Pulmonologists
31 years of experience
Video profile
Accepting new patients
Pulmonary Medicine Consultants
375 Municipal Dr
Ste 218
Richardson, TX 75080
972-680-0666
Locations and availability (3)

Education ?

Medical School Score
Wayne State University (1979)
  • Currently 1 of 4 apples

Awards & Distinctions ?

Awards  
Castle Connolly's Top Doctors™ (2012 - 2013)
Castle Connolly Top Doctors: Texas™ (2009)
Associations
American Board of Internal Medicine

Affiliations ?

Dr. Foster is affiliated with 16 hospitals.

Hospital Affilations

Score

Rankings

  • Methodist Dallas Medical Center
    Pulmonary Disease
    3500 W Wheatland Rd, Dallas, TX 75237
    • Currently 4 of 4 crosses
    Top 25%
  • Methodist Medical Center
    Pulmonary Disease
    1441 N Beckley Ave, Dallas, TX 75203
    • Currently 3 of 4 crosses
    Top 50%
  • Methodist Richardson Medical Center *
    Pulmonary Disease
    401 W Campbell Rd, Richardson, TX 75080
    • Currently 3 of 4 crosses
    Top 50%
  • North Central Medical Center
    Pulmonary Disease
    4500 Medical Center Dr, McKinney, TX 75069
    • Currently 3 of 4 crosses
    Top 50%
  • Medical Center Of Mckinney *
    Pulmonary Disease
    4500 Medical Center Dr, McKinney, TX 75069
    • Currently 3 of 4 crosses
    Top 50%
  • Medical Center Of Arlington
    Pulmonary Disease
    3301 Matlock Rd, Arlington, TX 76015
    • Currently 3 of 4 crosses
    Top 50%
  • Medical Center Of Plano
    Pulmonary Disease
    3901 W 15th St, Plano, TX 75075
    • Currently 2 of 4 crosses
  • Medical Center Of Lewisville
    Pulmonary Disease
    500 W Main St, Lewisville, TX 75057
    • Currently 2 of 4 crosses
  • Plano Specialty Hospital
    Pulmonary Disease
    1621 Coit Rd, Plano, TX 75075
    • Currently 1 of 4 crosses
  • IHS Hospital at Plano
    Pulmonary Disease
    1621 Coit Rd, Plano, TX 75075
    • Currently 1 of 4 crosses
  • Texas Health Presbyterian Hospital Of Dallas
    Pulmonary Disease
    8200 Walnut Hill Ln, Dallas, TX 75231
    • Currently 1 of 4 crosses
  • Plano Rehabilitation
  • Leland Medical Plaza
    2696 W Walnut St, Garland, TX 75042
  • Reliant Rehab
  • Plano Specialty
  • North Central Medical Center - West Park Campus
    130 S Central Expy, McKinney, TX 75070
  • * This information was reported to Vitals by the doctor or doctor's office.

    Publications & Research

    Dr. Foster has contributed to 10 publications.
    Title Enteropathogenic Escherichia Coli Effector Espf Interacts with Host Protein Abcf2.
    Date June 2007
    Journal Cellular Microbiology
    Excerpt

    Enteropathogenic Escherichia coli (EPEC) is a major causative agent of infant diarrhoea in developing countries. The EspF effector protein is injected from EPEC into host cells via a type III secretion system and is involved in the disruption of host intestinal barrier function. In addition, EspF is sorted to mitochondria and has a role in initiating the mitochondrial death pathway. To clarify the manner in which EspF affects host cells, we sought to identify eukaryotic EspF-binding proteins using affinity purification. Abcf2, a protein of unknown function and member of the ABC-transporter family, bound EspF in this assay. An interaction between EspF and Abcf2 was confirmed in a yeast two-hybrid system, by colocalization and by co-immunoprecipitation from EPEC-infected cells. Levels of Abcf2 were decreased in cells infected with EPEC in an EspF dose-dependent manner. Knock-down of Abcf2 expression by RNA interference increased EspF-induced caspase 9 and caspase 3 cleavage. In addition, Abcf2-knocked down cells showed increased caspase 3 cleavage upon treatment with the apoptosis inducing agent staurosporine. These results indicate that EspF induces or facilitates host cell death by targeting and interfering with the putative protective function of Abcf2.

    Title Silencing of Bak Ameliorates Apoptosis of Human Proximal Tubular Epithelial Cells by Escherichia Coli-derived Shiga Toxin 2.
    Date February 2006
    Journal Infection
    Excerpt

    BACKGROUND: Escherichia coli-derived Shiga toxin (Stx), the cause of the enteropathic hemolytic uremic syndrome, is a potent inducer of apoptotic cell death. The present study was performed to examine the hypothesis that Stx initiates apoptosis by activating the mitochondrial pathway involving mitochondrial-associated, pro-apoptotic Bcl-2 family proteins Bax and Bak. MATERIALS AND METHODS: To determine if Stx2-mediated apoptosis is dependent on Bax or Bak, a gene-silencing approach was employed using sequence-specific small interfering (si)RNA duplexes. Silencing of Bax and Bak protein expression in human renal proximal tubular epithelial (HK-2) cells and its effect on Shiga toxicity was assessed by immunofluorescence microscopy and Western blotting. RESULTS: Transfection of HK-2 cells, shown to be exquisitely sensitive to Stx, with siRNA duplexes successfully diminished Bak, but not Bax protein expression. In order to determine if silencing of pro-apoptotic gene expression affects Stx-induced apoptosis, HK-2 cells were transfected with Bak-specific or control siRNA, exposed to lethal concentrations of Stx2 and assessed for cleavage of poly(ADPribose) polymerase-1 (PARP) as a marker of apoptosis, using Western blot technology. We observed that siRNA-induced reduction of Bak expression levels correlated with decreased PARP cleavage. CONCLUSION: Results suggest that Stx-induced cell death involves pro-apoptotic Bak and that silencing of Bak gene expression affords partial protection against Stx-mediated apoptosis.

    Title Macrolide Antibiotics Modulate Erk Phosphorylation and Il-8 and Gm-csf Production by Human Bronchial Epithelial Cells.
    Date January 2006
    Journal American Journal of Physiology. Lung Cellular and Molecular Physiology
    Excerpt

    Macrolide antibiotics decrease proinflammatory cytokine production in airway cells from subjects with chronic airway inflammation. However, in subjects with chronic obstructive pulmonary disease, short-term azithromycin (AZM) therapy causes a transient early increase in the blood neutrophil oxidative burst followed by a decrease in inflammatory markers with longer administration. We studied the effects of clarithromycin (CAM) and AZM on proinflammatory cytokine production from normal human bronchial epithelial (NHBE) cells. CAM decreased IL-8 over the first 6 h and then significantly increased interleukin (IL)-8 at 12-72 h after exposure (P < 0.0001). AZM also increased IL-8 at 24 and 48 h, and CAM increased granulocyte-macrophage colony-stimulating factor at 48 h. In the presence of LPS, both CAM and AZM dose-dependently increased IL-8 secretion over 24 h, but after 5 days of exposure to 10 microg/ml CAM there is suppression of IL-8 (P < 0.001). PD-98059, an inhibitor of MAP kinase/ERK kinase, inhibited CAM-induced IL-8 (P < 0.0001) and GM-CSF (P < 0.01) release. The p38 MAP kinase inhibitor SB-203580 increased CAM-induced IL-8 release (P < 0.001), and the c-jun NH2-terminal kinase inhibitor SP-600125 had no effect on IL-8. At 120 min and 6 h, CAM increased phospho-ERK1/2 (pERK) but not phospho-p38 or phospho-JNK. Over the first 90 min, CAM at 10 microg/ml inhibited pERK and then increased pERK in parallel with measured IL-8 secretion. After daily CAM exposure for 5 days, both IL-8 and pERK returned to baseline. The p38 MAP kinase inhibitor, SB-203580 increased ERK phosphorylation and IL-8 secretion. These results suggest that macrolide antibiotics can differentially modulate proinflammatory cytokine secretion in NHBE cells, in part through ERK.

    Title Verotoxin (shiga Toxin) Sensitizes Renal Epithelial Cells to Increased Heme Toxicity: Possible Implications for the Hemolytic Uremic Syndrome.
    Date February 2005
    Journal Journal of the American Society of Nephrology : Jasn
    Excerpt

    Escherichia coli-derived verotoxins (VT; Shiga toxins) are causally related to the pathogenesis of enteropathic hemolytic uremic syndrome (HUS). Profound hemolysis is a defining feature of the disease, but it is not known whether the acute intravascular release of heme proteins contributes to HUS pathology. This study examined the biologic effects of hemin and VT by means of tubular epithelial-derived ACHN cells. Hemin at concentrations >/=200 microM caused cell rounding, spike formation, and detachment that was morphologically distinct from verocytotoxicity. VT caused apoptosis at concentrations >100 pM, as demonstrated by nuclear segmentation and poly(ADP-ribose) polymerase cleavage, whereas hemin-mediated injury of ACHN cells grown in serum-containing medium lacked attributes of programmed cell death. Pretreatment of ACHN monolayers with sublethal concentrations (1 to 10 pM) of VT for 12 to 18 h led to superadditive hemin-mediated cytotoxicity. This effect was not limited to ACHN cells, but was similarly noted in microvascular endothelial cells. Heme catabolism is regulated by (inducible) heme oxygenase-1 (HO-1). VT abrogated HO-1 expression in ACHN cells. Stimulation of cells for 6 h with CdCl(2), which markedly increased HO-1 expression before the addition of VT, blunted subsequent hemin injury. In conclusion, VT augments hemin-induced toxicity in renal tubular epithelial cells that can be reversed by prior induction of HO-1. It is proposed that VT subverts the physiologic defense against heme proteins by interfering with the regulated expression of HO-1 and that this mechanism contributes to the renal pathology in patients with Escherichia coli-associated HUS.

    Title Shiga Toxin 1-induced Activation of C-jun Nh(2)-terminal Kinase and P38 in the Human Monocytic Cell Line Thp-1: Possible Involvement in the Production of Tnf-alpha.
    Date January 2002
    Journal Journal of Leukocyte Biology
    Excerpt

    Shiga toxin-producing enterohemorrhagic E. coli infections cause bloody diarrhea, which may progress to life-threatening complications such as the hemolytic-uremic syndrome (HUS). HUS patients frequently have elevated levels of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) detectable in urine. Thus, sequelae may develop following the localized production of proinflammatory cytokines within the kidneys. A possible source of these cytokines are macrophages, which respond to the toxins by producing TNF-alpha. We have shown previously that THP-1 cells produce soluble TNF-alpha in response to the toxins, whose production requires host-cell tyrosine-kinase activity and toxin-enzymatic activity. To further examine signaling pathways involved in TNF-alpha expression, we determined that JNK1 and -2 and p38, but not ERK1 or -2, were phosphorylated following toxin exposure. Blockade of p38 activation reduced TNF-alpha production following Shiga toxin 1 treatment. Finally, we present a model of the ribotoxic stress response triggered in human macrophages by Shiga toxins.

    Title Shiga Toxin-induced Tumor Necrosis Factor Alpha Expression: Requirement for Toxin Enzymatic Activity and Monocyte Protein Kinase C and Protein Tyrosine Kinases.
    Date September 2000
    Journal Infection and Immunity
    Excerpt

    Infections with Shiga toxin (Stx)-producing bacteria cause bloody diarrhea which may progress to life-threatening complications, including acute renal failure and neurological abnormalities. The precise mechanism of disease progression is unclear, although evidence suggests that the localized production of the host proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-1 may exacerbate toxin-mediated vascular damage. Purified Stxs have been demonstrated to elicit proinflammatory cytokine synthesis from human peripheral blood mononuclear cells and monocytic cell lines in vitro. To understand toxin-monocyte interactions required for cytokine synthesis, we have treated differentiated THP-1 cells with purified wild-type toxins, enzymatic mutants, or B subunits and measured TNF-alpha production. Our data suggest that A subunit enzymatic activity is essential for cytokine production. THP-1 cells were treated with a series of protein kinase C (PKC), PKA, and protein tyrosine kinase inhibitors to examine the role of intracellular signaling molecules in Stx-mediated cytokine production. Treatment of cells with PKC and tyrosine kinase inhibitors blocked TNF-alpha secretion by Stx-stimulated THP-1 cells. Stx treatment directly activated PKC, which occurred at a point upstream of transcriptional activation of the gene encoding TNF-alpha.

    Title The Sézary Syndrome with Rapid Pulmonary Dissemination.
    Date August 1985
    Journal Cancer
    Excerpt

    The authors report the case of a patient with long-standing Sézary syndrome who developed the acute onset of bilateral pulmonary infiltration, severe hypoxemia, and hypotension. Initial diagnostic considerations centered around infection, but an open-lung biopsy revealed "mycosis fungoides" without evidence of an infectious process. The patient showed striking improvement when given vincristine and cyclophosphamide, but ultimately died 3 months later of a nonpulmonary catheter-related infection. This rare clinical association stresses the value of open lung biopsy as a diagnostic measure even in desperately ill individuals.

    Title Early Extubation After Coronary Artery Bypass: Brief Report.
    Date January 1985
    Journal Critical Care Medicine
    Excerpt

    We performed a prospective study of early post-coronary artery bypass graft (CABG) ventilator management and weaning. Sixty-three patients were studied consecutively; 27 were managed by the standard post-CABG weaning practice at this institution, and 36 were managed by respiratory therapists using a protocol with specific ventilation and weaning guidelines. The mean time to extubation was decreased by 41% using the protocol. Arterial blood gas sampling was reduced 42%. There were no deaths in either group. Physicians were alerted to problems necessitating interruption of the protocol in six of 36 patients studied. This protocol proved easy to follow and safe in the hands of respiratory therapists. It lowered costs and improved patient comfort.

    Title The Relationship of Respiratory Failure to the Oxygen Consumption Of, Lactate Production By, and Distribution of Blood Flow Among Respiratory Muscles During Increasing Inspiratory Resistance.
    Date February 1977
    Journal The Journal of Clinical Investigation
    Excerpt

    An animal model was developed to determine if blood flow to the respiratory muscles limits oxygen delivery and thus work output during inspiratory resistance. With incremental increases in the rate of work of breathing to 15 times the resting level, blood flow to the diaphragm rose exponentially 26-fold. Blood flow to other inspiratory and a few expiratory muscles increased to a much smaller extent, often only at the greater work loads. Cardiac output and blood pressure did not change. Arterial-venous oxygen content difference across the diaphragm became maximal at low work rates and thereafter all increases in oxygen delivery during higher work rates were accomplished by increments in blood flow. Oxygen consumption of the respiratory musculature calculated by blood flow times oxygen extraction increased exponentially with increasing work of breathing and was less than the increase in total body oxygen consumption at each work load. Hypoxemia and respiratory acidosis occurred when the animals inspired through the highest resistance; blood flow and oxygen consumption were even higher than that observed during previous resistances and there was no evidence of a shift to anaerobic metabolsim in blood lactate and pyruvate levels. Respiratory failure did not appear to be a consequence of insufficient blood flow in this model.

    Title The Uroflowmeter.
    Date May 1972
    Journal Paraplegia

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