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Miniaturization and Packaging of Implantable Biomedical Silicon Devices
Published in Simon Deleonibus, Convergence of More Moore, More Than Moore, and Beyond Moore, 2021
The biocompatibility of a material could be defined as its ability to coexist with a biological environment without causing undesirable effects in the frame of a specific biomedical application. To demonstrate biocompatibility, in vitro and in vivo tests have to be performed. Biological tests might vary depending on the category of material or the medical device. The International Standards Organization (ISO] established the standard ISO 10993 to homogenize the biological evaluation and testing of all classes of medical devices (MDs] that have direct or indirect contact with patients. In scientific literature, it has been mentioned that some materials are well known for their biocompatibility [22–25]. Nonetheless, biochemical contamination or different manufacturing processes can turn materials biocompatible into materials not suitable for medical implantation. For this reason, novel packaging materials must be tested, first in vitro, to assess their effects on cell viability and cellular morphology. The guideline ISO 10993-5 establishes that materials subject to in vitro cytotoxicity tests ought to be evaluated with a standard fibroblast cell culture (L929). A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen and plays a critical role in wound healing.
Current and Rising Concepts in Immunotherapy: Biopharmaceuti cals versus Nanomedicines
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
In many cases, TNF leads to necroptotic parenchymal cell death; for instance, keratinocytes form skin barriers, whereas hepatocytes form the parenchyma of the liver. Throughout different organs, many parenchymal cells are sensitive to MΦ-derived TNF, which fuels many types of inflammatory disease, including liver inflammation [3], rheumatoid arthritis [4], autoimmune disease [5], and psoriasis [6]. Biopharmaceuticals such as infliximab have changed the course of many chronic inflammatory diseases but are among the most expensive pharmaceuticals [7]. Under normal conditions, acute inflammation is terminated by a healing phase, whereas in chronic inflammation, immune cell mediators such as TNF lead to continuous tissue injury resulting in organ fibrosis and loss of function [8]. Fibrotic diseases with excessive extracellular matrix (ECM) growth are exerted by fibroblast-like cells. In the liver, these are hepatic stellate cells [9], and corresponding cell types also mediate skin [10] and cardiac scarring [11]. Fibroblasts produce different types of ECM proteins, the most abundant and popular ones being collagen. During fibrosis, collagen I is abundantly expressed [3], whereas in cancer, specific collagens, such as collagen IV, are generated, which stimulate cancer cell proliferation [12]. In summary, all organs have specific types of parenchymal, fibroblast-like, and immune cell subsets, which interact in disease.
Controlling both the constructive power and the destructive power of inflammation to promote repair and regeneration
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Ultimately, the success of wound healing is also determined by the balance between pro-regenerative extracellular matrix (ECM) formation and the formation of fibrotic scar tissue (Godwin et al. 2014). Fibroblasts are the critical cell type that shape the ECM environment during wounding and homeostasis and are highly responsive to inflammatory signaling. The profile of the inflammatory response is a major factor that influences the phenotype of fibroblasts and their role in fibrotic disease. The balance between the pro-fibrotic signals and the anti-fibrotic signals is, in turn, primarily shaped by the interactions between macrophages and T cells. If the microenvironment of the fibroblasts is pro-fibrotic, then these cells can differentiate into pro-fibrotic cells such as myofibroblasts, which secrete and participate in crosslinking ECM components into scar tissue. This fibrotic scar tissue is a major impediment to the migration and function of regeneration-competent cells and thus will thwart the regenerative process. The control of fibroblast function in wound repair, either targeting the fibroblast directly or by macrophage regulation and inflammation, has gained significant appreciation as an important point of intervention (Wynn 2008; Hinz et al. 2012; Wynn and Ramalingam 2012; Braga et al. 2015; Darby et al. 2015).
Polycaprolactone-gelatin membrane as a sealant biomaterial efficiently prevents postoperative anastomotic leakage with promoting tissue repair
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Gyeongjin Joo, Tamanna Sultana, Sohanur Rahaman, Sang Ho Bae, Hae Il Jung, Byong-Taek Lee
Cell proliferation is critical to maintain the biological performance of living body. Functionally active new cells replace the old or damaged cells base on endogenous regenerative capacities. L929 cell is a kind of fibroblast cell. The fibroblast cell synthesizes extracellular matrix and collagen so that it plays an important role in healing. One of the purposes of this study was healing of defected site. Therefore, developed membrane should be supportive to fibroblast cell attachment and viability. The relationship between L929 cells and membranes was evaluated via assessment of mitochondrial physiological functioning. The intensity of orange-colored formazan solution reacting with mitochondrial dehydrogenase in viable cells was measured after application of EZ-CYTOX reagent. All the four membranes (P1G1, P1G2, P1G3 and P1G4) and control showed similar growth trend at day 1 (Figure 4A). The cell proliferation rate on membranes was significantly reduced on day 3 compared with tissue cultured plate. The rapid hydrolytic degradation (Figure 3B) of hydrophilic gelatin from membranes rendered the scaffolds into bare PCL like structures which could be the reason for lowering the proliferation. Compared with other samples, the P1G4 sample showed the highest proliferation on day 7 (**p < 0.01). Although exponential cellular proliferation was observed in control group, the cytocompatibility of P1G4 membrane was within the safety proliferation margin (viability more than 80%) [54].
Chitosan-based nanoparticles as delivery-carrier for promising antimicrobial glycolipid biosurfactant to improve the eradication rate of Helicobacter pylori biofilm
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Muhammad Arif, Mohamed Sharaf, Sohaib Khan, Zhe Chi, Chen-Guang Liu
In view of the microbiological results, RL-NPs were selected for cytocompatibility evaluation given their effectiveness and validated functionality. Accordingly, the biological response to the developed RL-NPs was assayed in vitro with human fibroblasts. Fibroblasts, derived from mesenchymal precursors, are the most common cells of connective tissue, playing a fundamental structural role and contributing to the organizational tissue integrity by the secretion of precursors of the extracellular matrix [53]. Fibroblasts also play a relevant immunological role by sensing and responding to immunological initiators (e.g. damageassociated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) of endogenous or exogenous origin, being able to polarize into distinct phenotypes with secretomes that foster the immuno-inflammatory activation, as well as tissue healing and homeostasis [54].
Effect of poly(dimethylsiloxane)-block-poly(oligo (ethylene glycol) methacrylate) amphiphilic block copolymers on dermal fibroblast viability and proliferation
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Milad Ebtedaei, Kiyumars Jalili, Najibeh Alizadeh, Hakimeh Ghaleh, Farhang Abbasi
The PEG is a great water-soluble polymer and well-known non-toxic, which is desirable for wound healing materials. PEG permits the materials to maintain their great water swelling properties, whereas PDMS improves its surface to prevent protein adsorption [5]. Fibroblast cells are precious for their role in wound healing and are prevalent cells in connective tissue. The mechanism of action is migration of these cells to the injured tissue and deposition the collagen on the damaged site [6–8]. The wound fibroblasts endure phenotypic change to become proliferative myofibroblasts within the granulation tissue, this attends to increased collagen production and results in hypertrophic scar [9,10]. Apoptosis is another cellular process known to play a great role in scar formation. The apoptosis is a mechanism that plays a great role in the progress of granulation tissue into a scar [11]. The initiation of apoptosis is tightly regulated by activation mechanisms, because once apoptosis has begun, it inevitably leads to the death of the cell. The two well-known activation mechanisms are the intrinsic pathway and the extrinsic pathway [12,13]. A hypertrophic scar characterized by deposits of excessive amounts of collagen gives rise to a raised scar. The hypertrophic scarring in addition to causing physical shortcoming have the psychological and aesthetic effects on some patients that offend the patients more than physical disability [14,15].