tbuckley/cabot-search huggingface dataset:
Engineering biomaterials by inkjet printing of hydrogels with functional particulates
Authors: Cih Cheng, Eric J Williamson, George T.-C. Chiu, Bumsoo Han
Journal: Med-X (2024)

Abstract Hydrogels with particulates, including proteins, drugs, nanoparticles, and cells, enable the development of new and innovative biomaterials. Precise control of the spatial distribution of these particulates is crucial to produce advanced biomaterials. Thus, there is a high demand for manufacturing methods for particle-laden hydrogels. In this context, 3D printing of hydrogels is emerging as a promising method to create numerous innovative biomaterials. Among the 3D printing methods, inkjet printing, so-called drop-on-demand (DOD) printing, stands out for its ability to construct biomaterials with superior spatial resolutions. However, its printing processes are still designed by trial and error due to a limited understanding of the ink behavior during the printing processes. This review discusses the current understanding of transport processes and hydrogel behaviors during inkjet printing for particulate-laden hydrogels. Specifically, we review the transport processes of water and particulates within hydrogel during ink formulation, jetting, and curing. Additionally, we examine current inkjet printing applications in fabricating engineered tissues, drug delivery devices, and advanced bioelectronics components. Finally, the challenges and opportunities for next-generation inkjet printing are also discussed. Graphical Abstract
Bacterial diversity and specific taxa are associated with decolonization of carbapenemase-producing enterobacterales after fecal microbiota transplantation
Authors: Benjamin Davido, Andrea R. Watson, Pierre de Truchis, Gianluca Galazzo, Aurelien Dinh, Rui Batista, Elisabeth M. Terveer, Christine Lawrence, Hugues Michelon, Marion Jobard, Azzam Saleh-Mghir, Ed J. Kuijper, Silvia Caballero
Journal: Journal of Infection (2024)

We evaluated the effect of fecal microbiota transplantation (FMT) on the clearance of carbapenemase-producing Enterobacterales (CPE) carriage.
Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer
Authors: Hamzeh Kayhanian, William Cross, Suzanne E. M. van der Horst, Panagiotis Barmpoutis, Eszter Lakatos, Giulio Caravagna, Luis Zapata, Arne Van Hoeck, Sjors Middelkamp, Kevin Litchfield, Christopher Steele, William Waddingham, Dominic Patel, Salvatore Milite, Chen Jin, Ann-Marie Baker, Daniel C. Alexander, Khurum Khan, Daniel Hochhauser, Marco Novelli, Benjamin Werner, Ruben van Boxtel, Joris H. Hageman, Julian R. Buissant des Amorie, Josep Linares, Marjolijn J. L. Ligtenberg, Iris D. Nagtegaal, Miangela M. Laclé, Leon M. G. Moons, Lodewijk A. A. Brosens, Nischalan Pillay, Andrea Sottoriva, Trevor A. Graham, Manuel Rodriguez-Justo, Kai-Keen Shiu, Hugo J. G. Snippert, Marnix Jansen
Journal: Nature Genetics (2024)

Abstract Mismatch repair (MMR)-deficient cancer evolves through the stepwise erosion of coding homopolymers in target genes. Curiously, the MMR genes MutS homolog 6 ( MSH6) and MutS homolog 3 ( MSH3 ) also contain coding homopolymers, and these are frequent mutational targets in MMR-deficient cancers. The impact of incremental MMR mutations on MMR-deficient cancer evolution is unknown. Here we show that microsatellite instability modulates DNA repair by toggling hypermutable mononucleotide homopolymer runs in MSH6 and MSH3 through stochastic frameshift switching. Spontaneous mutation and reversion modulate subclonal mutation rate, mutation bias and HLA and neoantigen diversity. Patient-derived organoids corroborate these observations and show that MMR homopolymer sequences drift back into reading frame in the absence of immune selection, suggesting a fitness cost of elevated mutation rates. Combined experimental and simulation studies demonstrate that subclonal immune selection favors incremental MMR mutations. Overall, our data demonstrate that MMR-deficient colorectal cancers fuel intratumor heterogeneity by adapting subclonal mutation rate and diversity to immune selection.
Toward methodologies for motor imagery enhancement: a tDCS-BCI study
Authors: Diego Andrés Blanco Mora, Sybren Van Hoornweder, Kim van Dun, Stefanie Verstraelen, Koen Cuypers, Sergi Bermúdez i Badia, Raf Meesen
Journal: Brain-Computer Interfaces (2024)

Motor imagery (MI) becomes a powerful rehabilitation tool, particularly when combined with brain–computer interfaces (BCI). Therefore, methods to improve MI accuracy are a trending topic in the BCI field. Here, we examined the effects of transcranial direct current stimulation (tDCS) and MI priming on the MI signature in an EEG-based MI-BCI triple-blind study. Thirty healthy younger adults participated in this study and were designated to one of two priming groups: A bimanual tracking task and a MI task as primers for MI-BCI. During the performance of the primer task, participants received anodal and sham tDCS in two randomized sessions with a one-week wash-out period between sessions. Subsequently, participants performed an EEG-driven BCI-MI task. EEG time–frequency analyses revealed that desynchronization of the Beta Region precedes desynchronization in the Alpha Region, implying that the Beta frequency band might be best-suited to extract MI signatures as it could lead to faster MI-BCI. Contrary to our hypotheses, no effect of tDCS or priming task on EEG activity during the BCI-MI task was found. Future research should carefully consider the added value of tDCS and priming tasks BCI performance improvement. Electric field modeling studies and high-definition tDCS motor cortex stimulation might be promising avenues.
Multiple indicators of gut dysbiosis predict all-cause and cause-specific mortality in solid organ transplant recipients
Authors: J Casper Swarte, Shuyan Zhang, Lianne M Nieuwenhuis, Ranko Gacesa, Tim J Knobbe, Vincent E De Meijer, Kevin Damman, Erik A M Verschuuren, Tji C Gan, Jingyuan Fu, Alexandra Zhernakova, Hermie J M Harmsen, Hans Blokzijl, Stephan J L Bakker, Johannes R Björk, Rinse K Weersma
Journal: Gut (2024)

Gut microbiome composition is associated with multiple diseases, but relatively little is known about its relationship with long-term outcome measures. While gut dysbiosis has been linked to mortality risk in the general population, the relationship with overall survival in specific diseases has not been extensively studied. In the current study, we present results from an in-depth analysis of the relationship between gut dysbiosis and all-cause and cause-specific mortality in the setting of solid organ transplant recipients (SOTR).
Inference of Locus-Specific Population Mixtures From Linked Genome-Wide Allele Frequencies
Authors: Carlos S Reyna-Blanco, Madleina Caduff, Marco Galimberti, Christoph Leuenberger, Daniel Wegmann
Journal: Molecular Biology and Evolution (2024)

Abstract Admixture between populations and species is common in nature. Since the influx of new genetic material might be either facilitated or hindered by selection, variation in mixture proportions along the genome is expected in organisms undergoing recombination. Various graph-based models have been developed to better understand these evolutionary dynamics of population splits and mixtures. However, current models assume a single mixture rate for the entire genome and do not explicitly account for linkage. Here, we introduce TreeSwirl, a novel method for inferring branch lengths and locus-specific mixture proportions by using genome-wide allele frequency data, assuming that the admixture graph is known or has been inferred. TreeSwirl builds upon TreeMix that uses Gaussian processes to estimate the presence of gene flow between diverged populations. However, in contrast to TreeMix, our model infers locus-specific mixture proportions employing a hidden Markov model that accounts for linkage. Through simulated data, we demonstrate that TreeSwirl can accurately estimate locus-specific mixture proportions and handle complex demographic scenarios. It also outperforms related D- and f-statistics in terms of accuracy and sensitivity to detect introgressed loci.
Atypical melanocytes of an atypical Spitz tumour observed with optical super-high magnification dermoscopy
Authors: Maria Daviti, Ilias Papadimitriou, Elisa Cinotti, Aimilios Lallas
Journal: British Journal of Dermatology (2024)

A 64-year-old woman presented with a 6-mm pigmented lesion on her thigh. Dermatoscopy revealed the ‘starburst’ dermatoscopic pattern of a Spitzoid tumour. Before excision, the lesion was examined under ×400 magnification dermoscopy using the videoscope Fotofinder Medicam 1000 (Fotofinder System, Bad Birnbach, Germany) and in vivo Reflectance Confocal Microscopy (RCM) (Vivascope 1500®, MAVIG GmbH, Munich, Germany).
Selective delivery of imaging probes and therapeutics to the endoplasmic reticulum or Golgi apparatus: Current strategies and beyond
Authors: Hana Cho, Kang Moo Huh, Min Suk Shim, Yong-Yeon Cho, Joo Young Lee, Hye Suk Lee, Young Jik Kwon, Han Chang Kang
Journal: Advanced Drug Delivery Reviews (2024)
Germany's role in global health at a critical juncture
Authors: Christian Franz, Anna Holzscheiter, Ilona Kickbusch
Journal: The Lancet (2024)

In 2017, we set out-along with a larger group of authors-to assess Germany's contribution and potential leadership role in global health.We considered the ambitions and manifold efforts of Chancellor Angela Merkel's administration to become a trusted leader in global health governance and a reliable supporter of multilateral institutions, especially WHO.Based on the recommendations of our 2017 paper, in this Review we determine whether the country has indeed lived up to its vision and ambitions expressed in the Global Health Strategy adopted by the cabinet in 2020.Also, we outline what challenges Germany is now facing in a more complex global health environment and geopolitical situation, where leadership in the field is being redefined following the impact of the COVID-19 pandemic and amid broader shifts in the international order.
Optimizing early phase clinical trial washout periods: a report from the Therapeutic Advances in Childhood Leukemia and Lymphoma consortium
Authors: Eric S Schafer, Teresa Rushing, Kristine R Crews, Colleen Annesley, Susan I Colace, Nicole Kaiser, Lauren Pommert, Laura B Ramsey, Himalee S Sabnis, Kenneth Wong, Bill H Chang, Todd M Cooper, Nirali N Shah, Susan R Rheingold, Andrew E Place, Yueh-Yun Chi, Deepa Bhojwani, Alan S Wayne, M Brooke Bernhardt
Journal: JNCI Journal of the National Cancer Institute (2024)

The National Cancer Institute (NCI) issued a 2021 memorandum adopting the American Society of Clinical Oncology (ASCO) and Friends of Cancer Research (Friends) task force recommendations to broaden clinical study eligibility criteria. They recommended that washout periods be eliminated for most prior cancer therapy and when required to utilize evidence- and/or rationale-based criteria. The Therapeutic Advances in Childhood Leukemia and Lymphoma (TACL) consortium responded to this guidance.
Utility of uneven double-lumen catheter for difficult guidewire manipulation in endoscopic ultrasonography-guided pancreaticogastrostomy
Authors: Ayaka Machida, Yusuke Takasaki, Sho Takahashi, Akinori Suzuki, Shigeto Ishii, Toshio Fujisawa, Hiroyuki Isayama
Journal: Endoscopy (2024)

Endoscopic ultrasonography-guided pancreaticogastrostomy (EUS-PGS) is a challenging procedure, and the most difficult step is guidewire insertion to the appropriate portion. We report herein a case in which the guidewire was not advanced in the correct direction after puncture during EUS-PGS, and a double-lumen catheter was used to correct the direction of the guidewire.
Steatotic liver disease and HIV: an agenda for 2030
Authors: Juan M Pericàs, Anish K Arora, Carlotta Riebensahm, Alba Jiménez-Masip, Adrià Ramírez Mena, Trenton M White, Nikos Dedes, Giovanni Guaraldi, Annalisa Berzigotti, Gilles Wandeler, Meena B Bansal, Jordi Navarro, Jeffrey V Lazarus
Journal: The Lancet HIV (2024)
Rearrangements involving 11q23.3/KMT2A in adult AML: mutational landscape and prognostic implications – a HARMONY study
Authors: Alberto Hernández-Sánchez, Teresa González, Marta Sobas, Eric Sträng, Gastone Castellani, María Abáigar, Peter J. M. Valk, Ángela Villaverde Ramiro, Axel Benner, Klaus H. Metzeler, Raúl Azibeiro, Jesse M. Tettero, Joaquín Martínez-López, Marta Pratcorona, Javier Martínez Elicegui, Ken I. Mills, Christian Thiede, Guillermo Sanz, Konstanze Döhner, Michael Heuser, Torsten Haferlach, Amin T. Turki, Dirk Reinhardt, Renate Schulze-Rath, Martje Barbus, Jesús María Hernández-Rivas, Brian Huntly, Gert Ossenkoppele, Hartmut Döhner, Lars Bullinger
Journal: Leukemia (2024)

Abstract Balanced rearrangements involving the KMT2A gene ( KMT2A r) are recurrent genetic abnormalities in acute myeloid leukemia (AML), but there is lack of consensus regarding the prognostic impact of different fusion partners. Moreover, prognostic implications of gene mutations co-occurring with KMT2A r are not established. From the HARMONY AML database 205 KMT2A r adult patients were selected, 185 of whom had mutational information by a panel-based next-generation sequencing analysis. Overall survival (OS) was similar across the different translocations, including t(9;11)(p21.3;q23.3)/ KMT2A :: MLLT3 (p = 0.756). However, independent prognostic factors for OS in intensively treated patients were age &gt;60 years (HR 2.1, p = 0.001), secondary AML (HR 2.2, p = 0.043), DNMT3A -mut (HR 2.1, p = 0.047) and KRAS -mut (HR 2.0, p = 0.005). In the subset of patients with de novo AML &lt; 60 years, KRAS and TP53 were the prognostically most relevant mutated genes, as patients with a mutation of any of those two genes had a lower complete remission rate (50% vs 86%, p &lt; 0.001) and inferior OS (median 7 vs 30 months, p &lt; 0.001). Allogeneic hematopoietic stem cell transplantation in first complete remission was able to improve OS (p = 0.003). Our study highlights the importance of the mutational patterns in adult KMT2A r AML and provides new insights into more accurate prognostic stratification of these patients.
Epidemiology of childhood interstitial lung disease in France: the RespiRare cohort
Authors: Camille Fletcher, Alice Hadchouel, Caroline Thumerelle, Julie Mazenq, Manon Fleury, Harriet Corvol, Nouha Jedidi, Myriam Benhamida, Katia Bessaci, Tiphaine Bilhouee, Raphael Borie, Jacques Brouard, Aurélie Cantais, Annick Clement, Laurianne Coutier, Camille Cisterne, Pierrick Cros, Marie-Laure Dalphin, Christophe Delacourt, Eric Deneuville, Jean-Christophe Dubus, Carole Egron, Ralph Epaud, Michael Fayon, Aude Forgeron, Elsa Gachelin, François Galode, Isabelle Gertini, Lisa Giovannini-Chami, Pierre Gourdan, Tamazoust Guiddir, Audrey Herzog, Véronique Houdouin, Églantine Hullo, Pierre-Henri Jarreau, Guillame Labbé, Géraldine Labouret, Alice Ladaurade, Laurence Le Clainche Viala, Christophe Marguet, Alexandra Masson-Rouchaud, Caroline Perisson, Cinthia Rames, Philippe Reix, Marie-Catherine Renoux, Léa Roditis, Cyril Schweitzer, Aurélie Tatopoulos, Pascale Trioche-Eberschweiler, Françoise Troussier, Clémentine Vigier, Laurence Weiss, Marie Legendre, Camille Louvrier, Alix de Becdelievre, Aurore Coulomb, Chiara Sileo, Hubert Ducou le Pointe, Laureline Berteloot, Céline Delestrain, Nadia Nathan
Journal: Thorax (2024)

Interstitial lung disease in children (chILD) are rare and mostly severe lung diseases. Very few epidemiological data are available in limited series of patients. The aim of this study was to assess the prevalence and incidence of chILD in France.
Author Correction: ASS1 metabolically contributes to the nuclear and cytosolic p53-mediated DNA damage response
Authors: Lisha Qiu Jin Lim, Lital Adler, Emma Hajaj, Leandro R. Soria, Rotem Ben-Tov Perry, Naama Darzi, Ruchama Brody, Noa Furth, Michal Lichtenstein, Elizabeta Bab-Dinitz, Ziv Porat, Tevie Melman, Alexander Brandis, Sergey Malitsky, Maxim Itkin, Yael Aylon, Shifra Ben-Dor, Irit Orr, Amir Pri-Or, Rony Seger, Yoav Shaul, Eytan Ruppin, Moshe Oren, Minervo Perez, Jordan Meier, Nicola Brunetti-Pierri, Efrat Shema, Igor Ulitsky, Ayelet Erez
Journal: Nature Metabolism (2024)
Fibrinogen‐like 1: A hepatokine linking liver physiology to hematology
Authors: Jean Personnaz, Hervé Guillou, Léon Kautz
Journal: HemaSphere (2024)

A recent study identified the critical contribution of the hepatokine FGL1 to the regulation of iron metabolism during the recovery from anemia. FGL1 is secreted by hepatocytes in response to hypoxia to sequester BMP ligands and repress the transcription of the iron-regulatory hormone hepcidin. This process ensures the proper supply of iron to the bone marrow for new red blood cell synthesis and the restoration of physiological oxygen levels. FGL1 may therefore contribute to the recovery from common anemias and cause iron overload in chronic anemias with ineffective erythropoiesis, such as ß-thalassemia, dyserythropoietic anemia, and myelodysplastic syndromes. However, FGL1 has also been described as a regulator of hepatocyte proliferation, glucose homeostasis, and insulin signaling, as well as a mediator of liver steatosis and immune evasion. Chronic exposure to elevated levels of FGL1 during anemia may therefore have systemic metabolic effects besides iron regulation and erythropoiesis. Here, we are providing an overview of the proposed functions of FGL1 in physiology and pathophysiology.
Is it time to revise the fighting strategy toward type 2 diabetes? Sex and pollution as new risk factors
Authors: Michelangela Barbieri, Francesco Prattichizzo, Rosalba La Grotta, Giulia Matacchione, Lucia Scisciola, Rosaria Anna Fontanella, Giovanni Tortorella, Rosaria Benedetti, Vincenzo Carafa, Raffaele Marfella, Antonio Ceriello, Giuseppe Paolisso
Journal: Ageing Research Reviews (2024)

Diabetes mellitus, a metabolic condition affecting around 537 million individuals worldwide, poses significant challenges, particularly among the elderly population. The etiopathogenesis of type 2 diabetes (T2D) depends on a combination of the effects driven by advancing age, genetic background, and lifestyle habits, e.g. overnutrition. These factors influence the development of T2D differently in men and women, with an obvious sexual dimorphism possibly underlying the diverse clinical features of the disease in different sexes. More recently, environmental pollution, estimated to cause 9 million deaths every year, is emerging as a novel risk factor for the development of T2D. Indeed, exposure to atmospheric pollutants such as PM2.5, O3, NO2, and Persistent Organic Pollutants (POP)s, along with their combination and bioaccumulation, is associated with the development of T2D and obesity, with a 15 % excess risk in case of exposure to very high levels of PM2.5. Similar data are available for plasticizer molecules, e.g. bisphenol A and phthalates, emerging endocrine-disrupting chemicals. Even though causality is still debated at this stage, preclinical evidence sustains the ability of multiple pollutants to affect pancreatic function, promote insulin resistance, and alter lipid metabolism, possibly contributing to T2D onset and progression. In addition, preclinical findings suggest a possible role also for plastic itself in the development of T2D. Indeed, pioneeristic studies evidenced that micro- or nanoplastics (MNP)s, particles in the micro- or nano- range, promote cellular damage, senescence, inflammation, and metabolic disturbances, leading to insulin resistance and impaired glucose metabolism in animal and/or in vitro models. Here we synthesize recent knowledge relative to the association between air-related or plastic-derived pollutants and the incidence of T2D, discussing also the possible mechanistic links suggested by the available literature. We then anticipate the need for future studies in the field of candidate therapeutic strategies limiting pollution-induced damage in preclinical models, such as SGLT-2 inhibitors. We finally postulate that future guidelines for T2D prevention should consider pollution and sex an additional risk factors to limit the diabetes pandemic.
Exploring the Function of Epicardial Cells Beyond the Surface
Authors: David Wong, Julie Martinez, Pearl Quijada
Journal: Circulation Research (2024)

The epicardium, previously viewed as a passive outer layer around the heart, is now recognized as an essential component in development, regeneration, and repair. In this review, we explore the cellular and molecular makeup of the epicardium, highlighting its roles in heart regeneration and repair in zebrafish and salamanders, as well as its activation in young and adult postnatal mammals. We also examine the latest technologies used to study the function of epicardial cells for therapeutic interventions. Analysis of highly regenerative animal models shows that the epicardium is essential in regulating cardiomyocyte proliferation, transient fibrosis, and neovascularization. However, despite the epicardium's unique cellular programs to resolve cardiac damage, it remains unclear how to replicate these processes in nonregenerative mammalian organisms. During myocardial infarction, epicardial cells secrete signaling factors that modulate fibrotic, vascular, and inflammatory remodeling, which differentially enhance or inhibit cardiac repair. Recent transcriptomic studies have validated the cellular and molecular heterogeneity of the epicardium across various species and developmental stages, shedding further light on its function under pathological conditions. These studies have also provided insights into the function of regulatory epicardial-derived signaling molecules in various diseases, which could lead to new therapies and advances in reparative cardiovascular medicine. Moreover, insights gained from investigating epicardial cell function have initiated the development of novel techniques, including using human pluripotent stem cells and cardiac organoids to model reparative processes within the cardiovascular system. This growing understanding of epicardial function holds the potential for developing innovative therapeutic strategies aimed at addressing developmental heart disorders, enhancing regenerative therapies, and mitigating cardiovascular disease progression.
Mitochondrial Structure and Function in Human Heart Failure
Authors: Antentor Hinton, Steven M. Claypool, Kit Neikirk, Nanami Senoo, Celestine N. Wanjalla, Annet Kirabo, Clintoria R. Williams
Journal: Circulation Research (2024)

Despite clinical and scientific advancements, heart failure is the major cause of morbidity and mortality worldwide. Both mitochondrial dysfunction and inflammation contribute to the development and progression of heart failure. Although inflammation is crucial to reparative healing following acute cardiomyocyte injury, chronic inflammation damages the heart, impairs function, and decreases cardiac output. Mitochondria, which comprise one third of cardiomyocyte volume, may prove a potential therapeutic target for heart failure. Known primarily for energy production, mitochondria are also involved in other processes including calcium homeostasis and the regulation of cellular apoptosis. Mitochondrial function is closely related to morphology, which alters through mitochondrial dynamics, thus ensuring that the energy needs of the cell are met. However, in heart failure, changes in substrate use lead to mitochondrial dysfunction and impaired myocyte function. This review discusses mitochondrial and cristae dynamics, including the role of the mitochondria contact site and cristae organizing system complex in mitochondrial ultrastructure changes. Additionally, this review covers the role of mitochondria-endoplasmic reticulum contact sites, mitochondrial communication via nanotunnels, and altered metabolite production during heart failure. We highlight these often-neglected factors and promising clinical mitochondrial targets for heart failure.