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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 775 records · Page 43
All sourcesNASA NTRSDOE OSTI
DOE OSTI2015

Interactions of cullin3/KCTD5 complexes with both cytoplasmic and nuclear proteins: Evidence for a role in protein stabilization

Based on its specific interaction with cullin3 mediated by an N-terminal BTB/POZ homologous domain, KCTD5 has been proposed to function as substrate adapter for cullin3 based ubiquitin E3 ligases. In the present study we tried to validate this hypothesis through identification and characterization of additional KCTD5 interaction partners. For the replication protein MCM7, the zinc finger protein ZNF711 and FAM193B, a yet poorly characterized cytoplasmic protein, we could demonstrate specific interaction with KCTD5 both in yeast two-hybrid and co-precipitation studies in mammalian cells. Whereas trimeric complexes of cullin3 and KCTD5 with the respective KCTD5 binding partner were formed, KCTD5/cullin3 induced polyubiquitylation and/or proteasome-dependent degradation of these binding partners could not be demonstrated. On the contrary, KCTD5 or Cullin3 overexpression increased ZNF711 protein stability. - Highlights: • KCTD5 nuclear translocation depends upon M phase and protein oligomerization. • Identification of MCM7, ZNF711 and FAM193 as KCTD5 interaction partners. • Formation of trimeric complexes of KCTD5/cullin3 with MCM7, ZNF711 and FAM193B. • KCTD5 is not involved in polyubiquitylation of MCM7 replication factor. • The KCTD5/cullin3 complex stabilizes ZNF711 transcription factor.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes

Recent studies involving several viral systems have highlighted the importance of cellular intrinsic defense mechanisms through nuclear antiviral proteins that restrict viral propagation. These factors include among others components of PML nuclear bodies, the nuclear DNA sensor IFI16, and a potential restriction factor PHF13/SPOC1. For several nuclear replicating DNA viruses, it was shown that these factors sense and target viral genomes immediately upon nuclear import. In contrast to the anticipated view, we recently found that incoming adenoviral genomes are not targeted by PML nuclear bodies. Here we further explored cellular responses against adenoviral infection by focusing on specific conditions as well as additional nuclear antiviral factors. In line with our previous findings, we show that neither interferon treatment nor the use of specific isoforms of PML nuclear body components results in co-localization between incoming adenoviral genomes and the subnuclear domains. Furthermore, our imaging analyses indicated that neither IFI16 nor PHF13/SPOC1 are likely to target incoming adenoviral genomes. Thus our findings suggest that incoming adenoviral genomes may be able to escape from a large repertoire of nuclear antiviral mechanisms, providing a rationale for the efficient initiation of lytic replication cycle. - Highlights: • Host nuclear antiviral factors were analyzed upon adenovirus genome delivery. • Interferon treatments fail to permit PML nuclear bodies to target adenoviral genomes. • Neither Sp100A nor B targets adenoviral genomes despite potentially opposite roles. • The nuclear DNA sensor IFI16 does not target incoming adenoviral genomes. • PHF13/SPOC1 targets neither incoming adenoviral genomes nor genome-bound protein VII.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Fatty acid biosynthesis is involved in the production of hepatitis B virus particles

Hepatitis B virus (HBV) proliferates in hepatocytes after infection, but the host factors that contribute to the HBV lifecycle are poorly understood at the molecular level. We investigated whether fatty acid biosynthesis (FABS), which was recently reported to contribute to the genomic replication of hepatitis C virus, plays a role in HBV proliferation. We examined the effects of inhibitors of the enzymes in the FABS pathway on the HBV lifecycle by using recombinant HBV-producing cultured cells and found that the extracellular HBV DNA level, reflecting HBV particle production, was decreased by treatment with inhibitors suppressed the synthesis of long-chain saturated fatty acids with little cytotoxicity. The reduced HBV DNA level was reversed when palmitic acid, which is the product of fatty acid synthase (FAS) during FABS, was used simultaneously with the inhibitor. We also observed that the amount of intracellular HBV DNA in the cells was increased by FAS inhibitor treatment, suggesting that FABS is associated with HBV particle production but not its genome replication. This suggests that FABS might be a potent target for anti-HBV drug with a mode of action different from current HBV therapy. -- Highlights: •Inhibitors of ACC1 and FAS but not SCD1 decreased production of extracellular HBV DNA. •Products of FABS, long chain fatty acids, increased production of extracellular HBV DNA. •FAS inhibitor increased intracellular levels of HBV DNA and HBcAg. •FABS was suggested to contribute to HBV particle production without significant relation with secretory pathway of the cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Molecular dynamics simulations of Zika virus NS3 helicase: Insights into RNA binding site activity

America is still suffering with the outbreak of Zika virus (ZIKV) infection. Congenital ZIKV syndrome has already caused a public health emergency of international concern. However, there are still no vaccines to prevent or drugs to treat the infection caused by ZIKV. The ZIKV NS3 helicase (NS3h) protein is a promising target for drug discovery due to its essential role in viral genome replication. NS3h unwinds the viral RNA to enable the replication of the viral genome by the NS5 protein. NS3h contains two important binding sites: the NTPase binding site and the RNA binding site. Here, we used molecular dynamics (MD) simulations to study the molecular behavior of ZIKV NS3h in the presence and absence of ssRNA and the potential implications for NS3h activity and inhibition. Although there is conformational variability and poor electron densities of the RNA binding loop in various apo flaviviruses NS3h crystallographic structures, the MD trajectories of NS3h-ssRNA demonstrated that the RNA binding loop becomes more stable when NS3h is occupied by RNA. Our results suggest that the presence of RNA generates important interactions with the RNA binding loop, and these interactions stabilize the loop sufficiently that it remains in a closed conformation. This closed conformation likely keeps the ssRNA bound to the protein for a sufficient duration to enable the unwinding/replication activities of NS3h to occur. In addition, conformational changes of this RNA binding loop can change the nature and location of the optimal ligand binding site, according to ligand binding site prediction results. These are important findings to help guide the design and discovery of new inhibitors of NS3h as promising compounds to treat the ZIKV infection. - Highlights: • Ligand binding site predictions could provide useful insights into design of compounds to block ZIKV helicase activities. • Insights into dynamic features of NS3h and its interactions with ssRNA are provided through molecular dynamics simulations. • Presence of RNA generates stabilizing interactions with RNA binding loop of NS3h, which holds it in a closed conformation. • Closed conformation of the RNA binding loop keeps the ssRNA bound to the protein to enable the activity of NS3h.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

Protein kinase C downregulation induces senescence via FoxO3a inhibition in HCT116 and HEK293 cells

We investigated the impact of protein kinase C (PKC) on cellular senescence. The PKC activity and expression of conventional PKC (cPKC) and atypical PKC (aPKC) isoforms decreased during replicative senescence in IMR-90 cells. Forced inhibition of cPKC or aPKC induced the activation of senescence markers, including senescence-associated β-galactosidase activity and reactive oxygen species (ROS)-p53-p21{sup Cip1/WAF1} axis in HCT116 and HEK293 cells. PKC inhibition triggered the nuclear exportation of FoxO3a via stimulation of AKT-mediated phosphorylation of FoxO3a, and thereby decreased the transcription of FoxO3a target genes. Conversely, ectopic expression of the PKC isoforms led to stimulation of the nuclear import of FoxO3a and expression of the FoxO3a target genes. Ectopic FoxO3a expression attenuated ROS accumulation and senescent phenotypes induced by PKC inhibition. Therefore, this study suggests for the first time that downregulation of PKC induces senescence through the AKT-FoxO3a-ROS-p53-p21{sup Cip1/WAF1} pathway in HCT116 and HEK293 cells. - Highlights: • The activity and expression of PKC decreased during replicative senescence. • PKC downregulation induced senescence markers and ROS production. • PKC downregulation induced nuclear export of FoxO3a via AKT activation. • PKC downregulation reduced transcription of anti-oxidant genes. • PKC downregulation induces senescence via the AKT-FoxO3a-ROS pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Chlamydia pneumoniae exploits adipocyte lipid chaperone FABP4 to facilitate fat mobilization and intracellular growth in murine adipocytes

Highlights: • C. pneumoniae successfully infects and proliferates in murine adipocytes. • C. pneumoniae infection induces HSL-mediated lipolysis in adipocytes. • Inhibition of HSL abrogates intracellular growth of C. pneumoniae. • FABP4 is required for C. pneumoniae-induced fat mobilization and bacterial growth. • C. pneumoniae modulates host lipid metabolism to obtain ATP via β-oxidation. Fatty acid-binding protein 4 (FABP4), a cytosolic lipid chaperone predominantly expressed in adipocytes and macrophages, modulates lipid fluxes, trafficking, signaling, and metabolism. Recent studies have demonstrated that FABP4 regulates metabolic and inflammatory pathways, and in mouse models its inhibition can improve type 2 diabetes mellitus and atherosclerosis. However, the role of FABP4 in bacterial infection, metabolic crosstalk between host and pathogen, and bacterial pathogenesis have not been studied. As an obligate intracellular pathogen, Chlamydia pneumoniae needs to obtain nutrients such as ATP and lipids from host cells. Here, we show that C. pneumoniae successfully infects and proliferates in murine adipocytes by inducing hormone sensitive lipase (HSL)-mediated lipolysis. Chemical inhibition or genetic manipulation of HSL significantly abrogated the intracellular growth of C. pneumoniae in adipocytes. Liberated free fatty acids were utilized to generate ATP via β-oxidation, which C. pneumoniae usurped for its replication. Strikingly, chemical inhibition or genetic silencing of FABP4 significantly abrogated C. pneumoniae infection-induced lipolysis and mobilization of liberated FFAs, resulting in reduced bacterial growth in adipocytes. Collectively, these results demonstrate that C. pneumoniae exploits host FABP4 to facilitate fat mobilization and intracellular replication in adipocytes. This work uncovers a novel strategy used by intracellular pathogens for acquiring energy via hijacking of the host lipid metabolism pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

HMGB1 mediates HAdV-7 infection-induced pulmonary inflammation in mice

Highlights: • HMGB1 was associated with HAdV-7-induced lung inflammation and pathology. • HMGB1 promoted HAdV-7 replication and bound to TLR-4, TLR-9, and RAGE receptors. • Receptor engagement by HMGB1 activated NF-κB, inducing inflammatory mediators. • Thus, HMGB1 could serve as a therapeutic target in HAdV-7 infection. Human adenovirus (HAdV) is a common respiratory pathogen in children, with no safe and effective treatment currently available. HAdV type 7 (HAdV-7), in particular, causes severe pediatric pneumonia with a high incidence of sequelae and mortality. Clinical data and animal experiments suggest that HAdV-7-induced pneumonia promotes cell necrosis, releasing a large number of inflammatory mediators. In recent years, the high mobility group box-1 (HMGB1) protein, released by necrotic cells, has been shown to play important roles in several viral infections. Here, we show that HMGB1 levels gradually increased in the media supernatants of HAdV-7 infected A549 cells, starting at 12 h post-infection. In vivo, HMGB1 levels in BALF and mRNA levels in lung tissues significantly increased after 3 days of HAdV-7 infection. Among the HMGB1 receptor genes, TLR-4 and TLR-9 expression increased, and so did the receptor for advanced glycation end-products (RAGE). Interestingly, NF-κB levels also increased concomitantly. Conversely, when HMGB1 was blocked, the pathological scores from lung tissues, inflammatory mediator levels, and viral copy number all were reduced significantly; in addition, HMGB1-related signaling pathway molecules, namely TLR-4, TLR-9, RAGE, and NF-κB were also reduced. We conclude that HMGB1 promotes HAdV-7 replication and signals through TLR-4, TLR-9, and RAGE receptors to activate NF-κB, stimulating the release of inflammatory mediators and contributing to adenoviral pathology. Thus, HMGB1 could be used as a therapeutic target in HAdV-7 infection.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Distinct notch signaling expression patterns between nucleoside and nucleotide analogues treatment for hepatitis B virus infection

Highlights: • Notch signaling inhibited by nucleoside analogues treatment under HBV infection. • Upregulation of Notch signaling after nucleotide analogues administration. • Reduction of Foxp3 expression by both nucleotide and nucleoside analogues treatment. • Activation of phosphorylated mTORC2–Akt cascade after nucleotide analogue treatment. Nucleos(t)ide analogues therapies are currently approved for the treatment of chronic hepatitis B virus (HBV) infection, which effectively suppress HBV replication and correlate with the anti-HBV-specific immune response. Notch signaling serves pleiotropic roles in the immune system that also contribute to virus-specific immunity. In this study, we assessed Notch signal-related gene expression after administrating nucleoside or nucleotide analogues to HBV-replicating cells and clinical liver tissues. We found distinct Notch signaling expression patterns under nucleos(t)ide analogues therapies, with high expression for nucleotide analogues (adefovir pivoxil or tenofovir disoproxil fumarate) and low expression for nucleoside analogues (lamivudine or entecavir) in the presence of HBV infection. Furthermore, activation of mammalian target of rapamycin (mTOR)-Akt (Ser473) phosphorylation was also observed after nucleotide analogue treatment. In conclusion, nucleoside and nucleotide analogues displayed different patterns of Notch signaling activity under HBV infection, and the induction of mTORC2-Akt (Ser473) phosphorylation may contribute to nucleotide analogues-mediated Notch signaling activation.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

St6gal1 knockdown alters HBV life cycle in HepAD38 cells

Highlights: • Host glycosyltransferase machinery knockdown alters HBV rcDNA level. • Only St6gal1 knockdown reduced the HBV rcDNA level among treatments. • Viral protein expressions, except the X protein, were affected by St6gal1 knockdown. • HBV cccDNA and pgRNA levels among the treatments were unaffected. Complex glycans at the cell surface play important roles, and their alteration is known to modulate cellular activity. Previously, we found that HBV replication in HepAD38 altered cell-surface sialylated N-glycan through the upregulation of St6gal1, Mgat2, and Mgat4a expression. Here we studied the effects of knocking them down on HBV replication in HepAD38. Our results showed that St6gal1 knockdown (KD) reduced intracellular HBV rcDNA level by 90%, that Mgat2 KD did not change the intracellular HBV rcDNA level, and that Mgat4 KD increased the intracellular HBV rcDNA level by 19 times compared to Tet(−). The changes in intracellular rcDNA level were followed by the alteration of Pol and HBc expression. Our study suggests that St6gal1 KD contributes more to the HBV life cycle than Mgat2 or Mgat4a KD through the modification of intracellular L, Pol, and HBc expression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Transcriptome of porcine alveolar macrophages activated by interferon-gamma and lipopolysaccharide

The molecular repertoire of porcine alveolar macrophages (PAMs) is greatly affected by the microenvironment they are exposed to, and specifically by inflammatory cytokines, such as interferon gamma (IFN-γ) released by activated lymphocytes, and microbial products, such as lipopolysaccharide (LPS). In our previous study, we found that IFN-γ- and LPS-activated PAMs (M1) could inhibit porcine reproductive and respiratory syndrome virus (PRRSV) replication. In this study, comprehensive analysis of the expression profiles of the genes associated with the polarization of M0-type PAMs (resting) toward M1 phenotypes (activated by IFN-γ and LPS) led to the following main results: 1) 1551 and 1823 genes were upregulated or downregulated in M1-type PAMs, respectively, compared with M0-type PAMs; 2) Among these, genes encoding ASS1 and CRTAM were the most upregulated and downregulated, respectively; 3) Genes involved in cytokine-cytokine receptor interaction and the JAK/STAT signaling pathway were significantly upregulated, suggesting their critical role in cellular activation; and 4) Genes involved in antigen proteolysis and presentation (immunoproteasome subunits), and inhibition of virus replication (host restriction factors) were significantly upregulated, emphasizing the critical role of these cytokines in immunity. Thus, our results provide important information for future studies on the role of PAM polarization in modulation of infection.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2017

A historical survey of algorithms and hardware architectures for neural-inspired and neuromorphic computing applications

In this study, biological neural networks continue to inspire new developments in algorithms and microelectronic hardware to solve challenging data processing and classification problems. Here in this research, we survey the history of neural-inspired and neuromorphic computing in order to examine the complex and intertwined trajectories of the mathematical theory and hardware developed in this field. Early research focused on adapting existing hardware to emulate the pattern recognition capabilities of living organisms. Contributions from psychologists, mathematicians, engineers, neuroscientists, and other professions were crucial to maturing the field from narrowly-tailored demonstrations to more generalizable systems capable of addressing difficult problem classes such as object detection and speech recognition. Algorithms that leverage fundamental principles found in neuroscience such as hierarchical structure, temporal integration, and robustness to error have been developed, and some of these approaches are achieving world-leading performance on particular data classification tasks. Additionally, novel microelectronic hardware is being developed to perform logic and to serve as memory in neuromorphic computing systems with optimized system integration and improved energy efficiency. Key to such advancements was the incorporation of new discoveries in neuroscience research, the transition away from strict structural replication and towards the functional replication of neural systems, and the use of mathematical theory frameworks to guide algorithm and hardware developments.

97 MATHEMATICS AND COMPUTING↗
DOE OSTI2022

A guideline to document occupant behavior models for advanced building controls

The availability of computational power, and a wealth of data from sensors have boosted the development of model-based predictive control for smart and effective control of advanced buildings in the last decade. More recently occupant-behavior models have been developed for including people in the building control loops. However, while important objectives of scientific research are reproducibility and replicability of results, not all information is available from published documents. Therefore, the aim of this paper is to propose a guideline for a thorough and standardized occupant-behavior model documentation. For that purpose, the literature screening for the existing occupant behavior models in building control was conducted, and the occupant behavior modeling processes were studied to extract practices and gaps for each of the following phases: problem statement, data collection, and preprocessing, model development, model evaluation, and model implementation. Here, the literature screening pointed out that the current state-of-the-art on model documentation shows little unification, which poses a particular burden for the model application and replication in field studies. In addition to the standardized model documentation, this work presented a model-evaluation schema that enabled benchmarking of different models in field settings as well as the recommendations on how OB models are integrated with the building system.

Building control↗
DOE OSTI2023

Antiretroviral therapy reveals triphasic decay of intact SIV genomes and persistence of ancestral variants

The decay kinetics of HIV-1-infected cells are critical to understand virus persistence. We evaluated the frequency of simian immunodeficiency virus (SIV)-infected cells for 4 years of antiretroviral therapy (ART). The intact proviral DNA assay (IPDA) and an assay for hypermutated proviruses revealed short- and long-term infected cell dynamics in macaques starting ART ~1 year after infection. Intact SIV genomes in circulating CD4+T cells showed triphasic decay with an initial phase slower than the decay of the plasma virus, a second phase faster than the second phase decay of intact HIV-1, and a stable third phase reached after 1.6–2.9 years. Hypermutated proviruses showed bi- or mono-phasic decay, reflecting different selective pressures. Viruses replicating at ART initiation had mutations conferring antibody escape. With time on ART, viruses with fewer mutations became more prominent, reflecting decay of variants replicating at ART initiation. Collectively, these findings confirm ART efficacy and indicate that cells enter the reservoir throughout untreated infection.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2025

Sequential membrane- and protein-bound organelles compartmentalize genomes during phage infection

Many eukaryotic viruses require membrane-bound compartments for replication, but no such organelles are known to be formed by prokaryotic viruses. Bacteriophages of the Chimalliviridae family sequester their genomes within a phage-generated organelle, the phage nucleus, which is enclosed by a lattice of the viral protein ChmA. We show that inhibiting phage nucleus formation arrests infections at an early stage in which the injected phage genome is enclosed within a membrane-bound early phage infection (EPI) vesicle. Early phage genes are expressed from the EPI vesicle, demonstrating its functionality as a prokaryotic, transcriptionally active, membrane-bound organelle. We also show that the phage nucleus is essential, with genome replication beginning after the injected DNA is transferred from the EPI vesicle to the phage nucleus. Our results show that Chimalliviridae require two sophisticated subcellular compartments of distinct compositions and functions that facilitate successive stages of the viral life cycle.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2026

Structural insights into RNase H catalytic mechanism from room-temperature X-ray and neutron crystallography of apo- and RNA/DNA hybrid-bound enzyme

RNase H enzymes are sequence-nonspecific endonucleases that cleave RNA strands in RNA/DNA hybrid duplexes, an enzymatic process essential in DNA replication and repair in both prokaryotes and eukaryotes. Also, RNase H activity of the reverse transcriptase in human immunodeficiency viruses (HIV-1 and HIV-2) is indispensable for the viral replication cycle. RNase H enzymes play an central role in the development of gene therapies and are targets for novel antivirals. It is therefore of great importance to gain a detailed understanding of the RNase H catalytic mechanism to improve drug design. We utilized Bacillus halodurans RNase H1 (BhRNase H1) to shed light on its function and catalytic mechanism. Room-temperature neutron crystallography of the wild-type and inactive D132N mutant enzymes revealed that E109, belonging to the catalytic DEDD motif, can change its protonation state, allowing us to propose its role in the protonation of the leaving O3′ hydroxyl group of RNA. X-ray crystallography has demonstrated the ability of the RNA/DNA duplex to slide along the protein surface upon metal ion binding at site M A , transforming a product mimic into a Michaelis-like complex, which confirms an essential role of the M A metal ion in catalysis.

Enzyme mechanisms↗
DOE OSTI2017

Mapping environmental sensitivity: A systematic online approach to support environmental assessment and planning

Environmental sensitivity analysis provides a framework for systematically and objectively determining the potential for significant environmental impacts. The higher the natural or acquired sensitivity of the receiving environment, the less capable it is to cope with human-induced change. Given that sensitivity is context- and spatially-specific, Geographic Information Systems have been applied to develop an operational Webtool to analyse it. The Webtool enables a rapid and replicable spatial examination of environmental sensitivities and potential for land-use conflicts that supports Strategic Environmental Assessment and, ultimately, informed planning and decision-making. The novelty is on the provision of an online geoprocessing Widget that enables creation of context-specific maps. Pilot testing the Webtool in land-use and renewable energy planning through stakeholder engagement has validated its applicability. Stakeholders confirmed that it enables replicating and, in some cases, improving in-house SEA mapping processes while saving time and effort. However, its full reliance on publicly available spatial datasets renders completeness and resolution issues. The Webtool provides a critical starting-point for sectoral planning discussions and for developing plan/programme alternatives that avoid or minimise potentially incompatible or unsustainable zonings, while promoting consistency and transparency in impact assessment. - Highlights: •Sensitivity mapping can enhance baseline information for environmental assessments. •A novel online geoprocessing tool supports systematic sensitivity assessment. •It enables combining context-specific environmental criteria and value judgments. •Pilot testing it through stakeholder engagement has validated its applicability. •The tool promotes assessment consistency and transparency but data issues remain.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2016

Can developing countries leapfrog the centralized electrification paradigm?

Due to the rapidly decreasing costs of small renewable electricity generation 'systems, centralized power systems are no longer a necessary condition of universal access to modern energy services. Developing countries, where centralized electricity infrastructures are less developed, may be able to adopt these new technologies more quickly. We first review the costs of grid extension and distributed solar home systems (SHSs) as reported by a number of different studies. We then present a general analytic framework for analyzing the choice between extending the grid and implementing distributed solar home systems. Drawing upon reported grid expansion cost data for three specific regions, we demonstrate this framework by determining the electricity consumption levels at which the costs of provision through centralized and decentralized approaches are equivalent in these regions. We then calculate SHS capital costs that are necessary for these technologies provide each of five tiers of energy access, as defined by the United Nations Sustainable Energy for All initiative. Our results suggest that solar home systems can play an important role in achieving universal access to basic energy services. The extent of this role depends on three primary factors: SHS costs, grid expansion costs, and centralized generation costs. Given current technology costs, centralized systems will still be required to enable higher levels of consumption; however, cost reduction trends have the potential to disrupt this paradigm. By looking ahead rather than replicating older infrastructure styles, developing countries can leapfrog to a more distributed electricity service model. (C) 2016 International Energy Initiative. Published by Elsevier Inc. All rights reserved.

distributed electrification↗