Resume

• 2008

  Doctor of Philosophy (Ph.D.)

  I completed coursework and preliminary examination within the field of biomedical science

  specifically physiology. Additionally I developed and carried out an independent

  original investigation of the biophysical mechanisms underlying a neurophysiological phenomenon.

  Molecular Physiology & Biophysics

  Graduate Student Association (GSA)-Physiology Liaison;\nVP of Network Development

  Jefferson Business and Biotechnology (BizBio) Group

  Thomas Jefferson University

• 2004

  BS

  Applied Mathematics

  Columbia University Emergency Medical Services

  Columbia University Running Club

  Columbia Men's Ice Hockey

• Science

  Molecular Cloning

  Molecular Genetics

  Biochemistry

  Neuroscience

  Clinical Research

  Cell Culture

  Higher Education

  Matlab

  Due Diligence

  Editing

  Immunohistochemistry

  Cell Biology

  Data Analysis

  Lifesciences

  Research

  Electrophysiology

  Teaching

  Statistics

  Molecular Biology

  A Perspective on PhD Career Outlook: Training

  Mentoring and Utilizing a New Generation of STEM Doctoral Degrees

  As careers outside of academia become more accepted and increasingly diverse

  the career outlook for PhD students and postdoctoral fellows (postdocs) in science

  technology

  engineering and mathematics (STEM) continues to improve. However

  many academic institutions

  failing to adapt to the changing environment

  have inadequately prepared their students and postdocs for career placement in non-academic fields. Here we explore the obstacles in career planning

  \nprovide approaches to enhance career development

  and highlight examples of existing initiatives for change. By utilizing their unique skillset and emphasizing innovation and entrepreneurship

  STEM PhD graduates are poised to become the leaders of many different industries and extend the opportunities for future graduates. The goal of this work is to emphasize career opportunities outside of academia

  recognize inefficiencies in career planning and ultimately help current and future STEM PhD students and postdocs better prepare for future career success.

  A Perspective on PhD Career Outlook: Training

  Mentoring and Utilizing a New Generation of STEM Doctoral Degrees

  Manuel Covarrubias

  A-type voltage-gated K+ (Kv) channels self-regulate their activity by inactivating directly from the open state (open-state inactivation [OSI]) or by inactivating before they open (closed-state inactivation [CSI]). To determine the inactivation pathways

  it is often necessary to apply several pulse protocols

  pore blockers

  single-channel recording

  and kinetic modeling. However

  intrinsic hurdles may preclude the standardized application of these methods. Here

  we implemented a simple method inspired by earlier studies of Na+ channels to analyze macroscopic inactivation and conclusively deduce the pathways of inactivation of recombinant and native A-type Kv channels. We investigated two distinct A-type Kv channels expressed heterologously (Kv3.4 and Kv4.2 with accessory subunits) and their native counterparts in dorsal root ganglion and cerebellar granule neurons. This approach applies two conventional pulse protocols to examine inactivation induced by (a) a simple step (single-pulse inactivation) and (b) a conditioning step (double-pulse inactivation). Consistent with OSI

  the rate of Kv3.4 inactivation (i.e.

  the negative first derivative of double-pulse inactivation) precisely superimposes on the profile of the Kv3.4 current evoked by a single pulse because the channels must open to inactivate. In contrast

  the rate of Kv4.2 inactivation is asynchronous

  already changing at earlier times relative to the profile of the Kv4.2 current evoked by a single pulse. Thus

  Kv4.2 inactivation occurs uncoupled from channel opening

  indicating CSI. Furthermore

  the inactivation time constant versus voltage relation of Kv3.4 decreases monotonically with depolarization and levels off

  whereas that of Kv4.2 exhibits a J-shape profile. We also manipulated the inactivation phenotype by changing the subunit composition and show how CSI and CSI combined with OSI might affect spiking properties in a full computational model of the hippocampal CA1 neuron. This work unambiguously...

  Modeling-independent elucidation of inactivation pathways in recombinant and native A-type Kv channels.

  Manuel Covarrubias

  Gyorgy Panyi

  Tibor G. Szanto

  Voltage-gated K+ (Kv) channel activation depends on interactions between voltage sensors and an intracellular activation gate that controls access to a central pore cavity. Here

  we hypothesize that this gate is additionally responsible for closed-state inactivation (CSI) in Kv4.x channels. These Kv channels undergo CSI by a mechanism that is still poorly understood. To test the hypothesis

  we deduced the state of the Kv4.1 channel intracellular gate by exploiting the trap-door paradigm of pore blockade by internally applied quaternary ammonium (QA) ions exhibiting slow blocking kinetics and high-affinity for a blocking site. We found that inactivation gating seemingly traps benzyl-tributylammonium (bTBuA) when it enters the central pore cavity in the open state. However

  bTBuA fails to block inactivated Kv4.1 channels

  suggesting gated access involving an internal gate. In contrast

  bTBuA blockade of a Shaker Kv channel that undergoes open-state P/C-type inactivation exhibits fast onset and recovery inconsistent with bTBuA trapping. Furthermore

  the inactivated Shaker Kv channel is readily blocked by bTBuA. We conclude that Kv4.1 closed-state inactivation modulates pore blockade by QA ions in a manner that depends on the state of the internal activation gate.

  Closed-state inactivation involving an internal gate in Kv4.1 channels modulates pore blockade by intracellular quaternary ammonium ions

  Robert A. Reenan

  Rachel Maloney

  Mary Y. Ryan

  Channels

  Taylor & Francis

  RNA editing at four sites in eag

  a Drosophila voltage-gated potassium channel

  results in the substitution of amino acids into the final protein product that are not encoded by the genome. These sites and the editing alterations introduced are K467R (Site 1

  top of the S6 segment)

  Y548C

  N567D and K699R (Sites 2–4

  within the cytoplasmic C-terminal domain). We mutated these residues individually and expressed the channels in Xenopus oocytes. A fully edited construct (all four sites) has the slowest activation kinetics and a paucity of inactivation

  whereas the fully unedited channel exhibits the fastest activation and most dramatic inactivation. Editing Site 1 inhibits steady-state inactivation. Mutating Site 1 to the neutral residues resulted in intermediate inactivation phenotypes and a leftward shift of the peak current-voltage relationship. Activation kinetics display a Cole-Moore shift that is enhanced by RNA editing. Normalized open probability relationships for 467Q

  467R and 467K are superimposable

  indicating little effect of the mutations on steady-state activation. 467Q and 467R enhance instantaneous inward rectification

  indicating a role of this residue in ion permeation. Intracellular tetrabutylammonium blocks 467K significantly better than 467R. Block by intracellular

  but not extracellular

  tetraethylammonium interferes with inactivation. The fraction of inactivated current is reduced at higher extracellular Mg+2 concentrations

  and channels edited at Site 1 are more sensitive to changes in extracellular Mg+2 than unedited channels. These results show that even a minor change in amino acid side-chain chemistry and size can have a dramatic impact on channel biophysics

  and that RNA editing is important for fine-tuning the channel’s function.

  RNA editing in the eag potassium channel: biophysical consequences of editing a conserved S6 residue

  Columbia University EMS

  Mt. Laurel EMS

  Navigant

  New York Presbyterian Hospital

  Thomas Jefferson University

  New York

  NY

  Provided emergency medical care to the Columbia Campus and Morningside Heights Area as part of a New York State certified Emergency Medical Service; ran and directed the crew on the scene of incidents; responsible for all documentation and pre-hospital care reports; managed coordination between various New York City emergency responders (Fire Department

  Police

  Poison Control

  etc.) on scene.

  Crew Chief

  EMT-B

  Columbia University EMS

  Lawrenceville

  NJ

  Managing Consultant

  Navigant

  Graduate Student-Researcher

  Dept. of Neuroscience

  Greater Philadelphia Area

  Thomas Jefferson University

  New York

  NY

  Mentored by Arthur Smerling

  MD

  at Morgan Stanley Children's Hospital

  Department of Critical Care Medicine. Helped develop and conduct survey of bedside care as part of an initiative for infection prophylaxis among PICU patients. Executed retrospective clinical study of PICU patients.

  Researcher

  New York Presbyterian Hospital

  Greater Philadelphia Area

  Associate Director

  Navigant

  Lawrenceville

  NJ

  Senior Consultant

  Navigant

  Provided emergency medical care to Mount Laurel residents who activate the 911 system at the basic life support level. Made treatment and transport decisions during care of patient when advanced life support was unavailable. Attended special operations trainings including water rescue and HAZMAT and mass decontamination training.

  Mt. Laurel EMS