tbuckley/cabot-search huggingface dataset:
P09.31 The prognostic value of systemic inflammatory indices in recurrent Glioma treated with bevacizumab
Authors: A. Martínez-González, C. González Díaz, R. Cabrera, M. Lloret Sáez-Bravo, P. C. Lara
Journal: Neuro-Oncology (2017)

were analyzed for PFS and the use of ADs showed a statistically longer PFS with a pooled HR of 0.73 (95% CI 0.62-0.86;p< 0.01); However, among ADs, only bevacizumab (2752 PTS) demonstrated an improvement of PFS; indeed, the pooled HR for PFS for BEV studies was significant at HR = 0.6 (95% CI 0.5-0.7;p < 0.01), both alone (HR = 0.6; CI 95% 0.44-0.82;p < 0.01) or in combination to CT (HR = 0.6; 95% CI 0.4-0.7;p< 0.01), both as first-line treatment (HR = 0.65; 95% CI 0.52-0.83;p < 0.01) or in recurrent disease (HR = 0.51; 95% CI 0.43-0.61;p < 0.01).CONCLUSIONS: ADs did not improve OS in GBM PTS, both as first or second-line treatment.Among ADs, only BEV demonstrated a PFS benefit both as single agent or in combination with chemotherapy, both as first or second-line treatment.P09.
Therapeutic Rationale to Target Highly Expressed CDK7 Conferring Poor Outcomes in Triple-Negative Breast Cancer
Authors: Bo Li, Triona Ni Chonghaile, Yue Fan, Stephen F. Madden, Rut Klinger, Aisling E. O'Connor, Louise Walsh, Gillian O'Hurley, Girish Mallya Udupi, Jesuchristopher Joseph, Finbarr Tarrant, Emer Conroy, Alexander Gaber, Suet-Feung Chin, Helen A. Bardwell, Elena Provenzano, John Crown, Thierry Dubois, Sabine Linn, Karin Jirstrom, Carlos Caldas, Darran P. O'Connor, William M. Gallagher
Journal: Cancer Research (2017)

Abstract Triple-negative breast cancer (TNBC) patients commonly exhibit poor prognosis and high relapse after treatment, but there remains a lack of biomarkers and effective targeted therapies for this disease. Here, we report evidence highlighting the cell-cycle–related kinase CDK7 as a driver and candidate therapeutic target in TNBC. Using publicly available transcriptomic data from a collated set of TNBC patients (n = 383) and the METABRIC TNBC dataset (n = 217), we found CDK7 mRNA levels to be correlated with patient prognosis. High CDK7 protein expression was associated with poor prognosis within the RATHER TNBC cohort (n = 109) and the METABRIC TNBC cohort (n = 203). The highly specific CDK7 kinase inhibitors, BS-181 and THZ1, each downregulated CDK7-mediated phosphorylation of RNA polymerase II, indicative of transcriptional inhibition, with THZ1 exhibiting 500-fold greater potency than BS-181. Mechanistic investigations revealed that the survival of MDA-MB-231 TNBC cells relied heavily on the BCL-2/BCL-XL signaling axes in cells. Accordingly, we found that combining the BCL-2/BCL-XL inhibitors ABT-263/ABT199 with the CDK7 inhibitor THZ1 synergized in producing growth inhibition and apoptosis of human TNBC cells. Collectively, our results highlight elevated CDK7 expression as a candidate biomarker of poor prognosis in TNBC, and they offer a preclinical proof of concept for combining CDK7 and BCL-2/BCL-XL inhibitors as a mechanism-based therapeutic strategy to improve TNBC treatment. Cancer Res; 77(14); 3834–45. ©2017 AACR.
Exploratory analysis describing ultrasonic (US) evaluation of spleen size during peripheral blood progenitor cell (PBPC) mobilization by filgrastim in normal donors
Authors: P. J. Stiff, K. S. Hansen, L. Dreiling, M. Guo, A. S. Artz
Journal: Journal of Clinical Oncology (2009)

7102 Background: Filgrastim is used to mobilize CD34 + cells into the peripheral blood that are collected by apheresis for allogeneic transplantation. We prospectively evaluated spleen size during PBPC mobilization Methods: Donors ≥18 yrs eligible to be PBPC donors per institutional guidelines enrolled. Splenic assessments were done before, during, and after PBPC mobilization. Filgrastim dose and schedule and leukapheresis (LK) procedures were per local practice. Spleen size by US was measured in 3 dimensions: longitudinal (craniocaudal), transverse, and diagonal (perpendicular to transverse). Splenic volume was estimated by taking the cross-product of 3 dimensions and multiplying by 0.52, approximating an ellipse volume. Stiff (ASH 2007) reported the primary endpoint, fold change from baseline in splenic volume during mobilization. Exploratory analyses, including a linear regression evaluating the effect of age and baseline spleen size on fold-change, were performed. Results: 309 enrolled, median age 44yrs, 56% male. Median fold volume change from baseline to first LK was 1.47, resolving to near baseline 1 week after last LK. No significant clinical sequelae, including splenic rupture, were reported. Older donors appeared to have the smallest baseline spleen volume and the largest fold change (table). Linear regression analyses indicated age was a significant predictor for both baseline spleen volume (p=0.0031) and spleen volume fold change from baseline at first LK (p=0.0499). Conclusions: During mobilization, spleen volume transiently increased from baseline to day of 1st LK and returned to near baseline 1 week after last LK. Older donors tended to have smaller baseline splenic volume and greater fold changes in spleen size. Preclinical models suggest decreasing hematopoietic stem cell homing after mobilization with aging (Morrison 1996; Wagers 2002), which could result in splenic accumulation of progenitor and stem cells. [Table: see text] [Table: see text]
Trial of Transplantation of HCV-Infected Kidneys into Uninfected Recipients
Authors: David S Goldberg, Peter L Abt, Emily A Blumberg, Vivianna M Van Deerlin, Matthew Levine, K Rajender Reddy, Roy D Bloom, Susanna M Nazarian, Deirdre Sawinski, Paige Porrett, Ali Naji, Richard Hasz, Lawrence Suplee, Jennifer Trofe-Clark, Anna Sicilia, Maureen McCauley, Midhat Farooqi, Caren Gentile, Jennifer Smith, Peter P Reese
Journal: New England Journal of Medicine (2017)

An open-label pilot trial involving 10 patients shows that hepatitis C virus genotype 1–infected kidneys transplanted into HCV-negative recipients, followed by direct-acting antiviral therapy, can result in excellent allograft function with cure of HCV infection.
P17.15 IMRT based Hypofractionated Re-Irradiation of Progressive Glioblastoma: final analysis of results
Authors: N. Tanna, O. Kirmi
Journal: Neuro-Oncology (2017)

Background: Glioblastoma (GBM) is the commonest malignant brain tumour in adults. Current standard of care is concurrent ­chemo-radiotherapy and adjuvant chemotherapy, and either lomustine-based chemotherapy or temozolomide rechallenge at first relapse. There is no consensus on therapy after 1st line relapse chemotherapy, with a variety of approaches. There are case series in the literature on re-irradiation, but little consensus. He we report the results of using re-irradiation in a cohort of patient with relapsed GBM. Methods: We identified all patients treated at our centre with high-grade glioma from 1st January 2012 – 1st October 2016 who received chemo-radiotherapy and a second course of radiotherapy. Results: We identified 16 patients, of whom all had tissue sampling (13 sub-total resection; 3 biopsy) and radical chemo-radiotherapy (60Gy in 30 with concurrent Temozolamide) using IMRT. 4 stopped chemotherapy (1 sepsis, 1 rash & dyspnea, 2 thrombocytopenia). At relapse, 7 patients underwent further debulking surgery prior to chemotherapy. 12 patients received 2nd line chemo before re-irradiation (5x Procarbazine/Lomustine; 3x Lomustine; 1x Irinotecan; 1x Temozolamide; 1x Procarbazine/Lomustine/Vincristine; 1x Bevacizumab/Lomustine). 4 did not (2 thrombocytopenia, 1 clinical deterioration, 1 intolerance to chemo). Re-irradiation was delivered as 40Gy in 10 fractions for 15 patients (35 Gy in 10 fractions for one), using IMRT, with a median time of 34 weeks between starting primary radiotherapy and re-irradiation. CTV was defined as T1-contrast enhancing signal. PTV was CTV+3mm. Patients were routinely imaged with contrast-enhanced MRI at 1 and 4 months after the completion of re-irradiation. No patient developed radiological evidence of radionecrosis or toxicity beyond grade 2. According to RANO criteria, 12 patients were stable and one had 1 progressive disease at their first scan. 2 patients died from progressive disease less than 1 month after finishing re-irradiation. Median survival from completion of re-irradiation was 29 weeks (IQR 20-36). In all cases progression was noted at the primary disease site. Post-reirradiation, one patient enrolled in a phase 1 clinical trial, and 3 had 3rd line chemotherapy (1x Bevacixumab/Irinotecan, 1x Irinotecan only and 1x Lomustine). Conclusion: Reirradiation using IMRT for relapsed GBM has limited acute toxicity and in some patients offers a period of disease stability. Radionecrosis does not appear to be a significant issue given the life-expectancy of this cohort of patients. Optimal dose and sequencing of treatment remains unclear.
Inactivation of AP-1 proteins precedes the onset of radiation-induced lung damage
Authors: Michael G. Haase, Anke Klawitter, Gustavo B. Baretton
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

1302 

Radiation induced lung damage comprises inflammation as well as deregulation of cell damage repair and cell proliferation. AP-1 is an ubiquitous transcription factor involved in the regulation of inflammatory and proliferational processes. In this study, we investigated changes in the distribution and activity of AP-1 in the process of radiation induced lung damage and their underlying mechanisms. While there were no major changes in the cellular distribution of AP-1 proteins or mRNA, we found a loss of AP-1 DNA-binding activity 4.5 –5.5 weeks after irradiation. This was explained by a cleavage of the AP-1 proteins c-Jun and JunD producing fragments of ∼20 kDa unable to bind to DNA whereas the levels of their mRNA remained constant during that time period. Consistently, recombinant c-Jun was partially cleaved by extracts of irradiated lungs producing fragments of a similar size. In parallel, the mRNA of KGF, an AP-1 dependent gene, was down-regulated in the damaged lung. Since AP-1 is an ubiquitous transcription factor that is essential for cellular proliferation and differentiation, the functional inhibition of AP-1 is likely to play an important role in the pathogenesis of radiation induced lung damage.
Enteric-coated mycophenolate sodium versus azathioprine in patients with active systemic lupus erythematosus: a randomised clinical trial
Authors: Josep Ordi-Ros, Luis Sáez-Comet, Mercedes Pérez-Conesa, Xavier Vidal, Francesca Mitjavila, Antoni Castro Salomó, Jordi Cuquet Pedragosa, Vera Ortiz-Santamaria, Montserrat Mauri Plana, Josefina Cortés-Hernández
Journal: Annals of the Rheumatic Diseases (2017)

To compare the efficacy and safety of enteric-coated mycophenolate sodium (EC-MPS) versus azathioprine (AZA) in patients with active systemic lupus erythematosus (SLE) disease.A multicentre, 24-month, superiority, open-label, randomised controlled trial (NCT01112215) was conducted with 240 patients (120 per arm) receiving either EC-MPS (target dose: 1440 mg/day) or AZA (target dose: 2 mg/kg/day) in addition to prednisone and/or antimalarials. The primary endpoint was the proportion of patients achieving clinical remission, assessed by SLE Disease Activity Index 2000 (SLEDAI-2K) and British Isles Lupus Assessment Group (BILAG), at 3 and 24 months. Secondary endpoints included time to clinical remission, BILAG A and B flare rates, time to flare, corticosteroid reduction and adverse events (AEs).Proportion of patients achieving clinical remission (clinical SLEDAI=0) was higher in the EC-MPS group at 3 (32.5% vs 19.2%; treatment difference, 13.3 (CI 2.3 to 24), p=0.034) and 24 months (71.2% vs 48.3%; treatment difference, 22.9 (CI 10.4 to 34.4), p<0.001). EC-MPS was superior with respect to time to clinical remission (HR 1.43; 95% CI 1.07 to 1.91; p=0.017). BILAG A/B and B flares occurred more frequently in the AZA group (71.7% vs 50%, p=0.001 and 21.67% vs 8.3%, p=0.004, respectively). EC-MPS was superior with respect to time to first BILAG A/B (HR 1.81; 95% CI 1.3 to 2.56; p=0.0004) and BILAG A flare (HR 2.84; 95% CI 1.37 to 5.89; p=0.003). AEs were similar in both groups except for leucopenia that occurred more frequently with AZA.EC-MPS was superior to AZA in treating SLE and preventing further relapses.NCT01112215; Results.
P08.49 Sensitivity of glioma cell lines and normal human cultured astrocytes to modified isothiourea derivative (ZKK-13) and Caseine Kinase II inhibitors
Authors: E. B. Pucko, R. P. Ostrowski
Journal: Neuro-Oncology (2017)

Introduction: Glioblastoma multiforme (WHO grade IV) is the most aggressive primary brain tumour that is characterized by intratumoral heterogeneity, invasive growth and poor prognosis. The therapy of astroglial tumours remains still challenging. Promising group of compounds are derivatives of pentabromobenzylisothiouronium salt, which affect proliferation of some human cancer cells. Isothioureas are a class of amphiphilic compounds carrying a highly basic isothiourea group of pKa » 10. They exist in the protonated (cation) form, what is very important for molecular recognition of specific receptors. Second interesting class of compounds with a potential for cancer treatment are Caseine Kinase II (CK2) inhibitors. CK2 is an oncogenic protein kinase present in both the nucleus and cytoplasm of cells. The serine/threonine protein kinase CK2 modulates multiple signaling pathways involved in cell survival and function, and is therefore a promising drug target. The aim of this study was to evaluate the cytostatic effect of novel CK2 inhibitors and S-pentabromobenzylisothiourea derivative (ZKK-13) on cell lines of human glial tumours, as compared to normal human cultured astrocytes. Materials and Methods: We examined the cytostatic effect of selected modified isothiourea derivatives - pentabromobenzylisothioureas (ZKKs) including ZKK-13 and CK2 inhibitors against adult human glioblastoma cell line (T98G) and normal human cultured astrocytes. We analyzed cell viability (MTT metabolism assay), and conducted cell proliferation assay (Multisizer3; Beckman Coulter cell counter) after 24, 48 and 72 hours of incubation with investigated compounds. Results: In all experimental groups there was a marked decrease of a total cells number, especially after 48 and 72 hours of treatment. T98G cells treated with ZKK-13 showed a statistically significant decrease of proliferation rate at 10µM in comparison to the control cells. Inhibitor of kinase CK2 - 2- aminoethylamino-4,5,6,7- tetrabromo-1H- benzimidazole, appeared to be the most effective compound that exhibits a strong anti-proliferative effect on neoplastic astroglial cells in gliomas in vitro. Conclusions: The results show that CK2 inhibitors and S-pentabromobenzylisothiourea derivative have a potent antiproliferative efficacy against malignant glioma cells. It may offer a promising anti-tumour therapy, including treatment of glial cells-derived primary brain tumours. ACKNOWLEDGEMENT: The research was supported by the Foundation for the Development of Diagnostic and Therapy, Warsaw.
Triplicate Sputum Cultures for Efficacy Evaluation of Novel Antituberculosis Regimens
Authors: Andreas H. Diacon, Elana van Brakel, Nacer Lounis, Paul Meyvisch, Ben Van Baelen, Tine De Marez, Eilidh Jenkins, Brian Dannemann
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

in helping clinicians discriminate between states of health, contamination, colonization, and infection.Although in principle our metagenomic approach is capable of identifying nonbacterial pathogens, we have not yet established whether our current approach can detect fungal, viral, or protozoal pathogens in the lungs.Additional methodological work is needed to optimize the detection of microbial signal in host-DNA-rich respiratory specimens.Finally, further work is needed to streamline the bioinformatic analysis of metagenomic sequencing data before this approach can be scaled for testing in a clinical context.Pneumonia is a 21st-century problem, yet its diagnosis still relies on 19th-century tools.Our results demonstrate the feasibility and promise of introducing real-time metagenomics to our diagnostic arsenal.Clinical study is warranted, as the revolution in molecular microbiology has at last reached the bedside.
Joblessness and Lost Earnings after Acute Respiratory Distress Syndrome in a 1-Year National Multicenter Study
Authors: Biren B. Kamdar, Minxuan Huang, Victor D. Dinglas, Elizabeth Colantuoni, Till M. von Wachter, Ramona O. Hopkins, Dale M. Needham, L. Hudson, S. Gundel, C. Hough, M. Neff, K. Sims, A. Ungar, T. Watkins, J. Steingrub, M. Tidswell, E. Braden, L. DeSouza, C. Kardos, L. Kozikowski, S. Ouellette, K. Guntupalli, V. Bandi, C. Pope, C. Ross, R. Brower, H. Fessler, D. Hager, P. Mendez-Tellez, D. Needham, K. Oakjones, J. Sevransky, A. Workneh, C. Shanholtz, D. Herr, H. Howes, G. Netzer, P. Rock, A. Sampaio, J. Titus, P. Sloane, T. Beck, D. Highfield, S. King, B. Lee, N. Bolouri, H. P. Wiedemann, R. W. Ashton, D. A. Culver, T. Frederick, J. A. Guzman, J. J. Komara, A. J. Reddy, R. Hejal, M. Andrews, D. Haney, A. F. Connors, S. Lasalvia, J. D. Thornton, E. L. Warren, M. Moss, E. L. Burnham, L. Gray, J. Maloney, M. Mealer, I. Douglas, K. Overdier, K. Thompson, R. Wolken, S. Frankel, J. McKeehan, M. L. Warner, T. Bost, C. Higgins, K. Hodgin, N. MacIntyre, L. Brown, C. Cox, M. Gentile, J. Govert, N. Knudsen, S. Carson, L. Chang, S. Choudhury, W. Hall, J. Lanier, A. P. Wheeler, G. R. Bernard, M. Hays, S. Mogan, T. W. Rice, R. D. Hite, A. Harvey, P. E. Morris, M. Ragusky, P. Wright, S. Groce, J. McLean, A. Overton, J. Truwit, K. Enfield, M. Marshall, A. Morris, C. Grissom, A. Austin, S. Barney, S. Brown, J. Ferguson, H. Gallo, T. Graydon, E. Hirshberg, A. Jephson, N. Kumar, M. Lanspa, R. Miller, D. Murphy, J. Orme, A. Stowe, L. Struck, F. Thomas, D. Ward, P. Bailey, W. Beninati, L. Bezdjian, T. Clemmer, S. Rimkus, R. Tanaka, L. Weaver, C. Lawton, D. Hanselman, K. Sundar, W. Alward, C. Bishop, D. Eckley, D. Harris, T. Hill, B. Jensen, K. Ludwig, D. Nielsen, M. Pearce, M. A. Matthay, C. Calfee, B. Daniel, M. Eisner, O. Garcia, K. Kordesch, K. Liu, N. Shum, H. Zhou, M. W. Peterson, J. Blaauw, K. Van Gundy, R. Kallet, E. Johnson, T. Albertson, B. Morrissey, E. Vlastelin, B. deBoisblanc, A. Antoine, D. Charbonnet, J. Hunt, P. Lauto, A. Marr, G. Meyaski, C. Romaine, S. Brierre, J. Byrne, T. Jagneaux, C. LeBlanc, K. Moreau, C. Thomas, S. Jain, D. Taylor, L. Seoane, C. Hebert, J. Thompson, F. Simeone, J. Fearon, D. Schoenfeld, N. Dong, M. Guha, E. Hammond, P. Lazar, R. Morse, C. Oldmixon, N. Ringwood, E. Smoot, B. T. Thompson, R. Wilson, A. Harabin, S. Bredow, M. Waclawiw, G. Weinmann, R. G. Spragg, A. Slutsky, M. Levy, B. Markovitz, E. Petkova, C. Weijer, J. Sznajder, M. Begg, L. Gilbert-McClain, E. Israel, J. Lewis, S. McClave, P. Parsons
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Following acute respiratory distress syndrome (ARDS), joblessness is common but poorly understood.
P03.22 BRAF, FGFR1 and PDGFRA alterations in oligodendrogliomas - correlation with MAPK/mTOR pathway activation
Authors: C. Sarkar, A. Kumar, P. Pathak, S. Purkait, S. Nayak, M. Faruq, V. Suri, M. C. Sharma, A. Suri
Journal: Neuro-Oncology (2017)

Oligodendroglioma (ODGs) is relatively rare, comprising approximately 2.7% of all brain tumors. They have attracted great interest in both basic and clinical neurooncology because of having a better overall prognosis as compared to other diffuse gliomas. BRAF alterations and RTK alterations along with activation of mTOR and MAPK pathways have been identified in various glial tumors. However, these alterations and clinical outcome remain unexplored in ODGs. Hence, the aim of this study was to analyse, BRAF, FGFR1, PDGFRA related genetic alterations and MAPK-mTOR signaling pathway in oligodendroglioma (ODG). Based on 1p/19q co-deletion, IDH1 mutation, and ATRX immunostaining, 45 ODG cases were studied. BRAF-gain, BRAF-KIAA1549 fusion, FGFR1-TKD duplication and PDGFRA amplification were determined by quantitative real-time PCR. BRAF-V600E mutation was analysed by sanger sequencing and MAPK-mTOR pathway activation by Immunohistochemistry. BRAF-gain and BRAF -KIAA1549 fusion were detected in 40% and 23% of ODGs respectively. BRAF V600E mutation, FGFR1-TKD duplication and PDGFRA amplification had a low occurrence rate of 4%, 12% and 11%, respectively. Association of BRAF-gain with poor outcome and BRAF -KIAA149 fusion with better outcome was noted. MAPK/ERK pathway activation was detected in 71% of cases and was associated with BRAF-gain. Interestingly, all the cases harbouring FGFR1-TKD duplication showed MAPK/ERK pathway activation. mTOR pathway was however activated in a small subset of ODGs (12/45;27%). BRAF, FGFR1-TKD and PDGFRA alterations did not show significant association with grade and age. However, FGFR-TKD duplication was mainly reported in older age group (age >40 years)ODGs. Additionally, treatment of HS683 cell line with U0126, a MAPK inhibitor demonstrated decreased MAPK pathway activation and cell growth along with induced apoptosis. This study highlights the molecular heterogeneity in ODG, classified according to updated WHO classification 2016. Apart from earlier described biomarkers in ODGs, our findings implicate presence of BRAF and PDGFR-A and/or FGFR1-TKD duplication leading to MAPK-mTOR pathway activation, suggesting a pivotal role of these pathways in ODG tumorigenesis. Overall, we systematically characterised BRAF/FGFR/PDGFR alterations and consequent MAPK/mTOR pathway activation for the first time in ODGs. Importantly, in-vitro study indicates that targeted pharmacological inhibition of MAPK pathway may constitute a promising approach in the treatment of ODGs. As there are many agents known to inhibit MAPK pathways with few currently under investigation, a potentially bright future for further improved treatment of ODG patients holds promise.
Molecular Effects of Rituximab on CLL Cells In Vivo: Rapid Increase in Serum Interferon gamma, Induction of a Distinct Tumor Cell Gene Expression Signature and Loss of CD20 Expression.
Authors: Adrian Wiestner, Elinor Lee, Berengere Vire, Federica Gibellini, Ndegwa Njuguna, Yair Herishanu, Delong Liu, Peter Munson, Nalini Raghavachari, Therese White, Gerald E. Marti, Wyndham H. Wilson
Journal: Blood (2007)
A unique opportunity to use football to improve birth registration awareness and completeness in Nigeria
Authors: Olusesan Ayodeji Makinde, Clifford Obby Odimegwu, Funmilola M OlaOlorun
Journal: British Journal of Sports Medicine (2017)

Nigeria is a football-loving nation and has won silverware at international footballing events. By 2016, the country had won five of the under-17 world championships that had ever been held since the tournament’s inception in 1985 (16 tournaments). Brazil ranked next with number of three trophies. Nigeria also has the highest number of football players on the African continent, many of whom are youth.1 As at2006, there were over 6.5 million football players in the country, the eighth largest concentration of players in the world.1 

Age-related footballing events have been bedevilled by age fraud. Age fraud is a term for age fabrication or the use of false documentation to gain an advantage over opponents and has been described as the ‘biggest problem’ facing African football.2 Nigeria has been repeatedly accused of being involved in age fraud and several of its players have been disqualified from different events. The country was suspended by FIFA in 1989 and stripped of its hosting rights for the FIFA world youth championship in 1991 after three of the players who it presented in a previous contest had disparities in age …
Control of angiogenesis and host response by modulating the cell adhesion properties of an Elastin-Like Recombinamer-based hydrogel
Authors: Sebastian Manuel Staubli, Giulia Cerino, Israel Gonzalez De Torre, Matilde Alonso, Daniel Oertli, Friedrich Eckstein, Katharina Glatz, José Carlos Rodríguez Cabello, Anna Marsano
Journal: Biomaterials (2017)