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7. Religion et sentiments d'injustice dans les conflits intercommunautaires

Author

Soubiale, Nadège, Abassi, Z, Médiation, Information, Communication, Art (MICA), Université Bordeaux Montaigne, Roussiau, Nicolas, and Université, Bordeaux Montaigne

Subjects
[SHS] Humanities and Social Sciences, ComputingMilieux_MISCELLANEOUS, [SHS]Humanities and Social Sciences
Abstract

International audience

Published
2009

9. Glomerular injury

Author

Djudjaj, S., primary, Lue, H., additional, Urzinicok, T., additional, Engel, D., additional, Martin, I. V., additional, Buhl, E. M., additional, Floege, J., additional, Ostendorf, T., additional, Bernhagen, J., additional, Boor, P., additional, Cantaluppi, V., additional, Medica, D., additional, Mannari, C., additional, Figliolini, F., additional, Migliori, M., additional, Panichi, V., additional, Tetta, C., additional, Camussi, G., additional, Schulte, K., additional, Berger, K., additional, Sicking, E. M., additional, Jirak, P., additional, Thevissen, L., additional, Fuss, A., additional, Kriz, W., additional, Smeets, B., additional, Moeller, M. J., additional, Santhosh Kumar, V. R., additional, Kulkarni, O. P., additional, Darisipudi, N. M., additional, Mulay, S. R., additional, Anders, H.-J., additional, Assady, S., additional, Alter, J., additional, Litvak, M., additional, Ilan, N., additional, Vlodavsky, I., additional, and Abassi, Z., additional

Published
2013
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10. AKI - experimental models

Author

Lai, C.-F., primary, Lin, S.-L., additional, Chiang, W.-C., additional, Chen, Y.-M., additional, Kuo, M.-L., additional, Tsai, T.-J., additional, Hwang, H. S., additional, Choi, Y. A., additional, Park, K. C., additional, Yang, K. J., additional, Choi, H. S., additional, Kim, S. H., additional, Lee, S. J., additional, Chang, Y. K., additional, Kim, S. Y., additional, Yang, C. W., additional, Xiujuan, Z., additional, Yoshimura, R., additional, Matsuyama, M., additional, Chargui, J., additional, Touraine, J.-L., additional, Yoshimura, N., additional, Zulkarnaev, A. B., additional, Vasilenko, I. A., additional, Artemov, D. V., additional, Vatazin, A. V., additional, Park, S. K., additional, Kang, K. P., additional, Lee, S., additional, Kim, W., additional, Schneider, R., additional, Betz, B., additional, Moller-Ehrlich, K., additional, Wanner, C., additional, Sauvant, C., additional, Park, C. W., additional, Sohotnik, R., additional, Nativ, O., additional, Abbasi, A., additional, Awad, H., additional, Frajewicki, V., additional, Armaly, Z., additional, Heyman, S. N., additional, Abassi, Z., additional, Chen, P. Y., additional, Chen, B. L., additional, Yang, C. C., additional, Chiang, C. K., additional, Liu, S. H., additional, Abozahra, A. E., additional, Abd-Elkhabir, A. A., additional, Shokeir, A., additional, Hussein, A., additional, Awadalla, A., additional, Barakat, N., additional, Abdelaziz, A., additional, Yamaguchi, J., additional, Tanaka, T., additional, Eto, N., additional, Nangaku, M., additional, Quiros, Y., additional, Lopez-Hernandez, F. J., additional, Perez de Obanos, M. P., additional, Ruiz, J., additional, Lopez-Novoa, J. M., additional, Shin, H.-S., additional, Kim, M.-J., additional, Choi, Y.-J., additional, Ryu, E.-S., additional, Choi, H.-S., additional, Kang, D.-H., additional, Jankauskas, S. S., additional, Pevzner, I. B., additional, Zorova, L. D., additional, Babenko, V. A., additional, Morosanova, M. A., additional, Plotnikov, E. Y., additional, Zorov, D. B., additional, Huang, C.-Y., additional, Huang, T.-M., additional, Wu, V.-C., additional, Young, G.-H., additional, Chupyrkina, A. A., additional, Zorov, S. D., additional, Grande, J. P., additional, Hartono, S. P., additional, Knudsen, B. E., additional, Mederle, K., additional, Castrop, H., additional, Hocherl, K., additional, Iwakura, T., additional, Fujikura, T., additional, Ohashi, N., additional, Yasuda, H., additional, Fujigaki, Y., additional, Matsui, I., additional, Hamano, T., additional, Inoue, K., additional, Obi, Y., additional, Nakano, C., additional, Kusunoki, Y., additional, Tsubakihara, Y., additional, Rakugi, H., additional, Isaka, Y., additional, Shimomura, A., additional, Wallentin Guron, C., additional, Nguy, L., additional, Lundgren, J., additional, Grimberg, E., additional, Kashioulis, P., additional, Guron, G., additional, DiBona, G. F., additional, Nedergaard Mikkelsen, M., additional, Marcussen, N., additional, Saeed, A., additional, Edvardsson, K., additional, Lindberg, K., additional, Larsson, T., additional, Ito, K., additional, Nakashima, H., additional, Watanabe, M., additional, Abe, Y., additional, Ogahara, S., additional, Saito, T., additional, Albertoni, G., additional, Borges, F., additional, Schor, N., additional, Beresneva, O. N., additional, Parastayeva, M. M., additional, Kucher, A. G., additional, Ivanova, G. T., additional, Shved, N., additional, Rybakova, M. G., additional, Kayukov, I. G., additional, Smirnov, A. V., additional, Chen, J.-F., additional, Ni, H.-F., additional, Pan, M.-M., additional, Liu, H., additional, Xu, M., additional, Zhang, M.-H., additional, Liu, B.-C., additional, Kim, Y., additional, Choi, B. S., additional, Kim, Y. S., additional, Han, J. S., additional, Reis, L. A., additional, Christo, J. S., additional, Simoes, M. d. J., additional, Mulay, S. R., additional, Santhosh Kumar, V. R., additional, Kulkarni, O. P., additional, Darisipudi, M., additional, Lech, M., additional, Anders, H.-J., additional, Silachev, D. N., additional, Sola, A., additional, Jung, M., additional, Ventayol, M., additional, Mastora, C., additional, Buenestado, S., additional, Hotter, G., additional, Rong, S., additional, Shushakova, N., additional, Wensvoort, G., additional, Haller, H., additional, Gueler, F., additional, Morais, C., additional, Vesey, D. A., additional, Johnson, D. W., additional, Gobe, G. C., additional, Godo, M., additional, Kaucsar, T., additional, Revesz, C., additional, Hamar, P., additional, Cheng, Q., additional, Wen, J., additional, Ma, Q., additional, Zhao, J., additional, Castellano, G., additional, Stasi, A., additional, Di Palma, A. M., additional, Gigante, M., additional, Netti, G. S., additional, Curci, C., additional, Intini, A., additional, Divella, C., additional, Prattichizzo, C., additional, Fiaccadori, E., additional, Pertosa, G., additional, Grandaliano, G., additional, Gesualdo, L., additional, Wei, Q. W., additional, Jing, Q. Q., additional, Ying, N. J., additional, Dong, Q. Z., additional, Yong, G., additional, Pulkova, N. V., additional, Sukhikh, G. T., additional, Kim, S., additional, Lee, J., additional, Nam, N. J., additional, Na, K. Y., additional, Ma, S. K., additional, Joo, S. Y., additional, Kim, C. S., additional, Choi, J. S., additional, Bae, E. H., additional, Kim, S. W., additional, Cernaro, V., additional, Medici, M. A., additional, Donato, V., additional, Trimboli, D., additional, Lorenzano, G., additional, Santoro, D., additional, Montalto, G., additional, Buemi, M., additional, Longo, V., additional, Segreto, H. R. C., additional, Almeida, W., additional, Ramos, M. F., additional, Gomes, L., additional, Razvickas, C., additional, Gutberlet, M., additional, Meier, M., additional, Mengel, M., additional, Wacker, D., additional, Hueper, K., additional, Uzum, A., additional, Ersoy, R., additional, Cakalagaoglu, F., additional, Karaman, M., additional, Kolatan, E., additional, Sahin, O., additional, Yilmaz, O., additional, Cirit, M., additional, Inal, S., additional, Koc, E., additional, Okyay, G. U., additional, Pasaoglu, O., additional, Gonul, I., additional, Oyar, E., additional, Pasaoglu, H., additional, Guz, G., additional, Sabbatini, M., additional, Rossano, R., additional, Andreucci, M., additional, Pisani, A., additional, Riccio, E., additional, Choi, D. E., additional, Jeong, J. Y., additional, Kim, S. S., additional, Na, K.-R., additional, Lee, K. W., additional, Shin, Y. T., additional, Silva, A. F., additional, Teixeira, V. C., additional, Meszaros, K., additional, Koleganova-Gut, N., additional, Schaefer, F., additional, Ritz, E., additional, Walacides, D., additional, Ruskamp, N., additional, Schiffer, M., additional, Marom, O., additional, Haick, H., additional, Nakhoul, F., additional, Lv, L.-L., additional, Tang, R.-N., additional, Zhang, J.-D., additional, Ma, K.-L., additional, Chen, P.-S., additional, Ko, W.-J., additional, Misiara, G. P., additional, Coimbra, T. M., additional, Silva, G. E. B., additional, Costa, R. S., additional, Francescato, H. D. C., additional, Neto, M. M., additional, Dantas, M., additional, Olauson, H., additional, Amin, R., additional, Ponnusamy, A., additional, Goetz, R., additional, Mohammadi, M., additional, Canfield, A., additional, Kublickiene, K., additional, Rodriguez, J., additional, Reyes, E. P., additional, Cortes, P. P., additional, Fernandez, R., additional, Yoon, H. E., additional, Koh, E. S., additional, Chung, S., additional, Shin, S. J., additional, Pazzano, D., additional, Lupica, R., additional, Torre, F., additional, Costantino, G., additional, Prieto, M., additional, Gonzalez-Buitrago, J. M., additional, Lopez-Hernandez, F., additional, Morales, A. I., additional, Vicente-Vicente, L., additional, Ferreira, L., additional, Simoes, M. J., additional, Passos, C. d., additional, Schor, N. S., additional, Shimizu, M. H. M., additional, Canale, D., additional, de Braganca, A. C., additional, Andrade, L., additional, Luchi, W. M., additional, Seguro, A. C., additional, Goncalves, J., additional, Volpini, R. A., additional, Garrido, P., additional, Fernandes, J., additional, Ribeiro, S., additional, Vala, H., additional, Parada, B., additional, Alves, R., additional, Belo, L., additional, Costa, E., additional, Santos-Silva, A., additional, and Reis, F., additional

Published
2013
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13. Acute kidney injury - Experimental models

Author

Nagasaki, Y., primary, Yoshitomi, T., additional, Hirayama, A., additional, Schock-Kusch, D., additional, Xie, Q., additional, Shulhevich, Y., additional, Hesser, J., additional, Stsepankou, S., additional, Koenig, S., additional, Heinrich, R., additional, Pill, J., additional, Gretz, N., additional, Efrati, S., additional, Berman, S., additional, Abu-Hamad, R., additional, Siman-Tov, Y., additional, Weissgarten, J., additional, Kimura, T., additional, Takabatake, Y., additional, Takahashi, A., additional, Kaimori, J.-y., additional, Matsui, I., additional, Namba, T., additional, Kitamura, H., additional, Niimura, F., additional, Matsusaka, T., additional, Rakugi, H., additional, Isaka, Y., additional, Ito, K., additional, Watanabe, M., additional, Nakashima, H., additional, Abe, Y., additional, Ifuku, M., additional, Nishimura, S., additional, Saito, T., additional, Mulay, S. R., additional, Thomasova, D., additional, Ryu, M., additional, Anders, H.-J., additional, Nakayama, Y., additional, Ueda, S., additional, Yamagishi, S.-i., additional, Ando, R., additional, Kaida, Y., additional, Iwatani, R., additional, Fujimi, A., additional, Fukami, K., additional, Okuda, S., additional, Shin, Y. T., additional, Jeong, J. Y., additional, Jang, W. I., additional, Chung, S., additional, Choi, D. E., additional, Na, K. R., additional, Lee, K. W., additional, Mugitani, N., additional, Shimizu, Y., additional, Satake, K., additional, Suzuki, Y., additional, Horikoshi, S., additional, Tomino, Y., additional, Schneider, R., additional, Meusel, M., additional, Betz, B., additional, Wanner, C., additional, Koepsell, H., additional, Sauvant, C., additional, Dursun, B., additional, Abban, G., additional, Kucukatay, V., additional, Tufan, L., additional, Dodurga, Y., additional, Guclu, A., additional, Gok, D., additional, Vicente-Vicente, L., additional, Sanchez-Gonzalez, P. D., additional, Prieto, M., additional, Lopez-Novoa, J. M., additional, Lopez-Hernandez, F. J., additional, Morales, A. I., additional, Torres, A., additional, Dnyanmote, A., additional, Wu, W., additional, Nigam, S., additional, Wystrychowski, A., additional, Wystrychowski, W., additional, Kolodziejczyk, A., additional, Obuchowicz, E., additional, Wiecek, A., additional, Reis, L. A., additional, Borges, F. T., additional, Simoes, M. d. J., additional, Schor, N., additional, Mesnard, L., additional, Rafat, C., additional, Vandermeersch, S., additional, Nochy, D., additional, Garcon, L., additional, Callard, P., additional, Jouanneau, C., additional, Verpont, M.-C., additional, Hertig, A., additional, Rondeau, E., additional, Grosjean, F., additional, Torreggiani, M., additional, Esposito, V., additional, Mangione, F., additional, Serpieri, N., additional, Villa, L., additional, Sileno, G., additional, Marchi, G., additional, Fasoli, G., additional, Esposito, C., additional, Dal Canton, A., additional, Sancho-Martinez, S., additional, Striker, G., additional, Vlassara, H., additional, Zheng, F., additional, Park, D. J., additional, Kim, J. H., additional, Jung, M. H., additional, Seo, J. W., additional, Kim, H.-j., additional, Chang, S.-H., additional, Han, B.-G., additional, Yang, J.-W., additional, Yu, J.-M., additional, Choi, S.-O., additional, Christo, J. S., additional, Rusai, K., additional, Prokai, A., additional, Szebeni, B., additional, Meszaros, K., additional, Fekete, A., additional, Treszl, A., additional, Vannay, A., additional, Muller, V., additional, Reusz, G., additional, Heemann, U., additional, Tulassay, T., additional, Lutz, J., additional, Szabo, A. J., additional, Ranghino, A., additional, Bruno, S., additional, Grange, C., additional, Dolla, C., additional, Cantaluppi, V., additional, Biancone, L., additional, Tetta, C., additional, Segoloni, G. P., additional, Camussi, G., additional, Pinto, V., additional, Teixeira, V., additional, Almeida, W., additional, Fujikura, T., additional, Sun, Y., additional, Iwakura, T., additional, Yasuda, H., additional, Fujigaki, Y., additional, Simone, S., additional, Rascio, F., additional, Loverre, A., additional, Cosola, C., additional, Cariello, M., additional, Castellano, G., additional, Ditonno, P., additional, Schena, F. P., additional, Gesualdo, L., additional, Grandaliano, G., additional, Pertosa, G., additional, Choi, J.-Y., additional, Kim, J., additional, Jin, D.-C., additional, Cha, J.-H., additional, Kaynar, K., additional, Aliyazicioglu, R., additional, Ersoz, S., additional, Ulusoy, S., additional, Al, S., additional, Ozkan, G., additional, Cansiz, M., additional, Fuchs, T. C., additional, Emde, B., additional, Czasch, S., additional, von Landenberg, F., additional, Hewitt, P., additional, Abu-Salah, N., additional, Bishara, B., additional, Awad, H., additional, Ghrayeb, N., additional, Assady, S., additional, Armaly, Z., additional, Better, O., additional, and Abassi, Z., additional

Published
2011
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16. Adaptation to hypoxia in the diabetic rat kidney

Author

Rosenberger, C., primary, Khamaisi, M., additional, Abassi, Z., additional, Shilo, V., additional, Weksler-Zangen, S., additional, Goldfarb, M., additional, Shina, A., additional, Zibertrest, F., additional, Eckardt, K.-U., additional, Rosen, S., additional, and Heyman, S.N., additional

Published
2008
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24. Restoration of blood flow by using continuous perimuscular infiltration of plasmid DNA encoding subterranean mole rat Spalax ehrenbergi VEGF

Author

Roguin, A., primary, Avivi, A., additional, Nitecki, S., additional, Rubinstein, I., additional, Levy, N. S., additional, Abassi, Z. A., additional, Resnick, M. B., additional, Lache, O., additional, Melamed-Frank, M., additional, Joel, A., additional, Hoffman, A., additional, Nevo, E., additional, and Levy, A. P., additional

Published
2003
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41. The intrarenal endothelin system and hypertension.

Author

A, Abassi Z, S, Ellahham, J, Winaver, and A, Hoffman

Abstract

The kidney is both a source of endothelin (ET) generation and an important target organ of this peptide. The highest concentrations of ET-1 in the body exist in the renal medulla, where it mediates natriuretic and diuretic effects through the ET(B) receptor subtype. It is proposed that aberrations in the renal ET system may lead to sodium and water retention and subsequently to the development of hypertension.

Published
2001

43. Losartan improves the natriuretic response to ANF in rats with high-output heart failure.

Author

Abassi, Z A, Kelly, G, Golomb, E, Klein, H, and Keiser, H R

Abstract

During severe congestive heart failure (CHF), a number of sodium-retaining and vasoconstricting mechanisms are activated, including the renin-angiotensin-aldosterone system. In CHF, the renal effects of atrial natriuretic factor (ANF) are attenuated. The interaction of these endocrine factors is a major determinant of the clinical course of CHF. This study was designed to evaluate the role of the renin-angiotensin-aldosterone system in the development of avid sodium retention in CHF, induced in rats by creation of an aorto-caval fistula. Rats with aorto-caval fistula either compensate and maintain a normal sodium balance (UNaV > 1400 microEq/day) or decompensate and develop severe sodium retention (UNaV < 200 microEq/day), which leads to severe CHF. Chronic treatment with losartan, an angiotensin II receptor blocker, 10 mg/day, resulted in dramatic natriuresis (UNaV > 1000 microEQ/day) in decompensated rats, but not in compensated rats or controls. ANF infusion (50 micrograms/kg/hr) increased fractional sodium excretion 46-fold in compensated rats, but only 18-fold in decompensated rats. A similar pattern of responsiveness to ANF was observed in urinary cyclic GMP excretion. Chronic losartan treatment restored the natriuretic and urinary cyclic GMP excretion responses of decompensated rats to ANF. The improvement in the natriuretic response after losartan treatment was associated with a suppression of the previously elevated plasma aldosterone. These results demonstrate the pivotal role of angiotensin II in the development of sodium retention and of the blunted renal response to ANF in CHF, and indicate why losartan is useful therapy for cardiac edema.

Published
1994

44. Vascular endothelial growth factor (VEGF) fails to improve blood flow and to promote collateralization in a diabetic mouse ischemic hindlimb model

Author

Abassi Zaid A, Levy Nina S, Avivi Aaron, Nevo Eviatar, Rubinstein Irit, Nitecki Samy, Roguin Ariel, Sabo Edmond, Lache Orit, Frank Meira, Hoffman Aaron, and Levy Andrew P

Subjects
arteries, blood flow, collateral circulation, diabetes, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background Angiogenic therapy with vascular endothelial growth factor (VEGF) has been proposed as a treatment paradigm for patients suffering from an insufficiency of collateral vessels. Diabetes is associated with increase in the production of VEGF and therefore additional VEGF may not be beneficial. Accordingly, we sought to determine the efficacy of VEGF therapy to augment collateral formation and tissue perfusion in a diabetic mouse ischemic hindlimb model. Methods Diabetic and non-diabetic mice were studied in parallel for the efficacy of VEGF administration. Diabetes was induced with streptozotocin. Hindlimb ischemia was produced by severing the left iliac artery. An outlet tube from an osmotic infusion pump with placebo/ 500 micrograms of plasmid-DNA encoding VEGF was fenestrated and tunneled into the left quadriceps muscle. Results VEGF induced more rapid and complete restoration of blood flow in normal mice. However, in the setting of diabetes there was no difference between VEGF Vs. placebo in the rate or adequacy of flow restoration. There was a significant increase in smooth muscle actin and Factor-VIII antigen densities in diabetic animals and in animals which received VEGF. Conclusions Angiogenic therapy with VEGF in the setting of diabetes does not appear to have the beneficial effects seen in the absence of diabetes.

Published
2003

45. Compensated heart failure predisposes to outer medullary tubular injury: studies in rats.

Author

Goldfarb, Marina, Abassi, Zaid, Rosen, Seymour, Shina, Ahuva, Brezis, Mayer, Heyman, Samuel N., Goldfarb, M, Abassi, Z, Rosen, S, Shina, A, Brezis, M, and Heyman, S N

Subjects
*HEART failure, *ACUTE kidney failure, *ANIMAL models in research, *ANIMAL experimentation, *ARGININE, *BIOLOGICAL models, *VASODILATION, *CARDIOVASCULAR agents, *COMPARATIVE studies, *ENZYME inhibitors, *CARDIAC hypertrophy, *INDOMETHACIN, *KIDNEY tubules, *KIDNEYS, *RESEARCH methodology, *MEDICAL cooperation, *RATS, *RESEARCH, *RENAL circulation, *EVALUATION research, *VASOCONSTRICTION, *ACUTE kidney tubular necrosis, *DISEASE complications, *PHARMACODYNAMICS
Abstract

Background: Heart failure (HF) is considered a putative factor predisposing to acute renal failure (ARF). Since outer medullary hypoxic injury may play an important role in the pathogenesis of acute tubular necrosis, we explored the impact of experimental HF on the propensity to develop ARF with hypoxic medullary injury following the inhibition of prostaglandin and nitric oxide synthesis. Methods: Compensated, high-output HF was induced in Sprague-Dawley rats by aorto-caval fistula. At the eighth to ninth postoperative day, the rats were injected with indomethacin and N(omega) nitro-L-arginine methyl ester (L-NAME; ARF protocol) and were sacrificed 24 hours later for morphologic evaluation. Results: Kidney function comparably declined in HF-ARF rats and in control sham operated animals (CTR-ARF). Nevertheless, outer medullary hypoxic damage with medullary thick ascending limb (mTAL) necrosis occurred almost exclusively in the HF-ARF group (11 +/- 4% vs. 0.2 +/- 0.2% of tubules in CTR-ARF, P < 0.03). In a third group of HF animals subjected to vehicles only (HF-Nil), kidney function was preserved and renal morphology remained intact. Papillary-tip necrosis was consistently found in all animals subjected to indomethacin and L-NAME, irrespective of preconditioning. Morphometric evaluation disclosed that HF was not associated with mTAL hypertrophy. Conclusions: Incipient HF predisposes to hypoxic outer medullary injury, probably reflecting the impact of regional vasoconstrictive stimuli rather than tubular hypertrophy when protective local vasodilating mechanisms are hampered. The presence and extent of outer medullary hypoxic damage cannot be predicted from the functional derangement, which in the experimental settings may also represent prerenal azotemia or papillary damage. [ABSTRACT FROM AUTHOR]

Published
2001
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46. Expression of Renin-Angiotensin System Components in the Heart, Kidneys, and Lungs of Rats With Experimental Heart Failure

Author

Harry R. Keiser, Federico Pieruzzi, Zaid Abassi, Pieruzzi, F, Abassi, Z, and Keiser, H

Subjects
Male, medicine.medical_specialty, Angiotensin receptor, Heart disease, Blotting, Western, Gene Expression, Peptidyl-Dipeptidase A, Kidney, Polymerase Chain Reaction, Plasma renin activity, Rats, Sprague-Dawley, Renin-Angiotensin System, Physiology (medical), Internal medicine, Renin, Renin–angiotensin system, medicine, Animals, RNA, Messenger, Lung, Heart Failure, Receptors, Angiotensin, Animal, business.industry, Angiotensin II, Myocardium, Kidney metabolism, medicine.disease, Rats, medicine.anatomical_structure, Endocrinology, Heart failure, Rat, Cardiology and Cardiovascular Medicine, business
Abstract

Background Chronic activation of the renin-angiotensin system (RAS) plays an important role in the pathogenesis of heart failure. Increasing evidence indicates that other than the circulating RAS, a local RAS exists in several tissues, including the heart. The present study was carried out to quantify cardiac, renal, and pulmonary mRNA levels of renin, angiotensin-converting enzyme (ACE), and types 1 and 2 angiotensin II receptors (AT-1 and AT-2), in rats with different severities of heart failure. Methods and Results Heart failure was induced by the creation of an aortocaval fistula below the renal arteries. Rats with aortocaval fistula either compensate and maintain a normal sodium balance or decompensate and develop severe sodium retention. Six days after placement of the aortocaval fistula, heart weight (normalized to body weight) increased 35% ( P P P P P P Conclusions The development of heart failure is associated with a remarkable increase in the expression of a local RAS in the heart, which may contribute to the pathogenesis of this clinical syndrome.

Published
1995

47. Effects of polymerization on the hypertensive action of diaspirin cross-linked hemoglobin in rats

Author

Shaban Kotob, Zaid Abassi, Federico Pieruzzi, Majd Abouassali, Joseph C. Fratantoni, Harry R. Keiser, Abdu I. Alayash, Abassi, Z, Kotob, S, Pieruzzi, F, Abouassali, M, Keiser, H, Fratantoni, J, and Alayash, A

Subjects
Male, Cardiac output, Vascular smooth muscle, Hemodynamics, Blood Pressure, Polyethylene Glycol, Muscle, Smooth, Vascular, Blood substitute, Polyethylene Glycols, Rats, Sprague-Dawley, Hemoglobins, Heart Rate, Cardiac Output, Aorta, Chemistry, General Medicine, medicine.anatomical_structure, Cross-Linking Reagents, NG-Nitroarginine Methyl Ester, Enzyme Induction, Hypertension, Human, Glomerular Filtration Rate, medicine.medical_specialty, Endothelium, Cross-Linking Reagent, Pathology and Forensic Medicine, Blood Substitute, Blood Substitutes, Internal medicine, medicine, Animals, Humans, Hemodynamic, Hemoglobin, Analysis of Variance, Aspirin, Animal, Sodium, Stroke Volume, Surgery, Rats, Endocrinology, Blood pressure, Vascular resistance, Potassium, Rat, Vascular Resistance, Endothelium, Vascular, Nitric Oxide Synthase
Abstract

It is believed that the hypertensive effect of diaspirin crosslinked hemoglobin, a viable blood substitute, can be resolved by polymerization, which reduces the diffusion of this derivative into the interstitial space between nitric oxide-producing endothelium and the target vascular smooth muscle. We studied the systemic and renal responses to infusion of three cell-free human hemoglobins in anesthetized isovolemic rats: unmodified (HbA0), crosslinked (alpha-DBBF), and polymerized crosslinked (poly alpha-DBBF). HbA0 produced a significant increase in mean arterial blood pressure (MAP) throughout the 60-minute infusion. alpha-DBBF, on the other hand, produced a more marked and prolonged increase in MAP over 120 minutes. Only a moderate increase in MAP was observed in rats after a 30-minute infusion with poly alpha-DBBF. The extent of renal insufficiency produced by these proteins, as determined by the glomerular filtration rate, was in the following order: HbA0 > poly alpha-DBBF > alpha-DBBF. Infusion of poly alpha-DBBF, under hypovolemic but not isovolemic conditions in rats, produced an increase in heart rate, cardiac output, and stroke volume and a decrease in total peripheral resistance after 60 minutes. Chemical polymerization to increase the size of alpha-DBBF does not appear to improve its hemodynamic properties in rats, especially under partial exchange transfusion, a more clinically relevant indication for a hemoglobin-based blood substitute.

Published
1997

48. Pulmonary and renal neutral endopeptidase EC 3.4.24.11 in rats with experimental heart failure

Author

Shaban Kotob, Zaid Abassi, Harry R. Keiser, Federico Pieruzzi, Eliahu Golomb, Abassi, Z, Kotob, S, Golomb, E, Pieruzzi, F, and Keiser, H

Subjects
Male, medicine.medical_specialty, Molecular Sequence Data, Endogeny, Kidney, Polymerase Chain Reaction, Sodium balance, Rats, Sprague-Dawley, Downregulation and upregulation, Atrial natriuretic peptide, Internal medicine, Internal Medicine, medicine, Animals, RNA, Messenger, Neprilysin, Lung, chemistry.chemical_classification, Heart Failure, Alanine, Base Sequence, Animal, business.industry, medicine.disease, Rats, Blot, Endocrinology, Enzyme, chemistry, Heart failure, Rat, business
Abstract

Abstract Congestive heart failure is characterized by avid sodium retention and a blunted renal response to exogenous and endogenous atrial natriuretic peptide. Inhibition of neutral endopeptidase EC 3.4.24.11 , the main enzyme that degrades natriuretic peptides, produces a natriuretic response in different models of congestive heart failure. This raises the possibility that an increase in either the expression or activity of neutral endopeptidase is responsible for these phenomena. In the present study, we examined (1) the renal effects of SQ-28,603, a neutral endopeptidase inhibitor, in rats with moderate and severe congestive heart failure induced by an aortocaval fistula compared with sham controls, and (2) neutral endopeptidase expression and activity in the lungs and kidneys of these rats. Infusion of SQ-28,603 (40 mg/kg IV) induced a significant natriuretic response in normal rats and rats with moderate congestive heart failure. This response was blunted in rats with severe congestive heart failure. Surprisingly, renal neutral endopeptidase mRNA levels, assessed by quantitative reverse transcriptase–polymerase chain reaction; protein levels, assessed by Western blotting; and activity, assessed by gelatin gels, were comparable in all groups. Pulmonary neutral endopeptidase mRNA levels decreased by 45% in rats with severe congestive heart failure but not in rats with mild congestive heart failure. In addition, pulmonary neutral endopeptidase immunoreactivity levels and activity were significantly decreased in congestive heart failure in correlation with the severity of the disorder. We conclude that an increase in neutral endopeptidase expression or activity does not occur in rats with congestive heart failure, and therefore, an upregulation of neutral endopeptidase is unlikely to account for the blunted natriuretic response to the atrial natriuretic peptide and the positive sodium balance in congestive heart failure.

Published
1995

49. Effects of cyclosporin A on the synthesis, excretion, and metabolism of endothelin in the rat

Author

Federico Pieruzzi, Zaid Abassi, Farid Nakhoul, Harry R. Keiser, Abassi, Z, Pieruzzi, F, Nakhoul, F, and Keiser, H

Subjects
medicine.hormone, Male, medicine.medical_specialty, Molecular Sequence Data, Renal function, Biology, Endothelin-Converting Enzymes, Sulfonamide, Kidney, Endothelin, Nephrotoxicity, Endothelins, Rats, Sprague-Dawley, chemistry.chemical_compound, Internal medicine, Cyclosporin a, Metalloendopeptidase, Internal Medicine, medicine, Aspartic Acid Endopeptidase, Animals, Aspartic Acid Endopeptidases, Neprilysin, Creatinine, Sulfonamides, Base Sequence, Animal, Metalloendopeptidases, Bosentan, Recombinant Protein, Recombinant Proteins, Rats, Molecular Probe, medicine.anatomical_structure, Endocrinology, chemistry, Molecular Probes, Cyclosporine, Rat, Endothelin receptor
Abstract

Abstract Increasing evidence suggests that endothelin, a potent vasoconstrictor, is implicated in cyclosporin A (CsA)–induced nephrotoxicity. Increased levels of urinary and circulating endothelin have been described in CsA-treated humans and animals. The exact mechanisms by which CsA induces these increases are still unknown, and no data indicate whether these elevated levels reflect increased synthesis or decreased clearance of endothelin. In the present study, we investigated the effects of CsA administration (50 mg/kg per day IP for 6 days) to rats on plasma and urinary levels of endothelin; expression of endothelin-1 (ET-1), ET-3, and endothelin-converting enzyme in renal tissue; clearance of infused 125 I–ET-1; and degradation of 125 I–ET-1 by recombinant neutral endopeptidase. Rats given CsA for 6 days developed severe renal insufficiency, as shown by a 74% decrease in creatinine clearance rate (Ccr) ( P P P 125 I–ET-1 from the blood or the renal and pulmonary uptake of the peptide. Moreover, CsA did not affect the degradation of 125 I–ET-1 by highly purified recombinant neutral endopeptidase, a well-known endothelinase. Taken together, these data suggest that the elevated urinary endothelin levels obtained after CsA treatment originate from the kidney and reflect increased renal synthesis of ET-1. Moreover, the production of endothelin appears to be regulated at the mRNA transcription level, and expressions of ET-1 and ET-3 are regulated independently.

50. Patients with Gaucher disease display systemic elevation of ACE2, which is impacted by therapy status and genotype.

Author

Fokra A, Feldman HB, Kurolap A, Kinaneh S, Abassi Z, and Hershkovitz T

Abstract

Gaucher disease (GD) has a high carrier rate among Ashkenazi Jews.The most common disease-causing variant in this population N370S, is also prevalent pan-ethnically. This has led to speculations of some protective effect for carriers of this variant. During the recent COVID-19 pandemic, GD patients reportedly had a surprisingly low infection rate and mild symptoms considering their disease status. As SARS-CoV-2 gains entry into the cell via membrane-bound angiotensin-converting enzyme 2 (ACE2), we speculated that differences in levels of soluble ACE2 in GD patients could contribute to this protective state. While ACE is known to be elevated in GD, to our knowledge, ACE2 levels have not been explored. We measured serum and macrophage-bound levels of ACE and ACE2 by ELISA and western blot, respectively, in GD patients and age- and sex-matched controls. Our results reveal a significant elevation of both serum and macrophage-bound ACE and ACE2 in GD patients compared to healthy controls. This elevation appears to be mitigated by GD treatment. Moreover, the most robust ACE2 elevation was observed in N370S homozygotes, and was not effected by treatment. Since coronaviruses use the ACE2 receptor as a gateway for host cell entry, we speculate that elevated circulating ACE2 may serve as a decoy. This might explain the observed mild infections in GD patients during the COVID-19 pandemic., Competing Interests: Declaration of competing interest HBF received support from Genzyme for attending meetings, participation on a data safety monitoring board and ICGG scientific advisory board. TH received honoraria for lectures from Takeda. All other authors have no conflicts of interest to declare., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Published
2024
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