Education & Certifications
Bachelor of Science, Rice University, Biochemistry (2017)
Bachelor of Arts, Rice University, Medieval, Early Modern Studies (2017)
"Not Until I See My Other Doctor".
The Permanente journal
This story is based on a series of encounters between the author-a medical student-and a hospitalized patient with terminal cancer. Over multiple conversations, the narrator becomes closely acquainted with the patient's life and outlook, and helps her navigate an important decision regarding the course of her treatment. In the process, the narrator is given the opportunity to examine the limits of medicine and what matters to patients at the end of life.
View details for DOI 10.7812/TPP/19.033
View details for PubMedID 31852043
View details for PubMedCentralID PMC6907916
- Waiting for Jerry. The American journal of nursing 2020; 120 (3): 72
- Too much to do for death. Palliative & supportive care 2019: 1–2
- Dear Rachel. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2019: JCO1900978
- Deliverance, Their Way. Journal of palliative medicine 2019; 22 (12): 1614–15
- 2019 Hope Babette Tang Humanism in Healthcare Essay Contest: Third Place Medical Student Essay: The Hallmark Store. Academic medicine : journal of the Association of American Medical Colleges 2019; 94 (10): 1476–77
The wedding proposal.
Patient education and counseling
In this narrative essay, the author, a medical student, describes a patient who was nearing the end of her life and who feared passing away before she could witness her daughter's wedding. This story describes the lengths to which the medical team went to in order to address this concern, illustrating a particularly humanistic instance of what end-of-life care can mean.
View details for DOI 10.1016/j.pec.2019.11.006
View details for PubMedID 31744703
The Permanente journal
This short story is based on and told from the perspective of a patient the author encountered as a medical student. The story explores the thoughts of an elderly patient, who is hospitalized because of multiple organ failure, as she contemplates the voluntary refusal of food, fluid, and antibiotics. The patient weighs these options in light of her beliefs and experiences, and in the face of seemingly futile medicalization.
View details for DOI 10.7812/TPP/18.283
View details for PubMedID 31634109
- The lost art of letter writing. Palliative & supportive care 2019: 1–2
Inflammation-Stimulated Mesenchymal Stromal Cell-Derived Extracellular Vesicles Attenuate Inflammation.
Stem cells (Dayton, Ohio)
Extracellular vesicles (EVs) secreted by mesenchymal stromal cells (MSCs) have been proposed to be a key mechanistic link in the therapeutic efficacy of cells in response to cellular injuries through paracrine effects. We hypothesize that inflammatory stimulation of MSCs results in the release of EVs that have greater anti-inflammatory effects. The present study evaluates the immunomodulatory abilities of EVs derived from inflammation-stimulated and naive MSCs (MSCEv(+) and MSCEv, respectively) isolated using a current Good Manufacturing Practice (cGMP)-compliant tangential flow filtration (TFF) system. Detailed characterization of both EVs revealed differences in protein composition, cytokine profiles, and RNA content, despite similarities in size and expression of common surface markers. MSCEv(+) further attenuated release of pro-inflammatory cytokines in vitro when compared to MSCEv, with a distinctly different pattern of EV-uptake by activated primary leukocyte subpopulations. The efficacy of EVs was partially attributed to COX2/PGE2 expression. The present study demonstrates that inflammatory stimulation of MSCs renders release of EVs that have enhanced anti-inflammatory properties partially due to COX2/PGE2 pathway alteration. This article is protected by copyright. All rights reserved.
View details for PubMedID 29076623
Perturbations in Endothelial Dysfunction-Associated Pathways in the Nitrofen-Induced Congenital Diaphragmatic Hernia Model.
Journal of vascular research
2017; 55 (1): 26–34
Although it is well known that nitrofen induces congenital diaphragmatic hernia (CDH), including CDH-associated lung hypoplasia and pulmonary hypertension (PH) in rodents, the mechanism of pathogenesis remains largely unclear. It has been reported that pulmonary artery (PA) endothelial cell (EC) dysfunction contributes to the development of PH in CDH. Thus, we hypothesized that there is significant alteration of endothelial dysfunction-associated proteins in nitrofen-induced CDH PAs. Pregnant SD rats received either nitrofen or olive oil on gestational day 9.5. The newborn rats were sacrificed and divided into a CDH (n = 81) and a control (n = 23) group. After PA isolation, the expression of PA endothelial dysfunction-associated proteins was assessed on Western blot and immunostaining. We demonstrate that the expression of C-reactive protein and endothelin-1 and its receptors, ETA and ETB, were significantly increased in the CDH PAs. Levels of phosphorylated myosin light chain were significantly elevated, but those of phosphorylated endothelial nitric oxide synthase, caveolin-1, and mechanistic target of rapamycin were significantly decreased in the CDH PAs. In this work, we elucidate alterations in the expression of endothelial dysfunction-associated proteins specific to nitrofen-induced CDH rodent PAs, thereby advancing our understanding of the critical role of endothelial dysfunction-associated pathways in the pathogenesis of nitrofen-induced CDH.
View details for PubMedID 29216632
The Underlying Chemistry of Electronegative LDL's Atherogenicity
CURRENT ATHEROSCLEROSIS REPORTS
2014; 16 (8)
Electronegative low-density lipoprotein (LDL) found in human plasma is highly atherogenic, and its level is elevated in individuals with increased cardiovascular risk. In this review, we summarize the available data regarding the elevation of the levels of electronegative LDL in the plasma of patients with various diseases. In addition, we discuss the harmful effects and underlying mechanisms of electronegative LDL in various cell types. We also highlight the known biochemical properties of electronegative LDL that may contribute to its atherogenic functions, including its lipid and protein composition, enzymatic activities, and structural features. Given the increasing recognition of electronegative LDL as a potential biomarker and therapeutic target for the prevention of cardiovascular disease, key future goals include the development of a standard method for the detection of electronegative LDL that can be used in a large-scale population survey and the identification and testing of strategies for eliminating electronegative LDL from the blood.
View details for DOI 10.1007/s11883-014-0428-y
View details for Web of Science ID 000340523400002
View details for PubMedID 24890631
Gender disparity in LDL-induced cardiovascular damage and the protective role of estrogens against electronegative LDL
Increased levels of the most electronegative type of LDL, L5, have been observed in the plasma of patients with metabolic syndrome (MetS) and ST-segment elevation myocardial infarction and can induce endothelial dysfunction. Because men have a higher predisposition to developing coronary artery disease than do premenopausal women, we hypothesized that LDL electronegativity is increased in men and promotes endothelial damage.L5 levels were compared between middle-aged men and age-matched, premenopausal women with or without MetS. We further studied the effects of gender-influenced LDL electronegativity on aortic cellular senescence and DNA damage in leptin receptor-deficient (db/db) mice by using senescence-associated-β-galactosidase and γH2AX staining, respectively. We also studied the protective effects of 17β-estradiol and genistein against electronegative LDL-induced senescence in cultured bovine aortic endothelial cells (BAECs).L5 levels were higher in MetS patients than in healthy subjects (P < 0.001), particularly in men (P = 0.001). LDL isolated from male db/db mice was more electronegative than that from male or female wild-type mice. In addition, LDL from male db/db mice contained abundantly more apolipoprotein CIII and induced more BAEC senescence than did female db/db or wild-type LDL. In the aortas of db/db mice but not wild-type mice, we observed cellular senescence and DNA damage, and the effect was more significant in male than in female db/db mice. Pretreatment with 17β-estradiol or genistein inhibited BAEC senescence induced by male or female db/db LDL and downregulated the expression of lectin-like oxidized LDL receptor-1 and tumor necrosis factor-alpha protein.The gender dichotomy of LDL-induced cardiovascular damage may underlie the increased propensity to coronary artery disease in men.
View details for DOI 10.1186/1475-2840-13-64
View details for Web of Science ID 000334807000001
View details for PubMedID 24666525
View details for PubMedCentralID PMC3974745
- The Changing Image of Physician in Taiwan ASIAN SOCIAL SCIENCE 2013; 9 (4)