Publications

2018
Shangyu Hong, Wei Song, Peter-James H. Zushin, Bingyang Liu, Mark P. Jedrychowski, Amir I. Mina, Zhaoming Deng, Dimitrije Cabarkapa, Jessica A. Hall, Colin J. Palmer, Hassan Aliakbarian, John Szpyt, Steven P. Gygi, Ali Tavakkoli, Lydia Lynch, Norbert Perrimon, and Alexander S. Banks. 2018. “Phosphorylation of Beta-3 adrenergic receptor at serine 247 by ERK MAP kinase drives lipolysis in obese adipocytes.” Molecular MetabolismMolecular Metabolism, 12, Pp. 25-38.
Ayano C. Kohlgruber, Shani T. Gal-Oz, Nelson M. LaMarche, Moto Shimazaki, Danielle Duquette, Hung N. Nguyen, Amir I. Mina, Tyler Paras, Ali Tavakkoli, Ulrich von Andrian, Alexander S. Banks, Tal Shay, Michael B. Brenner, and Lydia Lynch. 2018. “γδ T cells producing interleukin-17A regulate adipose regulatory T cell homeostasis and thermogenesis.” Nature ImmunologyNature Immunology, 19, Pp. 464-474.Abstract
γδ T cells are situated at barrier sites and guard the body from infection and damage. However, little is known about their roles outside of host defense in nonbarrier tissues. Here, we characterize a highly enriched tissue-resident population of γδ T cells in adipose tissue that regulate age-dependent regulatory T cell (Treg) expansion and control core body temperature in response to environmental fluctuations. Mechanistically, innate PLZF+ γδ T cells produced tumor necrosis factor and interleukin (IL) 17 A and determined PDGFRα+ and Pdpn+ stromal-cell production of IL-33 in adipose tissue. Mice lacking γδ T cells or IL-17A exhibited decreases in both ST2+ Treg cells and IL-33 abundance in visceral adipose tissue. Remarkably, these mice also lacked the ability to regulate core body temperature at thermoneutrality and after cold challenge. Together, these findings uncover important physiological roles for resident γδ T cells in adipose tissue immune homeostasis and body-temperature control.
2017
Maria S. Asdourian, Meyha N. Swaroop, Hoda E. Sayegh, Cheryl L. Brunelle, Amir I. Mina, Hui Zheng, Melissa N. Skolny, and Alphonse G. Taghian. 2017. “Association Between Precautionary Behaviors and Breast Cancer–Related Lymphedema in Patients Undergoing Bilateral Surgery.” Journal of Clinical OncologyJournal of Clinical Oncology, 35, Pp. 3934-3941.Abstract
PurposeThis study examined the lifestyle and clinical risk factors for lymphedema in a cohort of patients who underwent bilateral breast cancer surgery.Patients and MethodsBetween 2013 and 2016, 327 patients who underwent bilateral breast cancer surgery were prospectively screened for arm lymphedema as quantified by the weight-adjusted volume change (WAC) formula. Arm perometry and subjective data were collected preoperatively and at regular intervals postoperatively. At the time of each measurement, patients completed a risk assessment survey that reported the number of blood draws, injections, blood pressure readings, trauma to the at-risk arm, and number of flights since the previous measurement. Generalized estimating equations were applied to ascertain the association among arm volume changes, clinical factors, and risk exposures.ResultsThe cohort comprised 327 patients and 654 at-risk arms, with a median postoperative follow-up that ranged from 6.1 to 68.2 months. Of the 654 arms, 83 developed lymphedema, defined as a WAC ≥ 10% relative to baseline. On multivariable analysis, none of the lifestyle risk factors examined through the risk assessment survey were significantly associated with increased WAC. Multivariable analysis demonstrated that having a body mass index ≥ 25 kg/m2 at the time of breast cancer diagnosis (P = .0404), having undergone axillary lymph node dissection (P = .0464), and receipt of adjuvant chemotherapy (P = .0161) were significantly associated with increased arm volume.ConclusionBlood pressure readings, blood draws, injections, and number or duration of flights were not significantly associated with increases in arm volume in this cohort. These findings may help to guide patient education about lymphedema risk reduction strategies for those who undergo bilateral breast cancer surgery.
Amir I Mina, Raymond A LeClair, Katherine B LeClair, David E Cohen, Louise Lantier, and Alexander S Banks. 2017. “CalR: A Web-based Analysis Tool for Indirect Calorimetry Experiments.” bioRxivbioRxiv.Abstract
We report a web-based tool for analysis of indirect calorimetry experiments which measure physiological energy balance. CalR easily imports raw data files, generates plots, and determines the most appropriate statistical tests for interpretation. Analysis with the general linear model (which includes ANOVA and ANCOVA) allows for flexibility to interpret experiments of obesity and thermogenesis. Users may also produce standardized output files of an experiment which can be shared and subsequently re-evaluated using CalR. This framework will provide the transparency necessary to enhance consistency and reproducibility in experiments of energy expenditure. CalR analysis software will greatly increase the speed and efficiency with which metabolic experiments can be organized, analyzed according to accepted norms, and reproduced, and will likely become a standard tool for the field. CalR is accessible at https://CalR.bwh.harvard.edu.
Colin J. Palmer, Raphael J. Bruckner, Joao A. Paulo, Lawrence Kazak, Jonathan Z. Long, Amir I. Mina, Zhaoming Deng, Katherine B. LeClair, Jessica A. Hall, Shangyu Hong, Peter-James H. Zushin, Kyle L. Smith, Steven P. Gygi, Susan Hagen, David E. Cohen, and Alexander S. Banks. 2017. “Cdkal1, a type 2 diabetes susceptibility gene, regulates mitochondrial function in adipose tissue.” Molecular MetabolismMolecular Metabolism, 6, Pp. 1212-1225.
Lawrence Kazak, Edward T. Chouchani, Gina Z. Lu, Mark P. Jedrychowski, Curtis J. Bare, Amir I. Mina, Manju Kumari, Song Zhang, Ivan Vuckovic, Dina Laznik-Bogoslavski, Petras Dzeja, Alexander S. Banks, Evan D. Rosen, and Bruce M. Spiegelman. 2017. “Genetic Depletion of Adipocyte Creatine Metabolism Inhibits Diet-Induced Thermogenesis and Drives Obesity.” Cell MetabolismCell Metabolism, 26, Pp. 660-671.e3.