Internists, Cardiologist (heart)
15 years of experience

Northwest Dallas
UT Southwestern Medical Center
5939 Harry Hines Blvd
Ste 935
Dallas, TX 75235
214-645-5505
Locations and availability (1)

Education ?

Medical School
Ain Shams University (1995)
Foreign school

Awards & Distinctions ?

Associations
American Board of Internal Medicine

Affiliations ?

Dr. Sadek is affiliated with 5 hospitals.

Hospital Affilations

Score

Rankings

  • Medical Center Of Arlington
    Cardiology
    3301 Matlock Rd, Arlington, TX 76015
    • Currently 4 of 4 crosses
    Top 25%
  • UT Southwestern University Hospital - Zale Lipshy
    5151 Harry Hines Blvd, Dallas, TX 75235
    • Currently 4 of 4 crosses
    Top 25%
  • Parkland Health & Hospital System
    Cardiology
    5201 Harry Hines Blvd, Dallas, TX 75235
    • Currently 4 of 4 crosses
    Top 25%
  • UT Southwestern University Hospital - St. Paul
    Cardiology
    5909 Harry Hines Blvd, Dallas, TX 75235
    • Currently 2 of 4 crosses
  • UT Southwestern St. Paul Hospital
  • Publications & Research

    Dr. Sadek has contributed to 12 publications.
    Title Transient Regenerative Potential of the Neonatal Mouse Heart.
    Date March 2011
    Journal Science (new York, N.y.)
    Excerpt

    Certain fish and amphibians retain a robust capacity for cardiac regeneration throughout life, but the same is not true of the adult mammalian heart. Whether the capacity for cardiac regeneration is absent in mammals or whether it exists and is switched off early after birth has been unclear. We found that the hearts of 1-day-old neonatal mice can regenerate after partial surgical resection, but this capacity is lost by 7 days of age. This regenerative response in 1-day-old mice was characterized by cardiomyocyte proliferation with minimal hypertrophy or fibrosis, thereby distinguishing it from repair processes. Genetic fate mapping indicated that the majority of cardiomyocytes within the regenerated tissue originated from preexisting cardiomyocytes. Echocardiography performed 2 months after surgery revealed that the regenerated ventricular apex had normal systolic function. Thus, for a brief period after birth, the mammalian heart appears to have the capacity to regenerate.

    Title The Distinct Metabolic Profile of Hematopoietic Stem Cells Reflects Their Location in a Hypoxic Niche.
    Date December 2010
    Journal Cell Stem Cell
    Excerpt

    Bone marrow transplantation is the primary therapy for numerous hematopoietic disorders. The efficiency of bone marrow transplantation depends on the function of long-term hematopoietic stem cells (LT-HSCs), which is markedly influenced by their hypoxic niche. Survival in this low-oxygen microenvironment requires significant metabolic adaptation. Here, we show that LT-HSCs utilize glycolysis instead of mitochondrial oxidative phosphorylation to meet their energy demands. We used flow cytometry to identify a unique low mitochondrial activity/glycolysis-dependent subpopulation that houses the majority of hematopoietic progenitors and LT-HSCs. Finally, we demonstrate that Meis1 and Hif-1alpha are markedly enriched in LT-HSCs and that Meis1 regulates HSC metabolism through transcriptional activation of Hif-1alpha. These findings reveal an important transcriptional network that regulates HSC metabolism.

    Title Bone-marrow-derived Side Population Cells for Myocardial Regeneration.
    Date October 2010
    Journal Journal of Cardiovascular Translational Research
    Excerpt

    Bone-marrow-derived stem cells have displayed the potential for myocardial regeneration in animal models as well as in clinical trials. Unfractionated bone marrow mononuclear cell (MNC) population is a heterogeneous group of cells known to include a number of stem cell populations. Cells in the side population (SP) fraction have a high capacity for differentiation into multiple lineages. In the current study, we investigated the role of murine and human bone-marrow-derived side population cells in myocardial regeneration. In these studies, we show that mouse bone-marrow-derived SP cells expressed the contractile protein, alpha-actinin, following culture with neonatal cardiomyocytes and after delivery into the myocardium following injury. Moreover, the number of green-fluorescent-protein-positive cells, of bone marrow side population origin, increased progressively within the injured myocardium over 90 days. Transcriptome analysis of these bone marrow cells reveals a pattern of expression consistent with immature cardiomyocytes. Additionally, the differentiation capacity of human granulocyte colony-stimulating factor stimulated peripheral blood stem cells were assessed following injection into injured rat myocardium. Bone marrow mononuclear cell and side population cells were both readily identified within the rat myocardium 1 month following injection. These human cells expressed human-specific cardiac troponin I as determined by immunohistochemistry as well as numerous cardiac transcripts as determined by polymerase chain reaction. Both human bone marrow mononuclear cells and human side population cells augmented cardiac systolic function following a modest drop in function as a result of cryoinjury. The augmentation of cardiac function following injection of side population cells occurred earlier than with bone marrow mononuclear cells despite the fact that the number of side population cells used was one tenth that of bone marrow mononuclear cells (9 x 10(5) cells per heart in the MNC group compared to 9 x 10(4) per heart in the SP group). These results support the hypotheses that rodent and human-bone-marrow derived side population cells are capable of acquiring a cardiac fate and that human bone-marrow-derived side population cells are superior to unfractionated bone marrow mononuclear cells in augmenting left ventricular systolic function following cryoinjury.

    Title Letter by Sadek and Garry Regarding Article, "iron-oxide Labeling and Outcome of Transplanted Mesenchymal Stem Cells in the Infarcted Myocardium".
    Date April 2008
    Journal Circulation
    Title Real Time Embolization of a Mitral Valve Vegetation.
    Date October 2007
    Journal Echocardiography (mount Kisco, N.y.)
    Title Rheumatic Manifestations of Psoriasis.
    Date June 2007
    Journal Clinical Rheumatology
    Excerpt

    Psoriatic arthritis was described as a distinct rheumatic disease in the 1960s, and subsequently grouped among the spondyloarthropathies. Recently, other rheumatic manifestations of psoriasis, such as enthesopathy and osteoperiostitis, were recognized. This study attempts to examine the rheumatological and radiological manifestations of Psoriasis and their association with skin and nail disease. Eighty-one psoriatic outpatients were interviewed consecutively during 6 months. Questionnaires and indices were carried out to assess the extent and severity of skin and nail involvement, as well as the activity and severity of peripheral and axial rheumatic manifestations. Radiological examination of the hands, feet, spine and pelvis was also done for all patients. Fifty-nine psoriatic outpatients (73%) had rheumatic manifestations clinically and/or radiologically (Psoriatic arthropathy "PsA"). Clinical peripheral arthritis was found in 14 (23.7%) of the patients with PsA, being oligoarticular in 11, polyarticular in two, and exclusively of the distal interphalangeal (DIP) joints in one patient. Sacroiliitis and/or spondylitis were found in 38 (64.4%), enthesopathy in 36 (61%), dactylitis in two (3.3%), radiological DIP involvement in 24 (40.6%), and radiological osteoperiostitis in 49 (83%) of patients with PsA. Most PsA patients had more than one rheumatic manifestation, while four patients (6.7%) had isolated enthesopathy without any other rheumatic manifestations. Subungual hyperkeratosis of the nails was significantly correlated with PsA (p<0.05), as well as with clinical arthritis, enthesopathy, and DIP involvement (p<0.01), while other types of skin and nail lesions were correlated with selected rheumatic manifestations. The performance of existing criteria for PsA was poor, as individual sets favored either sensitivity or specificity. Psoriatic arthropathy (PsA), occurring in about three-quarters of hospital outpatients with psoriasis, is more common than previously thought. More sensitive and specific criteria for the diagnosis and classification of PsA need to be developed, taking into account the recently described clinical and radiological manifestations.

    Title Inhibition of Cardiac Mitochondrial Respiration by Salicylic Acid and Acetylsalicylate.
    Date May 2005
    Journal Journal of Cardiovascular Pharmacology
    Excerpt

    Acetylsalicylate, the active ingredient in aspirin, has been shown to be beneficial in the treatment and prevention of cardiovascular disease. Because of the increasing frequency with which salicylates are used, it is important to more fully characterize extra- and intracellular processes that are altered by these compounds. Evidence is provided that treatment of isolated cardiac mitochondria with salicylic acid and to a lesser extent acetylsalicylate resulted in an increase in the rate of uncoupled respiration. In contrast, both compounds inhibited ADP-dependent NADH-linked (state 3) respiration to similar degrees. Under the conditions of our experiments, loss in state 3 respiration resulted from inhibition of the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase (KGDH). Kinetic analysis indicates that salicylic acid acts as a competitive inhibitor at the alpha-ketoglutarate binding site. In contrast, acetylsalicylate inhibited the enzyme in a noncompetitive fashion consistent with interaction with the alpha-ketoglutarate binding site followed by enzyme-catalyzed acetylation. The effects of salicylic acid and acetylsalicylate on cardiac mitochondrial function may contribute to the known cardioprotective effects of therapeutic doses of aspirin, as well as to the toxicity associated with salicylate overdose.

    Title Action of Some Micronutrients on the Infestation and Yield Components of Faba Bean by the Aphid, Aphis Craccivora Koch (aphididae, Homoptera) and the Leaf Miner, Liriomyza Trifolii (burgess) (agromyzidae, Diptera).
    Date April 2005
    Journal Communications in Agricultural and Applied Biological Sciences
    Excerpt

    Field experiments were carried out in the two growing seasons of 1999/2000 and 2000/2001 on faba bean (Vicia faba) plants in the Experimental Farm of Agriculture Research Station at Nubaria region, Alexandria, which is considered as a newly reclaimed calcareous soil. The present investigation aimed to evaluate the effect of spraying faba bean plants with certain micronutrients, i.e. Iron, Manganese and Zinc either in single double or triple combinations on the infestation by the aphid, Aphis craccivora Koch (Aphididae, Homoptera) and the leaf miner, Liriomyza trfolü (Burgess) (Agromyzidae, Diptera). The infestation by these insects was assessed using the parameters of Infestation grades as well as the injury indices. Faba bean plants cv. Giza Blanca were sprayed twice (45 and 66 days) after planting with the above-mentioned micronutrients. However, results of this investigation showed, with no doubt, that Mn, Zn and Fe individually or in double or triple combinations have increased to varied extents the infestation rates (%) of faba bean plants compared to the untreated ones. Such varied increases were mainly due to the metabolic roles of the used foliar sprays and their interactions, which indirectly affect the physio-biological actions of plants that may render them suitable for either A. craccivora or L. trifoii reproduction. This phenomenon might be also due to the different environmental factors. In both seasons, the relationship between nutrients applications and pests Infestation followed the same trend of increase in the percentages of infested plants. This assures and confirms the constant metabolic roles of such micronutrients. The biological seed weight (ton/fed.) was positively affected by the application of the used micronutrients. It is worth mentioning that the maximum response was observed in case of the triple treatment followed by the double and single treatments in a descending order. Application of the investigated micronutrients alone or in mixtures resulted in significant increases in yield and its components. Such increases were due to the fact that ions of Zn, Fe and Mn are cofactors of several enzymes, but rarely if ever with a high degree of specificity.

    Title Modulation of Mitochondrial Complex I Activity by Reversible Ca2+ and Nadh Mediated Superoxide Anion Dependent Inhibition.
    Date September 2004
    Journal Biochemistry
    Excerpt

    Complex I, a key component of the mitochondrial respiratory chain, exhibits diminished activity as a result of cardiac ischemia/reperfusion. Cardiac ischemia/reperfusion is associated with increases in the levels of mitochondrial Ca(2+) and pro-oxidants. In the current in vitro study, we sought evidence for a mechanistic link between Ca(2+), pro-oxidants, and inhibition of complex I utilizing mitochondria isolated from rat heart. Our results indicate that addition of Ca(2+) to solubilized mitochondria results in loss in complex I activity. Ca(2+) induced a maximum decrease in complex I activity of approximately 35% at low micromolar concentrations over a narrow physiologically relevant pH range. Loss in activity required reducing equivalents in the form of NADH and was not reversed upon addition of EGTA. The antioxidants N-acetylcysteine and superoxide dismutase, but not catalase, prevented inhibition, indicating the involvement of superoxide anion (O2(*-)) in the inactivation process. Importantly, the sulfhydryl reducing agent DTT was capable of fully restoring complex I activity implicating the formation of sulfenic acid and/or disulfide derivatives of cysteine in the inactivation process. Finally, complex I can reactivate endogenously upon Ca(2+) removal if NADH is present and the enzyme is allowed to turnover catalytically. Thus, the present study provides a mechanistic link between three alterations known to occur during cardiac ischemia/reperfusion, mitochondrial Ca(2+) accumulation, free radical production, and complex I inhibition. The reversibility of these processes suggests redox regulation of Ca(2+) handling.

    Title Cardiac Ischemia/reperfusion, Aging, and Redox-dependent Alterations in Mitochondrial Function.
    Date January 2004
    Journal Archives of Biochemistry and Biophysics
    Title Selective Inactivation of Redox-sensitive Mitochondrial Enzymes During Cardiac Reperfusion.
    Date November 2002
    Journal Archives of Biochemistry and Biophysics
    Excerpt

    Reperfusion of ischemic myocardial tissue results in an increase in mitochondrial free radical production and declines in respiratory activity. The effects of ischemia and reperfusion on the activities of Krebs cycle enzymes, as well as enzymes involved in electron transport, were evaluated to provide insight into whether free radical events are likely to affect enzymatic and mitochondrial function(s). An in vivo rat model was utilized in which ischemia is induced by ligating the left anterior descending coronary artery. Reperfusion, initiated by release of the ligature, resulted in a significant decline in NADH-linked ADP-dependent mitochondrial respiration as assessed in isolated cardiac mitochondria. Assays of respiratory chain complexes revealed reduction in the activities of complex I and, to a lesser extent, complex IV exclusively during reperfusion, with no alterations in the activities of complexes II and III. Moreover, Krebs cycle enzymes alpha-ketoglutarate dehydrogenase and aconitase were susceptible to reperfusion-induced inactivation with no decline in the activities of other Krebs cycle enzymes. The decline in alpha-ketoglutarate dehydrogenase activity during reperfusion was associated with a loss in native lipoic acid on the E2 subunit, suggesting oxidative inactivation. Inhibition of complex I in vitro promotes free radical generation. alpha-Ketoglutarate dehydrogenase and aconitase are uniquely susceptible to in vitro oxidative inactivation. Thus, our results suggest a scenario in which inhibition of complex I promotes free radical production leading to oxidative inactivation of alpha-ketoglutarate dehydrogenase and aconitase.

    Title Oxidative Modification and Inactivation of the Proteasome During Coronary Occlusion/reperfusion.
    Date September 2001
    Journal The Journal of Biological Chemistry
    Excerpt

    Restoration of blood flow to ischemic myocardial tissue results in an increase in the production of oxygen radicals. Highly reactive, free radical species have the potential to damage cellular components. Clearly, maintenance of cellular viability is dependent, in part, on the removal of altered protein. The proteasome is a major intracellular proteolytic system which degrades oxidized and ubiquitinated forms of protein. Utilizing an in vivo rat model, we demonstrate that coronary occlusion/reperfusion resulted in declines in chymotrypsin-like, peptidylglutamyl-peptide hydrolase, and trypsin-like activities of the proteasome as assayed in cytosolic extracts. Analysis of purified 20 S proteasome revealed that declines in peptidase activities were accompanied by oxidative modification of the protein. We provide conclusive evidence that, upon coronary occlusion/reperfusion, the lipid peroxidation product 4-hydroxy-2-nonenal selectively modifies 20 S proteasome alpha-like subunits iota, C3, and an isoform of XAPC7. Occlusion/reperfusion-induced declines in trypsin-like activity were largely preserved upon proteasome purification. In contrast, loss in chymotrypsin-like and peptidylglutamyl-peptide hydrolase activities observed in cytosolic extracts were not evident upon purification. Thus, decreases in proteasome activity are likely due to both direct oxidative modification of the enzyme and inhibition of fluorogenic peptide hydrolysis by endogenous cytosolic inhibitory protein(s) and/or substrate(s). Along with inhibition of the proteasome, increases in cytosolic levels of oxidized and ubiquitinated protein(s) were observed. Taken together, our findings provide insight into potential mechanisms of coronary occlusion/reperfusion-induced proteasome inactivation and cellular consequences of these events.


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