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Education ?

Medical School Score Rankings
The University of Texas Southwestern (1981)
Top 25%

Awards & Distinctions ?

American Board of Anesthesiology

Affiliations ?

Dr. Freeman is affiliated with 4 hospitals.

Hospital Affiliations



  • Medical Center Of Plano
    3901 W 15th St, Plano, TX 75075
  • Medical City Hosp
  • Presbyterian Plano Center For Diagnostics & Surger
    6020 W Parker Rd, Plano, TX 75093
  • Texas Health Center For Diagnostics And
  • Publications & Research

    Dr. Freeman has contributed to 5 publications.
    Title A Single Nucleotide Polymorphism in Mgea5 Encoding O-glcnac-selective N-acetyl-beta-d Glucosaminidase is Associated with Type 2 Diabetes in Mexican Americans.
    Date June 2005
    Journal Diabetes

    Excess O-glycosylation of proteins by O-linked beta-N-acetylglucosamine (O-GlcNAc) may be involved in the pathogenesis of type 2 diabetes. The enzyme O-GlcNAc-selective N-acetyl-beta-d glucosaminidase (O-GlcNAcase) encoded by MGEA5 on 10q24.1-q24.3 reverses this modification by catalyzing the removal of O-GlcNAc. We have previously reported the linkage of type 2 diabetes and age at diabetes onset to an overlapping region on chromosome 10q in the San Antonio Family Diabetes Study (SAFADS). In this study, we investigated menangioma-expressed antigen-5 (MGEA5) as a positional candidate gene. Twenty-four single nucleotide polymorphisms (SNPs), identified by sequencing 44 SAFADS subjects, were genotyped in 436 individuals from 27 families whose data were used in the original linkage report. Association tests indicated significant association of a novel SNP with the traits diabetes (P = 0.0128, relative risk = 2.77) and age at diabetes onset (P = 0.0017). The associated SNP is located in intron 10, which contains an alternate stop codon and may lead to decreased expression of the 130-kDa isoform, the isoform predicted to contain the O-GlcNAcase activity. We investigated whether this variant was responsible for the original linkage signal. The variance attributed to this SNP accounted for approximately 25% of the logarithm of odds. These results suggest that this variant within the MGEA5 gene may increase diabetes risk in Mexican Americans.

    Title Differentiation-inducing Quinolines As Experimental Breast Cancer Agents in the Mcf-7 Human Breast Cancer Cell Model.
    Date November 2004
    Journal Biochemical Pharmacology

    The purpose of this work is to develop agents for cancer differentiation therapy. We showed that five antiproliferative quinoline compounds in the National Cancer Institute database stimulated cell differentiation at growth inhibitory concentrations (3-14 microM) in MCF-7 human breast tumor cells in vitro. The differentiation-inducing quinolines caused lipid droplet accumulation, a phenotypic marker of differentiation, loss of Ki67 antigen expression, a cell cycle marker indicative of exit into G0, and reduced protein levels of the G1--S transcription factor, E2F1. The antimalarial quinolines, chloroquine, hydroxychloroquine and quinidine had similar effects in MCF-7 cells, but were 3-10 times less potent than the NSC compounds. NSC3852 and NSC86371 inhibited histone deacetylase (HDAC) activity in vitro and caused DNA damage and apoptosis in MCF-7 cells, consistent with their differentiation and antiproliferative activities. However, the HDAC assay results showed that for other compounds, direct HDAC enzyme inhibition was not required for differentiation activity. E2F1 protein was suppressed by all differentiation quinolines, but not by non-differentiating analogs, quinoline and primaquine. At equivalent antiproliferative concentrations, NSC69603 caused the greatest decrease in E2F1 protein (90%) followed by antimalarials quinidine and hydroxychloroquine. NSC69603 did not cause DNA damage. The other NSC compounds caused DNA damage and apoptosis and reduced E2F1 levels. The physicochemical properties of NSC3852, NSC69603, NSC86371, and NSC305819 predicted they are drug candidates suitable for development as experimental breast tumor cell differentiation agents. We conclude DNA damage and reductions in E2F1 protein are mechanistically important to the differentiation and antiproliferative activities of these quinoline drug candidates.

    Title Phosphatase Regulation of Gene Expression During Development of the Palate.
    Date September 2002
    Journal Life Sciences

    In mammalian cells, including those of the embryonic palate, the level of phosphorylation of cellular proteins at any given time reflects the activities of protein kinases and protein phosphatases. Both protein phosphatase-1 (PP-1) and PP-2A inhibit cAMP-mediated increases in transcription by dephosphorylating CREB at ser-133. Western blot analysis indicated that protein phosphatase 1 (PP-1) was expressed constitutively in palatal tissue during its development. Expression of PP-2A was regulated developmentally with maximal expression on gestational day (gd) 14. Densitometric scanning revealed a 30% increase in expression from gd 13 to gd 14. Virtually all phosphatase activity in the tissue extracts could be inhibited by 5 microM okadaic acid, demonstrating that PP-1 and PP-2A account for all detectable ser/thr protein phosphatase activity present in the developing palate. Moreover, no significant differences in PP-1 and PP-2A activities were observed during the period of palate development. Treatment of primary cultures of murine embryonic palate mesenchymal (MEPM) cells with forskolin (20 microM) to elevate intracellular cAMP levels, resulted in a time-dependent increase in CREB ser-133 phosphorylation and a corresponding time dependent decrease in PP-1 and PP-2A levels. Moreover, treatment of MEPM cells with okadaic acid resulted in a dramatic increase in basal CREB ser-133 phosphorylation. This suggests that PP-1 activity may contribute to transcriptional regulation of CREB and that PP-1 and PP-2A are regulated differentially by cAMP. Treatment of MEPM cells with TGF beta 1 (1 ng/ml) under conditions of TGF beta-induced CREB phosphorylation resulted in no effect on the expression of either PP-1 or PP-2A proteins and no significant alterations in total basal protein phosphatase activity. These results demonstrate that transcriptional regulation of CREB in embryonic palatal issue is dependent on the coordinate activity of specific kinases and phosphatases.

    Title Intubation Technique--a Health Hazard for the Anesthesiologist.
    Date April 1986
    Journal Anesthesiology
    Title Recurrence of Pulsus Alternans After Fentanyl Injection in a Patient with Aortic Stenosis and Congestive Heart Failure.
    Date January 1986
    Journal Canadian Anaesthetists' Society Journal

    Following aortic valve replacement in a patient with aortic stenosis and cardiac failure, marked pulsus alternans recurred immediately after intravenous injection of 0.5 mg fentanyl, without concomitant changes in heart rate, mean left atrial pressure, or the electrocardiogram. Pulsus alternans is known to occur in association with heart failure and aortic stenosis, but has not been reported previously in response to anaesthetic drugs. Mechanisms of pulsus alternans are discussed, and the possible contributory role of fentanyl is considered.

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