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1.

001-es BibID:BIBFORM028392
Első szerző:Balla György (csecsemő és gyermekgyógyász, neonatológus)
Cím:Ferritin : a cytoprotective antioxidant strategem of endothelium / Balla G., Jacob H. S., Balla J., Rosenberg M., Nath K., Apple F., Eaton J. W., Vercellotti G. M.
Dátum:1992
Megjegyzések:Phagocyte-mediated oxidant damage to vascular endothelium is likely involved in various vasculopathies including atherosclerosis and pulmonary leak syndromes such as adult respiratory distress syndrome. We have shown that heme, a hydrophobic iron chelate, is rapidly incorporated into endothelial cells where, after as little as 1 h, it markedly aggravates cytotoxicity engendered by polymorphonuclear leukocyte oxidants or hydrogen peroxide (H2O2). In contrast, however, if cultured endothelial cells are briefly pulsed with heme and then allowed to incubate for a prolonged period (16 h), the cells become highly resistant to oxidant-mediated injury and to the accumulation of endothelial lipid peroxidation products. This protection is associated with the induction within 4 h of mRNAs for both heme oxygenase and ferritin. After 16 h heme oxygenase and ferritin have increased approximately 50-fold and 10-fold, respectively. Differential induction of these proteins determined that ferritin is probably the ultimate cytoprotectant. Ferritin inhibits oxidant-mediated cytolysis in direct relation to its intracellular concentration. Apoferritin, when added to cultured endothelial cells, is taken up in a dose-responsive manner and appears as cytoplasmic granules by immunofluorescence; in a similar dose-responsive manner, added apoferritin protects endothelial cells from oxidant-mediated cytolysis. Conversely, a site-directed mutant of ferritin (heavy chain Glu62----Lys; His65----Gly) which lacks ferroxidase activity and is deficient in iron sequestering capacity, is completely ineffectual as a cytoprotectant. We conclude that endothelium and perhaps other cell types may be protected from oxidant damage through the iron sequestrant, ferritin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Biological Chemistry. - 267 : 25 (1992), p. 18148-18153. -
További szerzők:Jacob, Harry S. Balla József (1959-) (belgyógyász, nephrológus) Rosenberg, M. Nath, Karl Apple, F. Eaton, John W. Vercellotti, Gregory M.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM041562
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Role of heme, heme oxygenase and ferritin in free radical mediated vascular endothelial cell injury / József Balla, Gregory M. Vercellotti, Karl A. Nath, John W. Eaton, John D. Belcher, Harry S. Jacob, György Balla
Dátum:1994
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Megjelenés:Free Radicals in the Environment, Medicine and Toxicology : Critical Aspects and Current Highlights / ed. by H. Nohl, H. Esterbauer, C. Rice-Evans. - p. 429-466.
További szerzők:Vercellotti, Gregory M. Nath, Karl Eaton, John W. Belcher, John D. Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM041560
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Heme oxygenase and ferritin induction as a protective vessel wall endothelial cell response against free radical stress / J. Balla, G. M. Vercellotti, J. W. Eaton, H. S. Jacob, Gy. Balla
Dátum:1993
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Megjelenés:Oxygen Free Radicals and Scavengers in the Natural Sciences / eds. Gy. Mózsik, I. Emerit, J. Fehér, B. Matkovics, Á. Vincze. - p. 123-126.
További szerzők:Vercellotti, Gregory M. Eaton, John W. Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM040628
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Endothelial cell heme oxygenase and ferritin induction in rat lung by hemoglobin in vivo / Balla J., Nath K., Balla G., Juckett M. B., Jacob H. S., Vercellotti G. M.
Dátum:1995
ISSN:0002-9513
Megjegyzések:Iron-derived reactive oxygen species play an important role in the pathogenesis of various vascular disorders including vasculitis, atherosclerosis, and capillary leak syndromes such as the adult respiratory distress syndrome (ARDS). We have suggested that acute incorporation of the heme moiety of hemoglobin released from red blood cells into endothelium could provide catalytically active iron to the vasculature. Adaptation to chronic heme stress involves the induction of heme oxygenase and ferritin; the latter provides cytoprotection against free radicals in vitro. The present studies examine the bioavailability of heme, derived from hemoglobin, to induce heme oxygenase and ferritin in rat lungs in vivo. Intravenous injection of methemoglobin, but not oxyhemoglobin, increases total lung heme oxygenase mRNA approximately fivefold after 16 h. Accompanying this mRNA induction, expression of total lung heme oxygenase enzyme activity is also markedly enhanced. In situ hybridization for heme oxygenase reveals mRNA accumulation in the lung microvascular endothelium, implying incorporation of heme into endothelial cells. Similarly, methemoglobin significantly increases the ferritin protein content of rat lungs and in parallel, ferritin light-chain mRNA increases approximately 1.6-fold, whereas heavy-chain mRNA is upregulated by approximately 1.9-fold. Immunoreactive ferritin is present in lung microvascular endothelium after methemoglobin treatment, suggesting incorporation of heme iron into pulmonary vasculature. Subcutaneous injection of Sn-protoporphyrin IX, a competitive inhibitor of heme oxygenase, does not affect methemoglobin-induced ferritin synthesis in lungs. We speculate that methemoglobin, which might be generated by activated leukocytes in ARDS associated with disseminated interavascular coagulation, can provide heme iron to lung microvascular endothelium to induce heme oxygenase and ferritin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American journal of physiology. Lung cellular and molecular physiology. - 268 : 2 Pt1 (1995), p. L321-L327. -
További szerzők:Nath, Karl Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Juckett, Mark B. Jacob, Harry S. Vercellotti, Gregory M.
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5.

001-es BibID:BIBFORM040465
035-os BibID:PMID:1308986
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Endothelial cell heme oxygenase and ferritin induction by heme proteins : a possible mechanism limiting shock damage / J. Balla, H. S. Jacob, Gy. Balla, K. Nath, G. M. Vercellotti
Dátum:1992
Megjegyzések:Acutely, hemin sensitizes endothelial cells to oxidants but chronically protects the endothelium through the induction of ferritin. By releasing its heme, methemoglobin can sensitize endothelial cells in a fashion similar to free hemin. Furthermore, prolonged incubation with the endothelium allows methemoglobin to induce heme oxygenase and ferritin and concomitantly to modulate oxidant-mediated cytotoxicity. Methemoglobin but not hemoglobin, metmyoglobin or cytochrome c induces heme oxygenase and ferritin. Heme needs to be released from methemoglobin, since sodium cyanide, haptoglobin, and hemopexin inhibit the induction of these proteins. Neutrophils can oxidize hemoglobin to methemoglobin, which can subsequently induce both heme oxygenase and ferritin. We speculate that in shock with disseminated intravascular coagulation, marginated PMNs oxidize hemoglobin to heme-releasing methemoglobin. If critical defenses such as haptoglobin and hemopexin are overwhelmed, heme enters the endothelin cells, sensitizing them to oxidant damage. Endothelial cell adaptation via heme-induced heme oxygenase and ferritin production might limit ultimate progression to pulmonary and other vascular leak syndromes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
egyetemen (Magyarországon) készült közlemény
Megjelenés:Transactions of the Association of American Physicians. - 105 (1992), p. 1-6. -
További szerzők:Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Nath, Karl Vercellotti, Gregory M.
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6.

001-es BibID:BIBFORM040454
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Heme oxygenase and ferritin induction in kidney and endothelium to prevent oxidant damage / J. Balla, Gy. Balla, H. S. Jacob, G. M. Vercellotti, K. Nath
Dátum:1994
Tárgyszavak:Orvostudományok Klinikai orvostudományok előadáskivonat
Megjelenés:22nd Congress of International Society of Internal Medicine : abstract book. - p. 225-228.
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jacob, Harry S. Vercellotti, Gregory M. Nath, Karl
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7.

001-es BibID:BIBFORM040463
035-os BibID:PMID:8036736
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Oxidized low-density lipoproteins and endothelium : oral vitamin E supplementation prevents oxidized low-density lipoprotein-mediated vascular injury / József Balla, John D. Belcher, György Balla, Harry S. Jacob, Gregory M. Vercellotti
Dátum:1993
Megjegyzések:Vitamin E supplements may decrease the incidence of myocardial infarction by inhibiting LDL oxidation to atherogenic moieties. We previously reported that hemin is a potent and relevant lipophilic source of iron that can rapidly intercalate into LDL, catalyzing its oxidation and promoting its cytolysis of endothelium. The effects of oral vitamin E on heme-catalyzed LDL oxidation and resulting endothelial damage were studied in 10 volunteers who received daily 800 I.U. of vitamin E with or without vitamin C (1000 mg) for 2 weeks. Prior, during, and 2 weeks after supplementation, plasma LDL was isolated and its number of alpha-tocopherol molecules, resistance to heme-catalyzed oxidation, and ability to damage porcine aortic endothelial cells were assayed. Vitamin E supplementation doubled the lag phase of LDL peroxidation as compared to control (104 +/- 18 vs. 58 +/- 11 min; p < 0.001) accompanied by an increase in alpha-tocopherol content of LDL particles (26 +/- 6 vs. 11 +/- 2 mol/mol; p < 0.001). Most intriguingly, LDL-mediated endothelial cell cytotoxicity was prevented (3 +/- 2% vs. 42 +/- 12%; p < 0.001). After a 2-week washout period, LDL alpha-tocopherol content, the lag time of LDL oxidation, and oxidized LDL-mediated cytolysis all returned to baseline levels. To determine whether supplements of vitamin E and vitamin C beneficially synergize in these effects, we monitored several volunteers on daily vitamin E alone or vitamin C alone. Vitamin E alone (at doses as low as 400 I.U./day) affected all measurements in a manner identical to that when it was taken with vitamin C. Vitamin C alone had no significant effect on these measurements. We conclude: dietary vitamin E supplementation provides cytoprotection against LDL oxidation-mediated endothelial cell injury, but this salutary effect is rapidly lost after supplementation is stopped.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Transactions of the Association of American Physicians. - 106 (1993), p. 128-133. -
További szerzők:Belcher, John D. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jacob, Harry S. Vercellotti, Gregory M.
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8.

001-es BibID:BIBFORM028399
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Endothelial-cell heme uptake from heme proteins : induction of sensitization and desensitization to oxidant damage / J. Balla, H. S. Jacob, G. Balla, K. Nath, J. W. Eaton, G. M. Vercellotti
Dátum:1993
Megjegyzések:Iron-derived reactive oxygen species are implicated in the pathogenesis of various vascular disorders including atherosclerosis, vasculitis, and reperfusion injury. The present studies examine whether heme, when liganded to physiologically relevant proteins as in hemoglobin, can provide potentially damaging iron to intact endothelium. We demonstrate that reduced ferrohemoglobin, while relatively innocuous to cultured endothelial cells, when oxidized to ferrihemoglobin (methemoglobin), greatly amplifies oxidant (H2O2)-mediated endothelial-cell injury. Drawing upon our previous observation that free heme similarly primes endothelium for oxidant damage, we posited that methemoglobin, but not ferrohemoglobin, releases its hemes that can then be incorporated into endothelial cells. In support, cultured endothelial cells exposed to methemoglobin--in contrast to exposure to ferrohemoglobin, cytochrome c, or metmyoglobin--rapidly increased their heme oxygenase mRNA and enzyme activity, thereby supporting heme uptake; ferritin production was also markedly increased after such exposure, thus attesting to eventual incorporation of Fe. These cellular methemoglobin effects were inhibited by the heme-scavenging protein hemopexin and by haptoglobin or cyanide, agents that strengthen the liganding between heme and globin. If the endothelium is exposed to methemoglobin for a more prolonged period (16 hr), it accumulates large amounts of ferritin; concomitantly, and presumably associated with iron sequestration by this protein, the endothelium converts from hypersusceptible to hyperresistant to oxidative damage. We conclude that when oxidation of hemoglobin facilitates release of its heme groups, catalytically active iron is provided to neighboring tissue environments. The effect of this relinquished heme on the vasculature is determined both by extracellular factors--i.e., plasma proteins, such as haptoglobin and hemopexin--as well as intracellular factors, including heme oxygenase and ferritin. Acutely, if both extra- and intracellular defenses are overwhelmed, cellular toxicity arises; chronically, when ferritin is induced, resistance to oxidative injury may supervene.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Proceedings of the National Academy of Sciences of the United States of America. - 90 : 20 (1993), p. 9285-9289. -
További szerzők:Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Nath, Karl Eaton, John W. Vercellotti, Gregory M.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM023040
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Ferriporphyrins and endothelium : a 2-edged sword-promotion of oxidation and induction of cytoprotectants / Balla, J., Balla, G., Jeney, V., Kakuk, G., Jacob, H. S., Vercellotti, G. M.
Dátum:2000
ISSN:0006-4971
Megjegyzések:Heme arginate infusions blunt the symptoms of patients with acute intermittent porphyria without evidence of the vascular or thrombotic side effects reported for hematin, To provide a rationale for heme arginate's safety, the present study examined the effects of various ferriporphyrins to sensitize human endothelial cells to free radical injury and to induce heme oxygenase and ferritin expression. Heme arginate, unlike hematin, did not amplify oxidant-induced cytotoxicity mediated by hydrogen peroxide (5.3 +/- 2.4 versus 62.3 +/- 5.3% Cr-51 release, P < .0001) or by activated neutrophils (14.4 +/- 2.9 versus 41.1 +/- 6.0%, P < .0001), Nevertheless, heme arginate efficiently entered endothelial cells similarly to hematin, since both markedly induced heme oxygenase mRNA (more than 20-fold increase) and enzyme activity. Even with efficient permeation, endothelial cell ferritin content was only minimally increased by heme arginate compared with a 10-fold induction by hematin; presumably less free iron was derived from heme arginate despite up-regulation of heme oxygenase, Hematin is potentially vasculopathic by its marked catalysis of oxidation of low-density lipoprotein (LDL) to endothelial-toxic moieties, Heme arginate was significantly less catalytic. Heme arginate-conditioned LDL was less than half as cytotoxic to endothelial cells as hematin-conditioned LDL (P < .004), It is concluded that heme arginate may be less vasculotoxic than hematin since it is an effective heme oxygenase gene regulator but a less efficient free radical catalyst.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Blood. - 95 : 11 (2000), p. 3442-3450. -
További szerzők:Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jeney Viktória (1971-) (vegyész, kémia tanár) Kakuk György (1938-2018) (belgyógyász) Jacob, Harry S. Vercellotti, Gregory M.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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10.

001-es BibID:BIBFORM002292
Első szerző:Balla József (belgyógyász, nephrológus)
Cím:Heme, heme oxygenase and ferritin : how the vascular endothelium survives (and dies) in an iron-rich environment / J. Balla, G. M. Vercellotti, V. Jeney, A. Yachie, Zs. Varga, H. S. Jacob, J. W. Eaton, Gy. Balla
Dátum:2007
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Antioxidants and Redox Signaling 9 : 12 (2007), p. 2119-2137. -
További szerzők:Vercellotti, Gregory M. Jeney Viktória (1971-) (vegyész, kémia tanár) Yachie, Akihiro Varga Zsuzsa (1951-) (biokémikus, nephrológus) Jacob, Harry S. Eaton, John W. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus)
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11.

001-es BibID:BIBFORM040462
035-os BibID:PMID:8241098
Első szerző:Belcher, John D.
Cím:Vitamin E, LDL, and endothelium : brief oral vitamin supplementation prevents oxidized LDL-mediated vascular injury in vitro / J. D. Belcher, J. Balla, G. Balla, D. R. Jacobs Jr., M. Gross, H. S. Jacob, G. M. Vercellotti
Dátum:1993
Megjegyzések:In previously reported in vitro studies, we found that heme, a physiologically widespread hydrophobic iron compound, can rapidly generate oxidized low-density lipoprotein (LDL), which then becomes cytotoxic to cultured vascular endothelial cells; both LDL oxidation and endothelial cytotoxicity were inhibited by incubation with exogenous alpha-tocopherol (vitamin E) or ascorbic acid (vitamin C). Seeking relevance to in vivo conditions, we performed a study in which 10 human volunteers were given daily antioxidant supplements of 800 IU of DL-alpha-tocopherol acetate alone or in combination with 1000 mg of ascorbic acid for 2 weeks. LDL resistance to heme oxidation ex vivo, as measured by the lag time for conjugated-diene formation, increased by as much as threefold from a mean +/- SD of 58 +/- 11 to 104 +/- 18 minutes (P < .001); LDL alpha-tocopherol increased from 11 +/- 2 to 26 +/- 6 molecules per LDL particle (P < .001); and most impressively, cytotoxicity to porcine aortic endothelial cells incubated with LDL conditioned with heme plus H2O2 or with copper was completely prevented (cytotoxicity before supplementation was 42 +/- 12%, decreasing after supplementation to 3 +/- 2%, P < .001). These measurements reverted to their presupplement levels within 2 weeks after participants stopped taking antioxidant supplements and were reproduced in 4 subjects taking 800 IU of DL-alpha-tocopherol acetate supplements alone but not in the same subjects taking 1000 mg ascorbic acid supplements alone. In conclusion, oral vitamin E supplementation increases LDL alpha-tocopherol content, increases LDL resistance to oxidation, and decreases the cytotoxicity of oxidized LDL to cultured vascular endothelial cells.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Arteriosclerosis, Thrombosis, and Vascular Biology 13 : 12 (1993), p. 1779-1789. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jacobs, D. R., Jr. Gross, M. Jacob, Harry S. Vercellotti, Gregory M.
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DOI
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12.

001-es BibID:BIBFORM040457
035-os BibID:PMID:8221666
Első szerző:Cermak, Jaroslav
Cím:Tumor cell heme uptake induces ferritin synthesis resulting in altered oxidant sensitivity : possible role in chemotherapy efficacy / Jaroslav Cermak, József Balla, Harry S. Jacob, György Balla, Helen Enright, Karl Nath, Gregory M. Vercellotti
Dátum:1993
ISSN:0008-5472
Megjegyzések:Neovascularization and hemorrhage are common features of malignant tumors. We wondered whether hemoglobin derived from extravasated RBC deposits heme-derived iron into the tumor, which could modulate the sensitivity of cancer cells to oxidant-mediated injury. A brief exposure (1 h) of 51Cr-radiolabeled breast cancer cells (BT-20) but not colon cancer cells (Caco-2) to hemin (10 microM) or FeSO4 (10 microM) significantly enhances cytotoxicity mediated by 0.5 mM hydrogen peroxide (H2O2). Associated with Caco-2 resistance, these cells were found to be enriched in the endogenous iron chelator, ferritin. If cellular ferritin is even further increased through 1 h incubation (24 h prior to H2O2 exposure) of both cell types with hemin, FeSO4, or exogenous spleen apoferritin itself (24 h), marked resistance to H2O2-mediated cytotoxicity is manifest. Under several conditions, the sensitivity of tumor cells to oxidant-mediated lysis is inversely proportional to their ferritin content. Pretreatment of BT-20 and Caco-2 cells with hemin or FeSO4 rapidly increases H-ferritin mRNA but only slightly increases L-ferritin mRNA; nevertheless, large increases in overall ferritin content of iron-exposed cells result. Data analogous to those with H2O2-mediated cytotoxicity were obtained in studies of bleomycin-engendered DNA strand breakage and cell damage, i.e., brief treatment of BT-20 cells with both hemin or FeSO4 significantly increases their sensitivity to bleomycin (100 micrograms/ml), whereas treatment followed by 24 h incubation with media alone significantly protects against bleomycin toxicity. We speculate that acute exposure of tumors to iron (e.g., derived from heme-proteins in hemorrhagic cancerous lesions) may increase sensitivity of some cancer cells, particularly those relatively low in endogenous ferritin, to oxidant-mediated lysis. In contrast, repeated, more chronic, exposure effector cells or chemotherapeutic agents, an effect derived from their increased synthesis and accumulation of the intracellular iron scavenger, ferritin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Cancer Research 53 : 21 (1993), p. 5308-5313. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Enright, Helen Nath, Karl Vercellotti, Gregory M.
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