A Mediator-Free Multi-Ply Biofuel Cell Using an Interfacial Assembly between Hydrophilic Enzymes and Hydrophobic Conductive Oxide Nanoparticles with Pointed Apexes.

Biofuel cells (BFCs) based on enzymatic electrodes hold great promise as power sources for biomedical devices. However, their practical use is hindered by low electron transfer efficiency and poor operational stability of enzymatic electrodes. Here, a novel mediator-free multi-ply BFC that overcomes these limitations and exhibits both substantially high-power output and long-term operational stability is presented. The approach involves the utilization of interfacial interaction-induced assembly between hydrophilic glucose oxidase (GOx) and hydrophobic conductive indium tin oxide nanoparticles (ITO NPs) with distinctive shapes, along with a multi-ply electrode system. For the preparation of the anode, GOx and oleylamine-stabilized ITO NPs with bipod/tripod type are covalently assembled onto the host fiber electrode composed of multi-walled carbon nanotubes and gold (Au) NPs. Remarkably, despite the contrasting hydrophilic and hydrophobic properties, this interfacial assembly approach allows for the formation of nanoblended GOx/ITO NP film, enabling efficient electron transfer within the anode. Additionally, the cathode is prepared by sputtering Pt onto the host electrode. Furthermore, the multi-ply fiber electrode system exhibits unprecedented high-power output (≈10.4 mW cm-2 ) and excellent operational stability (2.1 mW cm-2 , ≈49% after 60 days of continuous operation). The approach can provide a basis for the development of high-performance BFCs.

The mitophagy receptor NIX induces vIRF-1 oligomerization and interaction with GABARAPL1 for the promotion of HHV-8 reactivation-induced mitophagy.

Recently, viruses have been shown to regulate selective autophagy for productive infections. For instance, human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), activates selective autophagy of mitochondria, termed mitophagy, thereby inhibiting antiviral innate immune responses during lytic infection in host cells. We previously demonstrated that HHV-8 viral interferon regulatory factor 1 (vIRF-1) plays a crucial role in lytic replication-activated mitophagy by interacting with cellular mitophagic proteins, including NIX and TUFM. However, the precise molecular mechanisms by which these interactions lead to mitophagy activation remain to be determined. Here, we show that vIRF-1 binds directly to mammalian autophagy-related gene 8 (ATG8) proteins, preferentially GABARAPL1 in infected cells, in an LC3-interacting region (LIR)-independent manner. Accordingly, we identified key residues in vIRF-1 and GABARAPL1 required for mutual interaction and demonstrated that the interaction is essential for mitophagy activation and HHV-8 productive replication. Interestingly, the mitophagy receptor NIX promotes vIRF-1-GABARAPL1 interaction, and NIX/vIRF-1-induced mitophagy is significantly inhibited in GABARAPL1-deficient cells. Moreover, a vIRF-1 variant defective in GABARAPL1 binding substantially loses the ability to induce vIRF-1/NIX-induced mitophagy. These results suggest that NIX supports vIRF-1 activity as a mitophagy mediator. In addition, we found that NIX promotes vIRF-1 aggregation and stabilizes aggregated vIRF-1. Together, these findings indicate that vIRF-1 plays a role as a viral mitophagy mediator that can be activated by a cellular mitophagy receptor.

Genome-Wide Pathway Exploration of the Epidermidibacterium keratini EPI-7T.

Functional cosmetics industries using skin microbiome screening and beneficial materials isolated from key microorganisms are receiving increasing attention. Since Epidermidibacterium keratini EPI-7T was first discovered in human skin, previous studies have confirmed that it can produce a new pyrimidine compound, 1,1'-biuracil, having anti-aging effects on human skin. Therefore, we conducted genomic analyses to judge the use value of E. keratini EPI-7T and provide up-to-date information. Whole-genome sequencing analysis of E. keratini EPI-7T was performed to generate new complete genome and annotation information. E. keratini EPI-7T genome was subjected to comparative genomic analysis with a group of closely-related strains and skin flora strains through bioinformatic analysis. Furthermore, based on annotation information, we explored metabolic pathways for valuable substances that can be used in functional cosmetics. In this study, the whole-genome sequencing (WGS) and annotation results of E. keratini EPI-7T were improved, and through comparative analysis, it was confirmed that the E. keratini EPI-7T has more metabolite-related genes than comparison strains. In addition, we annotated the vital genes for biosynthesis of 20 amino acids, orotic acid, riboflavin (B2) and chorismate. In particular, we were able to prospect that orotic acid could accumulate inside E. keratini EPI-7T under uracil-enriched conditions. Therefore, through a genomics approach, this study aims to provide genetic information for the hidden potential of E. keratini EPI-7T and the strain development and biotechnology utilization to be conducted in further studies.

Multifaceted roles of TAX1BP1 in autophagy.

TAX1BP1 is a selective macroautophagy/autophagy receptor that plays a central role in host defense to pathogens and in regulating the innate immune system. TAX1BP1 facilitates the xenophagic clearance of pathogenic bacteria such as Salmonella typhimurium and Mycobacterium tuberculosis and regulates TLR3 (toll-like receptor 3)-TLR4 and DDX58/RIG-I-like receptor (RLR) signaling by targeting TICAM1 and MAVS for autophagic degradation respectively. In addition to these canonical autophagy receptor functions, TAX1BP1 can also exert multiple accessory functions that influence the biogenesis and maturation of autophagosomes. In this review, we will discuss and integrate recent findings related to the autophagy function of TAX1BP1 and highlight outstanding questions regarding its functions in autophagy and regulation of innate immunity and host defense.Abbreviations: ATG: autophagy related; CALCOCO: calcium binding and coiled-coil domain; CC: coiled-coil; CHUK/IKKα: conserved helix-loop-helix ubiquitous kinase; CLIR: noncanonical LC3-interacting region; GABARAP: gamma-aminobutyric acid receptor associated protein; HTLV-1: human T-lymphotropic virus 1; IFN: interferon; IL1B/IL1ß: interleukin 1 beta; LIR: LC3-interacting region; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAPK/JNK: mitogen-activated protein kinase; mATG8: mammalian Atg8 homolog; MAVS: mitochondrial antiviral signaling protein; MEF: mouse embryonic fibroblast; MTB: Mycobacterium tuberculosis; MYD88: myeloid differentiation primary response gene 88; NBR1: NBR1, autophagy cargo receptor; NFKB/NF-κB: nuclear factor of kappa light polypeptide gene enhancer in B cells; OPTN: optineurin; Poly(I:C): polyinosinic:polycytidylic acid; PTM: post-translational modification; RB1CC1: RB1-inducible coiled-coil 1; RIPK: receptor (TNFRSF)-interacting serine-threonine kinase; RLR: DDX58/RIG-I-like receptor; RSV: respiratory syncytia virus; SKICH: SKIP carboxyl homology; SLR: SQSTM1 like receptor; SQSTM1: sequestosome 1; TAX1BP1: Tax1 (human T cell leukemia virus type I) binding protein 1; TBK1: TANK-binding kinase 1; TICAM1: toll-like receptor adaptor molecule 1; TLR: toll-like receptor; TNF: tumor necrosis factor; TNFAIP3: TNF alpha induced protein 3; TNFR: tumor necrosis factor receptor; TOM1: target of myb1 trafficking protein; TRAF: TNF receptor-associated factor; TRIM32: tripartite motif-containing 32; UBD: ubiquitin binding domain; ZF: zinc finger.

Herpesvirus lytic infection-induced mitophagy via viral interferon regulatory factor 1.

Viral control of mitochondria via mitophagy has a dampening effect on mitochondrion-mediated innate immune responses. We previously found that human herpesvirus 8 (HHV-8) could activate mitophagy via its lytic gene product vIRF-1 (viral interferon regulatory factor 1). Mechanistically, we previously demonstrated that vIRF-1 interacts with the mitophagic proteins BNIP3L (BCL2 interacting protein 3 like) and TUFM (Tu translation elongation factor, mitochondrial). Despite these significant findings, however, the precise molecular mechanisms underlying vIRF-1-activated mitophagy, particularly with core components of the autophagy machinery, remained to be fully elucidated. We recently reported that vIRF-1 binds preferentially and directly to GABARAPL1 (GABA type A receptor associated protein like 1) in a noncanonical manner, and this interaction is essential for virus-productive replication. Furthermore, we found that BNIP3L is a crucial factor that promotes vIRF-1 oligomerization and associated mitophagy activation, including GABARAPL1 interaction with vIRF-1 and TUFM dimerization. Together, our findings deepen our understanding of lytic infection-induced mitophagy and provide the key protein-protein interactions involved in vIRF-1-mediated mitophagy.

A Real-Time Detection Device for the Rapid Quantification of Skin Casual Sebum Using the Oil Red O Staining Method.

The human skin sebum suggests that it (along with other epidermal surface lipids) plays a role in skin barrier formation, the moderation of cutaneous inflammation, and antimicrobial defense. Various methods have been developed for collecting and measuring skin sebum. We tested methods of detection using "color intensity", by staining the skin casual sebum. This process was conducted in three steps; first, the selection of materials for sebum collection; second, staining the collected sebum; third, the development of a device that can measure the level of stained sebum. A plastic film was used to effectively collect sebum that increased with the replacement time of the sebum. In addition, the collected sebum was stained with Oil Red O (ORO) and checked with RGB; as a result, the R2 value was higher than 0.9. It was also confirmed that the correlation value was higher than 0.9 in the comparison result with Sebumeter®, which is a common standard technology. Finally, it was confirmed that the R2 value was higher than 0.9 in the detection value using the sensor. In conclusion, we have proven the proof of concept (PoC) for this method, and we would like to introduce an effective sebum measurement method that differs from the existing method.

Rapid identification of SARS-CoV-2 in the point-of-care using digital PCR-based Dr. PCR™ Di20K COVID-19 Detection Kit without viral RNA extraction.

BACKGROUND: Since COVID-19 was declared the pandemic by the WHO, it has continued to spread. There is a need for rapid, efficient, and accurate diagnostic kits and techniques to control its spread. OBJECTIVE: The diagnostic capability of the qRT-PCR-based Real-Q 2019-nCoV Detection Kit and dPCR-based Dr. PCR™ Di20K COVID-19 Detection Kit was compared and evaluated. METHODS: Diagnostic tests for COVID-19 were performed using two different COVID-19 kits and 301 individual specimens with confirmed COVID-19 positive/negative at the government-accredited medical institution. Assessment of diagnostic capability was measured through diagnostic sensitivity, specificity, Cohen's Kappa coefficient, and dilutional linearity tests. RESULTS: The COVID-19 diagnostic test results using two kits and 301 individual specimens perfectly matched the pre-diagnosis results of the medical institution. In addition, the measurement results of diagnostic sensitivity and specificity were "1", indicating high diagnostic capability. Cohen's Kappa coefficient value is "1", which means that the diagnosis concordance between the two kits is "Almost Perfect". As a result of dilutional linearity tests to evaluate their detection capability, both kits were measured with very high detection reliability. CONCLUSION: Here, we propose that the dPCR-based Dr. PCR™ Di20K COVID-19 Detection Kit has the advantages of the dPCR method reported in the previous study and is suitable for point-of-care testing (POCT) by overcoming the limitations of space, test time, cross-over contamination, and biosafety due to omitting RNA extraction process.

Autophagy-competent mitochondrial translation elongation factor TUFM inhibits caspase-8-mediated apoptosis.

Mitochondria support multiple cell functions, but an accumulation of dysfunctional or excessive mitochondria is detrimental to cells. We previously demonstrated that a defect in the autophagic removal of mitochondria, termed mitophagy, leads to the acceleration of apoptosis induced by herpesvirus productive infection. However, the exact molecular mechanisms underlying activation of mitophagy and regulation of apoptosis remain poorly understood despite the identification of various mitophagy-associated proteins. Here, we report that the mitochondrial translation elongation factor Tu, a mitophagy-associated protein encoded by the TUFM gene, locates in part on the outer membrane of mitochondria (OMM) where it acts as an inhibitor of altered mitochondria-induced apoptosis through its autophagic function. Inducible depletion of TUFM potentiated caspase-8-mediated apoptosis in virus-infected cells with accumulation of altered mitochondria. In addition, TUFM depletion promoted caspase-8 activation induced by treatment with TNF-related apoptosis-inducing ligand in cancer cells, potentially via dysregulation of mitochondrial dynamics and mitophagy. Importantly, we revealed the existence of and structural requirements for autophagy-competent TUFM on the OMM; the GxxxG motif within the N-terminal mitochondrial targeting sequences of TUFM was required for self-dimerization and mitophagy. Furthermore, we found that autophagy-competent TUFM was subject to ubiquitin-proteasome-mediated degradation but stabilized upon mitophagy or autophagy activation. Moreover, overexpression of autophagy-competent TUFM could inhibit caspase-8 activation. These studies extend our knowledge of mitophagy regulation of apoptosis and could provide a novel strategic basis for targeted therapy of cancer and viral diseases.

Diagnostic evaluation of qRT-PCR-based kit and dPCR-based kit for COVID-19.

BACKGROUND: Coronavirus disease of 2019 (COVID-19) is well known as a fatal disease, first discovered at Wuhan in China, ranging from mild to death, such as shortness of breath and fever. Early diagnosis of COVID-19 is a crucial point in preventing global prevalence. OBJECTIVE: We aimed to evaluate the diagnostic competency and efficiency with the Allplex™ 2019-nCoV Assay kit and the Dr. PCR 20 K COVID-19 Detection kit, designed based on the qRT-PCR and dPCR technologies, respectively. METHODS: A total of 30 negative and 20 COVID-19 positive specimens were assigned to the diagnostic test by using different COVID-19 diagnosis kits. Diagnostic accuracy was measured by statistical testing with sensitivity, specificity, and co-efficiency calculations. RESULTS: Comparing both diagnostic kits, we confirmed that the diagnostic results of 30 negative and 20 positive cases were the same pre-diagnostic results. The diagnostic statistics test results were perfectly matched with value (1). Cohen's Kappa coefficient was demonstrated that the given kits in two different ways were "almost perfect" with value (1). In evaluating the detection capability, the dilutional linearity experiments substantiate that the Dr. PCR 20 K COVID-19 Detection kit could detect SARS-CoV-2 viral load at a concentration ten times lower than that of the Allplex™ 2019-nCoV Assay kit. CONCLUSIONS: In this study, we propose that the dPCR diagnosis using LOAA dPCR could be a powerful method for COVID-19 point-of-care tests requiring immediate diagnosis in a limited time and space through the advantages of relatively low sample concentration and small equipment size compared to conventional qRT-PCR.

Development of a Glucose Sensor Based on Glucose Dehydrogenase Using Polydopamine-Functionalized Nanotubes.

The electrochemical-based detection of glucose is widely used for diagnostic purposes and is mediated by enzyme-mediated signal transduction mechanisms. For such applications, recent attention has focused on utilizing the oxygen-insensitive glucose dehydrogenase (GDH) enzyme in place of the glucose oxidase (GOx) enzyme, which is sensitive to oxygen levels. Currently used Ru-based redox mediators mainly work with GOx, while Ru(dmo-bpy)2Cl2 has been proposed as a promising mediator that works with GDH. However, there remains an outstanding need to improve Ru(dmo-bpy)2Cl2 attachment to electrode surfaces. Herein, we report the use of polydopamine-functionalized multi-walled carbon nanotubes (PDA-MWCNTs) to effectively attach Ru(dmo-bpy)2Cl2 and GDH onto screen-printed carbon electrodes (SPCEs) without requiring a cross-linker. PDA-MWCNTs were characterized by Fourier transform infrared (FT-IR) spectroscopy, Raman spectroscopy, and thermal gravimetric analysis (TGA), while the fabrication and optimization of Ru(dmo-bpy)2Cl2/PDA-MWCNT/SPCEs were characterized by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) measurements. The experimental results demonstrate a wide linear range of glucose-concentration-dependent responses and the multi-potential step (MPS) technique facilitated the selective detection of glucose in the presence of physiologically relevant interfering species, as well as in biological fluids (e.g., serum). The ease of device fabrication and high detection performance demonstrate a viable pathway to develop glucose sensors based on the GDH enzyme and Ru(dmo-bpy)2Cl2 redox mediator and the sensing strategy is potentially extendable to other bioanalytes as well.

Herpesvirus Regulation of Selective Autophagy.

Selective autophagy has emerged as a key mechanism of quality and quantity control responsible for the autophagic degradation of specific subcellular organelles and materials. In addition, a specific type of selective autophagy (xenophagy) is also activated as a line of defense against invading intracellular pathogens, such as viruses. However, viruses have evolved strategies to counteract the host's antiviral defense and even to activate some proviral types of selective autophagy, such as mitophagy, for their successful infection and replication. This review discusses the current knowledge on the regulation of selective autophagy by human herpesviruses.

Pentacyanoammineferrate-Based Non-Enzymatic Electrochemical Biosensing Platform for Selective Uric Acid Measurement.

The electrochemical-based detection of uric acid (UA) is widely used for diagnostic purposes. However, various interfering species such as ascorbic acid, dopamine, and glucose can affect electrochemical signals, and hence there is an outstanding need to develop improved sensing platforms to detect UA with high selectivity. Herein, we report a pentagonal mediator-based non-enzymatic electrochemical biosensing platform to selectively measure UA in the presence of interfering species. The working electrode was fabricated by electrodepositing polymerized 1-vinylimidazole (PVI), which has an imidazole ligand, onto indium tin oxide (ITO), and then conjugating nickel ions to the PVI-coated ITO electrode. Electrode performance was characterized by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) measurements and integrated together with pentacyanoammineferrate, which can bind to the amine groups of UA and function as an electron transferring mediator. The experimental results showed a wide linear range of UA concentration-dependent responses and the multi-potential step (MPS) technique facilitated selective detection of UA in the presence of physiologically relevant interfering species. Altogether, these findings support that pentacyanoammineferrate-based non-enzymatic electrodes are suitable biosensing platforms for the selective measurement of UA, and such approaches could potentially be extended to other bioanalytes as well.

Novel Functions and Virus-Host Interactions Implicated in Pathogenesis and Replication of Human Herpesvirus 8.

Human herpesvirus 8 (HHV-8) is classified as a γ2-herpesvirus and is related to Epstein-Barr virus (EBV), a γ1-herpesvirus. One important aspect of the γ-herpesviruses is their association with neoplasia, either naturally or in animal model systems. HHV-8 is associated with B-cell-derived primary effusion lymphoma (PEL) and multicentric Castleman's disease (MCD), endothelial-derived Kaposi's sarcoma (KS), and KSHV inflammatory cytokine syndrome (KICS). EBV is also associated with a number of B-cell malignancies, such as Burkitt's lymphoma, Hodgkin's lymphoma, and posttransplant lymphoproliferative disease, in addition to epithelial nasopharyngeal and gastric carcinomas. Despite the similarities between these viruses and their associated malignancies, the particular protein functions and activities involved in key aspects of virus biology and neoplastic transformation appear to be quite distinct. Indeed, HHV-8 specifies a number of proteins for which counterparts had not previously been identified in EBV, other herpesviruses, or even viruses in general, and these proteins are believed to play vital functions in virus biology and to be involved centrally in viral pathogenesis. Additionally, a set of microRNAs encoded by HHV-8 appears to modulate the expression of multiple host proteins to provide conditions conductive to virus persistence within the host and possibly contributing to HHV-8-induced neoplasia. Here, we review the molecular biology underlying these novel virus-host interactions and their potential roles in both virus biology and virus-associated disease.

The E3/E4 ubiquitin conjugation factor UBE4B interacts with and ubiquitinates the HTLV-1 Tax oncoprotein to promote NF-κB activation.

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), and the neurological disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax protein persistently activates the NF-κB pathway to enhance the proliferation and survival of HTLV-1 infected T cells. Lysine 63 (K63)-linked polyubiquitination of Tax provides an important regulatory mechanism that promotes Tax-mediated interaction with the IKK complex and activation of NF-κB; however, the host proteins regulating Tax ubiquitination are largely unknown. To identify new Tax interacting proteins that may regulate its ubiquitination we conducted a yeast two-hybrid screen using Tax as bait. This screen yielded the E3/E4 ubiquitin conjugation factor UBE4B as a novel binding partner for Tax. Here, we confirmed the interaction between Tax and UBE4B in mammalian cells by co-immunoprecipitation assays and demonstrated colocalization by proximity ligation assay and confocal microscopy. Overexpression of UBE4B specifically enhanced Tax-induced NF-κB activation, whereas knockdown of UBE4B impaired Tax-induced NF-κB activation and the induction of NF-κB target genes in T cells and ATLL cell lines. Furthermore, depletion of UBE4B with shRNA resulted in apoptotic cell death and diminished the proliferation of ATLL cell lines. Finally, overexpression of UBE4B enhanced Tax polyubiquitination, and knockdown or CRISPR/Cas9-mediated knockout of UBE4B attenuated both K48- and K63-linked polyubiquitination of Tax. Collectively, these results implicate UBE4B in HTLV-1 Tax polyubiquitination and downstream NF-κB activation.

Two-Ply Carbon Nanotube Fiber-Typed Enzymatic Biofuel Cell Implanted in Mice.

Implantable devices have emerged as a promising industry. It is inevitable that these devices will require a power source to operate in vivo. Thus, to power implantable medical devices, biofuel cells (BFCs) that generate electricity using glucose without an external power supply have been considered. Although implantable BFCs have been developed for application in vivo, they are limited by their bulky electrodes and low power density. In the present study, we attempted to apply to living mice an implantable enzymatic BFC (EBFC) that was previously reported to be a high-power EBFC comprising carbon nanotube yarn electrodes. To improve their mechanical properties and for convenient implantation, the electrodes were coated with Nafion and twisted into a micro-sized, two-ply, one-body system. When the two-ply EBFC system was implanted in the abdominal cavity of mice, it provided a high-power density of 0.3 mW/cm2. The two-ply EBFC system was injected through a needle using a syringe without surgery and the inflammatory response in vivo initially induced by the injection of the EBFC system was attenuated after 7 days, indicating the biocompatibility of the system in vivo.

Author Correction: Performance of a glucose-reactive enzyme-based biofuel cell system for biomedical applications.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Activation of NIX-mediated mitophagy by an interferon regulatory factor homologue of human herpesvirus.

Viral control of mitochondrial quality and content has emerged as an important mechanism for counteracting the host response to virus infection. Despite the knowledge of this crucial function of some viruses, little is known about how herpesviruses regulate mitochondrial homeostasis during infection. Human herpesvirus 8 (HHV-8) is an oncogenic virus causally related to AIDS-associated malignancies. Here, we show that HHV-8-encoded viral interferon regulatory factor 1 (vIRF-1) promotes mitochondrial clearance by activating mitophagy to support virus replication. Genetic interference with vIRF-1 expression or targeting to the mitochondria inhibits HHV-8 replication-induced mitophagy and leads to an accumulation of mitochondria. Moreover, vIRF-1 binds directly to a mitophagy receptor, NIX, on the mitochondria and activates NIX-mediated mitophagy to promote mitochondrial clearance. Genetic and pharmacological interruption of vIRF-1/NIX-activated mitophagy inhibits HHV-8 productive replication. Our findings uncover an essential role of vIRF-1 in mitophagy activation and promotion of HHV-8 lytic replication via this mechanism.

Performance of a glucose-reactive enzyme-based biofuel cell system for biomedical applications.

A glucose-reactive enzyme-based biofuel cell system (EBFC) was recently introduced in the scientific community for biomedical applications, such as implantable artificial organs and biosensors for drug delivery. Upon direct contact with tissues or organs, an implanted EBFC can exert effects that damage or stimulate intact tissue due to its byproducts or generated electrical cues, which have not been investigated in detail. Here, we perform a fundamental cell culture study using a glucose dehydrogenase (GDH) as an anode enzyme and bilirubin oxidase (BOD) as a cathode enzyme. The fabricated EBFC had power densities of 15.26 to 38.33 nW/cm2 depending on the enzyme concentration in media supplemented with 25 mM glucose. Despite the low power density, the GDH-based EBFC showed increases in cell viability (~150%) and cell migration (~90%) with a relatively low inflammatory response. However, glucose oxidase (GOD), which has been used as an EBFC anode enzyme, revealed extreme cytotoxicity (~10%) due to the lethal concentration of H2O2 byproducts (~1500 µM). Therefore, with its cytocompatibility and cell-stimulating effects, the GDH-based EBFC is considered a promising implantable tool for generating electricity for biomedical applications. Finally, the GDH-based EBFC can be used for introducing electricity during cell culture and the fabrication of organs on a chip and a power source for implantable devices such as biosensors, biopatches, and artificial organs.

Stretchable Fiber Biofuel Cell by Rewrapping Multiwalled Carbon Nanotube Sheets.

The fiber-type biofuel cell is attractive as an implantable energy source because the fiber can modify various structures and the wound can be stitched like a suture. In addition, in daily life, the biofuel cell is forced by human motion, and stretchability is a critical requirement for real applications. Therefore, we introduce a new type of highly stretchable, stable, soft fiber biofuel cell with microdiameter dimensions as an energy harvester. The completed biofuel cell operated well in fluids similar to human fluids, such as 20 mM phosphate-buffered 0.14 M NaCl solution (39.5 mW/cm2) and human serum (36.6 µW/cm2). The fiber-type biofuel cell can be reversibly stretched up to 100% in tensile direction while producing sustainable electrical power. In addition, the unique rewrapping structure, which traps the enzyme between multiwalled carbon nanotube sheets, enormously enhanced the stability of the biofuel cell when the biofuel cell was repeatedly stretched (the power density retention increased from 63 to 99%) and operated in human serum (the power density retention increased from 29 to 86%). The fiber can be easily woven into various structures, such as McKibben braid yarn, and scaled up by series and parallel connections.