Henry H. Ruiz, PhD, Postdoctoral Fellow

Henry H. Ruiz, PhDHenry H. Ruiz obtained his B.A. in Neuroscience and Psychology and a M.A. in Behavioral Neuroscience for Queens College and earned his Doctorate (PhD) degree from the Graduate Center of the City University of New York (CUNY). During his graduate career, Dr. Ruiz studied the intricate association between heightened sympathetic nervous system (SNS) activity, inflammation and behavioral perturbations. During his thesis, Dr. Ruiz compared and validated different protocol of the dextran sodium sulfate rodent model of colitis and identified rearing behavior as a potential readout for visceral discomfort in mice.

In 2014, Dr. Ruiz joined Dr. Christoph Buettner’s laboratory at the Mount Sinai School of Medicine where he developed an expertise in metabolic phenotyping using an array of dynamic metabolic tests as well as in transgenic breeding and large colony management. During this training period, Dr. Ruiz identified impaired brain insulin signaling, specifically in the hypothalamus, as a major link between Alzheimer’s disease (AD) and obesity/diabetes.

Dr. Ruiz has now joined the Diabetes Research Program where his goal is to characterize in detail the expression of the receptor for advanced glycation endproducts (RAGE) in the central nervous system and determine whether RAGE action in the central nervous system is a major contributor to obesity and/or diabetes.

 

Publications

  1. Fischer K, Ruiz HH, Jhun K, Finan B, Oberlin DJ, C Van der Heide V, Kalinovich AV, Petrovic N, Wolf Y, Clemmensen C, Shin AC, Divanovic S, Brombacher F, Glasmacher E, Keipert S, Jastroch M, Nagler J, Schramm KW, Medrikova D, Collden G, Woods SC, Herzig S, Homann D,  Jung S, Nedergaard J, Cannon B, Tschöp MH,  Müller TD*, Buettner C*. (2017). Alternatively activated macrophages are unable to synthesize catecholamines and do not contribute to adipose tissue adaptive thermogenesis. Nature Medicine (accepted).
  2. Shah N, Ruiz HH, Lalazar Y, Zafar U, Freda PU, Post KD, Buettner C, Geer EB. (2016). Pro-inflammatory cytokines remain elevated despite long-term remission in Cushing's disease: a prospective study. Clin Endocrinol (Oxf). 2016 Sep 15. doi: 10.1111/cen.13230.
  3. Ruiz HH, Chi T, Lindtner C, Hsieh W, Shin A.C, Ehrlich M, Gandy S, Buettner C. (2016). Increased susceptibility to metabolic dysregulation in a mouse model of Alzheimer's disease is associated with impaired hypothalamic insulin signaling and elevated BCAA levels. Alzheimer’s and Dementia. 8: 851-861.
  4. Knight EM, Ruiz HH, Kim SH, Harte JC, Hsieh W, Glabe C, Klein WL, Attie AD, Buettner C, Ehrlich ME, Gandy S. (2016). Unexpected partial correction of metabolic and behavioral phenotypes of Alzheimer's APP/PSEN1 mice by gene targeting of diabetes/Alzheimer's-related Sorcs1. Acta Neuropathologica Communications. 4: 16.
  5. Jeong JH, Lee DK, Blouet C, Ruiz HH, Buettner C, Chua S Jr, Schwartz GJ, Jo YH. (2015). Cholinergic neurons in the dorsomedial hypothalamus regulate mouse brown adipose tissue metabolism. Molecular Metabolism. 4(6): 483-492.
  6. Krellman J, Ruiz HH, Marciano V, Mondrow B, Croll SD. (2014). Behavioral and neuroanatomical abnormalities in pleiotrophin knockout mice. PLoS One. 9(7): e100597.
  7. Seiverling L, Pantelides M, Ruiz HH, Sturmey P. (2009). The Effect of Behavioral Skills Training with General-Case Training on Staff Chaining of Child Vocalizations within Natural Language Paradigm. The Journal of Behavioral Interventions, 25: 53–75.