Dr. Prakasha Kempaiah is a Associate Professor at the Center for Global Health(CGH), Department of Internal Medicine. Dr. Kempaiah received his PhD from the Institute for HumanGenetics, University of Goettingen, Germany. During his PhD dissertation, he worked on areas caused bygenetic disorders using animal models. Dr. Kempaiah's PhD thesis work on protein transduction domainmediated recombinant protein supplementation therapy for Rett-syndrome resulted in two disclosures beingfiled. He also has completed one year of certificate course in Clinical and Translational Research (CTR) at UNM with an emphasis on biostatistics, global health and clinical research. He is trained in the field of genetics, cell biology, biochemistry, animal models and infectious diseases with skills set in the areas of genetic diagnostics, cloning, cell culture, parasite culture, proteinexpression, flow cytometry, genotyping, functional genomics, genome wide association study (GWAS), geneexpression arrays, custom array design, high density data analysis, pathways network analysis andbiostatistics. Dr. Kempaiah is also well versed in using several genetics and genomics analysis tools such asSPSS, HPlus, Haploview, GeneSpring, Golden Helix SVS suite, GeneGo, analyzing genotypes, haplotypes,and high density GWAS and gene expression data. Dr. Kempaiah is an editorial board member of OpenJournal of Apoptosis, Human Parasitic Diseases, Journal of Life Medicine, AIMS Genetics, Asian Council ofScience Editors and Journal of Public Health & Epidemiology. He is also an invited peer-reviewer for HumanParasitic Diseases, Gene Regulation and Systems Biology, Cancer Cell International,Breast Cancer,Biotechnology Progress, Journal of Cell Death, Immunology and Immunogenetics Insights, Gene Expression toGenetical Genomics and Cancer Informatics and other journals.
His research projects includes: (1), determining the relationship between the immunomodulatory aspect of immuneresponse genes and promoter polymorphism (SNPs and VNTRs), functional changes, downstream effects onmodulator production, and SMA manifestation; (2), determining the suitability of Glutamine as a therapeuticagent in children with malaria to target HSP70 production and improve the therapeutic effects of anti-malarialsin combination with glutamine; (3), GWAS using Illumina Omni-2.5 array, human Immunochip and wholegenome transcriptome arrays to identify important markers, CNVs and candidates gene pathways thatcondition development of SMA; (4), malaria parasite cultures for anti-malarial drug screening and to isolatehemozoin (PfHz) and testing its immunomodulatory activities using in-vitro cultures; (5), elucidating themolecular mechanisms of inflammatory-derived inefficient erythropoiesis using CD34+ hematopoieticprogenitor’s cells isolated from umbilical specimens; (6), Identifying natural and pharmacological compoundsto stimulate inflammatory mediators altered during SMA such as interlukin-12 using in-vitro cultures treatedwith PfHz.
