Docality.com Logo
 
Dr. Donovan  Harper  Dc image

Dr. Donovan Harper Dc

5031 Ford Pkwy Suite 112
Bessemer AL 35022
205 255-5428
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 2085
NPI: 1346269040
Taxonomy Codes:
111NS0005X

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy

Conditions

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

None Found

Publications

Identification of seven new prostate cancer susceptibility loci through a genome-wide association study. - Nature genetics
Prostate cancer (PrCa) is the most frequently diagnosed cancer in males in developed countries. To identify common PrCa susceptibility alleles, we previously conducted a genome-wide association study in which 541,129 SNPs were genotyped in 1,854 PrCa cases with clinically detected disease and in 1,894 controls. We have now extended the study to evaluate promising associations in a second stage in which we genotyped 43,671 SNPs in 3,650 PrCa cases and 3,940 controls and in a third stage involving an additional 16,229 cases and 14,821 controls from 21 studies. In addition to replicating previous associations, we identified seven new prostate cancer susceptibility loci on chromosomes 2, 4, 8, 11 and 22 (with P = 1.6 x 10(-8) to P = 2.7 x 10(-33)).
Multiple loci on 8q24 associated with prostate cancer susceptibility. - Nature genetics
Previous studies have identified multiple loci on 8q24 associated with prostate cancer risk. We performed a comprehensive analysis of SNP associations across 8q24 by genotyping tag SNPs in 5,504 prostate cancer cases and 5,834 controls. We confirmed associations at three previously reported loci and identified additional loci in two other linkage disequilibrium blocks (rs1006908: per-allele OR = 0.87, P = 7.9 x 10(-8); rs620861: OR = 0.90, P = 4.8 x 10(-8)). Eight SNPs in five linkage disequilibrium blocks were independently associated with prostate cancer susceptibility.
Depressogenic cognitive styles: predictive validity, information processing and personality characteristics, and developmental origins. - Behaviour research and therapy
Two of the major cognitive theories of depression, the theory of Beck [Beck, A. T. (1967). Depression: clinical, experimental and theoretical aspects. New York: Harper & Row. and Beck, A. T. (1987) Cognitive models of depression. Journal of Cognitive Psychotherapy: an International Quarterly, 1, 5-37] and the hopelessness theory [Abramson, Metalsky, & Alloy, (1989) Hopelessness depression: a theory-based subtype of depression. Psychological Review, 96, 358-372], include the hypothesis that particular negative cognitive styles increase individuals' likelihood of developing episodes of depression, in particular, a cognitively mediated subtype of depression, when they encounter negative life events. The Temple-Wisconsin Cognitive Vulnerability to Depression (CVD) project is a two-site, prospective longitudinal study designed to test this cognitive vulnerability hypothesis, as well as the other etiological hypotheses of Beck's and the hopelessness theories of depression. In this article, based on CVD project findings to date, we review evidence that the hypothesized depressogenic cognitive styles do indeed confer vulnerability for clinically significant depressive disorders and suicidality. In addition, we present evidence regarding moderators of these depressogenic cognitive styles, the information processing and personality correlates of these styles and the possible developmental antecedents of these styles. We end with a consideration of future research directions and the clinical implications of cognitive vulnerability to depression.
Paternal or Maternal Uniparental Disomy of Chromosome 16 Resulting in Homozygosity of a Mutant Allele Causes Fanconi Anemia. - Human mutation
Fanconi anemia (FA) is a rare inherited disorder caused by pathogenic variants in one of 19 FANC genes. FA patients display congenital abnormalities, and develop bone marrow failure, and cancer susceptibility. We identified homozygous mutations in four FA patients and, in each case, only one parent carried the obligate mutant allele. FANCA and FANCP/SLX4 genes, both located on chromosome 16, were the affected recessive FA genes in three and one family respectively. Genotyping with short tandem repeat markers and SNP arrays revealed uniparental disomy (UPD) of the entire mutation-carrying chromosome 16 in all four patients. One FANCA patient had paternal UPD, whereas FA in the other three patients resulted from maternal UPD. These are the first reported cases of UPD as a cause of FA. UPD indicates a reduced risk of having another child with FA in the family and has implications in prenatal diagnosis.© 2016 WILEY PERIODICALS, INC.
Enhancement of HIV-1 infection and intestinal CD4+ T cell depletion ex vivo by gut microbes altered during chronic HIV-1 infection. - Retrovirology
Early HIV-1 infection is characterized by high levels of HIV-1 replication and substantial CD4 T cell depletion in the intestinal mucosa, intestinal epithelial barrier breakdown, and microbial translocation. HIV-1-induced disruption of intestinal homeostasis has also been associated with changes in the intestinal microbiome that are linked to mucosal and systemic immune activation. In this study, we investigated the impact of representative bacterial species that were altered in the colonic mucosa of viremic HIV-1 infected individuals (HIV-altered mucosal bacteria; HAMB) on intestinal CD4 T cell function, infection by HIV-1, and survival in vitro. Lamina propria (LP) mononuclear cells were infected with CCR5-tropic HIV-1BaL or mock infected, exposed to high (3 gram-negative) or low (2 gram-positive) abundance HAMB or control gram-negative Escherichia coli and levels of productive HIV-1 infection and CD4 T cell depletion assessed. HAMB-associated changes in LP CD4 T cell activation, proliferation and HIV-1 co-receptor expression were also evaluated.The majority of HAMB increased HIV-1 infection and depletion of LP CD4 T cells, but gram-negative HAMB enhanced CD4 T cell infection to a greater degree than gram-positive HAMB. Most gram-negative HAMB enhanced T cell infection to levels similar to that induced by gram-negative E. coli despite lower induction of T cell activation and proliferation by HAMB. Both gram-negative HAMB and E. coli significantly increased expression of HIV-1 co-receptor CCR5 on LP CD4 T cells. Lipopolysaccharide, a gram-negative bacteria cell wall component, up-regulated CCR5 expression on LP CD4 T cells whereas gram-positive cell wall lipoteichoic acid did not. Upregulation of CCR5 by gram-negative HAMB was largely abrogated in CD4 T cell-enriched cultures suggesting an indirect mode of stimulation.Gram-negative commensal bacteria that are altered in abundance in the colonic mucosa of HIV-1 infected individuals have the capacity to enhance CCR5-tropic HIV-1 productive infection and depletion of LP CD4 T cells in vitro. Enhanced infection appears to be primarily mediated indirectly through increased expression of CCR5 on LP CD4 T cells without concomitant large scale T cell activation. This represents a novel mechanism potentially linking intestinal dysbiosis to HIV-1 mucosal pathogenesis.
Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans. - Human molecular genetics
Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same region.© The Author 2015. Published by Oxford University Press.

Map & Directions

5031 Ford Pkwy Suite 112 Bessemer, AL 35022
View Directions In Google Maps

Nearby Doctors

5751 Pocahontas Rd Ste A
Bessemer, AL 35022
205 774-4242
985 9Th Ave Sw Suite X02
Bessemer, AL 35022
205 817-7870
985 9Th Ave Sw Suite 404
Bessemer, AL 35022
205 818-8475
985 9Th Ave Sw Ste 201
Bessemer, AL 35022
205 818-8555
5751 Pocahontas Rd Ste A Suite 5
Bessemer, AL 35022
205 774-4242
985 9Th Ave Southwest Suite 201 Pob
Bessemer, AL 35022
205 819-9339
6250 Park South Dr
Bessemer, AL 35022
205 255-5440
5031 Ford Pkwy Ste 113 Eagle Vision Eye Care
Bessemer, AL 35022
205 242-2733
985 9Th Ave Sw Ste 201
Bessemer, AL 35022
205 818-8555