ijrobp.2014.11.028

    View details for Web of Science ID 000351734000015

    View details for PubMedID 25659885

  • Dosimetric Modeling of Central Liver Toxicity After SBRT to the Liver 56th Annual Meeting of the American-Society-for-Radiation-Oncology Osmundson, E., Wu, Y., Bazan, J. G., Koong, A. C., Chang, D. T. ELSEVIER SCIENCE INC. 2014: S382–S382
  • Statin-associated Autoimmune Myopathies: A Pathophysiologic Spectrum CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES Wu, Y., Lach, B., Provias, J. P., Tarnopolsky, M. A., Baker, S. K. 2014; 41 (5): 638-647

    Abstract

    Statins have recently been reported to cause a rare autoimmune inflammatory and/or necrotic myopathy that begins or persists after drug cessation.We report on 26 patients seen at a neuromuscular centre between 2005 and 2011 who demonstrated muscle weakness/myalgias and creatine kinase elevations during or after statin treatment with continuation of signs and symptoms despite statin withdrawal.All patients were treated with immunosuppressive therapy with good response; all improved biochemically and 86% improved clinically. Sixty-five percent of patients who attempted to taper off immunosuppressive therapy relapsed. We report on a novel finding whereby five of the seven patients who underwent multiple biopsies throughout their disease demonstrated a transformation of their histological diagnosis, with four progressing from having myofibre necrosis with minimal or no inflammation to a diagnosis of polymyositis.This study offers preliminary evidence that statin-associated necrotizing myopathy and statin-associated polymyositis may not be separate entities but are part of the same pathophysiological spectrum. Both entities respond well to immunosuppression.

    View details for DOI 10.1017/cjn.2014.22

    View details for Web of Science ID 000347654100016

    View details for PubMedID 25373816

  • Six novel mutations in the myophosphorylase gene in patients with McArdle disease and a family with pseudo-dominant inheritance pattern MOLECULAR GENETICS AND METABOLISM Wu, Y., Weber, J. L., Vladutiu, G. D., Tarnopolsky, M. A. 2011; 104 (4): 587-591

    Abstract

    McArdle disease is an autosomal recessive glycogenosis due to deficiency of the enzyme myophosphorylase. It results from homozygous or compound heterozygous mutations in the gene for this enzyme, PYGM. We report six novel mutations in the PYGM gene based upon sequencing data including three missense mutations (p.D51G, p.P398L, and p.N648Y), one nonsense mutation (p.Y75X), one frame-shift mutation (p.Y114SfsX181), and one amino acid deletion (p.Y53del) in six patients with McArdle disease. We also report on a Caucasian family that appeared to transmit McArdle disease in an autosomal dominant manner. In order to evaluate the potential pathogenicity of the sequence variants, we performed in silico analysis using PolyPhen-2 and SIFT BLink, along with species conservation analysis using UCSC Genome Browser. The above mutations were all predicted to be disease associated with high probability and with at least the same level of certainty as several confirmed mutations. The current data add to the list of pathogenic mutations in the PYGM gene associated with McArdle disease.

    View details for DOI 10.1016/j.ymgme.2011.08.012

    View details for Web of Science ID 000298021400023

    View details for PubMedID 21880526