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Copy Writing
Clear copy about scientific products and how to use them.
Grant Writing
Making the big ideas shine while strictly adhering to grant requirements.
Paper Editing
Results: a cleaner paper with more room for data... and improved odds for acceptance.
Web Design
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Portfolio
Grant
Genetics & Cell Culture
NIH Grant
Biochemistry & Gene-Editing
Poster
Physiology & mRNA expression
Paper Review
Biochemistry & Yeast Screening
Software How-To Guide
Data Analysis & Programming
Science Explainer
Genetics & CRISPR
NIH-style Grant
The following sections are included as writing samples: specific aims, significance, innovation, approach, and future directions. For a 1-page writing sample, see the specific aims section on page 2.
Cystic fibrosis (CF) is caused by mutation of a single gene: CFTR. Bacterial infection contributes to CF lung disease via tissue-damaging inflammation and neutrophil-dominated immune response. Mechanisms linking CFTR mutation to this characteristic CF immune response are not well elucidated. Epigenetic changes (ie. alterations to chromatin that do not affect DNA sequence) associated with mutant CFTR may provide a mechanistic link. I propose to look genome-wide for altered regulation in CF using a better cell model than previously available.
This F-31 grant was funded by the NICHD (a branch of the NIH). The following sections are included as writing samples: introduction, specific aims, research strategy, project summary/abstract, and project narrative. For a 1-page writing sample, see the specific aims section on page 3.
The airway epithelial cells of patients with cystic fibrosis release excessive inflammatory signals that help precipitate lung disease. This proposal will elucidate mechanisms behind excessive inflammatory signaling as well as the potential for clinical reversibility.
This poster won an honorable mention cash prize in the graduate student poster presentation competition at the Case Western Reserve University Research ShowCASE.
Cystic fibrosis is a disease caused by mutations in the gene CFTR. Maintenance of a normal body mass index is a clinical goal for people with cystic fibrosis because it is associated with better lung function. Low body mass index is typically attributed to lung disease and nutrient malabsorption. In the cystic fibrosis mice, however, lean body type is present despite lack of lung disease and nutrient malabsorption. This poster examines whether CFTR dysfunction in fat tissue could play a role in the lean body type of cystic fibrosis mice.
This is an in-depth (5 page) review of a paper published in Nature Genetics .
Amyotrophic lateral sclerosis (ALS) is a disease of progressive motor neuron loss. One tenth of ALS cases are inherited; the others are sporadic with no identified cause. Hyper-excitation of motor neurons and free radical damage are hypothesized to lead to ALS. In support of this hypothesis, inhibiting motor neuron excitation with the drug riluzole inhibits motor neuron degeneration. Riluzole is currently the only treatment that slows disease course1. However, newly discovered drug targets, such as TDP-43, guide the search for other treatments.
