Severe hepatic sinusoidal obstruction associated with oxaliplatin-based chemotherapy in patients with metastatic colorectal cancer

Background: In advanced metastatic colorectal adenocarcinoma, the addition of a neo-adjuvant systemic treatment to surgery might translate into a survival advantage, although this is yet to be confirmed by ongoing randomized trials. The objective of this study was to assess the effects of preoperative systemic chemotherapy on the morphology of non-tumoral liver. Patients and methods: A large series of surgically resected liver metastases (n = 153) was selected. Light microscopy, electron microscopy, and immunohistochemistry using antibodies against endothelial cells (CD31) and hepatic stellate cells (α-SM actin, CRBP-1) were performed to identify sinusoidal wall integrity. Results: We found that 44 (51%) of the 87 post-chemotherapic liver resection specimens had sinusoidal dilatation and hemorrhage, related to rupture of the sinusoidal barrier. In contrast, the 66 livers treated by surgery alone remained normal. In 21 out of the 44 post-chemotherapy patients (48%), perisinusoidal and veno-occlusive fibrosis also developed. Sinusoidal injury persisted several months after end of chemotherapy, and fibrosis may progress. Development of lesions was strongly correlated to the use of oxaliplatin; 34 out of 43 patients (78%) treated with this drug showed striking sinusoidal alterations. Conclusions: Systemic neo-adjuvant chemotherapy in metastatic colorectal cancer frequently causes morphological lesions involving hepatic microvasculature. Sinusoidal obstruction, complicated by perisinusoidal fibrosis and veno-occlusive lesion of the non-tumoral liver revealed by this study, should be included in the list of the adverse side-effects of colorectal systemic chemotherapy, in particular related to the use of oxaliplati

Importance of histological tumor response assessment in predicting the outcome in patients with colorectal liver metastases treated with neo-adjuvant chemotherapy followed by liver surgery

Background: The purpose of the study was to characterize histological response to chemotherapy of hepatic colorectal metastases (HCRM), evaluate efficacy of different chemotherapies on histological response, and determine whether tumor regression grading (TRG) of HCRM predicts clinical outcome. Patients and methods: TRG was evaluated on 525 HCRM surgically resected from 181 patients, 112 pretreated with chemotherapy. Disease-free survival (DFS) and overall survival (OS) were correlated to TRG. Results: Tumor regression was characterized by fibrosis overgrowing on tumor cells, decreased necrosis, and tumor glands (if present) at the periphery of HCRM. With irinotecan/5-fluorouracil (5-FU), major (MjHR), partial (PHR), and no (NHR) histological tumor regression were observed in 17%, 13%, and 70% of patients, respectively. With oxaliplatin/5-FU, MjHR, PHR, and NHR were observed in 37%, 45%, and 18% of patients, respectively. Five patients, treated with oxaliplatin, had complete response in all their metastases. MjHR was associated with an improved 3-year DFS compared with PHR or NHR. MjHR and PHR were associated with an improved 5-year OS compared with NHR. Conclusion: Histological tumor regression of HCRM to chemotherapy corresponds to fibrosis overgrowth and not to increase of necrosis. TRG should be considered when evaluating efficacy of chemotherapy for HCRM. Histological tumor regression was most common among oxaliplatin-treated patients and associated with better clinical outcom

Analysis of two human pre-ribosomal factors, bystin and hTsr1, highlights differences in evolution of ribosome biogenesis between yeast and mammals

Recent studies reveal that maturation of the 40S ribosomal subunit precursors in mammals includes an additional step during processing of the internal transcribed spacer 1 (ITS1), when compared with yeast Saccharomyces cerevisiae, even though the protein content of the pre-40S particle appears to be the same. Here, we examine by depletion with siRNA treatment the function of human orthologs of two essential yeast pre-ribosomal factors, hEnp1/bystin and hTsr1. Like their yeast orthologs, bystin is required for efficient cleavage of the ITS1 and further processing of this domain within the pre-40S particles, whereas hTsr1 is necessary for the final maturation steps. However, bystin depletion leads to accumulation of an unusual 18S rRNA precursor, revealing a new step in ITS1 processing that potentially involves an exonuclease. In addition, pre-40S particles lacking hTsr1 are partially retained in the nucleus, whereas depletion of Tsr1p in yeast results in strong cytoplasmic accumulation of pre-40S particles. These data indicate that ITS1 processing in human cells may be more complex than currently envisioned and that coordination between maturation and nuclear export of pre-40S particles has evolved differently in yeast and mammalian cells

Pilocarpine-Induced Status Epilepticus in Rats Involves Ischemic and Excitotoxic Mechanisms

The neuron loss characteristic of hippocampal sclerosis in temporal lobe epilepsy patients is thought to be the result of excitotoxic, rather than ischemic, injury. In this study, we assessed changes in vascular structure, gene expression, and the time course of neuronal degeneration in the cerebral cortex during the acute period after onset of pilocarpine-induced status epilepticus (SE). Immediately after 2 hr SE, the subgranular layers of somatosensory cortex exhibited a reduced vascular perfusion indicative of ischemia, whereas the immediately adjacent supragranular layers exhibited increased perfusion. Subgranular layers exhibited necrotic pathology, whereas the supergranular layers were characterized by a delayed (24 h after SE) degeneration apparently via programmed cell death. These results indicate that both excitotoxic and ischemic injuries occur during pilocarpine-induced SE. Both of these degenerative pathways, as well as the widespread and severe brain damage observed, should be considered when animal model-based data are compared to human pathology

Antimicrobial resistance among migrants in Europe: a systematic review and meta-analysis

BACKGROUND: Rates of antimicrobial resistance (AMR) are rising globally and there is concern that increased migration is contributing to the burden of antibiotic resistance in Europe. However, the effect of migration on the burden of AMR in Europe has not yet been comprehensively examined. Therefore, we did a systematic review and meta-analysis to identify and synthesise data for AMR carriage or infection in migrants to Europe to examine differences in patterns of AMR across migrant groups and in different settings. METHODS: For this systematic review and meta-analysis, we searched MEDLINE, Embase, PubMed, and Scopus with no language restrictions from Jan 1, 2000, to Jan 18, 2017, for primary data from observational studies reporting antibacterial resistance in common bacterial pathogens among migrants to 21 European Union-15 and European Economic Area countries. To be eligible for inclusion, studies had to report data on carriage or infection with laboratory-confirmed antibiotic-resistant organisms in migrant populations. We extracted data from eligible studies and assessed quality using piloted, standardised forms. We did not examine drug resistance in tuberculosis and excluded articles solely reporting on this parameter. We also excluded articles in which migrant status was determined by ethnicity, country of birth of participants' parents, or was not defined, and articles in which data were not disaggregated by migrant status. Outcomes were carriage of or infection with antibiotic-resistant organisms. We used random-effects models to calculate the pooled prevalence of each outcome. The study protocol is registered with PROSPERO, number CRD42016043681. FINDINGS: We identified 2274 articles, of which 23 observational studies reporting on antibiotic resistance in 2319 migrants were included. The pooled prevalence of any AMR carriage or AMR infection in migrants was 25·4% (95% CI 19·1-31·8; I2 =98%), including meticillin-resistant Staphylococcus aureus (7·8%, 4·8-10·7; I2 =92%) and antibiotic-resistant Gram-negative bacteria (27·2%, 17·6-36·8; I2 =94%). The pooled prevalence of any AMR carriage or infection was higher in refugees and asylum seekers (33·0%, 18·3-47·6; I2 =98%) than in other migrant groups (6·6%, 1·8-11·3; I2 =92%). The pooled prevalence of antibiotic-resistant organisms was slightly higher in high-migrant community settings (33·1%, 11·1-55·1; I2 =96%) than in migrants in hospitals (24·3%, 16·1-32·6; I2 =98%). We did not find evidence of high rates of transmission of AMR from migrant to host populations. INTERPRETATION: Migrants are exposed to conditions favouring the emergence of drug resistance during transit and in host countries in Europe. Increased antibiotic resistance among refugees and asylum seekers and in high-migrant community settings (such as refugee camps and detention facilities) highlights the need for improved living conditions, access to health care, and initiatives to facilitate detection of and appropriate high-quality treatment for antibiotic-resistant infections during transit and in host countries. Protocols for the prevention and control of infection and for antibiotic surveillance need to be integrated in all aspects of health care, which should be accessible for all migrant groups, and should target determinants of AMR before, during, and after migration. FUNDING: UK National Institute for Health Research Imperial Biomedical Research Centre, Imperial College Healthcare Charity, the Wellcome Trust, and UK National Institute for Health Research Health Protection Research Unit in Healthcare-associated Infections and Antimictobial Resistance at Imperial College London

Human Induced Pluripotent Stem Cells Differentiation into Oligodendrocyte Progenitors and Transplantation in a Rat Model of Optic Chiasm Demyelination

BACKGROUND: This study aims to differentiate human induced pluripotent stem cells (hiPSCs) into oligodendrocyte precursors and assess their recovery potential in a demyelinated optic chiasm model in rats. METHODOLOGY/PRINCIPAL FINDINGS: We generated a cell population of oligodendrocyte progenitors from hiPSCs by using embryoid body formation in a defined medium supplemented with a combination of factors, positive selection and mechanical enrichment. Real-time polymerase chain reaction and immunofluorescence analyses showed that stage-specific markers, Olig2, Sox10, NG2, PDGFRα, O4, A2B5, GalC, and MBP were expressed following the differentiation procedure, and enrichment of the oligodendrocyte lineage. These results are comparable with the expression of stage-specific markers in human embryonic stem cell-derived oligodendrocyte lineage cells. Transplantation of hiPSC-derived oligodendrocyte progenitors into the lysolecithin-induced demyelinated optic chiasm of the rat model resulted in recovery from symptoms, and integration and differentiation into oligodendrocytes were detected by immunohistofluorescence staining against PLP and MBP, and measurements of the visual evoked potentials. CONCLUSIONS/SIGNIFICANCE: These results showed that oligodendrocyte progenitors generated efficiently from hiPSCs can be used in future biomedical studies once safety issues have been overcome

Cardiac-Oxidized Antigens Are Targets of Immune Recognition by Antibodies and Potential Molecular Determinants in Chagas Disease Pathogenesis

Trypanosoma cruzi elicits reactive oxygen species (ROS) of inflammatory and mitochondrial origin in infected hosts. In this study, we examined ROS-induced oxidative modifications in the heart and determined whether the resultant oxidized cardiac proteins are targets of immune response and of pathological significance in Chagas disease. Heart biopsies from chagasic mice, rats and human patients exhibited, when compared to those from normal controls, a substantial increase in protein 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), carbonyl, and 3-nitrotyrosine (3-NT) adducts. To evaluate whether oxidized proteins gain antigenic properties, heart homogenates or isolated cardiomyocytes were oxidized in vitro and one- or two-dimensional gel electrophoresis (2D-GE)/Western blotting (WB) was performed to investigate the proteomic oxidative changes and recognition of oxidized proteins by sera antibodies in chagasic rodents (mice, rats) and human patients. Human cardiomyocytes exhibited LD50 sensitivity to 30 µM 4-HNE and 100 µM H2O2 at 6 h and 12 h, respectively. In vitro oxidation with 4-HNE or H2O2 resulted in a substantial increase in 4-HNE- and carbonyl-modified proteins that correlated with increased recognition of cardiac (cardiomyocytes) proteins by sera antibodies of chagasic rodents and human patients. 2D-GE/Western blotting followed by MALDI-TOF-MS/MS analysis to identify cardiac proteins that were oxidized and recognized by human chagasic sera yielded 82 unique proteins. We validated the 2D-GE results by enzyme-linked immunosorbent assay (ELISA) and WB and demonstrated that oxidation of recombinant titin enhanced its immunogenicity and recognition by sera antibodies from chagasic hosts (rats and humans). Treatment of infected rats with phenyl-α-tert-butyl nitrone (PBN, antioxidant) resulted in normalized immune detection of cardiac proteins associated with control of cardiac pathology and preservation of heart contractile function in chagasic rats. We conclude that ROS-induced, cardiac-oxidized antigens are targets of immune recognition by antibodies and molecular determinants for pathogenesis during Chagas disease

Nucleolus: the fascinating nuclear body

Nucleoli are the prominent contrasted structures of the cell nucleus. In the nucleolus, ribosomal RNAs are synthesized, processed and assembled with ribosomal proteins. RNA polymerase I synthesizes the ribosomal RNAs and this activity is cell cycle regulated. The nucleolus reveals the functional organization of the nucleus in which the compartmentation of the different steps of ribosome biogenesis is observed whereas the nucleolar machineries are in permanent exchange with the nucleoplasm and other nuclear bodies. After mitosis, nucleolar assembly is a time and space regulated process controlled by the cell cycle. In addition, by generating a large volume in the nucleus with apparently no RNA polymerase II activity, the nucleolus creates a domain of retention/sequestration of molecules normally active outside the nucleolus. Viruses interact with the nucleolus and recruit nucleolar proteins to facilitate virus replication. The nucleolus is also a sensor of stress due to the redistribution of the ribosomal proteins in the nucleoplasm by nucleolus disruption. The nucleolus plays several crucial functions in the nucleus: in addition to its function as ribosome factory of the cells it is a multifunctional nuclear domain, and nucleolar activity is linked with several pathologies. Perspectives on the evolution of this research area are proposed

Effects of Climate and Atmospheric Nitrogen Deposition on Early to Mid-Term Stage Litter Decomposition Across Biomes

open263siWe acknowledge support by the German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig, funded by the German Research Foundation (FZT 118), Scientific Grant Agency VEGA(GrantNo.2/0101/18), as well as by the European Research Council under the European Union’s Horizon 2020 Research and Innovation Program (Grant Agreement No. 677232)Litter decomposition is a key process for carbon and nutrient cycling in terrestrial ecosystems and is mainly controlled by environmental conditions, substrate quantity and quality as well as microbial community abundance and composition. In particular, the effects of climate and atmospheric nitrogen (N) deposition on litter decomposition and its temporal dynamics are of significant importance, since their effects might change over the course of the decomposition process. Within the TeaComposition initiative, we incubated Green and Rooibos teas at 524 sites across nine biomes. We assessed how macroclimate and atmospheric inorganic N deposition under current and predicted scenarios (RCP 2.6, RCP 8.5) might affect litter mass loss measured after 3 and 12 months. Our study shows that the early to mid-term mass loss at the global scale was affected predominantly by litter quality (explaining 73% and 62% of the total variance after 3 and 12 months, respectively) followed by climate and N deposition. The effects of climate were not litter-specific and became increasingly significant as decomposition progressed, with MAP explaining 2% and MAT 4% of the variation after 12 months of incubation. The effect of N deposition was litter-specific, and significant only for 12-month decomposition of Rooibos tea at the global scale. However, in the temperate biome where atmospheric N deposition rates are relatively high, the 12-month mass loss of Green and Rooibos teas decreased significantly with increasing N deposition, explaining 9.5% and 1.1% of the variance, respectively. The expected changes in macroclimate and N deposition at the global scale by the end of this century are estimated to increase the 12-month mass loss of easily decomposable litter by 1.1-3.5% and of the more stable substrates by 3.8-10.6%, relative to current mass loss. In contrast, expected changes in atmospheric N deposition will decrease the mid-term mass loss of high-quality litter by 1.4-2.2% and that of low-quality litter by 0.9-1.5% in the temperate biome. Our results suggest that projected increases in N deposition may have the capacity to dampen the climate-driven increases in litter decomposition depending on the biome and decomposition stage of substrate.openKwon T.; Shibata H.; Kepfer-Rojas S.; Schmidt I.K.; Larsen K.S.; Beier C.; Berg B.; Verheyen K.; Lamarque J.-F.; Hagedorn F.; Eisenhauer N.; Djukic I.; Caliman A.; Paquette A.; Gutierrez-Giron A.; Petraglia A.; Augustaitis A.; Saillard A.; Ruiz-Fernandez A.C.; Sousa A.I.; Lillebo A.I.; Da Rocha Gripp A.; Lamprecht A.; Bohner A.; Francez A.-J.; Malyshev A.; Andric A.; Stanisci A.; Zolles A.; Avila A.; Virkkala A.-M.; Probst A.; Ouin A.; Khuroo A.A.; Verstraeten A.; Stefanski A.; Gaxiola A.; Muys B.; Gozalo B.; Ahrends B.; Yang B.; Erschbamer B.; Rodriguez Ortiz C.E.; Christiansen C.T.; Meredieu C.; Mony C.; Nock C.; Wang C.-P.; Baum C.; Rixen C.; Delire C.; Piscart C.; Andrews C.; Rebmann C.; Branquinho C.; Jan D.; Wundram D.; Vujanovic D.; Adair E.C.; Ordonez-Regil E.; Crawford E.R.; Tropina E.F.; Hornung E.; Groner E.; Lucot E.; Gacia E.; Levesque E.; Benedito E.; Davydov E.A.; Bolzan F.P.; Maestre F.T.; Maunoury-Danger F.; Kitz F.; Hofhansl F.; Hofhansl G.; De Almeida Lobo F.; Souza F.L.; Zehetner F.; Koffi F.K.; Wohlfahrt G.; Certini G.; Pinha G.D.; Gonzlez G.; Canut G.; Pauli H.; Bahamonde H.A.; Feldhaar H.; Jger H.; Serrano H.C.; Verheyden H.; Bruelheide H.; Meesenburg H.; Jungkunst H.; Jactel H.; Kurokawa H.; Yesilonis I.; Melece I.; Van Halder I.; Quiros I.G.; Fekete I.; Ostonen I.; Borovsk J.; Roales J.; Shoqeir J.H.; Jean-Christophe Lata J.; Probst J.-L.; Vijayanathan J.; Dolezal J.; Sanchez-Cabeza J.-A.; Merlet J.; Loehr J.; Von Oppen J.; Loffler J.; Benito Alonso J.L.; Cardoso-Mohedano J.-G.; Penuelas J.; Morina J.C.; Quinde J.D.; Jimnez J.J.; Alatalo J.M.; Seeber J.; Kemppinen J.; Stadler J.; Kriiska K.; Van Den Meersche K.; Fukuzawa K.; Szlavecz K.; Juhos K.; Gerhtov K.; Lajtha K.; Jennings K.; Jennings J.; Ecology P.; Hoshizaki K.; Green K.; Steinbauer K.; Pazianoto L.; Dienstbach L.; Yahdjian L.; Williams L.J.; Brigham L.; Hanna L.; Hanna H.; Rustad L.; Morillas L.; Silva Carneiro L.; Di Martino L.; Villar L.; Fernandes Tavares L.A.; Morley M.; Winkler M.; Lebouvier M.; Tomaselli M.; Schaub M.; Glushkova M.; Torres M.G.A.; De Graaff M.-A.; Pons M.-N.; Bauters M.; Mazn M.; Frenzel M.; Wagner M.; Didion M.; Hamid M.; Lopes M.; Apple M.; Weih M.; Mojses M.; Gualmini M.; Vadeboncoeur M.; Bierbaumer M.; Danger M.; Scherer-Lorenzen M.; Ruek M.; Isabellon M.; Di Musciano M.; Carbognani M.; Zhiyanski M.; Puca M.; Barna M.; Ataka M.; Luoto M.; H. Alsafaran M.; Barsoum N.; Tokuchi N.; Korboulewsky N.; Lecomte N.; Filippova N.; Hlzel N.; Ferlian O.; Romero O.; Pinto-Jr O.; Peri P.; Dan Turtureanu P.; Haase P.; Macreadie P.; Reich P.B.; Petk P.; Choler P.; Marmonier P.; Ponette Q.; Dettogni Guariento R.; Canessa R.; Kiese R.; Hewitt R.; Weigel R.; Kanka R.; Cazzolla Gatti R.; Martins R.L.; Ogaya R.; Georges R.; Gaviln R.G.; Wittlinger S.; Puijalon S.; Suzuki S.; Martin S.; Anja S.; Gogo S.; Schueler S.; Drollinger S.; Mereu S.; Wipf S.; Trevathan-Tackett S.; Stoll S.; Lfgren S.; Trogisch S.; Seitz S.; Glatzel S.; Venn S.; Dousset S.; Mori T.; Sato T.; Hishi T.; Nakaji T.; Jean-Paul T.; Camboulive T.; Spiegelberger T.; Scholten T.; Mozdzer T.J.; Kleinebecker T.; Runk T.; Ramaswiela T.; Hiura T.; Enoki T.; Ursu T.-M.; Di Cella U.M.; Hamer U.; Klaus V.; Di Cecco V.; Rego V.; Fontana V.; Piscov V.; Bretagnolle V.; Maire V.; Farjalla V.; Pascal V.; Zhou W.; Luo W.; Parker W.; Parker P.; Kominam Y.; Kotrocz Z.; Utsumi Y.Kwon T.; Shibata H.; Kepfer-Rojas S.; Schmidt I.K.; Larsen K.S.; Beier C.; Berg B.; Verheyen K.; Lamarque J.-F.; Hagedorn F.; Eisenhauer N.; Djukic I.; Caliman A.; Paquette A.; Gutierrez-Giron A.; Petraglia A.; Augustaitis A.; Saillard A.; Ruiz-Fernandez A.C.; Sousa A.I.; Lillebo A.I.; Da Rocha Gripp A.; Lamprecht A.; Bohner A.; Francez A.-J.; Malyshev A.; Andric A.; Stanisci A.; Zolles A.; Avila A.; Virkkala A.-M.; Probst A.; Ouin A.; Khuroo A.A.; Verstraeten A.; Stefanski A.; Gaxiola A.; Muys B.; Gozalo B.; Ahrends B.; Yang B.; Erschbamer B.; Rodriguez Ortiz C.E.; Christiansen C.T.; Meredieu C.; Mony C.; Nock C.; Wang C.-P.; Baum C.; Rixen C.; Delire C.; Piscart C.; Andrews C.; Rebmann C.; Branquinho C.; Jan D.; Wundram D.; Vujanovic D.; Adair E.C.; Ordonez-Regil E.; Crawford E.R.; Tropina E.F.; Hornung E.; Groner E.; Lucot E.; Gacia E.; Levesque E.; Benedito E.; Davydov E.A.; Bolzan F.P.; Maestre F.T.; Maunoury-Danger F.; Kitz F.; Hofhansl F.; Hofhansl G.; De Almeida Lobo F.; Souza F.L.; Zehetner F.; Koffi F.K.; Wohlfahrt G.; Certini G.; Pinha G.D.; Gonzlez G.; Canut G.; Pauli H.; Bahamonde H.A.; Feldhaar H.; Jger H.; Serrano H.C.; Verheyden H.; Bruelheide H.; Meesenburg H.; Jungkunst H.; Jactel H.; Kurokawa H.; Yesilonis I.; Melece I.; Van Halder I.; Quiros I.G.; Fekete I.; Ostonen I.; Borovsk J.; Roales J.; Shoqeir J.H.; Jean-Christophe Lata J.; Probst J.-L.; Vijayanathan J.; Dolezal J.; Sanchez-Cabeza J.-A.; Merlet J.; Loehr J.; Von Oppen J.; Loffler J.; Benito Alonso J.L.; Cardoso-Mohedano J.-G.; Penuelas J.; Morina J.C.; Quinde J.D.; Jimnez J.J.; Alatalo J.M.; Seeber J.; Kemppinen J.; Stadler J.; Kriiska K.; Van Den Meersche K.; Fukuzawa K.; Szlavecz K.; Juhos K.; Gerhtov K.; Lajtha K.; Jennings K.; Jennings J.; Ecology P.; Hoshizaki K.; Green K.; Steinbauer K.; Pazianoto L.; Dienstbach L.; Yahdjian L.; Williams L.J.; Brigham L.; Hanna L.; Hanna H.; Rustad L.; Morillas L.; Silva Carneiro L.; Di Martino L.; Villar L.; Fernandes Tavares L.A.; Morley M.; Winkler M.; Lebouvier M.; Tomaselli M.; Schaub M.; Glushkova M.; Torres M.G.A.; De Graaff M.-A.; Pons M.-N.; Bauters M.; Mazn M.; Frenzel M.; Wagner M.; Didion M.; Hamid M.; Lopes M.; Apple M.; Weih M.; Mojses M.; Gualmini M.; Vadeboncoeur M.; Bierbaumer M.; Danger M.; Scherer-Lorenzen M.; Ruek M.; Isabellon M.; Di Musciano M.; Carbognani M.; Zhiyanski M.; Puca M.; Barna M.; Ataka M.; Luoto M.; H. Alsafaran M.; Barsoum N.; Tokuchi N.; Korboulewsky N.; Lecomte N.; Filippova N.; Hlzel N.; Ferlian O.; Romero O.; Pinto-Jr O.; Peri P.; Dan Turtureanu P.; Haase P.; Macreadie P.; Reich P.B.; Petk P.; Choler P.; Marmonier P.; Ponette Q.; Dettogni Guariento R.; Canessa R.; Kiese R.; Hewitt R.; Weigel R.; Kanka R.; Cazzolla Gatti R.; Martins R.L.; Ogaya R.; Georges R.; Gaviln R.G.; Wittlinger S.; Puijalon S.; Suzuki S.; Martin S.; Anja S.; Gogo S.; Schueler S.; Drollinger S.; Mereu S.; Wipf S.; Trevathan-Tackett S.; Stoll S.; Lfgren S.; Trogisch S.; Seitz S.; Glatzel S.; Venn S.; Dousset S.; Mori T.; Sato T.; Hishi T.; Nakaji T.; Jean-Paul T.; Camboulive T.; Spiegelberger T.; Scholten T.; Mozdzer T.J.; Kleinebecker T.; Runk T.; Ramaswiela T.; Hiura T.; Enoki T.; Ursu T.-M.; Di Cella U.M.; Hamer U.; Klaus V.; Di Cecco V.; Rego V.; Fontana V.; Piscov V.; Bretagnolle V.; Maire V.; Farjalla V.; Pascal V.; Zhou W.; Luo W.; Parker W.; Parker P.; Kominam Y.; Kotrocz Z.; Utsumi Y

Strategic research agenda for biomedical imaging

This Strategic Research Agenda identifies current challenges and needs in healthcare, illustrates how biomedical imaging and derived data can help to address these, and aims to stimulate dedicated research funding efforts. Medicine is currently moving towards a more tailored, patient-centric approach by providing personalised solutions for the individual patient. Innovation in biomedical imaging plays a key role in this process as it addresses the current needs for individualised prevention, treatment, therapy response monitoring, and image-guided surgery. The use of non-invasive biomarkers facilitates better therapy prediction and monitoring, leading to improved patient outcomes. Innovative diagnostic imaging technologies provide information about disease characteristics which, coupled with biological, genetic and -omics data, will contribute to an individualised diagnosis and therapy approach. In the emerging field of theranostics, imaging tools together with therapeutic agents enable the selection of best treatments and allow tailored therapeutic interventions. For prenatal monitoring, the use of innovative imaging technologies can ensure an early detection of malfunctions or disease. The application of biomedical imaging for diagnosis and management of lifestyle-induced diseases will help to avoid disease development through lifestyle changes. Artificial intelligence and machine learning in imaging will facilitate the improvement of image interpretation and lead to better disease prediction and therapy planning. As biomedical imaging technologies and analysis of existing imaging data provide solutions to current challenges and needs in healthcare, appropriate funding for dedicated research is needed to implement the innovative approaches for the wellbeing of citizens and patients