Sina was born in Tehran, Iran and raised in Zanjan, Iran. He came out to Massachusetts to attend Harvard University where he obtained his undergraduate degree cum laude in Neuroscience with a secondary in Economics. In college, Sina conducted wet-lab research under the supervision of Dr. Hugo Bellen, worked as a legal intern in Levy Firestone Muse LLP, and served as a research assistant for Drs. Francis Shen, Steven Levitsky, and Jennifer Hochschild. Sina moved to California (by bike!) to begin medical school at Stanford where he is currently exploring clinical and research opportunities in functional neurosurgery and interventional psychiatry. Outside of medical school, Sina is an avid cyclist and currently rides with the Stanford Cycling Team. Sina also enjoys going on walks, doing yoga, listening to audiobooks, and learning to cook.
Honors & Awards
Sally and Cresap Moore Prize for energy and enthusiasm for interdisciplinary learning, Harvard University (2021)
John Harvard Scholarship for outstanding academic achievement, Harvard University (2020)
Harvard Foundation recognition for notable contributions to intercultural and race relations, Harvard University (2019)
Loss- or Gain-of-Function Mutations in ACOX1 Cause Axonal Loss via Different Mechanisms
2020; 106 (4): 589-+
ACOX1 (acyl-CoA oxidase 1) encodes the first and rate-limiting enzyme of the very-long-chain fatty acid (VLCFA) β-oxidation pathway in peroxisomes and leads to H2O2 production. Unexpectedly, Drosophila (d) ACOX1 is mostly expressed and required in glia, and loss of ACOX1 leads to developmental delay, pupal death, reduced lifespan, impaired synaptic transmission, and glial and axonal loss. Patients who carry a previously unidentified, de novo, dominant variant in ACOX1 (p.N237S) also exhibit glial loss. However, this mutation causes increased levels of ACOX1 protein and function resulting in elevated levels of reactive oxygen species in glia in flies and murine Schwann cells. ACOX1 (p.N237S) patients exhibit a severe loss of Schwann cells and neurons. However, treatment of flies and primary Schwann cells with an antioxidant suppressed the p.N237S-induced neurodegeneration. In summary, both loss and gain of ACOX1 lead to glial and neuronal loss, but different mechanisms are at play and require different treatments.
View details for DOI 10.1016/j.neuron.2020.02.021
View details for Web of Science ID 000535696300009
View details for PubMedID 32169171
View details for PubMedCentralID PMC7289150
The relation between pica and iron deficiency in children in Zanjan, Islamic Republic of Iran: a case-control study
EASTERN MEDITERRANEAN HEALTH JOURNAL
2017; 23 (6): 404-407
The aim of this case-control study was to determine the frequency of pica and its relationship with iron deficiency in children in Zanjan. We selected 872 children and determined the frequency of pica. We selected students who did not have pica of the same age and sex, and in the same class as our cases as a control group. Both groups were evaluated for iron deficiency anaemia. Among the 57 students (6.7%) who had pica, there was no significant relationship with sex (P > 0.05). The most common types of pica were soil (62.3%) and paper (31.2%). The frequency of anaemia among cases was greater than in controls, although the difference was not statistically significant. The serum iron/total iron binding capacity ratio ≤ 0.15 did not differ significantly between the 2 groups. We did not find any association between pica and anaemia and/or iron deficiency (P > 0.05).
View details for Web of Science ID 000410076000003
View details for PubMedID 28836652