Obstetricians & Gynecologists
42 years of experience

Accepting new patients
Medical Clinic of North Texas
809 W Randol Mill Rd
Ste A
Arlington, TX 76012
817-277-7133
Locations and availability (2)

Education ?

Medical School Score Rankings
University of Alabama at Birmingham (1968)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Associations
American Board of Obstetrics and Gynecology

Affiliations ?

Dr. Jeffers is affiliated with 12 hospitals.

Hospital Affilations

Score

Rankings

  • Texas Health Harris Methodist Hospital Fort Worth
    1301 Pennsylvania Ave, Fort Worth, TX 76104
    • Currently 4 of 4 crosses
    Top 25%
  • Texas Health Harris Methodist Hospital Southwest Fort Worth
    6100 Harris Pkwy, Fort Worth, TX 76132
    • Currently 4 of 4 crosses
    Top 25%
  • Harris Methodist H E B
    1600 Hospital Pkwy, Bedford, TX 76022
    • Currently 4 of 4 crosses
    Top 25%
  • Texas Health Presbyterian Hospital Of Dallas
    8200 Walnut Hill Ln, Dallas, TX 75231
    • Currently 3 of 4 crosses
    Top 50%
  • Texas Health Arlington Memorial Hospital
    800 W Randol Mill Rd, Arlington, TX 76012
    • Currently 3 of 4 crosses
    Top 50%
  • Texas Health Harris Methodist Hospital Azle
    108 Denver Trl, Azle, TX 76020
    • Currently 3 of 4 crosses
    Top 50%
  • Usmd Surgical Hospital Of Arlington
    801 W Interstate 20, Arlington, TX 76017
    • Currently 1 of 4 crosses
  • Usmd
  • Harris Methodist - Springwood
    1608 Hospital Pkwy, Bedford, TX 76022
  • TX Health Arlington
  • Texas Health Fort Worth
  • Harris Continued Care Hospital
    1301 Pennsylvania Ave, Fort Worth, TX 76104
  • Publications & Research

    Dr. Jeffers has contributed to 18 publications.
    Title Bid, Bim, and Puma Are Essential for Activation of the Bax- and Bak-dependent Cell Death Program.
    Date December 2010
    Journal Science (new York, N.y.)
    Excerpt

    Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in vivo evidence demonstrating an essential role of the proteins BID, BIM, and PUMA in activating BAX and BAK. Bid, Bim, and Puma triple-knockout mice showed the same developmental defects that are associated with deficiency of Bax and Bak, including persistent interdigital webs and imperforate vaginas. Genetic deletion of Bid, Bim, and Puma prevented the homo-oligomerization of BAX and BAK, and thereby cytochrome c-mediated activation of caspases in response to diverse death signals in neurons and T lymphocytes, despite the presence of other BH3-only molecules. Thus, many forms of apoptosis require direct activation of BAX and BAK at the mitochondria by a member of the BID, BIM, or PUMA family of proteins.

    Title Stepwise Activation of Bax and Bak by Tbid, Bim, and Puma Initiates Mitochondrial Apoptosis.
    Date January 2010
    Journal Molecular Cell
    Excerpt

    While activation of BAX/BAK by BH3-only molecules (BH3s) is essential for mitochondrial apoptosis, the underlying mechanisms remain unsettled. Here we demonstrate that BAX undergoes stepwise structural reorganization leading to mitochondrial targeting and homo-oligomerization. The alpha1 helix of BAX keeps the alpha9 helix engaged in the dimerization pocket, rendering BAX as a monomer in cytosol. The activator BH3s, tBID/BIM/PUMA, attack and expose the alpha1 helix of BAX, resulting in secondary disengagement of the alpha9 helix and thereby mitochondrial insertion. Activator BH3s remain associated with the N-terminally exposed BAX through the BH1 domain to drive homo-oligomerization. BAK, an integral mitochondrial membrane protein, has bypassed the first activation step, explaining why its killing kinetics are faster than those of BAX. Furthermore, death signals initiated at ER induce BIM and PUMA to activate mitochondrial apoptosis. Accordingly, deficiency of Bim/Puma impedes ER stress-induced BAX/BAK activation and apoptosis. Our study provides mechanistic insights regarding the spatiotemporal execution of BAX/BAK-governed cell death.

    Title The Problem with Large Diameter Metal-on-metal Acetabular Cup Inclination.
    Date August 2009
    Journal Bulletin of the Nyu Hospital for Joint Diseases
    Excerpt

    Large diameter metal-on-metal hip bearings have proven to be clinically successful in active patients, but, in a small number, they are associated with elevated wear and high metal ion levels when cup inclination angles are too steep and the version is too extreme, or either alone. Based on the geometry of six different commercially available large diameter metal-on-metal acetabular components, this study demonstrated that the critical bearing surface operates at an angle up to 16 masculine greater than the cup face inclination. Due to geometry alone, measured cup inclination is not the angle that most surgeons perceive it to be. We strongly recommend when employing large diameter metal-on-metal bearings that lower inclination and version angles are targeted to prevent excessive wear.

    Title Selection Against Puma Gene Expression in Myc-driven B-cell Lymphomagenesis.
    Date September 2008
    Journal Molecular and Cellular Biology
    Excerpt

    The p53 tumor suppressor pathway limits oncogenesis by inducing cell cycle arrest or apoptosis. A key p53 target gene is PUMA, which encodes a BH3-only proapoptotic protein. Here we demonstrate that Puma deletion in the Emu-Myc mouse model of Burkitt lymphoma accelerates lymphomagenesis and that approximately 75% of Emu-Myc lymphomas naturally select against Puma protein expression. Furthermore, approximately 40% of primary human Burkitt lymphomas fail to express detectable levels of PUMA and in some tumors this is associated with DNA methylation. Burkitt lymphoma cell lines phenocopy the primary tumors with respect to DNA methylation and diminished PUMA expression, which can be reactivated following inhibition of DNA methyltransferases. These findings establish that PUMA is silenced in human malignancies, and they suggest PUMA as a target for the development of novel chemotherapeutics.

    Title Cement Mantle Fatigue Failure in Total Hip Replacement: Experimental and Computational Testing.
    Date July 2007
    Journal Journal of Biomechanics
    Excerpt

    One possible loosening mechanism of the femoral component in total hip replacement is fatigue cracking of the cement mantle. A computational method capable of simulating this process may therefore be a useful tool in the preclinical evaluation of prospective implants. In this study, we investigated the ability of a computational method to predict fatigue cracking in experimental models of the implanted femur construct. Experimental specimens were fabricated such that cement mantle visualisation was possible throughout the test. Two different implant surface finishes were considered: grit blasted and polished. Loading was applied to represent level gait for two million cycles. Computational (finite element) models were generated to the same geometry as the experimental specimens, with residual stress and porosity simulated in the cement mantle. Cement fatigue and creep were modelled over a simulated two million cycles. For the polished stem surface finish, the predicted fracture locations in the finite element models closely matched those on the experimental specimens, and the recorded stem displacements were also comparable. For the grit blasted stem surface finish, no cement mantle fractures were predicted by the computational method, which was again in agreement with the experimental results. It was concluded that the computational method was capable of predicting cement mantle fracture and subsequent stem displacement for the structure considered.

    Title Hierarchical Regulation of Mitochondrion-dependent Apoptosis by Bcl-2 Subfamilies.
    Date January 2007
    Journal Nature Cell Biology
    Excerpt

    Although the BCL-2 family constitutes a crucial checkpoint in apoptosis, the intricate interplay between these family members remains elusive. Here, we demonstrate that BIM and PUMA, similar to truncated BID (tBID), directly activate BAX-BAK to release cytochrome c. Conversely, anti-apoptotic BCL-2-BCL-X(L)-MCL-1 sequesters these 'activator' BH3-only molecules into stable complexes, thus preventing the activation of BAX-BAK. Extensive mutagenesis of BAX-BAK indicates that their activity is not kept in check by BCL-2-BCL-X(L)-MCL-1. Anti-apoptotic BCL-2 members are differentially inactivated by the remaining 'inactivator' BH3-only molecules including BAD, NOXA, BMF, BIK/BLK and HRK/DP5. BAD displaces tBID, BIM or PUMA from BCL-2-BCL-X(L) to activate BAX-BAK, whereas NOXA specifically antagonizes MCL-1. Coexpression of BAD and NOXA killed wild-type but not Bax, Bak doubly deficient cells or Puma deficient cells with Bim knockdown, indicating that activator BH3-only molecules function downstream of inactivator BH3-only molecules to activate BAX-BAK. Our data establish a hierarchical regulation of mitochondrion-dependent apoptosis by various BCL-2 subfamilies.

    Title Targeted Deletion of Puma Attenuates Cardiomyocyte Death and Improves Cardiac Function During Ischemia-reperfusion.
    Date July 2006
    Journal American Journal of Physiology. Heart and Circulatory Physiology
    Excerpt

    The p53-upregulated modulator of apoptosis (Puma), a BH3-only member of the Bcl-2 protein family, is required for p53-dependent and -independent forms of apoptosis and has been implicated in the pathomechanism of several diseases, including cancer, acquired immunodeficiency syndrome, and ischemic brain disease. The role of Puma in cardiomyocyte death, however, has not been analyzed. On the basis of the ability of Puma to integrate diverse cell death stimuli, we hypothesized that Puma might be critical for cardiomyocyte death upon ischemia-reperfusion (I/R) of the heart. Here we show that hypoxia-reoxygenation of isolated cardiomyocytes led to an increase in Puma mRNA and protein levels. Moreover, if Puma was delivered by an adenoviral construct, cardiomyocytes died by apoptosis. Under ATP-depleted conditions, however, Puma overexpression primarily induced necrosis, suggesting that Puma is involved in the development of both types of cell death. Consistent with these findings, targeted deletion of Puma in a mouse model attenuated both apoptosis and necrosis. When the Langendorff ex vivo I/R model was used, infarcts were approximately 50% smaller in Puma(-/-) than in wild-type mice. As a result, after I/R, cardiac function was significantly better preserved in Puma(-/-) mice than in their wild-type littermates. Our study thus establishes Puma as an essential mediator of cardiomyocyte death upon I/R injury and offers a novel therapeutic target to limit cell loss in ischemic heart disease.

    Title On the Importance of Considering Porosity when Simulating the Fatigue of Bone Cement.
    Date October 2005
    Journal Journal of Biomechanical Engineering
    Excerpt

    Fatigue cracking in the cement mantle of total hip replacement has been identified as a possible cause of implant loosening. Retrieval studies and in vitro tests have found porosity in the cement may facilitate fatigue cracking of the mantle. The fatigue process has been simulated computationally using a finite element/continuum damage mechanics (FE/CDM) method and used as a preclinical testing tool, but has not considered the effects of porosity. In this study, experimental tensile and four-point bend fatigue tests were performed. The tensile fatigue S-N data were used to drive the computational simulation (FE/CDM) of fatigue in finite element models of the tensile and four-point bend specimens. Porosity was simulated in the finite element models according to the theory of elasticity and using Monte Carlo methods. The computational fatigue simulations generated variability in the fatigue life at any given stress level, due to each model having a unique porosity distribution. The fracture site also varied between specimens. Experimental validation was achieved for four-point bend loading, but only when porosity was included. This demonstrates that the computational simulation of fatigue, driven by uniaxial S-N data can be used to simulate nonuniaxial loadcases. Further simulations of bone cement fatigue should include porosity to better represent the realities of experimental models.

    Title Damage Accumulation, Fatigue and Creep Behaviour of Vacuum Mixed Bone Cement.
    Date July 2005
    Journal Biomaterials
    Excerpt

    The behaviour of bone cement under fatigue loading is of interest to assess the long-term in vivo performance. In this study, uniaxial tensile fatigue tests were performed on CMW-1 bone cement. Acoustic emission sensors and an extensometer were attached to monitor damage accumulation and creep deformation respectively. The S-N data exhibited the scatter synonymous with bone cement fatigue, with large pores generally responsible for premature failure; at 20 MPa specimens failed between 2 x 10(3) and 2 x 10(4) load cycles, while at 7 MPa specimens failed from 3 x 10(5) load cycles but others were still intact after 3 x 10(6) load cycles. Acoustic emission data revealed a non-linear accumulation of damage with respect to time, with increasing non-linearity at higher stress levels. The damage accumulation process was not continuous, but occurred in bursts separated by periods of inactivity. Damage in the specimen was located by acoustic emissions, and allowed the failure site to be predicted. Acoustic emission data were also used to predict when failure was not imminent. When this was the case at 3 million load cycles, the tests were terminated. Creep strain was plotted against the number of load cycles and a linear relationship was found when a double logarithmic scale was employed. This is the first time a brand of cement has been characterised in such detail, i.e. fatigue life, creep and damage accumulation. Results are presented in a manner that allows direct comparison with published data for other cements. The data can also be used to characterise CMW-1 in computational simulations of the damage accumulation process. Further evidence is provided for the condition-monitoring capabilities of the acoustic emission technique in orthopaedic applications.

    Title Puma is an Essential Mediator of P53-dependent and -independent Apoptotic Pathways.
    Date May 2004
    Journal Cancer Cell
    Excerpt

    Puma encodes a BH3-only protein that is induced by the p53 tumor suppressor and other apoptotic stimuli. To assess its physiological role in apoptosis, we generated Puma knockout mice by gene targeting. Here we report that Puma is essential for hematopoietic cell death triggered by ionizing radiation (IR), deregulated c-Myc expression, and cytokine withdrawal. Puma is also required for IR-induced death throughout the developing nervous system and accounts for nearly all of the apoptotic activity attributed to p53 under these conditions. These findings establish Puma as a principal mediator of cell death in response to diverse apoptotic signals, implicating Puma as a likely tumor suppressor.

    Title P53-independent Functions of the P19(arf) Tumor Suppressor.
    Date October 2000
    Journal Genes & Development
    Excerpt

    The p19(ARF) tumor suppressor antagonizes Mdm2 to induce p53-dependent cell cycle arrest. Individual TKO (triple knock out) mice nullizygous for ARF, p53, and Mdm2 develop multiple tumors at a frequency greater than those observed in animals lacking both p53 and Mdm2 or p53 alone, demonstrating that p19(ARF) can act independently of the Mdm2-p53 axis in tumor surveillance. Reintroduction of ARF into TKO mouse embryo fibroblasts (MEFs), but not into those lacking both p53 and ARF, arrested the cell division cycle in the G1 phase. Inhibition of the retinoblastoma protein had no effect on the ability of ARF to arrest TKO MEFs. Thus, in the absence of Mdm2, p19(ARF) interacts with other targets to inhibit cell proliferation.

    Title The Role of C5 and T-cell Receptor Vb Genes in Susceptibility to Collagen-induced Arthritis.
    Date August 1991
    Journal Immunogenetics
    Excerpt

    Collagen-induced arthritis (CIA) is a rodent arthritis model in which immunization with heterologous type II collagen induces an inflammatory polyarthritis. Susceptibility to the disease is mediated by major histocompatibility complex (MHC) genes as well as genes at other loci. Previous studies of the SWR/J mouse strain, which is resistant to CIA despite bearing the susceptible H-2q haplotype, have suggested that this resistance is the result of a deletion of T-cell receptor (Tcr) Vb gene segments which is carried by this strain. Other studies have implicated a deficiency in complement component C5 as the cause for the resistance. In order to assess the relative importance of these two genes in susceptibility to CIA, and to provide an estimate of the number of independent genes involved in the disease, we analyzed 196 F2 progeny of a (DBA/1 x SWR/J) cross for arthritis susceptibility, and expression of both C5 and Tcr genes. Thirty of the F2 progeny developed arthritis. All of the arthritic mice had at least one copy of the wild-type C5 allele, while the Tcr-Vb haplotypes were distributed in Mendelian fashion. These results demonstrate that C5 sufficiency is an absolute requirement for CIA, but that Tcr-Vb genes located within the SWR deletion have little influence. Genetic analysis of the incidence rate suggests that there is polygenic control of susceptibility to CIA and that in addition to H-2, 5-6 other independent loci (including C5) may be involved.

    Title Measurement of Hospital Cost Variation: Case Mix, Service Intensity, and Input Productivity Factors.
    Date August 1975
    Journal Health Services Research
    Title A Critique of the Hew "white Paper" on Health Care Economics.
    Date June 1975
    Journal Hospital Progress
    Title Medical Services--demand Versus Need and the Concept of Shortage: Rejoinder.
    Date February 1974
    Journal American Journal of Public Health
    Title On the Demand Versus Need for Medical Services and the Concept of "shortage".
    Date March 1971
    Journal American Journal of Public Health
    Title Quantum Optics of Traveling-wave Attenuators and Amplifiers.
    Date
    Journal Physical Review. A
    Title Crack Initiation Processes in Acrylic Bone Cement.
    Date
    Journal Journal of Biomedical Materials Research. Part A
    Excerpt

    A major constraint in improving the understanding of the micromechanics of the fatigue failure process and, hence, in optimizing bone cement performance is found in the uncertainties associated with monitoring the evolution of the internal defects that are believed to dominate in vivo failure. The present study aimed to synthesize high resolution imaging with complementary damage monitoring/detection techniques. As a result, evidence of the chronology of failure has been obtained. The earliest stages of crack initiation have been captured and it is proposed that, in the presence of a pore, crack initiation may occur away from the pore due to the combined influence of pore morphology and the presence of defects within regions of stress concentration. Furthermore, experimental evidence shows that large agglomerations of BaSO(4) are subject to microcracking during fatigue, although in the majority of cases, these are not the primary cause of failure. It is proposed that cracks may then remain contained within the agglomerations because of the clamping effect of the matrix during volumetric shrinkage upon curing. (c) 2008 Wiley Periodicals, Inc. J Biomed Mater Res, 2008.


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