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1. Intracranial pressure monitoring in patients with acute brain injury in the intensive care unit (SYNAPSE-ICU): an international, prospective observational cohort study

Author

F. Maldonado, E.D. Amundarain, S. Tsikriki, S. Yasin Wayhs, H. Berty Gutiérrez, A. Gritsan, P. Gradisek, Raimund Helbok, A. Efthymiou, Ankur Luthra, A. Marudi, A. Cotoia, L. Lencastre, Karim Asehnoune, Stefan Wolf, C. Thompson, Federico Pozzi, C. Hawthorne, M. Anglada, C. Vrettou, D. Glorieux, P. Kafle, M. Sekhon, R. Freitas, W. Sellami, Nino Stocchetti, Rafael Badenes, E. Provaznikova, G. Audibert, A. Blandino Ortiz, L. Rajbanshi, Hasin Afzal Ahmed, P. Kurtz, F. Magni, J. Thomsen, C. Diakaki, R. Pérez-Araos, E.E. Stamou, Marco Carbonara, K. Kojder, K. Vrbica, E. Picetti, L. Mebis, M.I. Gonzalez Perez, M.O. Holm, B. Pons, B. Monleon, S. Silva, N. Kovac, E. Kontoudaki, H. Westy Hoffmeyer, K. Nilam, M. Jibaja, G. Nardai, P. Bresil, A. Gempeler, Kristina Fuest, A. Rigamonti, M. Abdelaty, C.Y. Chan, C. Iasonidou, Giuseppe Citerio, S. Khomiakov, C. Bonetti, Andrea Cortegiani, Hervé Quintard, G.A. Gasca López, Y.B. Roka, V. Buldini, Laura Galarza, T. Bajracharya, J. Kletecka, G.S. Shrestha, G. Kyriazopoulos, M.E. Giménez, S. Maskey, C. Pacheco, A. Giugni, A. Kolias, P. Cavaleiro, S.A. Ñamendys Silva, S. Grotheer, Samyuktha Anand, Y Arabi, R. Siviter, O. Idowu, Z. Olson, H.S. Eddelien, Paola Rebora, A. Soragni, R. Sonneville, M. Fencl, Demosthenes Makris, M. Casanova, Francesca Graziano, S. Del Bianco, M. F. García, L. Corral, P. Morelli, F. Villa, F. Assunção, O. Sabelnikovs, M. Reade, Anselmo Caricato, E. Palli, M. Lamperti, S. Van De Velde, Francesca Elli, B. Soyer, A. Giannopoulos, M. Grandis, M. Simoes, J.P. Miroz, Summit Dev Bloria, I. Calamai, P. Biston, Ilaria Alice Crippa, S.M. Zerbi, E. Bertellini, M. Smitt, N. Pantelas, P. Banco, K. Sharma, C. Gelormini, J. Dibu, H. Sapra, S. Kozar, D. Gupta, P. Duque, Sanjeev Sivakumar, I. Brunetti, S.M. Krieg, S. Abed Maillard, A. Lores, M. Levin, Fabio Silvio Taccone, P. Lavicka, J.B. Andersen, R. Cinotti, Jean Louis Vincent, V. Davidovich, Geert Meyfroidt, P. Forjan, M. Škoti, G. Koukoulitsios, A. Dimoula, I. Seppelt, Ahmad Ozair, J.H. Mejia-Mantilla, Lara Prisco, M. Celaya Lopez, M. Fumale, R. Lightfoot, Rajeev Chauhan, R. Mendoza, J.M. Montes, A. Izzi, G. Domeniconi, E. Stival, J. Padilla Juan, C. Gakuba, V. Blazquez, A. Alsudani, K. Tánczos, D.H. Kandamby, L. Albrecht, L.J.Y. Dominguez, Carlo Giussani, Muhammed Elhadi, B. Majholm, E. Mouloudi, Jose I. Suarez, S.F. Ribaric, M.C. Casadio, L.L. Rivera, L. Pariente, W. Videtta, M. Lucca, Guillaume Besch, D. Olson, M.D. Arias Verdu, R. Soley, A. Lindner, Mauro Oddo, M.C. Quartarone, M.M. Khan, P. López Ojeda, Ainhoa Serrano, H.P. Shum, E. Ioannoni, T. Egmose Larsen, A. Motta, E. Favre Eva, S. Muehlschlegel, D. Pearson, A. Caillard, J. Skola, B. Kilapong, Nidhi Panda, Irene Aragão, D. Batista, J.L. Pinedo Portilla, Chiara Robba, Donald E. G. Griesdale, N. Dovbysh, Stefan J. Schaller, E.D. Hallt, N. Milivojevic, V. Spatenkova, J. Roberts, Robba, Chiara, Graziano, Francesca, Rebora, Paola, Elli, Francesca, Giussani, Carlo, Oddo, Mauro, Meyfroidt, Geert, Helbok, Raimund, Taccone, Fabio S, Prisco, Lara, Vincent, Jean-Loui, Suarez, Jose I, Stocchetti, Nino, Citerio, Giuseppe, Abdelaty, M., Abed Maillard, S., Ahmed, H., Albrecht, L., Alsudani, A., Amundarain, E.D., Anand, S., Andersen, J.B., Anglada, M., Arabi, Y, Aragao, I., Arias Verdu, M.D., Asehnoune, K., Assunção, F., Audibert, G., Badenes, R., Bajracharya, T., Banco, P., Batista, D., Bertellini, E., Berty Gutiérrez, H., Besch, G., Biston, P., Blandino Ortiz, A., Blazquez, V., Bloria, S., Bonetti, C., Bresil, P., Brunetti, I., Buldini, V., Caillard, A., Calamai, I., Carbonara, M., Caricato, A., Casadio, M.C., Casanova, M., Cavaleiro, P., Celaya Lopez, M., Chan, C.Y., Chauhan, R., Cinotti, R., Corral, L., Cortegiani, A., Cotoia, A., Crippa, I.A., Davidovich, V., Del Bianco, S., Diakaki, C., Dibu, J., Dimoula, A., Domeniconi, G., Dominguez, L.J.Y., Dovbysh, N., Duque, P., Eddelien, H.S., Efthymiou, A., Egmose Larsen, T., Elhadi, M., Favre Eva, E., Fencl, M., Forjan, P., Freitas, R., Fuest, K., Fumale, M., Gakuba, C., Galarza, L., García, M.F., Gasca López, G.A., Gelormini, C., Gempeler, A., Giannopoulos, A., Giménez, M.E., Giugni, A., Glorieux, D., Gonzalez Perez, M.I., Gradisek, P., Grandis, M., Griesdale, D., Gritsan, A., Grotheer, S., Gupta, D., Hallt, E.D., Hawthorne, C., Helbok, R., Holm, M.O., Iasonidou, C., Idowu, O., Ioannoni, E., Izzi, A., Jibaja, M., Kafle, P., Kandamby, D.H., Khan, M.M., Khomiakov, S., Kilapong, B., Kletecka, J., Kojder, K., Kolias, A., Kontoudaki, E., Koukoulitsios, G., Kovac, N., Kozar, S., Krieg, S.M., Kurtz, P., Kyriazopoulos, G., Lamperti, M., Lavicka, P., Lencastre, L., Levin, M., Lightfoot, R., Lindner, A., López Ojeda, P., Lores, A., Lucca, M., Luthra, A., Magni, F., Majholm, B., Makris, D., Maldonado, F., Marudi, A., Maskey, S., Mebis, L., Mejia-Mantilla, J.H., Mendoza, R., Milivojevic, N., Miroz, J.P., Monleon, B., Montes, J.M., Morelli, P., Motta, A., Mouloudi, E., Muehlschlegel, S., Ñamendys Silva, S.A., Nardai, G., Nilam, K., Olson, D., Ozair, A., Pacheco, C., Padilla Juan, J., Palli, E., Panda, N., Pantelas, N., Pariente, L., Pearson, D., Pérez-Araos, R., Picetti, E., Pinedo Portilla, J.L., Pons, B., Pozzi, F., Provaznikova, E., Quartarone, M.C., Quintard, H., Rajbanshi, L., Reade, M., Ribaric, S.F., Rigamonti, A., Rivera, L.L., Roberts, J., Roka, Y.B., Sabelnikovs, O., Sapra, H., Schaller, S.J., Sekhon, M., Sellami, W., Seppelt, I., Serrano, A., Sharma, K., Shrestha, G.S., Shum, H.P., Silva, S., Simoes, M., Sivakumar, S., Siviter, R., Skola, J., Škoti, M., Smitt, M., Soley, R., Sonneville, R., Soragni, A., Soyer, B., Spatenkova, V., Stamou, E.E., Stival, E., Olson, Z., Tánczos, K., Thompson, C., Thomsen, J., Tsikriki, S., Van De Velde, S., Videtta, W., Villa, F., Vrbica, K., Vrettou, C., Westy Hoffmeyer, H., Wolf, S., Yasin Wayhs, S., Zerbi, S.M., Robba, C, Graziano, F, Rebora, P, Elli, F, Giussani, C, Oddo, M, Meyfroidt, G, Helbok, R, Taccone, F, Prisco, L, Vincent, J, Suarez, J, Stocchetti, N, Citerio, G, and Investigators, SYNAPSE-ICU

Subjects
Male, Intracranial Pressure, Glasgow Outcome Scale, Malalties cerebrals, intensive care unit, law.invention, Cohort Studies, 0302 clinical medicine, law, Brain Injuries, Traumatic, Medicine, acute brain injury, Prospective Studies, Prospective cohort study, Unitats de cures intensives, Intracranial pressure, Intensive care units, Middle Aged, Intensive care unit, Intensive Care Units, Hypertension, Intracranial pressure monitoring, Female, Hipertensió, Brain diseases, Adult, medicine.medical_specialty, Critical Care, Traumatic brain injury, Intracranial pressure, monitoring, brain injury, 03 medical and health sciences, Internal medicine, Intensive care, Settore MED/41 - ANESTESIOLOGIA, Humans, Glasgow Coma Scale, Aged, Monitoring, Physiologic, business.industry, 030208 emergency & critical care medicine, ICP, medicine.disease, Brain Injuries, Neurology (clinical), Intracranial Hypertension, business, 030217 neurology & neurosurgery
Abstract

Background: The indications for intracranial pressure (ICP) monitoring in patients with acute brain injury and the effects of ICP on patients’ outcomes are uncertain. The aims of this study were to describe current ICP monitoring practises for patients with acute brain injury at centres around the world and to assess variations in indications for ICP monitoring and interventions, and their association with long-term patient outcomes. Methods: We did a prospective, observational cohort study at 146 intensive care units (ICUs) in 42 countries. We assessed for eligibility all patients aged 18 years or older who were admitted to the ICU with either acute brain injury due to primary haemorrhagic stroke (including intracranial haemorrhage or subarachnoid haemorrhage) or traumatic brain injury. We included patients with altered levels of consciousness at ICU admission or within the first 48 h after the brain injury, as defined by the Glasgow Coma Scale (GCS) eye response score of 1 (no eye opening) and a GCS motor response score of at least 5 (not obeying commands). Patients not admitted to the ICU or with other forms of acute brain injury were excluded from the study. Between-centre differences in use of ICP monitoring were quantified by using the median odds ratio (MOR). We used the therapy intensity level (TIL) to quantify practice variations in ICP interventions. Primary endpoints were 6 month mortality and 6 month Glasgow Outcome Scale Extended (GOSE) score. A propensity score method with inverse probability of treatment weighting was used to estimate the association between use of ICP monitoring and these 6 month outcomes, independently of measured baseline covariates. This study is registered with ClinicalTrial.gov, NCT03257904. Findings: Between March 15, 2018, and April 30, 2019, 4776 patients were assessed for eligibility and 2395 patients were included in the study, including 1287 (54%) with traumatic brain injury, 587 (25%) with intracranial haemorrhage, and 521 (22%) with subarachnoid haemorrhage. The median age of patients was 55 years (IQR 39–69) and 1567 (65%) patients were male. Considerable variability was recorded in the use of ICP monitoring across centres (MOR 4·5, 95% CI 3·8–4·9 between two randomly selected centres for patients with similar covariates). 6 month mortality was lower in patients who had ICP monitoring (441/1318 [34%]) than in those who were not monitored (517/1049 [49%]; p

Published
2021

2. Zinc-finger-based transcriptional repression of rhodopsin in a model of dominant retinitis pigmentosa

Author

Daniela Sanges, Valeria Marigo, Germana Meroni, Alberto Auricchio, Elena Marrocco, Claudio Mussolino, Ciro Bonetti, Enrico Maria Surace, Umberto Di Vicino, Mussolino, C., Sanges, D., Marrocco, E., Bonetti, C., Di Vicino, U., Marigo, V., Auricchio, A., Meroni, Germana, Surace, E. M., C., Mussolino, D., Sange, E., Marrocco, C., Bonetti, U., Di Vicino, V., Marigo, Auricchio, Alberto, G., Meroni, and Surace, Enrico Maria

Subjects
Rhodopsin, Transcription, Genetic, Gain‐of‐function, retinitis pigmentosa, transcriptional repression, zinc‐finger, zinc‐finger, Down-Regulation, Mice, Transgenic, Biology, 03 medical and health sciences, Mice, Gain‐of‐function, 0302 clinical medicine, Report, retinitis pigmentosa, Retinitis pigmentosa, transcriptional repression, medicine, Animals, Humans, zinc-finger, Allele, Gene, Psychological repression, 030304 developmental biology, Regulation of gene expression, Zinc finger, Genetics, 0303 health sciences, gain-of-function, Genetic Therapy, medicine.disease, Complementation, Mice, Inbred C57BL, Ophthalmoscopy, Repressor Proteins, RNA silencing, Disease Models, Animal, gene therapy, adeno-associated virus, Gene Knockdown Techniques, Molecular Medicine, 030217 neurology & neurosurgery
Abstract

Despite the recent success of gene-based complementation approaches for genetic recessive traits, the development of therapeutic strategies for gain-of-function mutations poses great challenges. General therapeutic principles to correct these genetic defects mostly rely on post-transcriptional gene regulation (RNA silencing). Engineered zinc-finger (ZF) protein-based repression of transcription may represent a novel approach for treating gain-of-function mutations, although proof-of-concept of this use is still lacking. Here, we generated a series of transcriptional repressors to silence human rhodopsin (hRHO), the gene most abundantly expressed in retinal photoreceptors. The strategy was designed to suppress both the mutated and the wild-type hRHO allele in a mutational-independent fashion, to overcome mutational heterogeneity of autosomal dominant retinitis pigmentosa due to hRHO mutations. Here we demonstrate that ZF proteins promote a robust transcriptional repression of hRHO in a transgenic mouse model of autosomal dominant retinitis pigmentosa. Furthermore, we show that specifically decreasing the mutated human RHO transcript in conjunction with unaltered expression of the endogenous murine Rho gene results in amelioration of disease progression, as demonstrated by significant improvements in retinal morphology and function. This zinc-finger-based mutation-independent approach paves the way towards a 'repression-replacement' strategy, which is expected to facilitate widespread applications in the development of novel therapeutics for a variety of disorders that are due to gain-of-function mutations.

Published
2011
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3. Mouse embryonic retina delivers information controlling cortical neurogenesis

Author

Ciro Bonetti, Enrico Maria Surace, Bonetti, C, and Surace, Enrico Maria

Subjects
Central Nervous System, Embryology, Time Factors, Mouse, Visual System, lcsh:Medicine, Mice, 0302 clinical medicine, Molecular Cell Biology, lcsh:Science, In Situ Hybridization, Visual Cortex, Cerebral Cortex, 0303 health sciences, Multidisciplinary, Neurogenesis, Gene Expression Regulation, Developmental, Anatomy, Animal Models, Immunohistochemistry, Sensory Systems, Corticogenesis, medicine.anatomical_structure, Cerebral cortex, Injections, Intraocular, Cell Division, Research Article, Central nervous system, Mitosis, Neurophysiology, Sensory system, Biology, Models, Biological, Cell Growth, Retina, 03 medical and health sciences, Model Organisms, Developmental Neuroscience, medicine, Animals, 030304 developmental biology, Colforsin, lcsh:R, Embryonic stem cell, Neuroanatomy, Visual cortex, Ki-67 Antigen, Bromodeoxyuridine, lcsh:Q, Neuroscience, 030217 neurology & neurosurgery, Developmental Biology
Abstract

The relative contribution of extrinsic and intrinsic mechanisms to cortical development is an intensely debated issue and an outstanding question in neurobiology. Currently, the emerging view is that interplay between intrinsic genetic mechanisms and extrinsic information shape different stages of cortical development [1]. Yet, whereas the intrinsic program of early neocortical developmental events has been at least in part decoded [2], the exact nature and impact of extrinsic signaling are still elusive and controversial. We found that in the mouse developing visual system, acute pharmacological inhibition of spontaneous retinal activity (retinal waves-RWs) during embryonic stages increase the rate of corticogenesis (cell cycle withdrawal). Furthermore, early perturbation of retinal spontaneous activity leads to changes of cortical layer structure at a later time point. These data suggest that mouse embryonic retina delivers long-distance information capable of modulating cell genesis in the developing visual cortex and that spontaneous activity is the candidate long-distance acting extrinsic cue mediating this process. In addition, these data may support spontaneous activity to be a general signal coordinating neurogenesis in other developing sensory pathways or areas of the central nervous system.

Published
2010

4. Inhibition of ocular neovascularization by hedgehog blockade

Author

Robin R. Ali, Aniello Vitale, Enrico Maria Surace, Ciro Bonetti, Gabriella Cotugno, Alberto Auricchio, Claudio Mussolino, Kamaljit S. Balaggan, Alessandra Tessitore, Surace, Enrico Maria, Balaggan, K. S., Tessitore, A., Mussolino, C., Cotugno, G., Bonetti, C., Vitale, A., Ali, R. R., and Auricchio, Alberto

Subjects
medicine.medical_specialty, animal structures, genetic structures, Cyclopamine, Angiogenesis, Neovascularization, Physiologic, Biology, Retina, Neovascularization, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Internal medicine, Drug Discovery, Genetics, medicine, Animals, Hedgehog Proteins, Sonic hedgehog, Molecular Biology, 030304 developmental biology, Pharmacology, 0303 health sciences, Neovascularization, Pathologic, Veratrum Alkaloids, Retinal, eye diseases, Up-Regulation, Vascular endothelial growth factor, Mice, Inbred C57BL, medicine.anatomical_structure, Endocrinology, Choroidal neovascularization, chemistry, 030220 oncology & carcinogenesis, embryonic structures, Cancer research, biology.protein, Molecular Medicine, sense organs, medicine.symptom
Abstract

Ocular neovascularization associated with proliferative diabetic retinopathy and age-related macular degeneration is the leading cause of severe visual loss in adults in developed countries. Physiological and pathological retinal angiogenesis may occur independently in postnatal life through the complex activation of pro- and antiangiogenic pathways. We report that the Sonic hedgehog (Shh) pathway is activated in the retina in animal models of retinal and choroidal neovascularization. We show that pharmacological inhibition of the Shh signaling pathway significantly reduces physiological retinal angiogenesis and inhibits pathological vascularization in both models. Under retinal hypoxic conditions, inhibition of the Shh pathway results in reduction of vascular endothelial growth factor (VEGF) level, along with that of Patched-1 (Ptch1), a canonical Shh target, thus placing Shh activation upstream of VEGF in experimental retinal neovascularization. Our data demonstrate the requirement of the Shh pathway for retinal angiogenesis and its inhibition as a potential therapeutic strategy targeting ocular neovascular disease.

Published
2005

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