Julia grew up in Fairfield County, Connecticut and graduated from the University of Connecticut in 2015 with a B.A., majoring in Psychology and minoring in Neuroscience. As an undergraduate she was a research assistant in Dr. Eiling Yee’s Psycholinguistics lab at the University of Connecticut, examining the relationship between embodied cognition and semantic memory. She also worked as a research assistant in Dr. Golda Ginsburg’s child and adolescent clinical psychiatry lab at the University of Connecticut Health Center, assisting in the development of a unified protocol for treatment of co-morbid disorders such as anxiety and depression.
Julia joined the lab in 2016 as a full-time research assistant, she is currently the Lab Manager of SPL and Research Coordinator for a project investigating affect regulation in women recently diagnosed with breast cancer. In her free time, Julia enjoys hiking, surfing, going to concerts and playing the violin.
Current Role at Stanford
Lab manager of the Stanford Psychophysiology Laboratory (SPL)
Education & Certifications
BA, University of Connecticut, Maj: Psychology, Min: Neuroscience (2015)
Service, Volunteer and Community Work
Crisis Textline Counselor, Crisis Textline (2/3/2017 - Present)
Redwood city, CA
Emotion, emotion regulation, counseling, clinical psychology, learning, exercise, sleep/circadian rhythm, ethology, SES, biological and societal impacts on brain development and plasticity
Milk sphingomyelin improves lipid metabolism and alters gut microbiota in high fat diet-fed mice
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
2016; 30: 93-101
High dietary fat intake can cause elevated serum and hepatic lipids, as well as contribute to gut dysbiosis, intestinal barrier dysfunction and increased circulating lipopolysaccharide (LPS). Dietary milk sphingomyelin (SM) has been shown to inhibit lipid absorption in rodents. We evaluated the effects of milk SM on lipid metabolism and LPS levels in C57BL/6J mice fed a high-fat diet for 4weeks and compared it with egg SM. Mice were fed a high-fat diet (45%kcal from fat) (CTL, n=10) or the same diet modified to contain 0.25% (wt/wt) milk SM (MSM, n=10) or 0.25% (wt/wt) egg SM (ESM, n=10). After 4weeks, MSM had gained significantly less weight and had reduced serum cholesterol compared to CTL. ESM had increases in serum cholesterol, triglycerides, phospholipids and SM compared to CTL. MSM significantly decreased, while ESM increased, hepatic triglycerides. This may have been related to induction of hepatic stearoyl-CoA desaturase-1 mRNA observed in ESM. MSM displayed intestinal and hepatic gene expression changes consistent with cholesterol depletion. MSM had significantly lower serum LPS compared to CTL, which may have been due to altered distal gut microbiota. Fecal Gram-negative bacteria were significantly lower, while fecal Bifidobacterium were higher, in MSM. These results suggest that milk SM is more effective than egg SM at combating the detrimental effects of a high-fat diet in mice. Additionally, distal gut microbiota is altered with milk SM and this may have contributed to the lower serum LPS observed.
View details for DOI 10.1016/j.jnutbio.2015.12.003
View details for Web of Science ID 000374347300010
View details for PubMedID 27012625
Black elderberry extract attenuates inflammation and metabolic dysfunction in diet-induced obese mice
BRITISH JOURNAL OF NUTRITION
2015; 114 (8): 1123-1131
Dietary anthocyanins have been shown to reduce inflammation in animal models and may ameliorate obesity-related complications. Black elderberry is one of the richest sources of anthocyanins. We investigated the metabolic effects of anthocyanin-rich black elderberry extract (BEE) in a diet-induced obese C57BL/6J mouse model. Mice were fed either a low-fat diet (n 8), high-fat lard-based diet (HFD; n 16), HFD+0·25 % (w/w) BEE (0·25 %-BEE; n 16) or HFD+1·25 % BEE (1·25 %-BEE; n 16) for 16 weeks. The 0·25 % BEE (0·034 % anthocyanin, w/w) and 1·25 % BEE (0·17 % anthocyanin, w/w) diets corresponded to estimated anthocyanin doses of 20-40 mg and 100-200 mg per kg of body weight, respectively. After 16 weeks, both BEE groups had significantly lower liver weights, serum TAG, homoeostasis model assessment and serum monocyte chemoattractant protein-1 compared with HFD. The 0·25 %-BEE also had lower serum insulin and TNFα compared with HFD. Hepatic fatty acid synthase mRNA was lower in both BEE groups, whereas PPARγ2 mRNA and liver cholesterol were lower in 1·25 %-BEE, suggesting decreased hepatic lipid synthesis. Higher adipose PPARγ mRNA, transforming growth factor β mRNA and adipose tissue histology suggested a pro-fibrogenic phenotype that was less inflammatory in 1·25 %-BEE. Skeletal muscle mRNA expression of the myokine IL-6 was higher in 0·25 %-BEE relative to HFD. These results suggest that BEE may have improved some metabolic disturbances present in this mouse model of obesity by lowering serum TAG, inflammatory markers and insulin resistance.
View details for DOI 10.1017/S0007114515002962
View details for Web of Science ID 000362974700004
View details for PubMedID 26314315