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Do stock returns respond to physical and transition climate risks? Evidence from emerging BRICS economies

Saqib A, Hussain I, Mefteh-Wali S

J Environ Manage, 2024 Dec;372:123303.
PMID: 39561456 DOI: 10.1016/j.jenvman.2024.123303

This study examines how stock market returns in emerging BRICS economies respond to growing physical and transition climate risks. To capture the physical climate risk, we use the frequency of natural disasters, the number of people affected by natural disasters, temperature anomaly, and precipitation anomaly. For transition risk, we included two climate-policy uncertainty measures. First, we conduct a panel-level analysis using a cross-sectionally augmented autoregressive distributed lag model. Second, for country-level analysis, we applied the augmented autoregressive distributed lag model to the monthly dataset from January-2000 to March-2023. The empirical results show that an increase in transition climate risk causes a significant and negative shock to stock returns, both in the short- and long-term in the panel and across each BRICS country. Second, we find that physical climate risk indicators have a significant and negative impact on stock returns in China, India, and South Africa, but not in Brazil or Russia. We conclude that the impact of physical climate risk on stock returns is country-specific, and that the impact of transition climate risk is widespread. These findings provide important insights for investors, regulators, hedgers, portfolio managers, and policymakers regarding policy formulation and future investment strategies.
Guinea pig genital tract lipidome reveals in vivo and in vitro regulation of phosphatidylcholine 16:0/18:1 and contribution to Chlamydia trachomatis serovar D infectivity

Wali S, Gupta R, Yu JJ, Mfuh A, Gao X, Guentzel MN, et al.

Metabolomics, 2016 Apr;12(4).
PMID: 27642272

INTRODUCTION: Chlamydia trachomatis (Ct), is the leading cause of sexually transmitted infections worldwide. Host transcriptomic- or proteomic profiling studies have identified key molecules involved in establishment of Ct infection or the generation of anti Ct-immunity. However, the contribution of the host metabolome is not known.
OBJECTIVES: The objective of this study was to determine the contribution of host metabolites in genital Ct infection.
METHODS: We used high-performance liquid chromatography-mass spectrometry, and mapped lipid profiles in genital swabs obtained from female guinea pigs at days 3, 9, 15, 30 and 65 post Ct serovar D intravaginal infection.
RESULTS: Across all time points assessed, 13 distinct lipid species including choline, ethanolamine and glycerol were detected. Amongst these metabolites, phosphatidylcholine (PC) was the predominant phospholipid detected from animals actively shedding bacteria i.e., at 3, 9, and 15 days post infection. However, at days 30 and 65 when the animals had cleared the infection, PC was observed to be decreased compared to previous time points. Mass spectrometry analyses of PC produced in guinea pigs (in vivo) and 104C1 guinea pig cell line (in vitro) revealed distinct PC species following Ct D infection. Amongst these, PC 16:0/18:1 was significantly upregulated following Ct D infection (p < 0.05, >twofold change) in vivo and in vitro infection models investigated in this report. Exogenous addition of PC 16:0/18:1 resulted in significant increase in Ct D in Hela 229 cells.
CONCLUSION: This study demonstrates a role for host metabolite, PC 16:0/18:1 in regulating genital Ct infection in vivo and in vitro.

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