Browse Health
Surgical Specialist
18 years of experience
Video profile
Accepting new patients

Education ?

Medical School Score
Texas Tech University (1992)
  • Currently 2 of 4 apples

Awards & Distinctions ?

Associations
American Board of Surgery

Affiliations ?

Dr. Deeb is affiliated with 9 hospitals.

Hospital Affilations

Score

Rankings

  • Covenant Medical Center
    3615 19th St, Lubbock, TX 79410
    • Currently 4 of 4 crosses
    Top 25%
  • Lubbock Heart Hospital
    4810 N Loop 289, Lubbock, TX 79416
    • Currently 4 of 4 crosses
    Top 25%
  • Covenant Children's Hospital
    3610 21st St, Lubbock, TX 79410
    • Currently 2 of 4 crosses
  • Covenant Hospital Levelland
    1900 College Ave, Levelland, TX 79336
    • Currently 2 of 4 crosses
  • Covenant Hospital Plainview
    2601 Dimmitt Rd, Plainview, TX 79072
    • Currently 1 of 4 crosses
  • University Medical Center - Lubbock
  • Swat Surgical Associates
  • Lincoln County Medical Center
  • University Medical Center
  • Publications & Research

    Dr. Deeb has contributed to 6 publications.
    Title Pentoxifylline Ameliorates Lithium-pilocarpine Induced Status Epilepticus in Young Rats.
    Date July 2008
    Journal Epilepsy & Behavior : E&b
    Excerpt

    The neuroprotective effects of pentoxifylline (PTX) against lithium-pilocarpine (Li-Pc)-induced status epilepticus (SE) in young rats are described. Animals treated with PTX (0, 20, 40, and 60 mg/kg) before induction of SE were examined for latency to and frequency of SE, behavioral changes, oxidative stress, neurochemical alterations in the hippocampus and striatum, and histological abnormalities in the hippocampus. Treatment with PTX significantly ameliorated the frequency and severity of epileptic seizures in a dose-dependent manner. Our behavioral studies using the elevated plus-maze, rotarod, and water maze tests suggested a significant reduction in anxiety, enhanced motor performance, and improved learning and memory in PTX-treated rats. Li-Pc-induced neuronal cell loss and sprouting of mossy fibers in the hippocampus were also attenuated by PTX. The neuroprotective activity of PTX was accompanied by reduction in oxidative stress and reversal of SE-induced depletion of dopamine and 5-hydroxytryptamine in hippocampus and striatum. The results of this study provide a good rationale to explore the prophylactic/therapeutic potential of PTX in SE.

    Title Heuristic Haptic Texture for Surgical Simulations.
    Date November 2004
    Journal Studies in Health Technology and Informatics
    Excerpt

    Generation of credible force feedback renderings adds the sense of touch crucial for the development of a realistic virtual surgical environment. However, a number of difficulties must be overcome before this can be achieved. One of the problems is the paucity of data on the in-vivo tissue compliance properties needed to generate acceptable output forces. Without this "haptic texture," the sense of touch component remains relatively primitive and unrealistic. Current research in the quantitative analysis of biomechanics of living tissue, including collection of in-vivo tissue compliance data using specialized sensors, has made tremendous progress. However, integration of all facets of biomechanical data in order to transfer them into haptic texture remains a very difficult problem. For this reason, we are attempting to create a library of heuristic haptic textures of anatomical structures. The library of heuristic haptic textures will capture the expert's sense of feel for selected anatomical structures and will be used to convey the sense of touch for surgical training simulations. Once the techniques for converting biomechanical data into haptic texture become more robust, this library can be used as a benchmark to verify theoretical computational models used for generating output forces in haptic devices.

    Title Volumetric Virtual Body Structures.
    Date November 2004
    Journal Studies in Health Technology and Informatics
    Excerpt

    Understanding the visuospatial aspects of anatomic structures is one of the most important goals of gross anatomy. Creation of realistic three-dimensional structures of human anatomy has thus been a goal of medical doctors and computer scientists. In this paper, we describe a PC/NT based system in which a user can easily select anatomical structures to be created, along with the chosen connected structures. The system then constructs a three-dimensional volumetric model, a virtual body structure, slice-by-slide. Once the virtual structure is assembled it is possible to "walk" through the volume with coronal, sagittal, and transverse views, or at any angle. The dynamic nature of the system is unique in that it allows for real time choice of volumetric body structures to be created, their rapid generation, and the ability to manipulate the resulting visualization.

    Title Adrenal Hemorrhage in a Pediatric Burn Patient.
    Date October 2001
    Journal Burns : Journal of the International Society for Burn Injuries
    Excerpt

    Adrenal hemorrhage with subsequent insufficiency is a rare complication in the burn patient. The case of a previously healthy 3-year-old Latin American male who was a victim of child abuse is presented. He suffered a submersion injury in hot water leading to a 45% total body surface area burn. An acute deterioration on the 7th post burn day was unresponsive to standard inotropic support and cardiopulmonary resuscitation. Post mortem examination revealed bilateral adrenal hemorrhage that had not been present 2 days earlier. To the authors' knowledge, this is the first reported case in a pediatric burn patient. The clinical manifestations of adrenal insufficiency vary widely and can be easily confused with sepsis. High index of suspicion is necessary for early diagnosis and treatment. Serum cortisol level should be checked and steroid therapy implemented if sepsis syndrome is unresponsive to standard therapy in this setting. This early intervention may be the key to improved survival of the burn patient with a sudden unexplained deterioration resistant to well established resuscitation methods.

    Title Tolerance to Beta,beta'-iminodipropionitrile (idpn)-induced Neurobehavioural and Vestibular Toxicity in Diabetic Rats.
    Date June 1999
    Journal Journal of Applied Toxicology : Jat
    Excerpt

    The present investigation was undertaken to study the neurotoxic effects of beta,beta'-iminodipropionitrile (IDPN) in normal, diabetic and insulin-treated diabetic rats. Sprague-Dawley male rats were divided into five groups: control, IDPN, diabetes, diabetes plus IDPN and diabetes plus insulin plus IDPN. The diabetes was induced with a single i.p. injection of streptozotocin (50 mg kg(-1)). One month after the induction of diabetes, the rats were treated with IDPN (100 mg kg(-1), i.p.) daily for 11 days. One of the diabetic groups treated with IDPN also received daily injection of insulin (25 U kg(-1), s.c.), 1 h before IDPN. The rats were observed daily for abnormal head movements and circling. The grip strength of the forelimbs was also measured. In the IDPN group the dyskinetic symptoms appeared on the 8th day, whereas the onset of dyskinesia was on the 12th day in IDPN-treated diabetic rats. The incidence and severity of dyskinesia were significantly higher in IDPN-treated normal (non-diabetic) rats as compared to IDPN-treated diabetic rats. The treatment of diabetic rats with insulin normalized striatal dopamine (DA) turnover but partially reversed diabetes-induced protection against IDPN dyskinesia. There was severe degeneration of sensory hair cells in crista ampullaris of IDPN-treated normal rats, whereas the diabetic rats showed significant protection against IDPN-induced vestibular hair cell degeneration. In conclusion, our study clearly demonstrates that diabetic rats are resistant to IDPN-induced neurobehavioural and vestibular toxicity. The results also show that diabetes-induced protection against IDPN-induced dyskinesia can be partially reversed by insulin. The mechanism behind the decreased vulnerability of diabetic animals to IDPN remains to be resolved. Further studies are warranted to investigate this paradoxical phenomenon.

    Title Dipyridamole Potentiates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (mptp)-induced Experimental Parkinsonism in Mice.
    Date
    Journal Parkinsonism & Related Disorders
    Excerpt

    Adenosine is an endogenous neuromodulator which alters neuronal excitability and firing rate. In recent years there has been growing interest in the manipulation of adenosine levels to understand the pathophysiology of various diseases. Dipyridamole (DPM) is a potent adenosine transport inhibitor that causes a several-fold increase in brain adenosine concentration. The present study was undertaken to investigate the effect of DPM on MPTP-induced neurotoxicity. Mice weighing 30 +/- 3 g were administered with MPTP (30 mg/kg, i.p.) daily for 5 days. DPM was given daily 1 h before MPTP in doses of 250, 500 and 1000 mg/kg body weight, (P.O.) respectively, in three different groups of mice for 7 days. Twenty four hours after the last dose of DPM, the animals were observed for neurobehavioral changes including locomotor activity and pole descending time. Immediately after behavioral studies, all the animals were sacrificed and brains were isolated for biochemical studies. The treatment of mice with MPTP or DPM individually produced no significant change in mobility or spasticity; however, the combination of these drugs produced significant bradykinesia. There was no incidence of mortality when the mice were treated with MPTP or DPM individually, though the combination of MPTP and DPM produced significant mortality which was proportional to the doses of the later drug. The treatment of mice with MPTP produced significant depletion of striatal dopamine and glutathione. Concomitant treatment of DPM with MPTP further reduced the striatal glutathione level without affecting dopamine. The result of this study shows the ability of DPM to potentiate MPTP-induced neurobehavioral toxicity and mortality in mice. Further studies are warranted to determine the role of adenosine in experimental and clinical Parkinson's disease.

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