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31 results on '"Netti, G. S."'

1. Pentraxin-3-mediated complement activation in a swine model of renal ischemia/reperfusion injury

Author

Divella, C., Stasi, A., Franzin, R., Rossini, M., Pontrelli, P., Sallustio, F., Netti, G. S., Ranieri, E., Lacitignola, L., Staffieri, F., Crovace, A. M., Lucarelli, G., Ditonno, P., Battaglia, M., Daha, M. R., van der Pol, P., van Kooten, C., Grandaliano, Giuseppe, Gesualdo, L., Stallone, G., Castellano, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Divella, C., Stasi, A., Franzin, R., Rossini, M., Pontrelli, P., Sallustio, F., Netti, G. S., Ranieri, E., Lacitignola, L., Staffieri, F., Crovace, A. M., Lucarelli, G., Ditonno, P., Battaglia, M., Daha, M. R., van der Pol, P., van Kooten, C., Grandaliano, Giuseppe, Gesualdo, L., Stallone, G., Castellano, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Pentraxins are a family of evolutionarily conserved pattern recognition molecules with pivotal roles in innate immunity and inflammation, such as opsonization of pathogens during bacterial and viral infections. In particular, the long Pentraxin 3 (PTX3) has been shown to regulate several aspects of vascular and tissue inflammation during solid organ transplantation. Our study investigated the role of PTX3 as possible modulator of Complement activation in a swine model of renal ischemia/reperfusion (I/R) injury. We demonstrated that I/R injury induced early PTX3 deposits at peritubular and glomerular capillary levels. Confocal laser scanning microscopy revealed PTX3 deposits co-localizing with CD31+ endothelial cells. In addition, PTX3 was associated with infiltrating macrophages (CD163), dendritic cells (SWC3a) and myofibroblasts (FSP1). In particular, we demonstrated a significant PTX3-mediated activation of classical (C1q-mediated) and lectin (MBL-mediated) pathways of Complement. Interestingly, PTX3 deposits co-localized with activation of the terminal Complement complex (C5b-9) on endothelial cells, indicating that PTX3-mediated Complement activation occurred mainly at the renal vascular level. In conclusion, these data indicate that PTX3 might be a potential therapeutic target to prevent Complement-induced I/R injury.

Published
2021

2. mTOR inhibition improves mitochondria function/biogenesis and delays cardiovascular aging in kidney transplant recipients with chronic graft dysfunction

Author

Infante, B., Bellanti, F., Correale, M., Pontrelli, P., Franzin, R., Leo, S., Calvaruso, M., Mercuri, S., Netti, G. S., Ranieri, E., Brunetti, N. D., Grandaliano, G., Gesualdo, L., Serviddio, G., Castellano, G., Stallone, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Infante, B., Bellanti, F., Correale, M., Pontrelli, P., Franzin, R., Leo, S., Calvaruso, M., Mercuri, S., Netti, G. S., Ranieri, E., Brunetti, N. D., Grandaliano, G., Gesualdo, L., Serviddio, G., Castellano, G., Stallone, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

CVD remains the major cause of mortality with graft functioning in Kidney transplant recipients (KTRs), with an estimated risk of CV events about 50-fold higher than in the general population. Many strategies have been considered to reduce the CV risk such as the use of mTOR inhibitors. We evaluate whether chronic mTOR inhibition might influence CV aging in KTRs studying the molecular mechanisms involved in this effect. We retrospectively analyzed 210 KTRs with stable graft function on therapy with CNI and mycophenolic acid (Group A, 105 pts.), or with CNI and mTORi (Everolimus, Group B, 105 pts.). The presence of mTOR inhibitor in immunosuppressive therapy was associated to increase serum levels of Klotho with concomitant reduction in FGF-23, with a significant decrease in left ventricular mass. In addition, KTRs with mTORi improved mitochondrial function/biogenesis in PBMC with more efficient oxidative phosphorylation, antioxidant capacity and glutathione peroxidase activity. Finally, group B KTRs presented reduced levels of inflammaging markers such as reduced serum pentraxin-3 and p21ink expression in PBMC. In conclusion, we demonstrated that mTOR inhibition in immunosuppressive protocols prevents the occurrence and signs of CV aging in KTRs.

Published
2021

3. Modulation of complement activation by pentraxin-3 in prostate cancer

Author

Stallone, G., Netti, G. S., Cormio, L., Castellano, G., Infante, B., Pontrelli, P., Divella, C., Selvaggio, O., Spadaccino, F., Ranieri, E., Sanguedolce, F., Pennella, A., Gesualdo, L., Carrieri, G., Grandaliano, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Stallone, G., Netti, G. S., Cormio, L., Castellano, G., Infante, B., Pontrelli, P., Divella, C., Selvaggio, O., Spadaccino, F., Ranieri, E., Sanguedolce, F., Pennella, A., Gesualdo, L., Carrieri, G., Grandaliano, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Pentraxin 3 (PTX3) is an essential component of the innate immune system and a recognized modulator of Complement cascade. The role of Complement system in the pathogenesis of prostate cancer has been largely underestimated. The aim of our study was to investigate the role of PTX3 as possible modulator of Complement activation in the development of this neoplasia. We performed a single center cohort study; from January 2017 through December 2018, serum and prostate tissue samples were obtained from 620 patients undergoing prostate biopsy. A group of patients with benign prostatic hyperplasia (BPH) underwent a second biopsy within 12–36 months demonstrating the presence of a prostate cancer (Group A, n = 40) or confirming the diagnosis of BPH (Group B, N = 40). We measured tissue PTX3 protein expression together with complement activation by confocal microscopy in the first and second biopsy in group A and B patients. We confirmed that that PTX3 tissue expression in the first biopsy was increased in group A compared to group B patients. C1q deposits were extensively present in group A patients co-localizing and significantly correlating with PTX3 deposits; on the contrary, C1q/PTX3 deposits were negative in group B. Moreover, we found a significantly increased expression of C3a and C5a receptors within resident cells in group A patient. Interestingly, C1q/PTX3 deposits were not associated with activation of the terminal Complement complex C5b-9; moreover, we found a significant increase of Complement inhibitor CD59 in cancer tissue. Our data indicate that PTX3 might play a significant pathogenic role in the development of this neoplasia through recruitment of the early components of Complement cascade with hampered activation of terminal Complement pathway associated with the upregulation of CD59. This alteration might lead to the PTX3-mediated promotion of cellular proliferation, angiogenesis and insensitivity to apoptosis possible leading to cancer cell i

Published
2020

4. IgE-mediated immune response and antibody-mediated rejection

Author

Rascio, F., Pontrelli, P., Netti, G. S., Manno, E., Infante, B., Simone, S., Castellano, G., Ranieri, E., Seveso, M., Cozzi, E., Gesualdo, L., Stallone, G., Grandaliano, Giuseppe, Grandaliano G. (ORCID:0000-0003-1213-2177), Rascio, F., Pontrelli, P., Netti, G. S., Manno, E., Infante, B., Simone, S., Castellano, G., Ranieri, E., Seveso, M., Cozzi, E., Gesualdo, L., Stallone, G., Grandaliano, Giuseppe, and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Background and objectives Active antibody-mediated rejection is the main cause of kidney transplant loss, sharing with SLE the alloimmune response and the systemic activation of the IFN-a pathway. IgE-mediated immune response plays a key role in the development of SLE nephritis and is associated with IFN-a secretion. The aim of our study was to investigate IgE-mediated immune response in antibody-mediated rejection. Design, setting, participants, & measurements This was a cross-sectional study of 56 biopsy-proven antibodymediated rejection study participants, 80 recipients with normal graft function/histology (control), 16 study participants with interstitial fibrosis/tubular atrophy, and six participants with SLE. We evaluated graft IgE deposition, tryptase (a mast cell marker), and CD203 (a specific marker of activated basophils) by immunofluorescence/confocal microscopy. In addition, we measured serum concentration of human myxovirus resistance protein 1, an IFN-a–induced protein, and anti-HLA IgE. Results We observed a significantly higher IgE deposition in tubules and glomeruli in antibody-mediated rejection (1766679 pixels) and SLE (1495643 pixels) compared with interstitial fibrosis/tubular atrophy (5826122 pixels) and control (253650 pixels). Patients with antibody-mediated rejection, but not control patients and patients with interstitial fibrosis/tubular atrophy, presented circulating anti-HLA IgE antibodies, although with a low mean fluorescence intensity. In addition, immunofluorescence revealed the presence of both mast cells and activated basophils in antibody-mediated rejection but not in control and interstitial fibrosis/tubular atrophy. The concentration of circulating basophils was significantly higher in antibody-mediated rejection compared with control and interstitial fibrosis/tubular atrophy. MxA serum levels were significantly higher in antibodymediated rejection compared with control and correlated with the extent of IgE deposition. Concl

Published
2020

5. Altered phosphorylation of cytoskeleton proteins in peripheral blood mononuclear cells characterizes chronic antibody-mediated rejection in kidney transplantation

Author

Rocchetti, M. T., Rascio, F., Castellano, G., Fiorentino, M., Netti, G. S., Spadaccino, F., Ranieri, E., Gallone, A., Gesualdo, L., Stallone, G., Pontrelli, P., Grandaliano, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Rocchetti, M. T., Rascio, F., Castellano, G., Fiorentino, M., Netti, G. S., Spadaccino, F., Ranieri, E., Gallone, A., Gesualdo, L., Stallone, G., Pontrelli, P., Grandaliano, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Chronic antibody-mediated rejection (CAMR) is the major cause of kidney transplant failure. The molecular mechanisms underlying this event are still poorly defined and this lack of knowledge deeply influences the potential therapeutic strategies. The aim of our study was to analyze the phosphoproteome of peripheral blood mononuclear cells (PBMCs), to identify cellular signaling networks differentially activated in CAMR. Phosphoproteins isolated from PBMCs of biopsy proven CAMR, kidney transplant recipients with normal graft function and histology and healthy immunocompetent individuals, have been investigated by proteomic analysis. Phosphoproteomic results were confirmed by Western blot and PBMCs’ confocal microscopy analyses. Overall, 38 PBMCs samples were analyzed. A differential analysis of PBMCs’ phosphoproteomes revealed an increase of lactotransferrin, actin-related protein 2 (ARPC2) and calgranulin-B in antibody-mediated rejection patients, compared to controls. Increased expression of phosphorylated ARPC2 and its correlation to F-actin filaments were confirmed in CAMR patients. Our results are the first evidence of altered cytoskeleton organization in circulating immune cells of CAMR patients. The increased expression of phosphorylated ARPC2 found in the PBMCs of our patients, and its association with derangement of F-actin filaments, might suggest that proteins regulating actin dynamics in immune cells could be involved in the mechanism of CAMR of kidney grafts.

Published
2020

6. LPS-binding protein modulates acute renal fibrosis by inducing pericyte-to-myofibroblast trans-differentiation through TLR-4 signaling

Author

Castellano, G., Stasi, A., Franzin, R., Sallustio, F., Divella, C., Spinelli, A., Netti, G. S., Fiaccadori, E., Cantaluppi, V., Crovace, A., Staffieri, F., Lacitignola, L., Grandaliano, G. (ORCID:0000-0003-1213-2177), Simone, S., Pertosa, G. B., Gesualdo, L., Castellano, G., Stasi, A., Franzin, R., Sallustio, F., Divella, C., Spinelli, A., Netti, G. S., Fiaccadori, E., Cantaluppi, V., Crovace, A., Staffieri, F., Lacitignola, L., Grandaliano, G. (ORCID:0000-0003-1213-2177), Simone, S., Pertosa, G. B., and Gesualdo, L.

Abstract

During sepsis, the increased synthesis of circulating lipopolysaccharide (LPS)-binding protein (LBP) activates LPS/TLR4 signaling in renal resident cells, leading to acute kidney injury (AKI). Pericytes are the major source of myofibroblasts during chronic kidney disease (CKD), but their involvement in AKI is poorly understood. Here, we investigate the occurrence of pericyte-to-myofibroblast trans-differentiation (PMT) in sepsis-induced AKI. In a swine model of sepsis-induced AKI, PMT was detected within 9 h from LPS injection, as evaluated by the reduction of physiologic PDGFRβ expression and the dysfunctional α-SMA increase in peritubular pericytes. The therapeutic intervention by citrate-based coupled plasma filtration adsorption (CPFA) significantly reduced LBP, TGF-β, and endothelin-1 (ET-1) serum levels, and furthermore preserved PDGFRβ and decreased α-SMA expression in renal biopsies. In vitro, both LPS and septic sera led to PMT with a significant increase in Collagen I synthesis and α-SMA reorganization in contractile fibers by both SMAD2/3-dependent and-independent TGF-β signaling. Interestingly, the removal of LBP from septic plasma inhibited PMT. Finally, LPS-stimulated pericytes secreted LBP and TGF-β and underwent PMT also upon TGF-β receptor-blocking, indicating the crucial pro-fibrotic role of TLR4 signaling. Our data demonstrate that the selective removal of LBP may represent a therapeutic option to prevent PMT and the development of acute renal fibrosis in sepsis-induced AKI.

Published
2019

7. LPS removal reduces CD80-mediated albuminuria in critically ill patients with gram-negative sepsis

Author

Netti, G. S., Sangregorio, F., Spadaccino, F., Staffieri, F., Crovace, A., Infante, B., Maiorano, A., Godeas, G., Castellano, G., Palma, A. M. D., Prattichizzo, C., Cotoia, A., Mirabella, L., Gesualdo, L., Cinnella, G., Stallone, G., Ranieri, E., Grandaliano, G., Grandaliano G. (ORCID:0000-0003-1213-2177), Netti, G. S., Sangregorio, F., Spadaccino, F., Staffieri, F., Crovace, A., Infante, B., Maiorano, A., Godeas, G., Castellano, G., Palma, A. M. D., Prattichizzo, C., Cotoia, A., Mirabella, L., Gesualdo, L., Cinnella, G., Stallone, G., Ranieri, E., Grandaliano, G., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

LPS-induced sepsis is a leading cause of acute kidney injury (AKI) in critically ill patients. LPS may induce CD80 expression in podocytes with subsequent onset of proteinuria, a risk factor for progressive chronic kidney disease (CKD) frequently observed after AKI. This study aimed to investigate the therapeutic efficacy of LPS removal in decreasing albuminuria through the reduction of podocyte CD80 expression. Between January 2015 and December 2017, 70 consecutive patients with Gram-negative sepsis-induced AKI were randomized to either have coupled plasma filtration and adsorption (CPFA) added to the standard care (n = 35) or not (n = 35). To elucidate the possible relationship between LPS-induced renal damage, proteinuria, and CD80 expression in Gram sepsis, a swine model of LPS-induced AKI was set up. Three hours after LPS infusion, animals were treated or not with CPFA for 6 h. Treatment with CPFA significantly reduced serum cytokines, C-reactive protein, procalcitonin, and endotoxin levels in patients with Gram-negative sepsis-induced AKI. CPFA significantly lowered also proteinuria and CD80 urinary excretion. In the swine model of LPS-induced AKI, CD80 glomerular expression, which was undetectable in control pigs, was markedly increased at the podocyte level in LPS-exposed animals. CPFA significantly reduced LPS-induced proteinuria and podocyte CD80 expression in septic pigs. Our data indicate that LPS induces albuminuria via podocyte expression of CD80 and suggest a possible role of timely LPS removal in preventing the maladaptive repair of the podocytes and the consequent increased risk of CKD in sepsis-induced AKI.

Published
2019

8. Serum Levels of BAFF and APRIL Predict Clinical Response in Anti-PLA2R-Positive Primary Membranous Nephropathy

Author

Netti, G. S., Infante, B., Spadaccino, F., Godeas, G., Corallo, M. G., Prisciandaro, C., Croce, L., Rotondi, M., Gesualdo, L., Stallone, G., Grandaliano, Giuseppe, Ranieri, E., Grandaliano G. (ORCID:0000-0003-1213-2177), Netti, G. S., Infante, B., Spadaccino, F., Godeas, G., Corallo, M. G., Prisciandaro, C., Croce, L., Rotondi, M., Gesualdo, L., Stallone, G., Grandaliano, Giuseppe, Ranieri, E., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Primary membranous nephropathy (PMN) is a renal-specific autoimmune disease caused by circulating autoantibodies that target glomerular podocyte antigens (PLA2R/THSD7A). However, very little is known on the molecular mechanisms controlling B cell response in this nephropathy. The present study was aimed at correlating the serum levels of B cell activators BAFF/BLyS and APRIL with the presence of anti-PLA2R antibodies in PMN patients and with long-term clinical outcome. To this aim, 51 patients with anti-PLA2R-positive biopsy-proven PMN and nephrotic range proteinuria (>3.5 g/24 hours) were enrolled between January 2009 and December 2015 and treated with conventional 6-month immunosuppressive therapy. After 6 months, 29 patients (56.9%) cleared circulating anti-PLA2R, while in remaining 22 (43.1%), they persisted. Intriguingly, in the first group, baseline serum levels of BAFF/BLyS and APRIL were significantly lower than those in the second one. Moreover, after 6 months of immunosuppressive therapy, an overall reduction in both cytokine serum levels was observed. However, in PMN patients with anti-PLA2R clearance, this reduction was more prominent, as compared with those with anti-PLA2R persistence. When related to clinical outcome, lower baseline BAFF/BLyS (<6.05 ng/mL) and APRIL (<4.20 ng/mL) serum levels were associated with significantly higher probability to achieve complete or partial remission after 24-month follow-up. After dividing the entire study cohort into three groups depending on both cytokine baseline serum levels, patients with both BAFF/BLyS and APRIL below the cut-off showed a significantly higher rate of complete or partial remission as compared with patients with only one cytokine above the cut-off, while the composite endpoint was achieved in a very low rate of patients with both cytokines above the cut-off. Taken together, these results provide new insights into the role of BAFF/BLyS and APRIL in both the pathogenesis of anti-PLA2R-pos

Published
2019

11. Aligned Nanofiber Topographies Enhance the Differentiation of Adult Renal Stem Cells into Glomerular Podocytes

Author

Sciancalepore, A. G., Moffa, M., Iandolo, D., Netti, G. S., Prattichizzo, C., Grandaliano, Giuseppe, Lucarelli, G., Cormio, L., Gesualdo, L., Pisignano, D., Grandaliano G. (ORCID:0000-0003-1213-2177), Sciancalepore, A. G., Moffa, M., Iandolo, D., Netti, G. S., Prattichizzo, C., Grandaliano, Giuseppe, Lucarelli, G., Cormio, L., Gesualdo, L., Pisignano, D., and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

The use of adult stem/progenitor cells is a challenge in current research about kidney functional regeneration. In this framework, material-induced stem cell differentiation can become a new paradigm to promote advances in therapies. Here, the effects of both isotropic and anisotropic fibrous topographies on the podocyte differentiation of adult renal stem cells (RSCs) from human donors are investigated. The proliferation rate of RSCs is analyzed, immunofluorescence and genetic analyses of specific podocyte markers (Wilms’ tumor 1 gene, nephrin, and podocin) are performed to assess the differentiation level on the scaffolds. The studied markers are over-expressed in RSCs cultured on aligned fibers compared to cells cultured on either protein-functionalized films or randomly oriented fibers. In addition, RSCs cultured on aligned fibers are found to differentiate toward podocyte precursors even in basal medium conditions, thus highlighting scaffold-induced commitment without exogenous chemicals or cellular reprogramming. Aligned polymer fiber scaffolds which provide instructive cues for RSC differentiation might lead to new biomimetic systems for renal stem cell engineering.

Published
2018

12. FO015LPS REMOVAL REDUCES CD80-MEDIATED MICROALBUMINURIA IN CRITICALLY ILL PATIENTS WITH GRAM-NEGATIVE SEPSIS PREVENTING ACUTE TO CHRONIC KIDNEY DISEASE TRANSITION

Author

Netti, G S, primary, Sangregorio, F, additional, Staffieri, F, additional, Crovace, A, additional, Infante, B, additional, Maiorano, A M, additional, Castellano, G, additional, Di Palma, A M, additional, Gesualdo, L, additional, Stallone, G, additional, Cinnella, G, additional, and Grandaliano, G, additional

Published
2018
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13. Semaphorin 3F expression is reduced in pregnancy complicated by preeclampsia. An observational clinical study

Author

Stallone, G., Matteo, M., Netti, G. S., Infante, B., Di Lorenzo, A., Prattichizzo, C., Carlucci, S., Trezza, F., Gesualdo, L., Greco, P., Grandaliano, Giuseppe, Grandaliano G. (ORCID:0000-0003-1213-2177), Stallone, G., Matteo, M., Netti, G. S., Infante, B., Di Lorenzo, A., Prattichizzo, C., Carlucci, S., Trezza, F., Gesualdo, L., Greco, P., Grandaliano, Giuseppe, and Grandaliano G. (ORCID:0000-0003-1213-2177)

Abstract

Background and objective Preeclampsia is a systemic disorder, affecting 2-10% of pregnancies, characterized by a deregulated pro-and anti-angiogenic balance. Semaphorin 3F is an angiogenesis inhibitor. We aimed to investigate whether semaphorin 3F expression is modulated in preeclampsia. Design, setting, participants, and measurements We performed two observational single center cohort studies between March 2013 and August 2014. In the first we enrolled 110 consecutive women, undergoing an elective cesarean section; in the second we included 150 consecutive women undergoing amniocentesis for routine clinical indications at 16-18 week of gestation. Semaphorin 3F concentration was evaluated in maternal peripheral blood, venous umbilical blood and amniotic fluid, along with its placenta protein expression at the time of delivery in the first study group and in the amniotic fluid at 16-18 weeks of gestation in the second study group. Results In the first study 19 patients presented at delivery with preeclampsia. Semaphorin 3F placenta tissue expression was significantly reduced in preeclampsia. In addition, semaphorin 3F level at delivery was significantly lower in serum, amniotic fluid and venous umbilical blood of preeclamptic patients compared with normal pregnant women. In the prospective cohort study 14 women developed preeclampsia. In this setting, semaphorin 3F amniotic level at 16-18 weeks of gestation was reduced in women who subsequently developed preeclampsia compared to women with a normal pregnancy. ROC curve analysis showed that semaphorin 3F amniotic levels could identify women at higher risk of preeclampsia. Conclusions Semaphorin 3F might represent a predictive biomarker of preeclampsia.

Published
2017

14. EXPERIMENTAL ACUTE KIDNEY INJURY

Author

Kuma, A., primary, Yamada, S., additional, Miyamoto, T., additional, Serino, R., additional, Tamura, M., additional, Otsuji, Y., additional, Kohno, K., additional, Cho, W. Y., additional, Kim, M.-G., additional, Jo, S.-K., additional, Kim, H. K., additional, Jado, J. C., additional, Humanes, B., additional, Lopez-Parra, V., additional, Camano, S., additional, Lara, J. M., additional, Cercenado, E., additional, Tejedor, A., additional, Lazaro, A., additional, Jansen, M., additional, Castellano, G., additional, Stasi, A., additional, Intini, A., additional, Gigante, M., additional, Di Palma, A. M., additional, Divella, C., additional, Netti, G. S., additional, Prattichizzo, C., additional, Pontrelli, P., additional, Crovace, A., additional, Staffieri, F., additional, Fiaccadori, E., additional, Brienza, N., additional, Grandaliano, G., additional, Pertosa, G. B., additional, Gesualdo, L., additional, Xanthopoulou, K., additional, Tsouchnikas, I., additional, Ouzounidis, G., additional, Kokaraki, G., additional, Lagoudaki, R., additional, Simeonidou, C., additional, Karkavelas, G., additional, Spandou, E., additional, Tsakiris, D., additional, Kallaras, K., additional, Schneider, R., additional, Meusel, M., additional, Betz, B. B., additional, Held, C., additional, Moller-Ehrlich, K., additional, Buttner-Herold, M., additional, Wanner, C., additional, Michael, G., additional, Sauvant, C., additional, Hosszu, A., additional, Antal, Z., additional, Hodrea, J., additional, Koszegi, S., additional, Banki, N. F., additional, Wagner, L., additional, Lenart, L., additional, Vannay, A., additional, Szabo, A. J., additional, Fekete, A., additional, Michael, A., additional, Faga, T., additional, Navarra, M., additional, Andreucci, M., additional, Lemoine, S., additional, Pillot, B., additional, Rabeyrin, M., additional, Varennes, A., additional, Ovize, M., additional, Juillard, L., additional, Gomes Santana, L., additional, Silva Almeida, W., additional, Schor, N., additional, Watanabe, M., additional, Fonseca, C. D., additional, Pessoa, E. A., additional, Mendonca, M. H., additional, Fernandes, S. M., additional, Borges, F. T., additional, Vattimo, M. F., additional, Ow, C. P. C., additional, Tassone, F., additional, Koeners, M. P., additional, Malpas, S. C., additional, Evans, R. G., additional, Alfarano, C., additional, Guardia, M.-A., additional, Lluel, P., additional, Palea, S., additional, Young, G.-H., additional, Wu, V.-C., additional, Choi, D. E., additional, Jeong, J. Y., additional, Chang, Y. K., additional, Chung, S., additional, Na, K. R., additional, Kim, S. S., additional, Lee, K. W., additional, Yang, Y., additional, Zhang, L., additional, Fu, P., additional, Zhao, Y., additional, Zhang, X., additional, Jadot, I., additional, Decleves, A.-E., additional, Colombaro, V., additional, Martin, B., additional, Voisin, V., additional, Habsch, I., additional, Deprez, E., additional, Nortier, J., additional, Caron, N., additional, Iwakura, T., additional, Fujikura, T., additional, Ohashi, N., additional, Yasuda, H., additional, Fujigaki, Y., additional, Vasco, C. F., additional, Vattimo, M. D. F. F., additional, Draibe, J., additional, Y ld r m, Y., additional, Aba, O., additional, Y lmaz, Z., additional, Kadiroglu, A. K., additional, Y lmaz, M. E., additional, Gul, M., additional, Ketani, A., additional, Colpan, L., additional, Neiva, L. B. d. M., additional, Suller Garcia, J., additional, Oliveira, A. S. d., additional, Naves, M. A., additional, Van Swelm, R. P. L., additional, Wetzels, J. F. M., additional, Verweij, V. G. M., additional, Laarakkers, C. M. M., additional, Pertijs, J. C. L. M., additional, Swinkels, D. W., additional, Masereeuw, R., additional, Sereno, J., additional, Rodrigues-Santos, P., additional, Vala, H., additional, Rocha-Pereira, P., additional, Fernandes, J., additional, Santos-Silva, A., additional, Teixeira, F., additional, Reis, F., additional, Altuntas, A., additional, Yilmaz, H. R., additional, Uz, E., additional, Demir, M., additional, Gokcimen, A., additional, Bayram, D. S., additional, Aksu, O., additional, Sezer, M. T., additional, Yang, K. H., additional, Jung, Y. J., additional, Kim, D., additional, Lee, A. S., additional, Lee, S., additional, Kang, K. P., additional, Park, S. K., additional, Kim, W., additional, Junglee, N. A., additional, Searell, C. R., additional, Jibani, M. M., additional, Macdonald, J. H., additional, Wu, C.-C., additional, Chen, C.-C., additional, Lu, K.-C., additional, Lin, Y.-F., additional, Estrela, G. R., additional, Wasinski, F., additional, Pereira, R., additional, Malheiros, D., additional, Camara, N. O. S., additional, Araujo, R. C., additional, Ramos, M. F., additional, Passos, C. d. S., additional, Razvickas, C. V., additional, Borges, F., additional, Ormanji, M., additional, Plotnikov, E., additional, Morosanova, M., additional, Pevzner, I., additional, Zorova, L., additional, Manskikh, V., additional, Skulachev, M., additional, Skulachev, V., additional, Zorov, D., additional, Pinto, C. F., additional, and Vattimo, M., additional

Published
2014
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15. 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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16. Experimental pathology

Author

Yi Chun, D. X., primary, Alexandre, H., additional, Edith, B., additional, Nacera, O., additional, Julie, P., additional, Chantal, J., additional, Eric, R., additional, Zhang, X., additional, Jin, Y., additional, Miravete, M., additional, Dissard, R., additional, Klein, J., additional, Gonzalez, J., additional, Caubet, C., additional, Pecher, C., additional, Pipy, B., additional, Bascands, J.-L., additional, Mercier-Bonin, M., additional, Schanstra, J., additional, Buffin-Meyer, B., additional, Claire, R., additional, Rigothier, C., additional, Richard, D., additional, Sebastien, L., additional, Moin, S., additional, Chantal, B., additional, Christian, C., additional, Jean, R., additional, Migliori, M., additional, Cantaluppi, V., additional, Mannari, C., additional, Medica, D., additional, Giovannini, L., additional, Panichi, V., additional, Goldwich, A., additional, Alexander, S., additional, Andre, G., additional, Amann, K., additional, Migliorini, A., additional, Sagrinati, C., additional, Angelotti, M. L., additional, Mulay, S. R., additional, Ronconi, E., additional, Peired, A., additional, Romagnani, P., additional, Anders, H.-J., additional, Chiang, W. C., additional, Lai, C. F., additional, Peng, W.-H., additional, Wu, C. F., additional, Chang, F.-C., additional, Chen, Y.-T., additional, Lin, S.-L., additional, Chen, Y. M., additional, Wu, K. D., additional, Lu, K.-S., additional, Tsai, T. J., additional, Virgine, O., additional, Qing Feng, F., additional, Zhang, S.-Y., additional, Dominique, D., additional, Vincent, A., additional, Marina, C., additional, Philippe, L., additional, Georges, G., additional, Pawlak, A., additional, Sahali, D., additional, Matsumoto, S., additional, Kiyomoto, H., additional, Ichimura, A., additional, Dan, T., additional, Nakamichi, T., additional, Tsujita, T., additional, Akahori, K., additional, Ito, S., additional, Miyata, T., additional, Xie, S., additional, Zhang, B., additional, Shi, W., additional, Yang, Y., additional, Nagasu, H., additional, Satoh, M., additional, Kidokoro, K., additional, Nishi, Y., additional, Ihoriya, C., additional, Kadoya, H., additional, Sasaki, T., additional, Kashihara, N., additional, Wu, C.-F., additional, Chou, Y.-H., additional, Duffield, J., additional, Rocca, C., additional, Gregorini, M., additional, Corradetti, V., additional, Valsania, T., additional, Bedino, G., additional, Bosio, F., additional, Pattonieri, E. F., additional, Esposito, P., additional, Sepe, V., additional, Libetta, C., additional, Rampino, T., additional, Dal Canton, A., additional, Omori, H., additional, Kawada, N., additional, Inoue, K., additional, Ueda, Y., additional, Yamamoto, R., additional, Matsui, I., additional, Kaimori, J., additional, Takabatake, Y., additional, Moriyama, T., additional, Isaka, Y., additional, Rakugi, H., additional, Wasilewska, A., additional, Taranta-Janusz, K., additional, Deebek, W., additional, Kuroczycka-Saniutycz, E., additional, Lee, A. S., additional, Lee, J. E., additional, Jung, Y. J., additional, Kang, K. P., additional, Lee, S., additional, Kim, W., additional, Arfian, N., additional, Emoto, N., additional, Yagi, K., additional, Nakayama, K., additional, Hartopo, A. B., additional, Nugrahaningsih, D. A., additional, Yanagisawa, M., additional, Hirata, K.-I., additional, Munoz-Felix, J. M., additional, Lopez-Novoa, J. M., additional, Martinez-Salgado, C., additional, Oujo, B., additional, Arevalo, M., additional, Bernabeu, C., additional, Perez-Barriocanal, F., additional, Jesper, K., additional, Nathalie, V., additional, Pierre, G., additional, Yi Chun, D. X., additional, Iyoda, M., additional, Shibata, T., additional, Matsumoto, K., additional, Shindo-Hirai, Y., additional, Kuno, Y., additional, Wada, Y., additional, Akizawa, T., additional, Schwartz, I., additional, Schwartz, D., additional, Prot Bertoye, C., additional, Terryn, S., additional, Claver, J., additional, Beghdadi, W. B., additional, Monteiro, R., additional, Blank, U., additional, Devuyst, O., additional, Daugas, E., additional, Van Beneden, K., additional, Geers, C., additional, Pauwels, M., additional, Mannaerts, I., additional, Van den Branden, C., additional, Van Grunsven, L. A., additional, Seckin, I., additional, Pekpak, M., additional, Uzunalan, M., additional, Uruluer, B., additional, Kokturk, S., additional, Ozturk, Z., additional, Sonmez, H., additional, Yaprak, E., additional, Furuno, Y., additional, Tsutsui, M., additional, Morishita, T., additional, Shimokawa, H., additional, Otsuji, Y., additional, Yanagihara, N., additional, Kabashima, N., additional, Ryota, S., additional, Kanegae, K., additional, Miyamoto, T., additional, Nakamata, J., additional, Ishimatsu, N., additional, Tamura, M., additional, Nakagawa, T., additional, Ichikawa, K., additional, Miyamoto, M., additional, Takabayashi, D., additional, Yamazaki, H., additional, Kakeshita, K., additional, Koike, T., additional, Kagitani, S., additional, Tomoda, F., additional, Hamashima, T., additional, Ishii, Y., additional, Inoue, H., additional, Sasahara, M., additional, El Machhour, F., additional, Kerroch, M., additional, Mesnard, L., additional, Chatziantoniou, C., additional, Dussaule, J.-C., additional, Inui, K., additional, Sasai, F., additional, Maruta, Y., additional, Nishiwaki, H., additional, Kawashima, E., additional, Inoue, Y., additional, Yoshimura, A., additional, Musacchio, E., additional, Priante, G., additional, Valvason, C., additional, Sartori, L., additional, Baggio, B., additional, Kim, J. H., additional, Gross, O., additional, Diana, R., additional, Gry, D. H., additional, Asimal, B., additional, Johanna, T., additional, Imke, S.-E., additional, Lydia, W., additional, Gerhard-Anton, M., additional, Hassan, D., additional, Cano, J. L., additional, Griera, M., additional, Olmos, G., additional, Martin, P., additional, Cortes, M. A., additional, Lopez-Ongil, S., additional, Rodriguez-Puyol, D., additional, DE Frutos, S., additional, Gonzalez, M., additional, Luengo, A., additional, Rodriguez-Puyol, M., additional, Calleros, L., additional, Lupica, R., additional, Lacquaniti, A., additional, Donato, V., additional, Maggio, R., additional, Mastroeni, C., additional, Lucisano, S., additional, Cernaro, V., additional, Fazio, M. R., additional, Quartarone, A., additional, Buemi, M., additional, Kacik, M., additional, Goedicke, S., additional, Eggert, H., additional, Hoyer, J. D., additional, Wurm, S., additional, Steege, A., additional, Banas, M., additional, Kurtz, A., additional, Banas, B., additional, Lasagni, L., additional, Lazzeri, E., additional, Romoli, S., additional, Schaefer, I., additional, Teng, B., additional, Worthmann, K., additional, Haller, H., additional, Schiffer, M., additional, Prattichizzo, C., additional, Netti, G. S., additional, Rocchetti, M. T., additional, Cormio, L., additional, Carrieri, G., additional, Stallone, G., additional, Grandaliano, G., additional, Ranieri, E., additional, Gesualdo, L., additional, Kucher, A., additional, Smirnov, A., additional, Parastayeva, M., additional, Beresneva, O., additional, Kayukov, I., additional, Zubina, I., additional, Ivanova, G., additional, Abed, A., additional, Schlekenbach, L., additional, Foglia, B., additional, Kwak, B., additional, Chadjichristos, C., additional, Queisser, N., additional, Schupp, N., additional, Brand, S., additional, Himer, L., additional, Szebeni, B., additional, Sziksz, E., additional, Saijo, S., additional, Kis, E., additional, Prokai, A., additional, Banki, N. F., additional, Fekete, A., additional, Tulassay, T., additional, Vannay, A., additional, Hegner, B., additional, Schaub, T., additional, Lange, C., additional, Dragun, D., additional, Klinkhammer, B. M., additional, Rafael, K., additional, Monika, M., additional, Anna, M., additional, Van Roeyen, C., additional, Boor, P., additional, Eva Bettina, B., additional, Simon, O., additional, Esther, S., additional, Floege, J., additional, Kunter, U., additional, Janke, D., additional, Jankowski, J., additional, Hayashi, M., additional, Takamatsu, I., additional, Horimai, C., additional, Yoshida, T., additional, Seno DI Marco, G., additional, Koenig, M., additional, Stock, C., additional, Reiermann, S., additional, Amler, S., additional, Koehler, G., additional, Fobker, M., additional, Buck, F., additional, Pavenstaedt, H., additional, Lang, D., additional, Brand, M., additional, Plotnikov, E., additional, Morosanova, M., additional, Pevzner, I., additional, Zorova, L., additional, Pulkova, N., additional, Zorov, D., additional, Wornle, M., additional, Ribeiro, A., additional, Belling, F., additional, Merkle, M., additional, Nakazawa, D., additional, Nishio, S., additional, Shibasaki, S., additional, Tomaru, U., additional, Akihiro, I., additional, Kobayashi, I., additional, Imanishi, Y., additional, Kurajoh, M., additional, Nagata, Y., additional, Yamagata, M., additional, Emoto, M., additional, Michigami, T., additional, Ishimura, E., additional, Inaba, M., additional, Wu, C.-C., additional, Lu, K.-C., additional, Chen, J.-S., additional, Chu, P., additional, Lin, Y.-F., additional, Eller, K., additional, Schroll, A., additional, Kirsch, A., additional, Huber, J., additional, Weiss, G., additional, Theurl, I., additional, Rosenkranz, A. R., additional, Zawada, A., additional, Rogacev, K., additional, Achenbach, M., additional, Fliser, D., additional, Held, G., additional, Heine, G. H., additional, Miyamoto, Y., additional, Iwao, Y., additional, Watanabe, H., additional, Kadowaki, D., additional, Ishima, Y., additional, Chuang, V. T. G., additional, Sato, K., additional, Otagiri, M., additional, Maruyama, T., additional, Iwatani, H., additional, Honda, D., additional, Noguchi, T., additional, Tanaka, M., additional, Tanaka, H., additional, Fukagawa, M., additional, Pircher, J., additional, Koppel, S., additional, Mannell, H., additional, Krotz, F., additional, Virzi, G. M., additional, Bolin, C., additional, Cruz, D., additional, Scalzotto, E., additional, De Cal, M., additional, Vescovo, G., additional, Ronco, C., additional, Grobmayr, R., additional, Lech, M., additional, Ryu, M., additional, Aoshima, Y., additional, Mizobuchi, M., additional, Ogata, H., additional, Kumata, C., additional, Nakazawa, A., additional, Kondo, F., additional, Ono, N., additional, Koiwa, F., additional, Kinugasa, E., additional, Freisinger, W., additional, Lale, N., additional, Lampert, A., additional, Ditting, T., additional, Heinlein, S., additional, Schmieder, R. E., additional, Veelken, R., additional, Nave, H., additional, Perthel, R., additional, Suntharalingam, M., additional, Bode-Boger, S., additional, Beutel, G., additional, Kielstein, J., additional, Rodrigues-Diez, R., additional, Rayego-Mateos, S., additional, Lavoz, C., additional, Stark Aroeira, L. G., additional, Orejudo, M., additional, Alique, M., additional, Ortiz, A., additional, Egido, J., additional, Ruiz-Ortega, M., additional, Oskar, W., additional, Rusan, C., additional, Padberg, J.-S., additional, Wiesinger, A., additional, Reuter, S., additional, Grabner, A., additional, Kentrup, D., additional, Lukasz, A., additional, Oberleithner, H., additional, Pavenstadt, H., additional, Kumpers, P., additional, Eberhardt, H. U., additional, Skerka, C., additional, Chen, Q., additional, Hallstroem, T., additional, Hartmann, A., additional, Kemper, M. J., additional, Zipfel, P. F., additional, N'gome-Sendeyo, K., additional, Fan, Q.-F., additional, Toblli, J., additional, Cao, G., additional, Giani, J. F., additional, Dominici, F. P., additional, Kim, J. S., additional, Yang, J. W., additional, Kim, M. K., additional, Han, B. G., additional, and Choi, S. O., additional

Published
2012
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17. Cell signalling / Growth factors

Author

Koenigshausen, E., primary, Ruetze, M., additional, Zierhut, U., additional, Potthoff, S. A., additional, Woznowski, M., additional, Stegbauer, J., additional, Quack, I., additional, Rump, L. C., additional, Sellin, L., additional, Worthmann, K., additional, Leitges, M., additional, Dittrich-Breiholz, O., additional, Kracht, M., additional, Haller, H., additional, Schiffer, M., additional, Koenigshausen, E., additional, Grabowski, S., additional, Gerbaulet, L., additional, Kabbany, S., additional, Kramann, R., additional, Schneider, R., additional, Couson, S., additional, Kunter, U., additional, Floege, J., additional, Gigante, M., additional, De Martino, M., additional, Cormio, L., additional, Prattichizzo, C., additional, Cavalcanti, E., additional, Netti, G. S., additional, Montemurno, E., additional, Mancini, V., additional, Battaglia, M., additional, Gesualdo, L., additional, Carrieri, G., additional, and Ranieri, E., additional

Published
2011
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18. Genetic diseases and molecular genetics

Author

Stekrova, J., primary, Reiterova, J., additional, Elisakova, V., additional, Merta, M., additional, Kohoutova, M., additional, Tesar, V., additional, Suvakov, S., additional, Damjanovic, T., additional, Dimkovic, N., additional, Pljesa, S., additional, Savic-Radojevic, A., additional, Pljesa-Ercegovac, M., additional, Matic, M., additional, Djukic, T., additional, Coric, V., additional, Simic, T., additional, Gigante, M., additional, d'Altilia, M., additional, Montemurno, E., additional, Schirinzi, A., additional, Bruno, F., additional, Netti, G. S., additional, Ranieri, E., additional, Stallone, G., additional, Infante, B., additional, Grandaliano, G., additional, Gesualdo, L., additional, Maritati, F., additional, Alberici, F., additional, Bonatti, F., additional, Oliva, E., additional, Sinico, R. A., additional, Moroni, G., additional, Leoni, A., additional, Gregorini, G., additional, Jeannin, G., additional, Possenti, S., additional, Tumiati, B., additional, Grasselli, C., additional, Brugnano, R., additional, Salvarani, C., additional, Fraticelli, P., additional, Pavone, L., additional, Pesci, A., additional, Guida, G., additional, Neri, T. M., additional, Buzio, C., additional, Malerba, G., additional, Martorana, D., additional, Vaglio, A., additional, Santucci, L., additional, Candiano, G., additional, Cremasco, D., additional, Tosetto, E., additional, Del Prete, D., additional, Bruschi, M., additional, Ghiggeri, G. M., additional, Anglani, F., additional, Rainone, F., additional, Soldati, L., additional, Terranegra, A., additional, Arcidiacono, T., additional, Aloia, A., additional, Dogliotti, E., additional, Vezzoli, G., additional, Maruniak-Chudek, I., additional, Zenker, M., additional, Chudek, J., additional, Obeidova, L., additional, Stekrova, J., additional, Lnenicka, P., additional, Iwanitskiy, L. V., additional, Krasnova, T. N., additional, Samokhodskaya, L. M., additional, Bernasconi, A. R., additional, Albarracin, L., additional, Liste, A. A., additional, Politei, J. M., additional, Heguilen, R. M., additional, Kaito, H., additional, Nozu, K., additional, Nakanishi, K., additional, Hashimura, Y., additional, Shima, Y., additional, Ninchoji, T., additional, Yoshikawa, N., additional, Iijima, K., additional, Matsuo, M., additional, Hur, E., additional, Gungor, O., additional, Bozkurt, D., additional, Bozgul, S. M. K., additional, Caliskan, H., additional, Dusunur, F., additional, Basci, A., additional, Akcicek, F., additional, Duman, S., additional, Li, Y., additional, Wang, C., additional, Nan, L., additional, Hruskova, Z., additional, Brabcova, I., additional, Lanska, V., additional, Honsova, E., additional, Hanzal, V., additional, Borovicka, V., additional, Rysava, R., additional, Zachoval, R., additional, Viklicky, O., additional, Miltenberger-Miltenyi, G., additional, Almeida, E., additional, Calado, J., additional, Carvalho, F., additional, Pereira, S., additional, Teixeira, C., additional, Jorge, S., additional, Viana, H., additional, Gomes da Costa, A., additional, Yang, C.-S., additional, Tseng, M.-H., additional, Yang, S.-S., additional, and Lin, S.-H., additional

Published
2011
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26. Proteinuria in the prognosis of IgA nephropathy.

Author

Aucella F, Netti GS, Piemontese M, Cincione IR, Infante B, and Gesualdo L

Subjects
Glomerulonephritis, IGA diagnosis, Humans, Prognosis, Proteinuria diagnosis, Proteinuria therapy, Glomerulonephritis, IGA complications, Proteinuria complications
Abstract

IgA Nephropathy (IgAN) is the most common lesion causing primary glomerulonephritis in the world. The main clinical predictors of progression are: elevated blood pressure, high histological score and proteinuria. Although elevated serum creatinine concentration at diagnosis, increased excretion of cytochines, age at onset, obesity and genetic factors may all influence clinical outcome, it is quite clear that proteinuria is the hallmark of renal damage in IgAN. Patients with IgAN and little or no proteinuria (<500 mg/day) have low risk of progression in the short term, while the rate of decline in renal function is 25-fold faster in those with sustained proteinuria >3 g/day. The product of duration (years) and urinary protein excretion (g/day) at the time of renal biopsy is more significantly correlated with progression. So, this so called proteinuria index may be a useful predictor for glomerular and interstitial histopathological changes and the fate of renal function in IgAN. The progression of IgAN may be slowed by antihypertensive and antiproteinuric therapy, such as angiotensin converting enzyme inhibitors and/or angiotensin II receptor blockers, that can minimize secondary glomerular injury. Proteinuria has been shown to be an adverse prognostic factor in IgAN, with a strong relationship between proteinuria and prognosis and established importance of remission. Consequently, targeting proteinuria may be a valid surrogate for individualized kidney protective therapy.

Published
2009

27. [Proteomics and the kidney: an innovative approach to the study of renal disease].

Author

Netti GS, Rocchetti MT, Papale M, Centra M, Centonze D, Di Paolo S, Ranieri E, and Gesualdo L

Subjects
Animals, Biomarkers urine, Biomedical Research, Humans, Kidney physiopathology, Kidney Diseases physiopathology, Kidney Diseases urine, Kidney Diseases diagnosis, Proteomics
Abstract

In the post human genome era, several ''omics'' fields are emerging. Proteomics has experienced a rapid growth in the recent past and has great potential for the future. Proteomic technologies are used with increasing frequency also in nephrology. The aim of this review is to examine the recent application of emerging proteomic technologies to the study of renal physiology and pathophysiology. We highlight the use in renal research of a number of available techniques including 2-dimensional gel electrophoresis, liquid chromatography/mass spectrometry, surface-enhanced laser desorption/ionization, and capillary electrophoresis/mass spectrometry. We examine the role, efficacy and diagnostic potential of the different proteomic approaches, focusing on current difficulties and potential solutions. The integrating role of bioinformatics and the need for standardized procedures for sample preservation and analysis and reporting of results are also discussed. Although the field is still in an embryonic stage, the knowledge gained up to now is important not only for a better understanding of renal physiology and pathophysiology, but also for the identification of disease markers and the development and follow-up of new therapies. This review gives an overview of proteomics, providing background information, outlining the scopes, highlighting the applications in nephrology, and reporting advantages and limitations.

Published
2008

28. [Biofilters and biosensors].

Author

Netti GS, Centonze D, and Gesualdo L

Subjects
Filtration instrumentation, Humans, Biosensing Techniques, Renal Dialysis instrumentation
Abstract

Sepsis is the leading cause of morbidity and mortality in intensive care units (ICU). Acute renal failure (ARF) is a common condition, affecting approximately 5% of all hospitalized patients and up to 20% of critically ill patients. The combination of ARF and sepsis is associated with 75% mortality. Hyperglycemia and an increase in plasma lactate concentration are markers of poor prognosis in patients with sepsis; they often precede the onset of multiple organ dysfunction and ARF. Direct online measurement by means of amperometric biosensors would allow the early detection of increasing levels of both glucose and lactate, as well as the possibility to maintain glucose within a well-defined range. Current standards of care in ARF require synthetic membranes that substitute the small solute clearance function of the renal glomerulus, but they do not replace the transport, metabolic and endocrine functions of the renal proximal tubule cells. The application of cell therapy to the successful process of hemofiltration may therefore improve the poor prognosis of patients with ARF in the ICU. An extracorporeal bioartificial kidney consisting of a conventional hemofilter connected to a renal tubule assist device has demonstrated both in animal models of ARF and in phase I/II clinical trials its ability to successfully replace the filtration, transport, metabolic, and endocrine functions of the kidney. To improve the outcome of septic patients with ARF, multidisciplinary interactions and cooperation between basic, clinical and industrial researchers are mandatory; the development of new artificial or biological devices may allow online monitoring of biological parameters and better treatment of septic syndrome and related systemic complications.

Published
2007

29. [Chemokines: possible therapeutic targets and useful clinical parameters in renal transplantation].

Author

Mazzinghi B, Netti GS, Lazzeri E, and Romagnani P

Subjects
Graft Rejection etiology, Humans, Postoperative Complications etiology, Renal Insufficiency, Chronic etiology, Chemokines drug effects, Chemokines physiology, Graft Rejection prevention & control, Kidney Transplantation, Postoperative Complications prevention & control, Renal Insufficiency, Chronic prevention & control
Abstract

Chemokines are a family of small, structurally related cytokines that regulate trafficking of different subsets of leukocytes, thus critically regulating inflammation. The chemokine system influences allograft biology at 3 main levels: 1) the process of ischemia-reperfusion injury, 2) the induction of transplant tolerance, and 3) the pathogenesis of acute rejection and chronic allograft nephropathy. Accordingly, following ischemia/reperfusion in a rat model, CXCR2 produced at the graft level attracts and activates granulocytes, which in turn promotes graft damage. Moreover, in some experimental models CCR4 recruits T regulatory cells and mediates transplant tolerance. Furthermore, the discovery of the involvement of CXCR3 in the induction of the alloresponse to transplant suggests that this chemokine receptor might represent an important target for treatment of both acute rejection and chronic allograft nephropathy. Indeed, CXCR3 ligands play a pivotal role in the initiation and amplification of host alloresponses and also alter vascular cell functions, which explains their critical role not only in the development of acute rejection, but also in the pathogenesis of chronic allograft nephropathy, where both immune- and nonimmune- mediated mechanisms are involved. Finally, we have recently demonstrated that the pretransplant serum level of the CXCR3 ligand IP-10/CXCL10 is a clinically useful parameter for the identification of subjects with a high risk of acute rejection, chronic allograft nephropathy, and graft failure. This simple test could contribute to the prevention of acute rejections and the individualization of immunosuppressive therapies.

Published
2007

30. [Renal neoplasms and renal transplantation: current problems and future perspectives].

Author

Carrieri G, Netti GS, Perrone A, Stallone G, Selvaggi FP, and Gesualdo L

Subjects
Carcinoma, Renal Cell diagnosis, Carcinoma, Renal Cell surgery, Early Diagnosis, Humans, Polycystic Kidney Diseases diagnosis, Polycystic Kidney Diseases surgery, Tissue Donors, Kidney Neoplasms diagnosis, Kidney Neoplasms surgery, Kidney Transplantation adverse effects
Abstract

Primary carcinomas of the kidney can develop in renal transplantation in four sets of circumstances: (1) detected in the donor, (2) detected as a pre-existing neoplasm in the recipient prior to transplantation, (3) as de novo malignancies arising post-transplantation in the native kidneys of the recipient, (4) or in the graft. In Italy, any renal mass detected during harvesting does not allow the use of any organs for transplantation; however, several reports from other countries have already shown the safety and efficacy of transplanting kidneys with small (<4 cm), unifocal, subcapsular tumors, after resecting the lesion at the back table and verifying the negativity of the surgical margins; this strategy could also be evaluated in Italy to expand the donor pool. Acquired cystic kidney disease (ACKD) is commonly observed in uremic patients undergoing chronic hemodialysis (HD); numerous studies have reported an increased prevalence of renal cell carcinoma (RCC) in association with this nephropathy. The use of ultrasound, computerized axial tomography (CAT) and magnetic resonance imaging (MRI) has greatly improved the ability to detect renal tumors at earlier stages associated with ACKD and the morbidity and mortality rate, in either uremic or transplant patients. RCC in the transplanted kidney is rare and, when recognized, requires nephrectomy. However, a conservative approach with nephron sparing surgery has been reported for selected cases as a useful strategy to treat renal carcinoma in the allograft.

Published
2004

31. [Nutcracker syndrome: a difficult case of recurrent gross hematuria].

Author

Di Palma AM, Netti GS, Papagno F, Antonica G, Ettorre GC, Prisco T, and Gesualdo L

Subjects
Adolescent, Aorta, Abdominal, Humans, Male, Mesenteric Arteries, Recurrence, Syndrome, Hematuria etiology, Renal Veins, Vascular Diseases complications, Vascular Diseases diagnosis
Abstract

Background: The Nutcracker Syndrome (NS) is an uncommon clinical condition caused by compression and entrapment of the renal vein (LRV) as it passes through the angle between the superior mesenteric artery (SMA) and the aorta (meso-aortic angle). Intermittent macrohematuria, left peripelvic and gonadal vein varices and aspecific abdominal pain may be common manifestations of this syndrome., Case-Report: A 15-year-old white boy developed recurrent macrohaematuria in June 2002. He had a history of upper respiratory infection prior the first episode of gross hematuria followed by 4 other episodes of macrohematuria 'sine causa'. Blood pressure and renal function were normal. Routine laboratory tests showed only an increase in serum LDH levels (901 IU/L) with negative Coombs' test, both direct and indirect, and absence of schistocytes in the blood smear. Renal ultrasonography showed normal kidneys while an intravenous pyelography showed a 'minus' in the right ureter. For this reason, a cystoscopy and a retrograde pielography were performed but resulted normal. A renal biopsy was carried out because of the presence of one episode of post-infective macrohaematuria, but light microscopy and immunofluorescence examinations were found to be normal. Renal ultrasonography and Color Doppler ultrasonography (CD-USG) oriented our diagnosis towards NS. An abdominal computerised tomography (CT) scan confirmed that the LRV was compressed between the aorta and the SMA., Conclusions: NS cannot be diagnosed with routine diagnostic methods. Endoscopic and radiological methods may provide some clues for the presence of NS, while CD-USG may be considered to be the first level non-invasive method for diagnosis. The sensitivity and specificity of this test for diagnosing NS is reported as being 78% and 94%, respectively. The best treatment available for this syndrome is still being debated.

Published
2004

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