Jason Kronenfeld holds a Bachelors of Science in Chemistry with minors in French and Math from The University of Arizona (Graduated May 2021, Summa Cum Laude with Honors). Jason spent his time at UArizona conducting research in Benjamin J. Renquist's group and working with Honors students as a Resident Assistant.
He joined the Renquist research group in 2017 where he has worked on projects related to lactation, metabolic rate, hyperinsulinemia and insulin resistance, asthma, and more. He led work on two projects. 1) Understanding the mechanism by which heat suppresses food intake as an effect of global warming. Increasing heat-stressed food intake is proposed to increase milk production in lactating mammals, increase animal efficiency, and decrease milk production costs. 2) Creating a novel approach to address glycemic control for treatment of type two diabetes mellitus – a collaboration with Dr. Khanna's research group to conduct in silico, in vivo, and in vitro testing of the novel approach.
In Fall 2021, Jason entered the Stanford University PhD program in chemistry, to be eventually followed with a post-doctoral fellowship with the ultimate goal of acting as a principal investigator in academia. He performs research in the DeSimone Lab focused on applications of high-resolution continuous liquid interface production (CLIP) under a National Science Foundation Graduate Research Fellowship. Outside of the lab, Jason is involved in research ethics and public communication initiatives as well as a student-led waltz performance group (Stanford Committee on Research, The Civilian, and the Viennese Ball Opening Committee, respectively).
Education & Certifications
BS, The University of Arizona, Chemistry (2021)
Single-digit-micrometer-resolution continuous liquid interface production.
2022; 8 (46): eabq2846
To date, a compromise between resolution and print speed has rendered most high-resolution additive manufacturing technologies unscalable with limited applications. By combining a reduction lens optics system for single-digit-micrometer resolution, an in-line camera system for contrast-based sharpness optimization, and continuous liquid interface production (CLIP) technology for high scalability, we introduce a single-digit-micrometer-resolution CLIP-based 3D printer that can create millimeter-scale 3D prints with single-digit-micrometer-resolution features in just a few minutes. A simulation model is developed in parallel to probe the fundamental governing principles in optics, chemical kinetics, and mass transport in the 3D printing process. A print strategy with tunable parameters informed by the simulation model is adopted to achieve both the optimal resolution and the maximum print speed. Together, the high-resolution 3D CLIP printer has opened the door to various applications including, but not limited to, biomedical, MEMS, and microelectronics.
View details for DOI 10.1126/sciadv.abq2846
View details for PubMedID 36383664
A Leak-Free Head-Out Plethysmography System to Accurately Assess Lung Function in Mice.
Journal of applied physiology (Bethesda, Md. : 1985)
Mice are a valuable model for elegant studies of complex, systems-dependent diseases, including pulmonary diseases. Current tools to assess lung function in mice are either terminal or lack accuracy. We set out to develop a low-cost, accurate, head-out variable-pressure plethysmography system to allow for repeated, non-terminal measurements of lung function in mice. Current head-out plethysmography systems are limited by air leaks that prevent accurate measures of volume and flow. We designed an inflatable cuff that encompasses the mouse's neck preventing air leak. We wrote corresponding software to collect and analyze the data, remove movement artifacts, and automatically calibrate each dataset. This software calculates inspiratory/expiratory volume, inspiratory/expiratory time, breaths per minute, mid-expiratory flow, and end-inspiratory pause. To validate the use, we established that our plethysmography system accurately measured tidal breathing, the bronchoconstrictive response to methacholine, sex and age associated changes in breathing, and breathing changes associated with house dust mite sensitization. Our estimates of volume, flow, and timing of breaths are in line with published estimates, we observed dose-dependent decreases in volume and flow in response to methacholine (P < 0.05), increased lung volume and decreased breathing rate with aging (P < 0.05), and that house dust mite sensitization decreased volume and flow (P <0.05) while exacerbating the methacholine induced increases in inspiratory and expiratory time (P < 0.05). We describe an accurate, sensitive, low-cost, head-out plethysmography system that allows for longitudinal studies of pulmonary disease in mice.
View details for DOI 10.1152/japplphysiol.00835.2021
View details for PubMedID 35608203
A critical role of hepatic GABA in the metabolic dysfunction and hyperphagia of obesity
2021; 35 (13): 109301
Hepatic lipid accumulation is a hallmark of type II diabetes (T2D) associated with hyperinsulinemia, insulin resistance, and hyperphagia. Hepatic synthesis of GABA, catalyzed by GABA-transaminase (GABA-T), is upregulated in obese mice. To assess the role of hepatic GABA production in obesity-induced metabolic and energy dysregulation, we treated mice with two pharmacologic GABA-T inhibitors and knocked down hepatic GABA-T expression using an antisense oligonucleotide. Hepatic GABA-T inhibition and knockdown decreased basal hyperinsulinemia and hyperglycemia and improved glucose intolerance. GABA-T knockdown improved insulin sensitivity assessed by hyperinsulinemic-euglycemic clamps in obese mice. Hepatic GABA-T knockdown also decreased food intake and induced weight loss without altering energy expenditure in obese mice. Data from people with obesity support the notion that hepatic GABA production and transport are associated with serum insulin, homeostatic model assessment for insulin resistance (HOMA-IR), T2D, and BMI. These results support a key role for hepatocyte GABA production in the dysfunctional glucoregulation and feeding behavior associated with obesity.
View details for DOI 10.1016/j.celrep.2021.109301
View details for Web of Science ID 000668072600010
View details for PubMedID 34192532
- Development of a GABA Transaminase Inhibitor That Does Not Penetrate the Blood-Brain Barrier The University of Arizona Honors College. Thesis Repository. 2021
Feed intake-dependent and -independent effects of heat stress on lactation and mammary gland development
JOURNAL OF DAIRY SCIENCE
2020; 103 (12): 12003-12014
With a growing population, a reliable food supply is increasingly important. Heat stress reduces livestock meat and milk production. Genetic selection of high-producing animals increases endogenous heat production, while climate change increases exogenous heat exposure. Both sources of heat exacerbate the risk of heat-induced depression of production. Rodents are valuable models to understand mechanisms conserved across species. Heat exposure suppresses feed intake across homeothermic species including rodents and production animal species. We assessed the response to early-mid lactation or late-gestation heat exposure on milk production and mammary gland development/function, respectively. Using pair-fed controls we experimentally isolated the feed intake-dependent and -independent effects of heat stress on mammary function and mass. Heat exposure (35°C, relative humidity 50%) decreased daily feed intake. When heat exposure occurred during lactation, hypophagia accounted for approximately 50% of the heat stress-induced hypogalactia. Heat exposure during middle to late gestation suppressed feed intake, which was fully responsible for the lowered mammary gland weight of dams at parturition. However, the impaired mammary gland function in heat-exposed dams measured by metabolic rate and lactogenesis could not be explained by depressed feed consumption. In conclusion, mice recapitulate the depressed milk production and mammary gland development observed in dairy species while providing insight regarding the role of feed intake. This opens the potential to apply genetic, experimental, and pharmacological models unique to mice to identify the mechanism by which heat is limiting animal production.
View details for DOI 10.3168/jds.2020-18675
View details for Web of Science ID 000603029300036
View details for PubMedID 33041042
- Determining the Role of Obesity and Muscarinic Signaling in Asthma WILEY. 2020
It's Strong, It's Stable, It's Streptavidin
FEDERATION AMER SOC EXP BIOL. 2015
View details for Web of Science ID 000361470500058