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High-probability grants
According to our matching algorithm, David R. Friedland is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2004 — 2008 |
Friedland, David R |
K08Activity Code Description: To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. |
Differential Gene Expression in the Cochlear Nucleus @ Medical College of Wisconsin
DESCRIPTION (provided by applicant): Approximately a half million Americans are severely deafened and 1 in 3 individuals over 65 demonstrates significant hearing loss. Rehabilitative options have improved in the ability to restore hearing levels however problems with discrimination, hearing in noise and tinnitus remain. Recent studies indicate that the central auditory system plays a significant role in these problems, however, precise anatomic and physiological correlation is lacking. We propose to define a genetic model of central auditory function to better understand normal and pathologic auditory processes. The fundamental hypothesis of this application is that the specialized anatomic and physiologic properties of the cochlear nucleus are reflected in the genes expressed by its neurons (i.e., the transcriptome). This study will use serial analysis of gene expression (SAGE) to characterize and quantify mRNA expressed within cochlear nucleus subdivisions and neurons. Modern bioinformatics techniques will be applied to identify unique, differentially expressed and novel genes in this auditory brain stem region. These genes will be localized to specific classes of cells and cochlear nucleus subdivisions by in situ hybridization and immuno-histochemistry. Similar genetic and localizing studies will also be performed on the multipolar class of cochlear nucleus neurons. These experiments will enable the correlation of physiologic and morphologic properties of the auditory system with specific genetic transcripts. The generation of a molecular profile of the cochlear nuclei will provide greater insight into the auditory system by demonstrating the fundamental mechanisms subserving signal processing. These data will also provide a powerful template upon which to test and design novel treatments for improving hearing, discrimination and tinnitus in a significant portion of the population.
|
0.943 |
2010 — 2011 |
Friedland, David R |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Microrna Regulation of Cholesteatoma Growth @ Medical College of Wisconsin
DESCRIPTION (provided by applicant): Cholesteatomas are benign growths typically arising in the outer and middle ears. These fairly common lesions represent a dysregulation of skin growth and cause localized temporal bone destruction. Cholesteatomas commonly cause chronic infection and often lead to hearing loss, dizziness or facial nerve paralysis. Complications of cholesteatoma include serious conditions such as meningitis and brain abscesses. There are no medical therapies for cholesteatoma and current treatment is surgical resection. Recurrences are common and most individuals with cholesteatoma will undergo multiple operations. The long-term goal of this study is to identify the mechanisms regulating cholesteatoma growth for the development of novel pharmacological treatments for this disorder. The relatively easy access of the middle ear to intratympanic drug delivery makes a topical inhibitor of cholesteatoma growth an attractive mode of primary or adjunctive therapy. Recent studies have shown that benign and malignant tumor growth is associated with alterations in human microRNA expression and activity. Although phylogenetically ancient, microRNAs have only recently been identified as potent regulators of protein translation. These small nucleotides (~22nt) bind to messenger RNA (mRNA) and down-regulate protein production by degrading the message or by blocking translation. Our preliminary studies show significant up-regulation of human microRNA-21 (hsa-mir-21) in cholesteatoma as compared to normal post-auricular skin. Hsa-mir-21 is up-regulated in many tumors including vestibular schwannoma, hepatocellular carcinoma and breast cancer. This microRNA is predicted to target PTEN, PDCD4 and TPM1 messenger RNA and to be regulated by STAT3. These proteins are involved in cell growth and tumor suppressor pathways. Using real-time RT-PCR, western blot analyses, and in situ hybridization we will explore the role of hsa-mir-21 in regulating cholesteatoma growth. Further, we will investigate the role of additional microRNAs in this disorder by high-throughput microRNA microarrays. A cell culture system will also be developed to test the potential of specific microRNA interfering molecules to inhibit cholesteatoma growth and proliferation. PUBLIC HEALTH RELEVANCE: Cholesteatomas are aggressive but benign lesions of the ear that commonly cause hearing loss and chronic infections. There are no medical treatments and repeated surgeries for removal are common in children and adults. This study seeks to identify novel regulators of cholesteatoma growth that may lead to pharmacological therapies and thus improve hearing outcomes and avoid serious medical and surgical complications.
|
0.943 |