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2. Inhibition of transcription factor NFAT activity in activated platelets enhances their aggregation and exacerbates gram-negative bacterial septicemia

Author

Poli, V, Di Gioia, M, Sola-Visner, M, Granucci, F, Frelinger, A, Michelson, A, Zanoni, I, Poli V., Di Gioia M., Sola-Visner M., Granucci F., Frelinger A. L., Michelson A. D., Zanoni I., Poli, V, Di Gioia, M, Sola-Visner, M, Granucci, F, Frelinger, A, Michelson, A, Zanoni, I, Poli V., Di Gioia M., Sola-Visner M., Granucci F., Frelinger A. L., Michelson A. D., and Zanoni I.

Abstract

During gram-negative septicemia, interactions between platelets and neutrophils initiate a detrimental feedback loop that sustains neutrophil extracellular trap (NET) induction, disseminated intravascular coagulation, and inflammation. Understanding intracellular pathways that control platelet-neutrophil interactions is essential for identifying new therapeutic targets. Here, we found that thrombin signaling induced activation of the transcription factor NFAT in platelets. Using genetic and pharmacologic approaches, as well as iNFATuation, a newly developed mouse model in which NFAT activation can be abrogated in a cell-specific manner, we demonstrated that NFAT inhibition in activated murine and human platelets enhanced their activation and aggregation, as well as their interactions with neutrophils and NET induction. During gram-negative septicemia, NFAT inhibition in platelets promoted disease severity by increasing disseminated coagulation and NETosis. NFAT inhibition also partially restored coagulation ex vivo in patients with hypoactive platelets. Our results define non-transcriptional roles for NFAT that could be harnessed to address pressing clinical needs.

Published
2022

3. An adjuvant strategy enabled by modulation of the physical properties of microbial ligands expands antigen immunogenicity

Author

Borriello, F, Poli, V, Shrock, E, Spreafico, R, Liu, X, Pishesha, N, Carpenet, C, Chou, J, Di Gioia, M, Mcgrath, M, Dillen, C, Barrett, N, Lacanfora, L, Franco, M, Marongiu, L, Iwakura, Y, Pucci, F, Kruppa, M, Ma, Z, Lowman, D, Ensley, H, Nanishi, E, Saito, Y, O'Meara, T, Seo, H, Dhe-Paganon, S, Dowling, D, Frieman, M, Elledge, S, Levy, O, Irvine, D, Ploegh, H, Williams, D, Zanoni, I, Borriello F., Poli V., Shrock E., Spreafico R., Liu X., Pishesha N., Carpenet C., Chou J., Di Gioia M., McGrath M. E., Dillen C. A., Barrett N. A., Lacanfora L., Franco M. E., Marongiu L., Iwakura Y., Pucci F., Kruppa M. D., Ma Z., Lowman D. W., Ensley H. E., Nanishi E., Saito Y., O'Meara T. R., Seo H. -S., Dhe-Paganon S., Dowling D. J., Frieman M., Elledge S. J., Levy O., Irvine D. J., Ploegh H. L., Williams D. L., Zanoni I., Borriello, F, Poli, V, Shrock, E, Spreafico, R, Liu, X, Pishesha, N, Carpenet, C, Chou, J, Di Gioia, M, Mcgrath, M, Dillen, C, Barrett, N, Lacanfora, L, Franco, M, Marongiu, L, Iwakura, Y, Pucci, F, Kruppa, M, Ma, Z, Lowman, D, Ensley, H, Nanishi, E, Saito, Y, O'Meara, T, Seo, H, Dhe-Paganon, S, Dowling, D, Frieman, M, Elledge, S, Levy, O, Irvine, D, Ploegh, H, Williams, D, Zanoni, I, Borriello F., Poli V., Shrock E., Spreafico R., Liu X., Pishesha N., Carpenet C., Chou J., Di Gioia M., McGrath M. E., Dillen C. A., Barrett N. A., Lacanfora L., Franco M. E., Marongiu L., Iwakura Y., Pucci F., Kruppa M. D., Ma Z., Lowman D. W., Ensley H. E., Nanishi E., Saito Y., O'Meara T. R., Seo H. -S., Dhe-Paganon S., Dowling D. J., Frieman M., Elledge S. J., Levy O., Irvine D. J., Ploegh H. L., Williams D. L., and Zanoni I.

Abstract

Activation of the innate immune system via pattern recognition receptors (PRRs) is key to generate lasting adaptive immunity. PRRs detect unique chemical patterns associated with invading microorganisms, but whether and how the physical properties of PRR ligands influence the development of the immune response remains unknown. Through the study of fungal mannans, we show that the physical form of PRR ligands dictates the immune response. Soluble mannans are immunosilent in the periphery but elicit a potent pro-inflammatory response in the draining lymph node (dLN). By modulating the physical form of mannans, we developed a formulation that targets both the periphery and the dLN. When combined with viral glycoprotein antigens, this mannan formulation broadens epitope recognition, elicits potent antigen-specific neutralizing antibodies, and confers protection against viral infections of the lung. Thus, the physical properties of microbial ligands determine the outcome of the immune response and can be harnessed for vaccine development.

Published
2022

5. Effective targeting of breast cancer stem cells by combined inhibition of Sam68 and Rad51

Author

Turdo, A., Gaggianesi, M., Di Franco, S., Veschi, V., D'Accardo, C., Porcelli, G., Lo Iacono, M., Pillitteri, I., Verona, F., Militello, G., Zippo, A., Poli, V., Fagnocchi, L., Beyes, S., Stella, S., Lattanzio, R., Faldetta, N., Lentini, V. L., Porcasi, R., Pistone, G., Bongiorno, M. R., Stassi, G., De Maria Marchiano, Ruggero, Todaro, M., De Maria R. (ORCID:0000-0003-2255-0583), Turdo, A., Gaggianesi, M., Di Franco, S., Veschi, V., D'Accardo, C., Porcelli, G., Lo Iacono, M., Pillitteri, I., Verona, F., Militello, G., Zippo, A., Poli, V., Fagnocchi, L., Beyes, S., Stella, S., Lattanzio, R., Faldetta, N., Lentini, V. L., Porcasi, R., Pistone, G., Bongiorno, M. R., Stassi, G., De Maria Marchiano, Ruggero, Todaro, M., and De Maria R. (ORCID:0000-0003-2255-0583)

Abstract

Breast cancer (BC) is the second cause of cancer-related deceases in the worldwide female population. Despite the successful treatment advances, 25% of BC develops resistance to current therapeutic regimens, thereby remaining a major hurdle for patient management. Current therapies, targeting the molecular events underpinning the adaptive resistance, still require effort to improve BC treatment. Using BC sphere cells (BCSphCs) as a model, here we showed that BC stem-like cells express high levels of Myc, which requires the presence of the multifunctional DNA/RNA binding protein Sam68 for the DNA-damage repair. Analysis of a cohort of BC patients displayed that Sam68 is an independent negative factor correlated with the progression of the disease. Genetic inhibition of Sam68 caused a defect in PARP-induced PAR chain synthesis upon DNA-damaging insults, resulting in cell death of TNBC cells. In contrast, BC stem-like cells were able to survive due to an upregulation of Rad51. Importantly, the inhibition of Rad51 showed synthetic lethal effect with the silencing of Sam68, hampering the cell viability of patient-derived BCSphCs and stabilizing the growth of tumor xenografts, including those TNBC carrying BRCA mutation. Moreover, the analysis of Myc, Sam68 and Rad51 expression demarcated a signature of a poor outcome in a large cohort of BC patients. Thus, our findings suggest the importance of targeting Sam68-PARP1 axis and Rad51 as potential therapeutic candidates to counteract the expansion of BC cells with an aggressive phenotype.

Published
2022

12. Lysosomal protease deficiency or substrate overload induces an oxidative-stress mediated STAT3-dependent pathway of lysosomal homeostasis

Author

Martínez-Fábregas, J., Prescott, A., Kasteren, S.I. van, Pedrioli, D.L., McLean, I., Moles, A., Reinheckel, T., Poli, V., and Watts, C.

Subjects
Mice, Knockout, STAT3 Transcription Factor, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Science, Janus Kinase 2, Article, Cell Line, Mice, Inbred C57BL, Lysosomal Storage Diseases, Mice, Oxidative Stress, Cysteine Endopeptidases, Cysteine Proteases, Lysosomes, Animals, Humans, Kidney Diseases, RNA Interference, lcsh:Q, RNA, Small Interfering, lcsh:Science
Abstract

Diverse cellular processes depend on the lysosomal protease system but how cells regulate lysosomal proteolytic capacity is only partly understood. We show here that cells can respond to protease/substrate imbalance in this compartment by de novo expression of multiple lysosomal hydrolases. This response, exemplified here either by loss of asparagine endopeptidase (AEP) or other lysosomal cysteine proteases, or by increased endocytic substrate load, is not dependent on the transcription factor EB (TFEB) but rather is triggered by STAT3 activation downstream of lysosomal oxidative stress. Similar lysosomal adaptations are seen in mice and cells expressing a constitutively active form of STAT3. Our results reveal how cells can increase lysosomal protease capacity under ‘fed’ rather than ‘starved’ conditions that activate the TFEB system. In addition, STAT3 activation due to lysosomal stress likely explains the hyperproliferative kidney disease and splenomegaly observed in AEP-deficient mice., How cells regulate their lysosomal proteolytic capacity is only partly understood. Here, the authors show that lysosomal protease deficiency or substrate overload induces lysosomal stress leading to activation of a STAT3-dependent, TFEB-independent pathway of lysosomal hydrolase expression.

Published
2019

13. High dose intravenous immune globulins and plasma exchange in Guillain-Barré Syndrome

Author

Ravasio, A., Pasquinelli, M., Dossi, B. Currò, Neri, W., Guidi, C., Gessaroli, M., Rasi, F., Fabbri, R., Mazzini, G., Rebucci, GG., Padoan, G., Callegarini, C., Ciucci, G., Guidi, AR., Facchini, G., Galeotti, M., Casmiro, M., Bianchedi, G., Tola, MR., Govoni, V., Granieri, E., Tralli, G., Tugnoli, V., Mussuto, V., D'Alessandro, R., Guarino, M., Baldrati, R., Laudadio, S., Sacquegna, T., Salvi, F., Ambrosetto, G., Sorgato, P., Ferrari, V., Gentilini, M., Colombo, A., Merelli, E., Miele, V., Lolli, V., Santangelo, M., Motti, L., Guidetti, D., Solimè, F., Granella, F., Pavesi, G., Allegri, I., Falco, L., Scaglioni, A., Montanari, E., Cammarata, S., Poli, V., Emilia-Romagna Study Group on Clinical and Epidemiological Problems in Neurology Italy, and Participating Centers

Published
1995
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14. ARTERIAL SWITCH OPERATION AND PLASMA BIOMARKERS: ANALYSIS AND CORRELATION WITH EARLY POSTOPERATIVE OUTCOMES

Author

Giordano R, Cantinotti M, Arcieri L, Poli V, Pak V, Murzi B., Giordano, R, Cantinotti, M, Arcieri, L, Poli, V, Pak, V, and Murzi, B.

Abstract

The aims of our study were to describe plasma brain natriuretic peptide (BNP), Troponin I (TnI), and Cystatin C (Cys-C) concentration kinetics in the postoperative period after arterial switch operation in neonate, and to test the correlation between the plasma biomarkers and early clinical outcomes. We prospectively enrolled 29 neonates who underwent ASO. All patients received Custodiol cardioplegia. Blood samples were collected preoperatively (one day before) and in the ICU immediately after admission, and then 6, 12, 24, and 48 h after surgery. TnI peak (mean 17.23 ± 7.0 ng/mL) occurred between the arrival in the ICU and the 6th hour, then we had a constant decrease. TnI had a good correlation with the inotropic support time (r = 0.560, p = 0.0015) and ICU time (r = 0.407, p = 0.028), less than with ventilation and Hospital stay (r = 0.37, p = 0.0451 and r = 0.385, p = 0.0404). BNP peak (mean 4773.79 ± 2724.52 ng/L) was in the preoperative time with a constant decrease after the operation and it had no significant correlations with clinical outcomes. The CyS-C had the highest preoperative values, which decreased during the operating phase, and then constantly increased upon arrival to the ICU with a peak at 48 h (mean 1.76 ± 0.35 mg/L). CyS-C peak had a good correlation with a plasmatic creatinine peak (r = 0.579, p = 0.0009) but not with other clinical outcomes. Our study demonstrated significant correlations between the Tnl peak and early clinical outcomes in neonates undergoing arterial switch operation. Other plasma biomarkers such as the BNP and CyS-C had no direct correlation.

Published
2017

17. STAT3 controls the long-term survival and phenotype of repair Schwann cells during nerve regeneration

Author

Benito, C, Davis, Cm, Gomez-Sanchez, Ja, Turmaine, M, Meijer, D, Poli, V, Mirsky, R, and Jessen, Kr.

Subjects
Male, STAT3 Transcription Factor, Schwann, Neuroscience (all), denervation, injury, Brain-Derived Neurotrophic Factor, Development/Plasticity/Repair, nerve, regeneration, repair, Animals, Female, Glial Cell Line-Derived Neurotrophic Factor, Mice, Peripheral Nerve Injuries, Schwann Cells, Nerve Regeneration, Phenotype, nervous system, Research Articles
Abstract

After nerve injury, Schwann cells convert to a phenotype specialized to promote repair. But during the slow process of axonal regrowth, these repair Schwann cells gradually lose their regeneration-supportive features and eventually die. Although this is a key reason for the frequent regeneration failures in humans, the transcriptional mechanisms that control long-term survival and phenotype of repair cells have not been studied, and the molecular signaling underlying their decline is obscure. We show, in mice, that Schwann cell STAT3 has a dual role. It supports the long-term survival of repair Schwann cells and is required for the maintenance of repair Schwann cell properties. In contrast, STAT3 is less important for the initial generation of repair Schwann cells after injury. In repair Schwann cells, we find that Schwann cell STAT3 activation by Tyr705 phosphorylation is sustained during long-term denervation. STAT3 is required for maintaining autocrine Schwann cell survival signaling, and inactivation of Schwann cell STAT3 results in a striking loss of repair cells from chronically denervated distal stumps. STAT3 inactivation also results in abnormal morphology of repair cells and regeneration tracks, and failure to sustain expression of repair cell markers, including Shh, GDNF, and BDNF. Because Schwann cell development proceeds normally without STAT3, the function of this factor appears restricted to Schwann cells after injury. This identification of transcriptional mechanisms that support long-term survival and differentiation of repair cells will help identify, and eventually correct, the failures that lead to the deterioration of this important cell population. SIGNIFICANCE STATEMENT Although injured peripheral nerves contain repair Schwann cells that provide signals and spatial clues for promoting regeneration, the clinical outcome after nerve damage is frequently poor. A key reason for this is that, during the slow growth of axons through the proximal parts of injured nerves repair, Schwann cells gradually lose regeneration-supporting features and eventually die. Identification of signals that sustain repair cells is therefore an important goal. We have found that in mice the transcription factor STAT3 protects these cells from death and contributes to maintaining the molecular and morphological repair phenotype that promotes axonal regeneration. Defining the molecular mechanisms that maintain repair Schwann cells is an essential step toward developing therapeutic strategies that improve nerve regeneration and functional recovery.

Published
2017

18. Diagnosis and management of myocardial involvement in systemic immune-mediated diseases: A position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease

Author

Caforio, A.L.P. Adler, Y. Agostini, C. Allanore, Y. Anastasakis, A. Arad, M. Böhm, M. Charron, P. Elliott, P.M. Eriksson, U. Felix, S.B. Garcia-Pavia, P. Hachulla, E. Heymans, S. Imazio, M. Klingel, K. Marcolongo, R. Matucci Cerinic, M. Pantazis, A. Plein, S. Poli, V. Rigopoulos, A. Seferovic, P. Shoenfeld, Y. Zamorano, J.L. Linhart, A.

Published
2017

19. THE ROLE OF AORTOPEXY IN YHE SURGICAL MANAGEMENT OF THE LEFT MAIN STEM BRONCHUS COMPRESSION FROM DESCENDING AORTA-LEFT PULMONARY ARTERY FORCEPS: RESULTS OF A TEN YEARS EXPERIENCE BY A DEDICATED TEAM

Author

Arcieri L, Giordano R, Serio P, Fainardi V, Di Maurizio M, Melo M, Poli V, Pak V, Maizza A, Baggi R, Moschetti R, Assanta N, Cantinotti M, Chiappa E, Noccioli B, Mirabile L, Murzi B, Arcieri, L, Giordano, R, Serio, P, Fainardi, V, Di Maurizio, M, Melo, M, Poli, V, Pak, V, Maizza, A, Baggi, R, Moschetti, R, Assanta, N, Cantinotti, M, Chiappa, E, Noccioli, B, Mirabile, L, and Murzi, B

Published
2015

20. SUPRA-ANNULAR MITRAL VALVE IMPLANTATION IN VERY SMALL CHILDREN

Author

Giordano R, Cantinotti M, Pak V, Arcieri L, Poli V, Assanta N, Moschetti R, Murzi B, Giordano, R, Cantinotti, M, Pak, V, Arcieri, L, Poli, V, Assanta, N, Moschetti, R, and Murzi, B

Abstract

Objective Mitral valve replacement (MVR) is a surgical option when mitral valvuloplasty is not feasible/successful. This study reviews our experience with MVR in very young children. Methods From July 2004 to January 2014, seven children (mean age 13.3-±-11.2 months; range 4 months to 35 months; mean body weight 6.0-±-2.2-kg) underwent MVR with a mechanical prosthesis in the supra-annular position. To provide better exposure in the left atrium, we performed in all but one case a biatrial transeptal incision according to Guiraudon. Six patients had congenital defects of the mitral valve and one had rheumatic. Six patients had undergone previous cardiosurgical procedures. Results All patients were implanted with a CarboMedics (CarboMedics, Austin, TX, USA) mechanical prosthesis. Mean prosthesis size was 19.0-±-3.1-mm (range 16 to 25). There were no cases of operative or late mortality. At follow-up (mean 67.1-±-34.8 months; range 25 to 108 months) two patients (28.6%) required reoperation both for thrombotic pannus formation over the disc at two and three months from first operation, respectively; only in one case was replacement necessary. Conclusion Supra-annular MVR may be considered a feasible secondary surgical option in children with a small annulus when mitral valvuloplasty is unsuccessful or unsuitable. Early and mid-term outcomes are acceptable but complications are not uncommon, especially related to thrombotic events.

Published
2015

21. SURGERY OF THE TRACHEA IN CHILDREN LESS THAN ONE YEAR OF AGE: MIDTERM RESULTS OF A DEDICATED TRACHEAL YEAM

Author

Arcieri L, Giordano R, Serio P, Fainardi V, Di Maurizio M, Melo M, Poli V, Pak V, Maizza A, Baggi R, Moschetti R, Assanta N, Cantinotti M, Chiappa E, Noccioli B, Mirabile L, Murzi B, Arcieri, L, Giordano, R, Serio, P, Fainardi, V, Di Maurizio, M, Melo, M, Poli, V, Pak, V, Maizza, A, Baggi, R, Moschetti, R, Assanta, N, Cantinotti, M, Chiappa, E, Noccioli, B, Mirabile, L, and Murzi, B

Published
2015

30. MYC agisce da fattore di riprogrammazione tumorale tramite induzione di uno stato di staminalità cellulare in cellule epiteliali umane della ghiandola mammaria

Author

Poli, V, POLI, VITTORIA, Poli, V, and POLI, VITTORIA

Abstract

Cancer is both a genetic and an epigenetic disease whose outcome is influenced by tumor microenvironment. These three determinants represent the major driving forces of tumorigenesis and cause the functional heterogeneity observed in most of the cancer types. Both normal and neoplastic cell populations are known to harbor subpopulations of Stem Cells (SCs) that can both self-renew and spawn more differentiated progeny that, in the case of cancer, forms the tumor bulk. For what concerns Cancer Stem Cells (CSCs), they are proposed to held most of the tumor initiating potential and a higher proportion of CSCs within a tumor often correlates with poorer prognosis. Accumulating evidences indicate that SCs transcriptional program of both normal and neoplastic tissues rely on common molecular regulators including important developmental signals, such as the WNT pathway, whose de-regulation is causative of tumor initiation. Given their importance in the maintenance and propagation of cancer, identifying the cell of origin of CSCs would represent a great opportunity for understanding the molecular mechanisms underlying the onset of tumorigenesis, thereby offering new therapeutic strategies. A likely scenario of how multistep tumorigenesis may proceeds is that pools of transit amplifying progenitor cells, that are mitotically more active and more numerous than SCs, may serve as targets of somatic and epigenetic alterations that would cause their de-differentiation, pushing them back to the SCs compartment. This emerging model is based upon recent findings that hierarchically organized cell populations are, at least in epithelial tissues such as the mammary gland, more plastic than previously imagined. In this view, cell transformation can be described as a cell reprogramming process toward a SC-like state, in which a committed cell has to over-come a number of epigenetic barriers, that normally stabilize it, in order to alter its identity. Although promising, the mechanisms t

Published
2016

31. HYPERTENSION IN ADULT AFTER OPERATION OF AORTIC COARCTATION

Author

Palma, G., Raffaele Giordano, Russolillo, V., Cioffi, S., Palumbo, S., Mucerino, M., Poli, V., Vosa, C., Palma, Gaetano, Giordano, R., Russolillo, V., Cioffi, S., Palumbo, S., Mucerino, M., Poli, V., and Vosa, Carlo

Abstract

Aim. The benefit of coarctation repair on the resolution of systolic hypertension in adults has been questioned. Methods. Between March 1997 and July 2009, 65 consecutive adult patients (≥16 years) underwent repair of aortic coarctation. There were 40 men (65%) and 25 women (35%) with a mean age of 22.3±4.8 years (range, 16 to 34 years). All patients had critical systolic blood hypertension (SBP ≥140 mmHg). SBP ranged from 140 to 205 mmHg, with a mean of 163.5±17.6 mmHg. The mean diastolic BP was 95.1±18.3 mmHg (range, 70 to 120 mmHg). Most patients (41/65, 74%) were on a regimen of at least one antihypertensive drug. Results. The patients were followed up after coarctation repair for 2 to 144 months (mean, 68±39 months). There was no death. No other major complications occurred. There have been no repeat interventions during follow-up. Four patients were lost to follow-up. Of the 61 patients with preoperative hypertension, 53 (87%) were normotensive (SBP

Published
2011

32. Sildenafil therapy for pulmonary hypertension before and after pediatric congenital heart surgery

Author

Gaetano Palma, Giordano, R., Russolillo, V., Cioffi, S., Palumbo, S., Mucerino, M., Poli, V., Vosa, C., Palma, G, Giordano, R, Russolillo, V, Cioffi, S, Palumbo, S, Mucerino, M, Poli, V, and Vosa, C

Abstract

Pulmonary hypertension associated with pediatric congenital heart defects is a major cause of postoperative morbidity and death. Sildenafil has been combined with inhaled nitric oxide to treat pulmonary hypertension. We retrospectively studied the pre- and postoperative effects of oral sildenafil as monotherapy in children with pulmonary hypertension who underwent surgery to correct congenital cardiac defects. From September 2005 through November 2009, 38 children with moderate-to-severe pulmonary arterial hypertension (pulmonary arterial/aortic pressure ratio, >0.7) underwent cardiac surgery at our institution. Fifteen patients were given sildenafil (0.35 mg/kg, every 4 hr) orally or through nasogastric tubes 1 week before and 1 week after surgery. Twentythree patients of comparable medical status were given sildenafil only upon the institution of cardiopulmonary bypass and for 1 week after surgery. Postoperatively, the 15 patients who were given preoperative sildenafil had significantly lower mean pulmonary arterial pressures (25.6 ± 3.1 vs 30.4 ± 5.7 mmHg; P=0.005) and pulmonary arterial/aortic pressure ratios (0.35 ± 0.05 vs 0.42 ± 0.07; P=0.002) than did the other 23 patients. The preoperative therapy also shortened cardiopulmonary bypass time, mechanical ventilation time, and lengths of intensive care unit and hospital stays. No sildenafil- related hypertensive crises or sequelae occurred. As monotherapy, oral sildenafil in low doses appears to control pulmonary hypertension safely and effectively in children undergoing operations to correct congenital heart defects, particularly when it is given both preoperatively and postoperatively. Further study is warranted.

Published
2011

33. IL POPOLAMENTO DELLA ROMAGNA E DELLE AREE LIMITROFE TRA LA FINE DELLA MEDIA ETÀ DEL BRONZO E L’ETÀ DEL BRONZO RECENTE

Author

CATTANI, MAURIZIO, DEBANDI, FLORENCIA INES, Poli V., Ravaglia M., Vaccari B, Cattani M., Debandi F., Poli V., Ravaglia M., and Vaccari B

Subjects
SOLAROLO, ETÀ DEL BRONZO, ROMAGNA
Abstract

Si presenta sinteticamente una valutazione delle segnalazioni relative alle fasi finali del Bronzo Medio e del Bronzo Recente in Romagna e nelle zone limitrofe per una ricostruzione delle dinamiche insediative e per un approfondimento dei reperti rinvenuti nel sito di Solarolo.

Published
2009

35. Trattamento chirurgico dell’interruzione dell’arco aortico

Author

Russolillo V., Cioffi S, Langella G, Giordano R., Pelella G., Poli V., Merlino E., Mucerino M., PALMA, GAETANO, VOSA, CARLO, Russolillo, V., Cioffi, S, Langella, G, Giordano, R., Pelella, G., Poli, V., Merlino, E., Mucerino, M., Palma, Gaetano, and Vosa, Carlo

Published
2007

37. La sostituzione valvolare in eta' pediatrica

Author

Russolillo V., Cioffi S., Merlino E., Farina G., Poli V., Caianiello G., Nava A., Tozzi R., PALMA, GAETANO, VOSA, CARLO, Russolillo, V., Cioffi, S., Merlino, E., Farina, G., Poli, V., Caianiello, G., Palma, Gaetano, Nava, A., Tozzi, R., and Vosa, Carlo

Published
2006

39. Moderated Poster session - Genetic, Epigenetic & Integrative480Inhibiting mitochondrial fission with Mdivi-1 directs cardiac differentiation of human induced pluripotent stem cells via protein kinase CK2481A novel role of tristetraprolin in preventing mitochondrial dysfunction in the heart against iron deficiency by optimizing expression of Rieske iron-sulfur protein482Different therapeutic approaches to downregulate the activation of the hepatic interleukin-6/stat3/complement pathway in two models of autoimmune myocarditis483In vitro and in vivo genome engineering of Dilated Cardiomyopathy caused by phospholamban R14 deletion.484Contractile dysfunction of induced pluripotent stem cell-derived cardiomyocytes from a duchenne muscular dystrophy patient485Cigarette smoking increases expression of the G protein-coupled receptor 15 mRNA by change in CpG methylation486Cardiogenic potential of iPSC from cardiac progenitor cells

Author

Lim, S, primary, Sato, T, primary, Marino, F, primary, Stillitano, F, primary, Pioner, JM, primary, Haase, T, primary, Pianezzi, E, primary, Sivakumaran, P, additional, Hernandez, D, additional, Wong, RCB, additional, Taylor, C, additional, Dusting, G, additional, Pebay, A, additional, Bayeva, M, additional, Chang, HC, additional, Shapiro, JS, additional, Yar, S, additional, Ardehali, H, additional, Camporeale, A, additional, Avalle, L, additional, Heymans, S, additional, Roman, B, additional, Kotelianski, V, additional, Poli, V, additional, Karakikes, I, additional, Nonnenmacher, M, additional, Ceholski, D, additional, Zhang, L, additional, Hulot, JS, additional, Cai, CL, additional, Kranias, EG, additional, Hajjar, RJ, additional, Racca, AW, additional, Klaiman, JM, additional, Guan, X, additional, Pabon, L, additional, Muskheli, V, additional, Macadangdang, J, additional, Kim, DH, additional, Mack, DL, additional, Childers, MK, additional, Tesi, C, additional, Poggesi, C, additional, Murry, CE, additional, Regnier, M, additional, Krause, J, additional, Mueller, C, additional, Stenzig, J, additional, Roethemeier, C, additional, Wild, PS, additional, Blankenberg, S, additional, Zeller, T, additional, Altomare, C, additional, Cervio, E, additional, Bolis, S, additional, Moccetti, T, additional, Camici, GG, additional, Barile, L, additional, and Vassalli, GG, additional

Published
2016
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43. Partial inhibition of gp130-Jak-Stat3 signaling prevents Wnt-ß-catenin-mediated intestinal tumor growth and regeneration

Author

Phesse, T., Buchert, M., Stuart, E., Flanagan, D., Faux, M., Afshar-Sterle, S., Walker, F., Zhang, H., Nowell, C., Jorissen, R., Tan, C., Hirokawa, Y., Eissmann, M., Poh, A., Malaterre, J., Pearson, H., Kirsch, D., Provero, P., Poli, V., Ramsay, R., Sieber, O., Burgess, A., Huszar, D., Vincan, Elizabeth, Ernst, M., Phesse, T., Buchert, M., Stuart, E., Flanagan, D., Faux, M., Afshar-Sterle, S., Walker, F., Zhang, H., Nowell, C., Jorissen, R., Tan, C., Hirokawa, Y., Eissmann, M., Poh, A., Malaterre, J., Pearson, H., Kirsch, D., Provero, P., Poli, V., Ramsay, R., Sieber, O., Burgess, A., Huszar, D., Vincan, Elizabeth, and Ernst, M.

Abstract

Copyright © 2014 American Association for the Advancement of Science. All Rights Reserved. Most colon cancers arise from somatic mutations in the tumor suppressor gene APC (adenomatous polyposis coli), and these mutations cause constitutive activation of the Wnt-to-ß-catenin pathway in the intestinal epithelium. Because Wnt-ß-catenin signaling is required for homeostasis and regeneration of the adult intestinal epithelium, therapeutic targeting of this pathway is challenging. We found that genetic activation of the cytokine-stimulated pathway mediated by the receptor gp130, the associated Jak (Janus kinase) kinases, and the transcription factor Stat3 (signal transducer and activator of transcription 3) was required for intestinal regeneration in response to irradiation-induced damage in wild-type mice and for tumorigenesis in Apc-mutant mice. Systemic pharmacological or partial genetic inhibition of gp130-Jak-Stat3 signaling suppressed intestinal regeneration, the growth of tumors in Apc-mutant mice, and the growth of colon cancer xenografts. The growth of Apc-mutant tumors depended on gp130-Jak-Stat3 signaling for induction of the polycomb repressor Bmi-1, and the associated repression of genes encoding the cell cycle inhibitors p16 and p21. However, suppression of gp130-Jak-Stat3 signaling did not affect Wnt-ß-catenin signaling or homeostasis in the intestine. Thus, these data not only suggest a molecular mechanism for how the gp130-Jak-Stat3 pathway can promote cancer but also provide a rationale for therapeutic inhibition of Jak in colon cancer.

Published
2014

44. Genomic and functional approaches as powerful tools to stratify human T-cell lymphoproliferative disorders and to identify relevant tumorigenic culprits

Author

Piva, Roberto, Pellegrino, Elisa, Agnelli, L, Grosso, V, Tamagno, I, Ferrantino, L, Cagnoni, G, Fornari, A, Novero, D, Poli, V, Zamò, A, Chiosi, M, Rosenwald, A, Müller Hermelink HK, Vermi, W, Facchetti, F, Fulciniti, F, De Chiara, A, Ponzoni, M, Doglioni, C, Piccaluga, Pp, Pileri, S, De Wolf Peeters, C, Neri, A, and Inghirami, Giorgio

Published
2008

45. C/EBPß blocks p65 phosphorylation and thereby NF-kB-mediated transcription in TNF-tolerant cells

Author

Zwergal, A., Quirling, M., Saugel, B., Huth, K.C., Sydlik, C., Poli, V., Neumeier, D., Ziegler-Heitbrock, L., and Brand, K.

Abstract

TNF is a major mediator of inflammation, immunity, and apoptosis. Pre-exposure to TNF reduces sensitivity to restimulation, a phenomenon known as tolerance, considered as protective in sepsis, but also as a paradigm for immunoparalysis. Earlier experiments in TNF-tolerant cells display inhibition of NF-kappaB-dependent IL-8 gene expression at the transcriptional level with potential involvement of C/EBPbeta. In this study, we have shown that a kappaB motive was sufficient to mediate transcriptional inhibition under TNF tolerance conditions in monocytic cells. Furthermore, in tolerant cells, TNF-induced NF-kappaB p65 phosphorylation was markedly decreased, which was accompanied by the formation of C/EBPbeta-p65 complexes. Remarkably, in C/EBPbeta(-/-) cells incubated under the conditions of TNF tolerance, neither impairment of transcription nor inhibition of p65 phosphorylation was observed. Finally, we showed that C/EBPbeta overexpression reduced p65-mediated transactivation and that association of C/EBPbeta with p65 specifically prevented p65 phosphorylation. Our data demonstrate that C/EBPbeta is an essential signaling component for inhibition of NF-kappaB-mediated transcription in TNF-tolerant cells and suggest that this is caused by blockade of p65 phosphorylation. These results define a new molecular mechanism responsible for TNF tolerance in monocytic cells that may contribute to the unresponsiveness seen in patients with sepsis.

Published
2006

46. Precipitation Estimation: from the RAO to Eurainsat and beyond

Author

Levizzani, V., Adamo, C., Alberoni, P. P., Antonini, A., Battaglia, A., Baptista, J. P. V. P., Bauer, P., Buzzi, A., Capacci, D., Caracciolo, C., Cattani, E., Celano, M., Cimini, D., Costa, M. J., Davolio, S., Dietrich, S., Fantini, M., Di Michele, S., Giuliani, G., Hinsman, D. E., Kästner, M., Khain, A., Kidd, C., Kidd, J., Kniveton, D., Lahav, R., Layberry, R., Lensky, I., PIERO MALGUZZI, Mantovani, S., Marzano, F. S., Maurizi, A., Medaglia, C. M., Melani, S., Meneguzzo, F., Messeri, G., Mugnai, A., Natali, S., Orlandi, A., Ortolani, A., Panegrossi, G., Pasqui, M., Pinori, S., Poli, V., Porcù, F., Prodi, F., Purdom, J. F. W., Rosenfeld, D., Sanderson, V., Schmelz, J., Smith, E. A., Solomon, R., Steinwagner, J., Tampieri, F., Tapiador, F. J., Tassa, A., Torricella, F., Tripoli, G. J., Turk, F. J., Vicente, G. A., and Villani, M. G.

Subjects
satellite, Dynamik der Atmosphäre, precipitation, MSG
Abstract

The key objective of the project "Use of the MSG SEVIRI channels in a combined SSM/I, TRMM and geostationary IR method for rapid updates of rainfall" is the development of algorithms for rapid-update of satellite rainfall estimations at the geostationary (GEO) scale. The new channels available with the Spinning Enhanced Visible and Infrared Imager (SEVIRI) radiometer in the visible (VIS), near infrared (NIR) and infrared (IR) portions of the spectrum provide new insights into the microphysical and dynamic structure of precipitating clouds thus allowing for a more precise identification of precipitation intensities. Passive microwave (PMW) radiometers on board low Earth orbiting (LEO) satellites are used to determine information on the vertical cloud structure. Key features of the new method(s) are: 1. Microphysical characterization of precipitating clouds with VIS/IR sensors; 2. Creation of cloud microphysical and radiative databases from cloud model outputs and aircraft penetrations; 3. Tuning of PMW algorithms for different cloud systems (maritime, continental, convective, stratiform,...); 4. Combination of data from different algorithms and application to a rapid updatecycle at the GEO scale. The project provided the background for EURAINSAT "European Satellite Rainfall Estimation and Monitoring at the Geostationary Scale", a research project co-funded by the Energy, Environment and Sustainable Development Programme of the European Commission within the topic "Development of generic Earth observation technologies". The project web site is accessible at http://www.isac.cnr.it/~eurainsat/. Moreover, it has represented the European framework for the launch of the International Precipitation Working Group (IPWG). A brief account of the major research and organizational results will be given in the following.

Published
2004

47. P381 THE ROLE OF SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION 3 (STAT3) IN CHOLESTASIS AND BILE ACID (BA) SYNTHESIS

Author

Svinka, J., primary, Stiedl, P., additional, Mair, M., additional, Claudel, T., additional, Einwallner, E., additional, Rampetsreiter, P., additional, Mikulits, W., additional, Marschall, H.U., additional, Hengstler, J., additional, Poli, V., additional, Esterbauer, H., additional, Casanova, E., additional, Sibilia, M., additional, Trauner, M., additional, and Eferl, R., additional

Published
2014
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49. Science and technology research and development in support to ITER and the Broader Approach at CEA

Author

Bécoulet, A., primary, Hoang, G.T., additional, Abiteboul, J., additional, Achard, J., additional, Alarcon, T., additional, Alba-Duran, J., additional, Allegretti, L., additional, Allfrey, S., additional, Amiel, S., additional, Ané, J.M., additional, Aniel, T., additional, Antar, G., additional, Argouarch, A., additional, Armitano, A., additional, Arnaud, J., additional, Arranger, D., additional, Artaud, J.F., additional, Audisio, D., additional, Aumeunier, M., additional, Autissier, E., additional, Azcona, L., additional, Back, A., additional, Bahat, A., additional, Bai, X., additional, Baiocchi, B., additional, Balaguer, D., additional, Balme, S., additional, Balorin, C., additional, Barana, O., additional, Barbier, D., additional, Barbuti, A., additional, Basiuk, V., additional, Baulaigue, O., additional, Bayetti, P., additional, Baylard, C., additional, Beaufils, S., additional, Beaute, A., additional, Bécoulet, M., additional, Bej, Z., additional, Benkadda, S., additional, Benoit, F., additional, Berger-By, G., additional, Bernard, J.M., additional, Berne, A., additional, Bertrand, B., additional, Bertrand, E., additional, Beyer, P., additional, Bigand, A., additional, Bonhomme, G., additional, Borel, G., additional, Boron, A., additional, Bottereau, C., additional, Bottollier-Curtet, H., additional, Bouchand, C., additional, Bouquey, F., additional, Bourdelle, C., additional, Bourg, J., additional, Bourmaud, S., additional, Brémond, S., additional, Bribiesca Argomedo, F., additional, Brieu, M., additional, Brun, C., additional, Bruno, V., additional, Bucalossi, J., additional, Bufferand, H., additional, Buravand, Y., additional, Cai, L., additional, Cantone, V., additional, Cantone, B., additional, Caprin, E., additional, Cartier-Michaud, T., additional, Castagliolo, A., additional, Belo, J., additional, Catherine-Dumont, V., additional, Caulier, G., additional, Chaix, J., additional, Chantant, M., additional, Chatelier, M., additional, Chauvin, D., additional, Chenevois, J., additional, Chouli, B., additional, Christin, L., additional, Ciazynski, D., additional, Ciraolo, G., additional, Clairet, F., additional, Clapier, R., additional, Cloez, H., additional, Coatanea-Gouachet, M., additional, Colas, L., additional, Colledani, G., additional, Commin, L., additional, Coquillat, P., additional, Corbel, E., additional, Corre, Y., additional, Cottet, J., additional, Cottier, P., additional, Courtois, X., additional, Crest, I., additional, Dachicourt, R., additional, Dapena Febrer, M., additional, Daumas, C., additional, de Esch, H.P.L., additional, De Gentile, B., additional, Dechelle, C., additional, Decker, J., additional, Decool, P., additional, Deghaye, V., additional, Delaplanche, J., additional, Delchambre-Demoncheaux, E., additional, Delpech, L., additional, Desgranges, C., additional, Devynck, P., additional, Dias Pereira Bernardo, J., additional, Dif-Pradalier, G., additional, Doceul, L., additional, Dong, Y., additional, Douai, D., additional, Dougnac, H., additional, Dubuit, N., additional, Duchateau, J.-L., additional, Ducobu, L., additional, Dugue, B., additional, Dumas, N., additional, Dumont, R., additional, Durocher, A., additional, Duthoit, F., additional, Ekedahl, A., additional, Elbeze, D., additional, Escarguel, A., additional, Escop, J., additional, Faïsse, F., additional, Falchetto, G., additional, Farjon, J., additional, Faury, M., additional, Fedorzack, N., additional, Féjoz, P., additional, Fenzi, C., additional, Ferlay, F., additional, Fiet, P., additional, Firdaouss, M., additional, Francisquez, M., additional, Franel, B., additional, Frauche, J., additional, Frauel, Y., additional, Futtersack, R., additional, Garbet, X., additional, Garcia, J., additional, Gardarein, J., additional, Gargiulo, L., additional, Garibaldi, P., additional, Garin, P., additional, Garnier, D., additional, Gauthier, E., additional, Gaye, O., additional, Geraud, A., additional, Gerome, M., additional, Gervaise, V., additional, Geynet, M., additional, Ghendrih, P., additional, Giacalone, I., additional, Gibert, S., additional, Gil, C., additional, Ginoux, S., additional, Giovannangelo, L., additional, Girard, S., additional, Giruzzi, G., additional, Goletto, C., additional, Goncalves, R., additional, Gonde, R., additional, Goniche, M., additional, Goswami, R., additional, Grand, C., additional, Grandgirard, V., additional, Gravil, B., additional, Grisolia, C., additional, Gros, G., additional, Grosman, A., additional, Guigue, J., additional, Guilhem, D., additional, Guillemaut, C., additional, Guillerminet, B., additional, Guimaraes Filho, Z., additional, Guirlet, R., additional, Gunn, J. P., additional, Gurcan, O., additional, Guzman, F., additional, Hacquin, S., additional, Hariri, F., additional, Hasenbeck, F., additional, Hatchressian, J.C., additional, Hennequin, P., additional, Hernandez, C., additional, Hertout, P., additional, Heuraux, S., additional, Hillairet, J., additional, Honore, C., additional, Hornung, G., additional, Houry, M., additional, Hunstad, I., additional, Hutter, T., additional, Huynh, P., additional, Icard, V., additional, Imbeaux, F., additional, Irishkin, M., additional, Isoardi, L., additional, Jacquinot, J., additional, Jacquot, J., additional, Jiolat, G., additional, Joanny, M., additional, Joffrin, E., additional, Johner, J., additional, Joubert, P., additional, Jourd'Heuil, L., additional, Jouve, M., additional, Junique, C., additional, Keller, D., additional, Klepper, C., additional, Kogut, D., additional, Kubič, M., additional, Labassé, F., additional, Lacroix, B., additional, Lallier, Y., additional, Lamaison, V., additional, Lambert, R., additional, Larroque, S., additional, Latu, G., additional, Lausenaz, Y., additional, Laviron, C., additional, Le, R., additional, Le Luyer, A., additional, Le Niliot, C., additional, Le Tonqueze, Y., additional, Lebourg, P., additional, Lefevre, T., additional, Leroux, F., additional, Letellier, L., additional, Li, Y., additional, Lipa, M., additional, Lister, J., additional, Litaudon, X., additional, Liu, F., additional, Loarer, T., additional, Lombard, G., additional, Lotte, P., additional, Lozano, M., additional, Lucas, J., additional, Lütjens, H., additional, Magaud, P., additional, Maget, P., additional, Magne, R., additional, Mahieu, J.-F., additional, Maini, P., additional, Malard, P., additional, Manenc, L., additional, Marandet, Y., additional, Marbach, G., additional, Marechal, J.-L., additional, Marfisi, L., additional, Marle, M., additional, Martin, C., additional, Martin, V., additional, Martin, G., additional, Martinez, A., additional, Martino, P., additional, Masset, R., additional, Mazon, D., additional, Mellet, N., additional, Mercadier, L., additional, Merle, A., additional, Meshcheriakov, D., additional, Messina, P., additional, Meyer, O., additional, Millon, L., additional, Missirlian, M., additional, Moerel, J., additional, Molina, D., additional, Mollard, P., additional, Moncada, V., additional, Monier-Garbet, P., additional, Moreau, D., additional, Moreau, M., additional, Moreau, P., additional, Morel, P., additional, Moriyama, T., additional, Motassim, Y., additional, Mougeolle, G., additional, Moulton, D., additional, Moureau, G., additional, Mouyon, D., additional, Naim Habib, M., additional, Nardon, E., additional, Négrier, V., additional, Nemeth, J., additional, Nguyen, C., additional, Nguyen, M., additional, Nicolas, L., additional, Nicolas, T., additional, Nicollet, S., additional, Nilsson, E., additional, N'Konga, B., additional, Noel, F., additional, Nooman, A., additional, Norscini, C., additional, Nouailletas, R., additional, Oddon, P., additional, Ohsako, T., additional, Orain, F., additional, Ottaviani, M., additional, Pagano, M., additional, Palermo, F., additional, Panayotis, S., additional, Parrat, H., additional, Pascal, J.-Y., additional, Passeron, C., additional, Pastor, P., additional, Patterlini, J., additional, Pavy, K., additional, Pecquet, A.-L., additional, Pégourié, B., additional, Peinturier, C., additional, Pelletier, T., additional, Peluso, B., additional, Petrzilka, V., additional, Peysson, Y., additional, Pignoly, E., additional, Pirola, R., additional, Pocheau, C., additional, Poitevin, E., additional, Poli, V., additional, Poli, S., additional, Pompon, F., additional, Porchy, I., additional, Portafaix, C., additional, Preynas, M., additional, Prochet, P., additional, Prou, M., additional, Ratnani, A., additional, Raulin, D., additional, Ravenel, N., additional, Renard, S., additional, Ricaud, B., additional, Richou, M., additional, Ritz, G., additional, Roche, H., additional, Roubin, P., additional, Roux, C., additional, Ruiz, K., additional, Sabathier, F., additional, Sabot, R., additional, Saille, A., additional, Saint-Laurent, F., additional, Sakamoto, R., additional, Salasca, S., additional, Salmon, T., additional, Samaille, F., additional, Sanchez, S., additional, Santagiustina, A., additional, Saoutic, B., additional, Sarazin, Y., additional, Sardain, P., additional, Schlosser, J., additional, Schneider, M., additional, Schwob, J., additional, Segui, J., additional, Seguin, N., additional, Selig, G., additional, Serret, D., additional, Signoret, J., additional, Simonin, A., additional, Soldaini, M., additional, Soler, B., additional, Soltane, C., additional, Song, S., additional, Sourbier, F., additional, Sparagna, J., additional, Spitz, P., additional, Spuig, P., additional, Storelli, A., additional, Strugarek, A., additional, Tamain, P., additional, Tena, M., additional, Theis, J., additional, Thomine, O., additional, Thouvenin, D., additional, Torre, A., additional, Toulouse, L., additional, Travère, J., additional, Tsitrone, E., additional, Turck, B., additional, Urban, J., additional, Vallet, J.-C., additional, Vallory, J., additional, Valognes, A., additional, Van Helvoirt, J., additional, Vartanian, S., additional, Verger, J.-M., additional, Vermare, L., additional, Vermare, C., additional, Vezinet, D., additional, Vicente, K., additional, Vidal, J., additional, Vignal, N., additional, Vigne, T., additional, Villecroze, F., additional, Villedieu, E., additional, Vincent, B., additional, Volpe, B., additional, Volpe, D., additional, Volpe, R., additional, Wagrez, J., additional, Wang, H., additional, Wauters, T., additional, Wintersdorff, O., additional, Wittebol, E., additional, Zago, B., additional, Zani, L., additional, Zarzoso, D., additional, Zhang, Y., additional, Zhong, W., additional, and Zou, X.L., additional

Published
2013
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