About MacSphere

MacSphere is McMaster University's Institutional Repository (IR). The purpose of an IR is to bring together all of a University's research under one umbrella, with an aim to preserve and provide access to that research. The research and scholarly output included in MacSphere has been selected and deposited by the individual university departments and centres on campus.

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Communities in MacSphere

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Recent Submissions

Low-carbon governmental policies and cost of debt: evidence from China
(2025-12) Zhao, Gang; Zhang, Jianhao; Jin, Justin; Nainar, Khalid; Michael Lee-Chin & Family Institute for Strategic Business Studies
This paper uses the staggered difference-in-differences design to investigate the effects of the low-carbon city pilot (LCCP) policy on the cost and underlying mechanisms of debt financing for enterprises. Our findings show that the LCCP significantly decreases the debt cost of enterprises through enhancements in Environmental, Social, and Governance (ESG) performance and the reduction of information asymmetry. Additional analysis indicates that the LCCP’s ability to reduce the cost of debt is particularly pronounced for firms with higher agency costs and those located in China’s eastern regions. This study offers evidence for assessing the effectiveness of low-carbon policies and suggests recommendations to policymakers seeking to enhance the design and implementation of LCCP, thereby contributing to the green development of enterprises and regions. Valuation Insight: A company’s impact on the environment is an important element in the value that it delivers. In China certain local governments introduced policies to facilitate the enterprise transition to low-carbon practices, standardizing reporting on greenhouse gas emissions and requiring the undertaking of green technological transformation. The paper finds that companies in these localities experienced significant decreases in debt costs through enhancements in ESG performance and the reduction of information asymmetry.
Corporate biodiversity exposure and the market response to earnings announcements
(2025-12) Akbari, Amir; Ng, Lilian; Wang, Tracy; Zhu, Nathan; Michael Lee-Chin & Family Institute for Strategic Business Studies
Biodiversity loss is increasingly recognized as a material financial risk to firms, yet little is known about how biodiversity-related exposure affects the way capital markets process earnings disclosures.We examine whether corporate biodiversity exposure (CBE), defined as the extent to which a firm’s polluting facilities are located near conservation-priority areas, shapes investors’ responses to earnings announcements. Drawing on the disclosure-processing-cost framework, we argue that CBE raises disclosure-processing costs at the integration stage by introducing spatially localized ecological and regulatory complexity, which makes it more difficult for investors to integrate reported earnings into valuation-relevant expectations of future cash flows. Consistent with this prediction, firms with higher CBE exhibit weaker earnings response coefficients, indicating attenuated market responsiveness to earnings announcements. These effects are amplified under greater ecological and regulatory uncertainty and attenuated in stronger information environments and under greater external monitoring. Exploiting staggered protected-area expansions in a stacked difference-in-differences design, we provide causal evidence that newly exposed firms experience a decline in earnings–return sensitivity. Overall, our findings identify biodiversity exposure as a place-based disclosure-processing friction and highlight how disclosure and governance shape the pricing of earnings announcements in the presence of ecological complexity. Valuation Insight: Exposure to potential biodiversity loss affects corporate value. The paper shows that, when a firm’s polluting activities are close to conservation priority areas, it becomes more difficult for investors to identify how relevant reported earnings are for future cash flows. Market response to earnings surprises decreases markedly. Biodiversity risk is not only an ecological or regulatory concern, but also a factor that can impair price discovery in capital markets.
Optimal portfolio with options
(2025-11) Jeon, Yoontae; Kan, Raymond; Li, Gang; Michael Lee-Chin & Family Institute for Strategic Business Studies
We propose a parsimonious framework to analyze the optimal asset allocation problem for a mean–variance investor who incorporates options into the portfolio. Building on the key insight that risk-neutral volatility often differs from physical volatility, we derive closed-form expressions for the optimal portfolio weights with options. The resulting economic gains are substantial and remain robust even when solvency constraints and transaction costs are considered. We then take the model to the data and show that the framework delivers superior out-of-sample performance for an investor trading the S&P 500 index and its options. Our approach underscores the importance of accounting for differences between physical and risk-neutral volatilities when constructing an optimal portfolio that includes options. Valuation Insight: A firm’s issue of options, other than benefiting the firm’s financial position, adds value by providing investors with an investment alternative that is not duplicated by holding the firm’s stock. The additional investment value from options occurs when basic assumptions leading to Black-Scholes options pricing are violated causing variability implied by the model to differ from actual volatility. The paper shows, in this realistic scenario, that investors may benefit substantially from adding options to their stock portfolio.
Evaluating Biomolecular and Biochemical Characteristics of Anti-Platelet Factor 4/Heparin Antibodies in Serological Subtypes of Heparin-Induced Thrombocytopenia
(2026) Kwok, Sarah
Heparin induced thrombocytopenia (HIT) is an adverse reaction to heparin (a commonly used anticoagulant), characterized by a low platelet count and potentially catastrophic thrombosis. Resembling HIT is vaccine-induced immune thrombocytopenia and thrombosis (VITT), which arose in response to the COVID-19 pandemic due to SARS-CoV-2 adenoviral vector-based vaccines. Both of these immune-mediated disorders are caused by antibodies against the chemokine, platelet-factor-4 (PF4/CXCL4), which activates platelets through the FcγIIa receptor, leading to the release of procoagulant platelet microparticles, reduction in platelet count level, and a high risk of venous and arterial thrombosis that can be severe and even fatal. There are two serological subtypes of HIT based on their platelet activation patterns in functional assays: classical heparin-dependent HIT (HD-HIT) antibodies that require heparin for platelet activation, and autoimmune heparin-independent HIT (HI-HIT) antibodies that do not require heparin for platelet activation. HI-HIT is a more severe subtype associated with higher rates of disseminated intravascular coagulation (DIC), more severe and prolonged thrombocytopenia (platelet count of <20 × 109/L), and persistence of symptoms after heparin cessation. Previous research in our laboratory found that HD-HIT and HI-HIT bound to different regions on PF4. Interestingly, in VITT, the precise anti-PF4 antibody epitopes correlated with clinical outcomes, such as whether the rare event of cerebral venous sinus thrombosis (CVST) occurred. Our research suggests that the precise antibody epitope targeted may be important for determining clinical outcomes in anti-PF4 disorders; by extension, we want to investigate whether this observation exists in HD-HIT and HI-HIT. In this thesis, we conducted an in-depth comparison of HD-HIT (n=16) and HI-HIT (n=20) subtypes at the level of anti-PF4/heparin epitopes, antibody binding affinity, antibody titre, and clinical outcomes. We used established methods to determine the anti-PF4/heparin epitopes for a large cohort of HIT patients to expand upon earlier preliminary work. We found that the combined HIT binding site on PF4 (n=36) was distinct from previously identified epitopes of monoclonal anti-PF4 antibodies, including the KKO, 5B9, VITT, and 1E12, as well as the heparin binding site. By gaining a deeper understanding of anti-PF4/heparin binding sites in HIT, we can potentially develop diagnostics that can target this shared binding region. Additionally, we found that HD-HIT and HI-HIT antibodies bind to very similar regions on PF4, which was contrary to our expectations, but agrees with our recent finding that HIT is driven by a pathogenic monoclonal IgG antibody. Rather than differences in anti-PF4/heparin epitopes, we provide evidence that HI-HIT antibodies have higher antibody affinities and titres compared with HD-HIT. Additionally, we found one amino acid residue (P37) that was significantly different in HIT patients with a platelet nadir above (n=6) and below (n=7) 50 x109 platelets/L, and we found seven residues (D7, L8, T16, V29, A39, K50, I64) that were significantly different between HIT patients with (n=8) and without (n=5) thrombotic complications. Overall, this suggests that separating HIT patients based on their platelet activation patterns in functional assays may not be as important as separating HIT patients based on clinical outcomes.
Electroencephelographic Biomarkers of Treatment Response to Transcranial Magnetic Stimulation for Major Depressive Disorder
(2026) Prokop-Millar, Shelby

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