Résumé relevant to Galenus LLC
for James C Poleman
Cleveland, Ohio and New Orleans, Louisiana
Collaboration / Headhunting inquiries welcome

Contact   Linkedin  Microsoft Academic  Pubmed

2000-2013: Laboratory Technician IV, Willard A. Birnbaum Cystic Fibrosis Research Center, the Department of Pediatrics, Case Western Reserve University School of Medicine.
Supervised by Mitchell Drumm, Ph.D, who worked with Francis Collins, M.D., Ph.D. (Now Director of N.I.H.), on identification of the gene causing Cystic Fibrosis (CF).
I came to CWRU with experience as a veterinary surgical nurse and hopes for Veterinary School, so I rarely strayed far from the CF Mouse. The first several years at Case were spent executing experiments utilizing a Murine model of acute or chronic Pseudomonas lung infection in mutant and transgenic mice. Experimental parameters included a panel of five inflammatory cytokines, but inflammation was not exciting me. 
I become increasingly enamored with metabolic biochemistry, nutrition and energy homeostasis and Mitch encouraged me to run with that ball-giving me plenty of projects to feed that curiosity. 
CF is not typically thought of as a disease of metabolism, but significant correlations recently found in Genome-wide association meta-analysis made this a compelling new avenue of investigation within the disease. Though I drifted from my original goal of going to veterinary school,  I maintained a strong relationship with the Institutional Animal Care and Use Committee and made AWA compliance and PHS policy a top priority for myself and the lab.

Absence of leptin signaling allows fat accretion in CF mice

American Journal of Physiology-Gastrointestinal and Liver Physiology

Aug 17, 2018

From the Abstract:

“To improve energy balance through increased caloric intake and reduced energy expenditure, we disrupted leptin signaling by crossing the db/db leptin receptor allele with mice carrying R117H Cftr mutation. Compared with db/db mice, absence of leptin signaling in CF mice (CF db/db) resulted in delayed and moderate hyperphagia with lower de novo lipogenesis and lipid deposition, producing only moderately obese CF mice. Greater body length was found in db/db mice, but not in CF db/db suggesting CF-dependent effect on bone growth.”

See Article

Altered de novo lipogenesis contributes to low adipose stores in cystic fibrosis mice.

American Journal of Physiology-Gastrointestinal and Liver Physiology

Jun 7, 2012

Though they exhibit exocrine pancreatic function (a concern in Cystic Fibrosis), mice with the F508del mutation in Cftr do not store adipose tissue at levels similar to their wild-type cohort. Hepatic transcriptome analysis, quantitative food intake, diet/fecal analysis to determine lipid absorption and tissues that have incorporated deuterium from labeled water are reviewed to suggest a model of hepatic de novo lipogenisis as down-regulated in cystic fibrosis which is independent of malabsorption or pancreatic enzyme activity. This may provide a reason that pancreatic enzyme replacement therapy does little to correct the cystic fibrosis growth phenotype.

See Article

Preferential Transfection of Tissue Macrophages Following Intravenous Administration of sec-R Targeted hCFTR DNA Enhances Survival of CF Mice Inoculated with Pseudomonas aeruginosa Agar Beads.

Molecular Therapy    1 May 2004

A Murine model of chronic Pseudomonas infection was used to test targeted  hCFTR delivery to tissue macrophages using compacted DNA complexes.

See Article

Other Projects:

Investigation of Energy Substrate Utilization in Cystic Fibrosis through indirect calorimetry.

Static as well as exercise protocols are used. Project supervised and strongly supported by Nicola Lai, Ph.D, CWRU Department of Biomedical Engineering, Modeling & Analysis of Physiological Systems.

Investigation of role of the Melanocortin 3 Receptor in Cystic Fibrosis.

Specifically concerning functional differences in F508del-affected Cftr.

Investigation of role of oxidative stress in intestinal obstruction through oxidation of Methionine (in Cystic Fibrosis).

or rather, lack of Methionine Sulfoxide reduction by Methionine Sulfoxide reductase-A, once Methionine has been oxidized.

Search for novel Cystic Fibrosis screening process though Red Blood Cell, Gadolinium(III) Chloride interaction

Investigation of activation of Acetyl-CoA carboxylase by AMP Kinase in Cystic Fibrosis.

As a technician in earlier days, I mostly appear in acknowledgements of published works.

Previous to this, I worked in a veterinary surgical suite (as mentioned) and a veterinary general practice which, together, comprise the entirety of my clinical and pharmacology experience.

I’ve also served as a Ohio Department of Agriculture-licensed aquatic biologist (#144759) for a lake & pond care company, gardened professionally, installed HVAC systems, managed an aquarium store, completed a brief internship at the Cleveland Zoo Aquatics Building, made pizzas for Chuck E. Cheese and tended bar on Bourbon St, New Orleans.