H William Strauss

Lucile Packard Children’s Hospital at Stanford, Palo Alto, CA, USA

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Publications (64)363.56 Total impact

  • Article: Attenuation of apoptosis by telmisartan in atherosclerotic plaques of apolipoprotein e-/- mice: evaluation using technetium 99m-annexin a5.
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    ABSTRACT: Technetium 99m (99mTc)-annexin A5, a marker of ongoing apoptosis, is supposed to be useful in the detection of metabolically active atheroma. The aim of this study was to determine the potential of 99mTc-annexin A5 for evaluating the therapeutic effects of an angiotensin II receptor type 1 blocker (ARB) (telmisartan) on atherosclerosis. Male apolipoprotein E-/- mice were divided into telmisartan-treated (3 mg/kg/d, n = 10) and control (n = 10) groups. After 16 to 21 weeks of treatment, 99mTc-annexin A5 was injected and cryostat sections of aortic tissues (n = 10-12/aorta) were prepared. The 99mTc-annexin A5 accumulation level in the plaques was evaluated by autoradiography. Serial sections of the plaques were histologically examined to identify the lesion phenotypes (normal vessels, early lesions, atheromatous lesions, and fibrotic lesions), plaque size, macrophage infiltration levels, and lipid deposition levels. Telmisartan treatment significantly decreased the plaque size (0.05 ± 0.05 vs 0.11 ± 0.08, mm2), macrophage infiltration level (0.02 ± 0.02 vs 0.03 ± 0.02, mm2), lipid deposition level (0.01 ± 0.01 vs 0.02 ± 0.02, mm2), and 99mTc-annexin A5 accumulation level (1.30 ± 1.09 vs 2.15 ± 1.91, × 10-6/g). 99mTc-annexin A5 accumulation levels in the plaques positively correlated with macrophage infiltration (r = .69, p < .05) and lipid deposition (r = .66, p < .05) levels. Apoptosis imaging with 99mTc-annexin A5 may be useful for evaluating the therapeutic effects of ARBs on atherosclerosis.
    Molecular Imaging 08/2013; 12(5):300-9. · 3.18 Impact Factor
  • Article: Recent Advances in the Molecular Imaging of Programmed Cell Death: Part II--Non-Probe-Based MRI, Ultrasound, and Optical Clinical Imaging Techniques.
    Francis G Blankenberg, H William Strauss
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    ABSTRACT: There is much that can be done to detect apoptosis and other forms of cell death with existing clinical modalities including ultrasound, MRI, and optical imaging without the need for current or new intravenous contrast agents. We will discuss how these widely available imaging technologies can readily be applied to the imaging of apoptosis in patients undergoing chemotherapy or radiation treatment. The limiting factor of course is the lack of knowledge of the optimal times after the start of treatment for the most accurate assessment of apoptosis and necrosis with each modality and specific technique. It is hoped that imaging studies that systematically look at treatment response can soon be performed to address these issues.
    Journal of Nuclear Medicine 11/2012; · 6.38 Impact Factor
  • Article: Recent Advances in the Molecular Imaging of Programmed Cell Death: Part I--Pathophysiology and Radiotracers.
    Francis G Blankenberg, H William Strauss
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    ABSTRACT: In humans, apoptosis (programmed cell death) is the most common form of cell death after necrosis. Apoptosis is a series of genetically preprogrammed biochemical and morphologic energy-requiring events that, after a specific external or internal stimulus, results in the physiologic disappearance of a cell via its self-disintegration and packaging of its contents into membrane vesicles called apoptotic bodies. Apoptotic bodies can readily be ingested, with their nutrients and even organelles recycled by neighboring cells or phagocytes without local inflammation. In contrast, necrosis is characterized by the primary loss of plasma membrane integrity and the uncontrolled release of a cell's contents, often causing local inflammation, tissue damage, and scarring. Alternate forms of cell death also exist, associated with specific molecular mechanisms involving enzymes, organelles, genes, external stimuli, or blockade of normal cell proliferation. In this review we will briefly outline the molecular mechanisms of apoptosis that can be imaged with radiotracers now under development.
    Journal of Nuclear Medicine 10/2012; · 6.38 Impact Factor
  • Article: Quantitative Determination of Apoptosis of Pancreatic β-Cells in a Murine Model of Type 1 Diabetes Mellitus.
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    ABSTRACT: Type 1 diabetes mellitus is characterized by a significant deficit in pancreatic β-cell mass, presumably caused by β-cell apoptosis. We investigated the incidence of β-cell apoptosis in streptozotocin-treated mice and nonobese diabetic (NOD) mice with (99m)Tc-annexin A5. Vehicle-treated mice, streptozotocin-treated mice, and NOD mice at the ages of 5, 9, 16, and 20 wk (5-8 mice per group) were injected with (99m)Tc-annexin A5 and sacrificed 6 h later for autoradiography, and the regional (99m)Tc-annexin A5 level in the pancreas was evaluated. Pancreatic islets were identified by insulin immunohistochemical staining, and apoptotic cells were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. The (99m)Tc-annexin A5 level in pancreatic islets was expressed as the percentage injected dose per area of pancreatic islets and normalized by animal body weight (%ID × 10(6)/mm(2)/kg). The level of apoptotic cells in pancreatic islets was expressed as the number of TUNEL-positive cells per area of pancreatic islets (cells/mm(2)). The (99m)Tc-annexin A5 accumulation level was significantly higher (2.5 ± 0.7 vs. 0.7 ± 0.1 %ID × 10(6)/mm(2)/kg, P < 0.05) and the number of TUNEL-positive cells was significantly higher (1,170 ± 535 vs. 5 ± 6 cells/mm(2), P < 0.05) in the pancreatic islets of the streptozotocin-treated mice than in those of the vehicle-treated mice. The (99m)Tc-annexin A5 accumulation level was significantly higher (1.1 ± 0.4 vs. 0.5 ± 0.1 %ID × 10(6)/mm(2)/kg, P < 0.05) and the number of TUNEL-positive cells was significantly higher (152 ± 82 vs. 4 ± 9 cells/mm(2), P < 0.05) in the pancreatic islets of 16-wk-old NOD mice than in those of 5-wk-old NOD mice. In addition, the level of (99m)Tc-annexin A5 correlated with the number of TUNEL-positive cells in the pancreatic islets of the streptozotocin-treated mice (r = 0.821, P < 0.001) and NOD mice (r = 0.721, P < 0.001). There is significant islet cell apoptosis with (99m)Tc-annexin A5 accumulation in the pancreas of both streptozotocin and NOD mice.
    Journal of Nuclear Medicine 08/2012; 53(10):1585-91. · 6.38 Impact Factor
  • Article: Treadmill exercise inducing mild to moderate ischemia has no significant effect on skeletal muscle or cardiac 18F-FDG uptake and image quality on subsequent whole-body PET scan.
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    ABSTRACT: We report the effects of treadmill exercise on (18)F-FDG uptake in skeletal muscles and image quality of torso PET and compare stress myocardial perfusion imaging patterns with myocardial (18)F-FDG uptake. There were 3 groups of patients: 48 patients underwent PET within 8 h after a treadmill test (Ex 8), 45 patients within 48 h after a treadmill test (Ex 48), and 34 patients without prior exercise. Mean workload (8.4 ± 2.3 [Ex 8] vs. 8.9 ± 2.6 metabolic equivalents [Ex 48]) was similar in both exercise groups. Muscle uptake was assessed by standardized uptake value. Myocardial uptake patterns were compared visually. Minor differences between patient groups were noted only for maximum standardized uptake value in quadriceps muscles. There was no correlation between perfusion defects and myocardial (18)F-FDG uptake patterns. Thus, treadmill exercise does not affect muscle (18)F-FDG uptake or image quality on subsequent PET. Cardiac (18)F-FDG uptake on torso PET scans is unrelated to myocardial perfusion status.
    Journal of Nuclear Medicine 05/2012; 53(6):917-21. · 6.38 Impact Factor
  • Article: Myocardial imaging for mitochondrial membrane potential.
    H William Strauss, Heiko Schöder
    JACC. Cardiovascular imaging 03/2012; 5(3):293-6. · 14.29 Impact Factor
  • Article: Myo-Myo: Yes, papa. Eating sugar? No, papa! Modulating the myocardial menu for imaging coronary inflammation...
    Jagat Narula, H William Strauss
    European Journal of Nuclear Medicine 09/2011; 38(11):2014-7. · 4.53 Impact Factor
  • Source
    Article: The Japanese tsunami and resulting nuclear emergency at the Fukushima Daiichi power facility: technical, radiologic, and response perspectives.
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    ABSTRACT: The Fukushima Daiichi nuclear power facility, in the Futaba District of the Fukushima Prefecture in Japan, was severely damaged by the earthquake and ensuing tsunami that struck off the northern coast of the island of Honshu on March 11, 2011. The resulting structural damage to the plant disabled the reactor's cooling systems and led to significant, ongoing environmental releases of radioactivity, triggering a mandatory evacuation of a large area surrounding the plant. The status of the facility continues to change, and permanent control of its radioactive inventory has not yet been achieved. The purpose of this educational article is to summarize the short-term chronology, radiologic consequences, emergency responses, and long-term challenges associated with this event. Although there is ongoing debate on preparedness before the event and the candor of responsible entities in recognizing and disclosing its severity, it largely appears that appropriate key actions were taken by the Japanese authorities during the event that should mitigate any radiologic health impact. These actions include an organized evacuation of over 200,000 inhabitants from the vicinity of the site and areas early in the emergency; monitoring of food and water and placement of radiation limits on such foodstuffs; distribution of stable potassium iodide; and systematic scanning of evacuees. However, the risk of additional fuel damage and of further, perhaps substantial, releases persists. The situation at the Fukushima Daiichi nuclear facility remains fluid, and the long-term environmental and health impact will likely take years to fully delineate.
    Journal of Nuclear Medicine 07/2011; 52(9):1423-32. · 6.38 Impact Factor
  • Article: Mobilizing the fountain of youth within.
    H William Strauss, Josef J Fox
    Journal of Nuclear Cardiology 03/2011; 18(3):396-7. · 2.67 Impact Factor
  • Article: The effect of posttherapy 131I SPECT/CT on risk classification and management of patients with differentiated thyroid cancer.
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    ABSTRACT: The objective of this study was to determine whether posttherapy (131)I SPECT/CT changed the need for additional cross-sectional imaging or modified the American Thyroid Association risk of recurrence classification. We performed planar imaging and SPECT/CT in a consecutive series of patients after (131)I therapy. Planar imaging and SPECT/CT were performed on 148 consecutive patients with thyroid carcinoma (125 papillary, 2 follicular, 8 Hürthle cell, and 13 poorly differentiated) approximately 5 d after the therapeutic administration of 1,739-8,066 MBq (47-218 mCi) of (131)I. The indication for treatment was postsurgical ablation (n = 109) or recurrent or metastatic disease with rising thyroglobulin levels (n = 39). SPECT/CT scans were obtained for all subjects for 1 bed position (38 cm), which included the neck and upper chest. Additional SPECT/CT scans of the abdomen or pelvis were acquired if suggestive findings were noted on planar images. All patients were treated in real time, according to the standard of care in our practice. At that time, clinical decisions regarding thyroid tumor classification were made by our multidisciplinary group based on all data, including operative findings, pathology, imaging, and thyroglobulin levels. In a retrospective analysis, planar and SPECT/CT images were interpreted independently, and sites of uptake were categorized as likely benign, malignant, or equivocal. An experienced thyroid endocrinologist used a combination of surgical histopathology and scan findings to determine whether additional cross-sectional imaging was required and determined if the imaging findings changed the patient's risk category. In 29 patients, 61 additional cross-sectional imaging studies were avoided using SPECT/CT, compared with medical decision making based on the planar images alone. In 7 of 109 postsurgical patients, SPECT/CT findings changed the initial American Thyroid Association risk of recurrence classification. The sensitivity of planar imaging and SPECT/CT for identification of focal (131)I uptake in the thyroid bed was similar in the postsurgical and recurrence cohorts. For metastatic disease in the neck, characterization of (131)I uptake by SPECT/CT in the postsurgical group was significantly better than that by planar scanning (P < 0.01). Among the 109 postsurgical patients, the characterization of iodine uptake in the lung, liver, and bone was also more accurate using SPECT/CT than planar scanning (P < 0.01). The CT portion of SPECT/CT demonstrated non-iodine-avid lesions in 32 of 148 patients. SPECT/CT data provided information that reduced the need for additional cross-sectional imaging in 29 patients (20%) and significantly altered the initial risk of recurrence estimates in 7 of 109 patients (6.4%), thereby altering patient management recommendations with regard to frequency and intensity of follow-up studies.
    Journal of Nuclear Medicine 09/2010; 51(9):1361-7. · 6.38 Impact Factor
  • Article: Metaiodobenzylguanidine imaging comes of age. A new arrow in the prognostic quiver for heart failure patients.
    Journal of the American College of Cardiology 05/2010; 55(20):2222-4. · 14.16 Impact Factor
  • Chapter: Molecular Imaging of Atherosclerotic Plaque Vulnerability: Comparison between 18F-FDG and 99mTc-Annexin A5
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    ABSTRACT: Macrophage infiltration, apoptosis, and lipid deposition greatly contribute to plaque vulnerability. Nuclear imaging provides at least two potential indicators to identify vulnerable plaques: 18F-fluorodeoxyglucose (FDG) as a marker of intraplaque inflammation and 99mTc-annexin A5 as a marker of apoptosis. In this article we summarize our recent study on the comparison of 18F-FDG and 99mTc-annexin A5 uptake in atherosclerotic lesions of the apolipoprotein E knockout (ApoE-/-) mouse, and briefly review previous studies on molecular imaging of atherosclerotic plaques using 18F-FDG and 99mTc-annexin A5. The intralesional distribution of 18F-FDG and 99mTc-annexin A5 was determined in male ApoE-/- mice. The mice were maintained on a high-fat diet after the age of 5 weeks. At 25 weeks. 18F-FDG or 99mTc-annexin A5 was injected and the aortas were harvested. Regional radioactivity distribution was compared in relation to Oil Red O staining. Both 18F-FDG and 99mTc-annexin A5 showed preferential uptakes into atherosclerotic lesions, with higher uptake levels for 18F-FDG than 99mTc-annexin A5. The regional uptake levels of these tracers were significantly correlated with the Oil Red O staining score. The uptake ratios of advanced lesions to early lesions were significantly higher for 99mTc-annexin A5 than for 18F-FDG. Previous studies have indicated that 18F-FDG and 99mTc-annexin A5 are useful for the detection of vulnerable atherosclerotic lesions. Our findings could further characterize these tracers as follows: the high aortic uptake level of 18F-FDG may offer higher sensitivity in lesion detection, whereas the preferential uptake of 99mTc-annexin A5 in advanced lesions suggests its potential for assessing the vulnerability of atherosclerotic plaques.
    12/2009: pages 69-77;
  • Article: One step closer to imaging vulnerable plaque in the coronary arteries.
    Josef J Fox, H William Strauss
    Journal of Nuclear Medicine 05/2009; 50(4):497-500. · 6.38 Impact Factor
  • Article: Resurrection of thallium-201 for myocardial perfusion imaging.
    H William Strauss, Dale Bailey
    JACC. Cardiovascular imaging 04/2009; 2(3):283-5. · 14.29 Impact Factor
  • Article: Prolonged high-fat feeding enhances aortic 18F-FDG and 99mTc-annexin A5 uptake in apolipoprotein E-deficient and wild-type C57BL/6J mice.
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    ABSTRACT: (18)F-FDG, a marker of the enhanced metabolism characteristic of activated inflammatory cells, and (99m)Tc-annexin A5, a marker of apoptosis, are both widely believed to be useful for the imaging of unstable atheroma (rupture-prone vulnerable plaques [VP]). Serum cholesterol functions as a proinflammatory factor, driving the formation of VP, and affects the immune responses of aortic tissues systemically. It is therefore reasonable to postulate that prolonged cholesterol loading may alter the aortic uptake of these tracers. Here, we evaluated the aortic uptake of (18)F-FDG and (99m)Tc-annexin A5 in apolipoprotein E-deficient (apoE(-/-)) and wild-type mice placed on high-fat diets. Male apoE(-/-) and wild-type (C57BL/6J) mice were maintained on high-fat diets after the age of 5 wk. Wild-type mice fed regular chow were used as controls. At the ages of 10, 18, and 25 wk (5-15 mice per group at each time point), mice were injected with (18)F-FDG or (99m)Tc-annexin A5 after 12 h of fasting. At 1 h after (18)F-FDG injection (or 2 h after (99m)Tc-annexin A5 injection), mice were sacrificed, and the aortas were removed for well-type scintillation counting of radioactivity. The results were expressed as percentage injected dose per gram of tissue and normalized by animal body weight [(ID%/g) x kg]. En face staining was then performed to assess the location and size (surface area) of the lipid pool within each aortic specimen. Concurrent blood samples were obtained to determine the plasma lipid profile of each group. No atherosclerotic lesions were found in wild-type mice regardless of the diet, whereas the lesion area progressively increased with age in apoE(-/-) mice. Mean plasma cholesterol levels remained stable with the regular diet in wild-type mice (73-78 mg/dL) but increased with cholesterol feeding in wild-type mice (143-179 mg/dL) and in apoE(-/-) mice (>1,300 mg/dL). Aortic tracer uptake [(ID%/g) x kg] remained stable with the regular diet in wild-type mice (0.054-0.053 and 0.021-0.023 for (99m)Tc-annexin A5) but increased with cholesterol feeding in wild-type mice (0.164 for (18)F-FDG and 0.036 for (99m)Tc-annexin A5 at 25 wk) and in apoE(-/-) mice (0.249 for (18)F-FDG and 0.047 for (99m)Tc-annexin A5 at 25 wk). The accumulation of (18)F-FDG and (99m)Tc-annexin A5 in aortic tissues is influenced not only by the progression of atherosclerotic disease but also by cholesterol loading over time.
    Journal of Nuclear Medicine 10/2008; 49(10):1707-14. · 6.38 Impact Factor
  • Article: Arithmetic of vulnerable plaques for noninvasive imaging.
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    ABSTRACT: Sudden cardiac death and acute myocardial infarction often occur as the first manifestation of coronary artery disease. Otherwise asymptomatic individuals with subclinical atherosclerosis almost always have a classic risk-factor profile and it is essential that they are identified before the occurrence of an acute coronary event. The ability to recognize such individuals requires the development of strategies that can localize unstable atherosclerotic lesions. Plaques that are vulnerable to rupture demonstrate distinct histological characteristics, including large plaque and necrotic core volumes, extensive remodeling of the vessel at the lesion site, and attenuated fibrous caps. Precise metrics of typical vulnerable atherosclerotic plaque dimensions will need to be defined to facilitate their identification by noninvasive imaging modalities.
    Nature Clinical Practice Cardiovascular Medicine 08/2008; 5 Suppl 2:S2-10. · 7.04 Impact Factor
  • Article: Stress myocardial perfusion imaging- the beginning...
    H William Strauss
    JACC. Cardiovascular imaging 04/2008; 1(2):238-40. · 14.29 Impact Factor
  • Article: Molecular imaging of atherosclerosis.
    Mark P S Dunphy, H William Strauss
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    ABSTRACT: Techniques are being developed for clinical molecular imaging of atherosclerosis to identify and characterize vulnerable plaques in each vascular territory. Molecular imaging encompasses multiple imaging modalities that depict cellular and subcellular processes. Molecular imaging can provide a "virtual histology" noninvasively about atherosclerotic disease, characterizing vascular lesions with markers of inflammation, angiogenesis, lipid metabolism, and more.
    Current Cardiology Reports 04/2008; 10(2):121-7.
  • Chapter: Imaging of Apoptosis
    Francis G. Blankenberg, H. William Strauss
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    ABSTRACT: Many diseases are associated with an abnormal increase or decrease in apoptosis (programmed cell death). A variety of newer drugs have been designed to enhance apoptosis (such as cancer therapy) or decrease programmed cell death (such as agents interrupting the immune inflammatory pathway in arthritis). Until recently apoptosis could be assessed only in vitro or by histological assay of biopsied material. To determine the effectiveness of therapy, it would be very helpful to have an in vivo imaging technique. Characteristic changes of apoptosis can be identified by ultrasound, magnetic resonance, and radionuclide approaches. The status of these approaches is outlined in this chapter with possible clinical uses listed in Table 1.
    12/2007: pages 303-316;
  • Article: Radiolabeled Monocyte Chemotactic Protein 1 for the detection of inflammation in experimental atherosclerosis.
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    ABSTRACT: Chemotactic peptides, such as Monocyte Chemotactic Protein 1 (MCP-1), play a key role in transendothelial migration of mononuclear cells during the development and progression of atherosclerotic disease. Because atherosclerotic plaques that are precursors of acute coronary events harbor abundant macrophage infiltration, we hypothesized that the detection of a high concentration of MCP-1 receptors on inflammatory cells should noninvasively identify vulnerable plaques. Atherosclerotic lesions were induced by balloon deendothelialization of the abdominal aorta, which was followed by a 0.5% cholesterol diet for 16 wk in 7 New Zealand White rabbits; 5 unmanipulated rabbits, fed normal chow for 16 wk, were used as controls. Radionuclide imaging was performed immediately after intravenous (99m)Tc-labeled MCP-1 administration and 3 h later. At the end of imaging session, aortas were explanted and submitted for estimation of quantitative MCP-1 uptake (in percentage injected dose per gram, %ID/g) and pathologic characterization. Atherosclerotic lesions were clearly visible in all hyperlipidemic animal gamma-imaging. No tracer uptake was seen in the control rabbits. The mean quantitative MCP-1 uptake in atherosclerotic lesions was 4-fold higher than that of the aortic specimens from the control rabbits (0.065 +/- 0.005 vs. 0.016 +/- 0.006; P < 0.0001). Histology confirmed a strong correlation between MCP-1 uptake and the number of macrophages in American Heart Association type II-IV lesions (r = 0.87, P < 0.0001). Noninvasive radionuclide imaging of inflammation is feasible by MCP-1 in experimentally induced atherosclerosis. It is proposed that detection of the extent of inflammation in advanced atherosclerotic plaques may allow identification of unstable plaques.
    Journal of Nuclear Medicine 12/2007; 48(11):1816-21. · 6.38 Impact Factor

Institutions

  • 2012
    • Lucile Packard Children’s Hospital at Stanford
      Palo Alto, CA, USA
  • 2004–2012
    • Memorial Sloan-Kettering Cancer Center
      • • Department of Radiology
      • • Department of Medical Physics
      • • Endocrinology Service
      New York City, NY, USA
  • 2008
    • University of California, Irvine
      Irvine, CA, USA
  • 2004–2008
    • Hokkaido University
      • • Department of Nuclear Medicine
      • • Graduate School of Medicine
      Sapporo-shi, Hokkaido, Japan
  • 2007
    • Rambam Medical Center
      • Department of Nuclear Medicine
      Haifa, Haifa District, Israel
  • 2004–2007
    • Kanazawa University
      • Department of Biotracer Medicine
      Kanazawa-shi, Ishikawa-ken, Japan
  • 2005
    • Centre Hospitalier Universitaire de Brest
      Brest, Brittany, France
  • 2003
    • Drexel University
      Philadelphia, PA, USA
    • Nikko Memorial Hospital
      Hitachi, Ibaraki-ken, Japan
  • 1999–2002
    • Stanford University
      • • Department of Cardiothoracic Surgery
      • • Department of Radiology
      Palo Alto, CA, USA
  • 2001
    • Department of Nuclear Medicine
      Nitra, Nitriansky Kraj, Slovakia