Hanqi (Caroline) Yao

All Publications

• Healthcare-Associated Clostridioides difficile Infection: Learning the Perspectives of Healthcare Workers to Build Successful Strategies. American journal of infection control Lev, V., Anbarchian, T., Yao, H., Bhat, A., Britt, P., Shieh, L. 2023

  Abstract

  BACKGROUND: Clostridioides difficile (C. difficile) is one of the most common healthcare-associated infections that negatively impacts patient care and healthcare costs. This study takes a unique approach to C. difficile infection (CDI) control by investigating key prevention obstacles through the perspectives of Stanford Health Care (SHC) frontline healthcare personnel.METHODS: An anonymous qualitative survey was distributed at SHC, focusing on knowledge and practice of CDI prevention guidelines, as well as education, communication, and perspectives regarding CDI at SHC.RESULTS: 112 survey responses were analyzed. Our findings unveiled gaps in personnel's knowledge of C. difficile diagnostic guidelines, and revealed a need for targeted communication and guideline-focused education. Healthcare staff shared preferences and recommendations, with the majority recommending enhanced communication of guidelines and information as a strategy for reducing CDI rates. The findings were then used to design and propose internal recommendations for SHC to mitigate the gaps found.DISCUSSION: Many guidelines and improvement strategies are based on strong scientific and medical foundations; however, it is important to ask whether these guidelines are effectively translated into practice. Frontline healthcare workers hold empirical perspectives that could be key in infection control.CONCLUSIONS: Our findings emphasize the importance of including frontline healthcare personnel in infection prevention decision-making processes and the strategies presented here can be applied to mitigating infections in different healthcare settings.

  View details for DOI 10.1016/j.ajic.2023.08.008

  View details for PubMedID 37579972

• Neurons that regulate mouse torpor NATURE Hrvatin, S., Sun, S., Wilcox, O. F., Yao, H., Lavin-Peter, A. J., Cicconet, M., Assad, E. G., Palmer, M. E., Aronson, S., Banks, A. S., Griffith, E. C., Greenberg, M. E. 2020; 583 (7814): 115-+

  Abstract

  The advent of endothermy, which is achieved through the continuous homeostatic regulation of body temperature and metabolism1,2, is a defining feature of mammalian and avian evolution. However, when challenged by food deprivation or harsh environmental conditions, many mammalian species initiate adaptive energy-conserving survival strategies-including torpor and hibernation-during which their body temperature decreases far below its homeostatic set-point3-5. How homeothermic mammals initiate and regulate these hypothermic states remains largely unknown. Here we show that entry into mouse torpor, a fasting-induced state with a greatly decreased metabolic rate and a body temperature as low as 20 °C6, is regulated by neurons in the medial and lateral preoptic area of the hypothalamus. We show that restimulation of neurons that were activated during a previous bout of torpor is sufficient to initiate the key features of torpor, even in mice that are not calorically restricted. Among these neurons we identify a population of glutamatergic Adcyap1-positive cells, the activity of which accurately determines when mice naturally initiate and exit torpor, and the inhibition of which disrupts the natural process of torpor entry, maintenance and arousal. Taken together, our results reveal a specific neuronal population in the mouse hypothalamus that serves as a core regulator of torpor. This work forms a basis for the future exploration of mechanisms and circuitry that regulate extreme hypothermic and hypometabolic states, and enables genetic access to monitor, initiate, manipulate and study these ancient adaptations of homeotherm biology.

  View details for DOI 10.1038/s41586-020-2387-5

  View details for Web of Science ID 000623830500002

  View details for PubMedID 32528180

  View details for PubMedCentralID PMC7449701