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Organoids are three‐dimensional self‐renewing and organizing clusters of cells that recapitulate the behavior and functionality of developed organs. Referred to as “organs in a dish,” organoids are invaluable biological models for disease modeling or drug screening. Currently, organoid culture commonly relies on an expensive and undefined tumor‐derived reconstituted basal membrane which hinders its application in high‐throughput screening, regenerative medicine, and diagnostics. Here, we introduce a novel engineered plant‐based nanocellulose hydrogel is introduced as a well‐defined and low‐cost matrix that supports organoid growth. Gels containing 0.1% nanocellulose fibers (99.9% water) are ionically crosslinked and present mechanical properties similar to the standard animal‐based matrix. The regulation of the osmotic pressure is performed by a salt‐free strategy, offering conditions for cell survival and proliferation. Cellulose nanofibers are functionalized with fibronectin‐derived adhesive sites to provide the required microenvironment for small intestinal organoid growth and budding. Comparative transcriptomic profiling reveals a good correlation with transcriptome‐wide gene expression pattern between organoids cultured in both materials, while differences are observed in stem cells‐specific marker genes. These hydrogels are tunable and can be combined with laminin‐1 and supplemented with insulin‐like growth factor (IGF‐1) to optimize the culture conditions. Nanocellulose hydrogel emerges as a promising matrix for the growth of organoids. Plant‐based nanocellulose hydrogel is introduced as a well‐defined and very low‐cost porous nanofibrous matrix that supports organoid growth. The mechanical, chemical, and biological properties of the gel are engineered to mimic the extracellular matrix (ECM), providing the required microenvironment for small intestinal organoid culture. This performant hydrogel is tunable with ECM‐derived components, emerging as a promising biomaterial for organoid systems.

Three-dimensional (3D) cancer models are invaluable tools designed to study tumour biology and new treatments. Pancreatic ductal adenocarcinoma (PDAC), one of the deadliest types of cancer, has been progressively explored with bioengineered 3D approaches by deconstructing elements of its tumour microenvironment. Here, we investigated the suitability of collagen-nanocellulose hydrogels to mimic the extracellular matrix of PDAC and to promote the formation of tumour spheroids and multicellular 3D cultures with stromal cells. Blending of type I collagen fibrils and cellulose nanofibres formed a matrix of controllable stiffness, which resembled the lower profile of pancreatic tumour tissues. Collagen-nanocellulose hydrogels supported the growth of tumour spheroids and multicellular 3D cultures, with increased metabolic activity and matrix stiffness. To validate our 3D cancer model, we tested the individual and combined effects of the anti-cancer compound triptolide and the chemotherapeutics gemcitabine and paclitaxel, resulting in differential cell responses. Our blended 3D matrices with tuneable mechanical properties consistently maintain the growth of PDAC cells and its cellular microenvironment and allow the screening of anti-cancer treatments.

Pancreatic cancer cells rely on glutamine to sustain their survival in the stiff and poorly vascularized tumor microenvironment (TME). Inhibiting glutamic‐oxaloacetic transaminase 1 (GOT1) is a strategy to target glutamine metabolism and impair cancer cell functions. However, it remains unclear how cellular and extracellular elements of the TME respond to GOT1 inhibition. We engineered a pancreatic TME model ‘on a dish’ and recreated the metabolic interactions. Stromal cells remodeled the extracellular matrix and upregulated metabolic programs, including glutamine metabolism, oxidative phosphorylation, and central carbon metabolism. Cell responses to GOT1 inhibition were modulated by TME elements, with reductions in cell viability and proliferation occurring only under tissue‐like conditions. GOT1 inhibition altered matrix organization by upregulating different matrix‐related proteins, while it did not enhance cell responses to cytotoxic drugs. Our findings uncover the metabolic crosstalk within the TME and show that metabolism‐targeting treatments directly impact stromal elements of pancreatic cancer. Using tumor tissue engineering, we recreated pancreatic cancer and found that inhibiting glutamic‐oxaloacetic transaminase 1 (GOT1) induces extracellular matrix remodeling and secretome rewiring, as well as promotes cell death.

Originality/value--It is the first study in the Brazilian insurance market that utilizes the loss reserve errors in a specific accruals model to jointly study their impacts and three motivations for managers' opportunistic behavior in relation to claims provisions.

Tissue engineering has produced innovative tools for cancer research. 3D cancer models based on molecularly designed biomaterials aim to harness the dimensionality and biomechanical and biochemical properties of tumour tissues. However, to date, despite the critical role that the extracellular matrix plays in cancer, only a minority of 3D cancer models are built on biomaterial-based matrices. Major reasons for avoiding this critical design feature are the difficulty in recreating the inherent complexity of the tumour microenvironment and the limited availability of practical analytical and validation techniques. Recent advances emerging at the interface of supramolecular chemistry, materials science and tumour biology are generating new approaches to overcome these boundaries and enable the design of physiologically relevant 3D models. Here, we discuss how these 3D systems are applied to deconstruct and engineer the tumour microenvironment, opening opportunities to model primary tumours, metastasis and responses to anticancer treatment. Biology can help to design materials and approaches for tumour tissue engineering. Biomaterials are a requisite for modelling cancer to rebuild tissue organization, composition and function. This Review discusses bioengineering strategies that recreate the pathophysiology of tumour tissues to address questions in cancer research.

Safe blood transfusion requires compatibility testing of donor and recipient to prevent potentially fatal transfusion reactions. Detection of immunoglobulin G (IgG) antibodies requires incubation at 37 °C, often for up to 15 minutes. Current incubation technology predominantly relies on slow thermal-gradient dependent conduction. Here, we present rapid optical heating via laser, where targeted illumination of a blood-antibody sample in a diagnostic gel card is converted into heat, via photothermal absorption. Our laser-incubator heats the 75 µL blood-antibody sample to 37 °C in under 30 seconds. We show that red blood cells act as photothermal agents under near-infrared laser incubation, triggering rapid antigen-antibody binding. We detect no significant damage to the cells or antibodies for laser incubations of up to fifteen minutes. We demonstrate laser-incubated immunohaematological testing to be both faster and more sensitive than current best practice — with clearly positive results seen from laser incubations of just 40 seconds.