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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 1,063 records · Page 59
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

Non-thermal plasma reduces periodontitis-induced alveolar bone loss in rats

Periodontitis, a chronic infectious disease induced by microbial biofilm, is one of the most common diseases worldwide. Scaling and root planning (SRP) has always been recognized as the typical treatment. However, the therapeutic efficiency is often limited due to the intraoperative bleeding and the limitations of instruments. Non-thermal atmospheric plasma (NTP) appears to be a potential tool for periodontitis due to its promising biofilm degradation and decontamination effects. In this study, we investigated the role of NTP, as an adjuvant approach for the treatment of ligature-induced periodontitis in rats. Herein we showed that SRP or SRP-NTP application attenuated the periodontitis-induced alveolar bone loss, reflected by the increased BV/TV value and the decreased CEJ-AB distance, which might be related to the lower detection rate of periodontal pathogen in SRP and SRP-NTP groups. Besides, SRP-NTP rats showed less bone loss and lower CEJ-AB distance than that of SRP group at 30d post treatment, indicating a more comprehensive and long-lasting effect of SRP-NTP. A remarkable decrease of osteoclast number and lower expression of RANKL was also detected in SRP-NTP rats. In addition, expression of inflammatory-related cytokines such as TNF-α and IL-1β decreased significantly in SRP-NTP group, while IL-10 level increased substantially. These results together illustrated that a combination of SRP and NTP treatment was an effective way to prevent periodontitis progress, which reduced alveolar bone loss and promoted periodontium restoration in ligature-induced periodontitis rats. In conclusion, non-thermal plasma treatment may be considered as a feasible and effective supplementary approach to control periodontitis.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

c-Myc-driven glycolysis via TXNIP suppression is dependent on glutaminase-MondoA axis in prostate cancer

Highlights: • c-Myc suppresses TXNIP transcription in a glutamine-dependent manner. • c-Myc induction of GLS1 is necessary for TXNIP suppression. • TXNIP represses glycolytic target genes broadly in c-Myc-driven cancers. • c-Myc and TXNIP levels are negatively associated in PCA tissues and predict patient outcome. Oncogenic c-Myc-induced metabolic reprogramming triggers cellular dependency on exogenous glucose and glutamine. Understanding how nutrients are used may provide new target for therapeutic intervention. We previously provided an alternate route to c-Myc-driven glucose metabolism via the repression of thioredoxin-interacting protein (TXNIP), which is a potent negative regulator of glucose uptake. Herein, we demonstrate that c-Myc suppression of TXNIP is predominantly through the activation of glutaminolysis via glutaminase (GLS1) in prostate cancer cells. Glutamine depletion blocked c-Myc-dependent reductions of TXNIP and its principal regulator MondoA transcriptional activity. Further, GLS1 inhibition by either siRNA or CB-839 resumed TXNIP expression that was repressed by c-Myc. The TXNIP promoter with mutant E-Box region, which was recognized by MondoA, failed to respond to c-Myc or GLS1, indicating c-Myc repression of TXNIP by GLS1 is predominantly through the blockage of MondoA activity. Especially, ectopic TXNIP expression decreased c-Myc-induce glucose uptake and lead to a broad range of glycolytic target gene suppressions. Thus TXNIP is a key adaptor for c-Myc-driven aerobic glycolysis. Supporting the biological significance of c-Myc and TXNIP, their reciprocal relationship are correlates with patient outcome and contributes to the aggressive phenotype in PCAs.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long noncoding RNA LINC00339 aggravates doxorubicin-induced cardiomyocyte apoptosis by targeting MiR-484

Highlights: • LncRNA LINC00339 was highly expressed in DOX stimulated primary rat cardiomyocytes and H9c2 cells. • Knockdown of LINC00339 significantly reduced primary rat cardiomyocytes and H9c2 cells proliferation and apoptosis. • LINC00339 acts as a critical pro-apoptosis lncRNA that aggravates DOX-induced cardiac remodeling by miR-484. Abnormally expressed long noncoding RNAs (lncRNAs) has been recognized as one of the key source in cardiac diseases. However, the role of lncRNA in doxorubicin (DOX)-induced cardiotoxicity remains largely unknown. In previous studies, we have screened some aberrantly expressed lncRNAs from an animal model for DOX-induced cardiotoxicity, and LINC00339 is one of the highly expressed lncRNA. In this study, we validated and further explored its regulatory mechanisms using in vitro model systems. Primary cultured myocardial cell (PC) and H9C2 cell line were treated with different concentrations of DOX and the expression of LINC00339 were markedly up-regulated. However, knockdown of endogenous LINC00339 by its siRNA improved cells proliferation activity and reduced cardiomyocyte apoptosis. Further experiments showed the opposite trend of expression between LINC00339 and miR-484. Bioinformatics analysis and luciferase reporter assay indicated that LINC00339 directly binds to miR-484. Moreover, miR-484 inhibitor abrogated the collagen synthesis inhibition induced by LINC00339. These findings reveal a novel function of the LINC00339/miR-484 axis in DOX-induced cardiotoxicity.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Paclitaxel promotes lung cancer cell apoptosis via MEG3-P53 pathway activation

Highlights: • Paclitaxel up-regulated the expression of long-chain non-coding RNA maternally expressed gene 3 and P53 in Non-small cell lung cancer cell A549 cell line. • Inhibition of maternally expressed gene 3 attenuated the antitumor activity of PTX. • Overexpression of maternally expressed gene 3 enhanced the anti-tumor activity of paclitaxel. • Maternally expressed gene 3 inhibited the proliferation of A549 cells by activating p53, and inhibition of maternally expressed gene 3 partially attenuated the cytotoxicity of paclitaxel via inhibition of P53. • Maternally expressed gene 3 plays an important role in Reactive oxygen species production and subsequently induces A549 cell death. Paclitaxel (PTX) is a first-line chemotherapy drug for advanced non-small cell lung cancer (NSCLC). The long-chain non-coding RNA maternally expressed gene 3 (MEG3) is a recognized tumor suppressor. This study aimed to explore the effects of PTX on the expression of MEG3 and its anti-tumor mechanism in lung cancer cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine cell proliferation. Quantitative polymerase chain reaction was used to determine the levels of MEG3 expressions. Western blot and immunofluorescence were used to detect protein levels. Small interfering RNA or pCDNA-MEG3 transfection was used to downregulate or upregulate MEG3 expression. Dichlorof luorescein diacetate was used to detect intracellular reactive oxygen species. Flow cytometry was used to analyze apoptosis. PTX significantly inhibited the proliferation of NSCLC cells and increased the expressions of MEG3 and P53. The downregulation of MEG3 attenuated PTX-induced cytotoxicity, whereas upregulation of MEG3 induced cell death and increased P53 expression. The inhibition of P53 caused no effect on the upstream MEG3 expression. Our results suggest that the MEG3-P53 pathway is involved in the apoptosis of A549 cells induced by PTX.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Prevention of acute liver injury by suppressing plasma kallikrein-dependent activation of latent TGF-β

Highlights: • TGF-β contributes to the pathogenesis of acute liver injury (ALI). • PLK-dependent TGF-β activation occurs in/around macrophages in ALI mice. • R58 latency associated protein-degradation products serve as an indicator for ALI. • Inhibiting PLK suppresses apoptosis and improves survival rate of ALI mice. Acute liver injury (ALI) is highly lethal acute liver failure caused by different etiologies. Transforming growth factor β (TGF-β) is a multifunctional cytokine and a well-recognized inducer of apoptotic and necrotic cell death in hepatocytes. Latent TGF-β is activated partly through proteolytic cleavage by a serine protease plasma kallikrein (PLK) between the R58 and L59 residues of its propeptide region. Recently, we developed a specific monoclonal antibody to detect the N-terminal side LAP degradation products ending at residue R58 (R58 LAP-DPs) that reflect PLK-dependent TGF-β activation. This study aimed to explore the potential roles of PLK-dependent TGF-β activation in the pathogenesis of ALI. We established a mouse ALI model via the injection of anti-Fas antibodies (Jo2) and observed increases in the TGF-β1 mRNA level, Smad3 phosphorylation, TUNEL-positive apoptotic hepatocytes and R58-positive cells in the liver tissues of Jo2-treated mice. The R58 LAP-DPs were observed in/around F4/80-positive macrophages, while macrophage depletion with clodronate liposomes partly alleviated the Jo2-induced liver injury. Blocking PLK-dependent TGF-β activation using either the serine proteinase inhibitor FOY305 or the selective PLK inhibitor PKSI-527 or blocking the TGF-β receptor-mediated signaling pathway using SB431542 significantly prevented Jo2-induced hepatic apoptosis and mortality. Furthermore, similar phenomena were observed in the mouse model of ALI with the administration of acetaminophen (APAP). In summary, R58 LAP-DPs reflecting PLK-dependent TGF-β activation may serve as a biomarker for ALI, and targeting PLK-dependent TGF-β activation has potential as a therapeutic strategy for ALI.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

The circular RNA circ-ITCH suppresses ovarian carcinoma progression through targeting miR-145/RASA1 signaling

Highlights: • A broad down-regulation of circ-ITCH and a worse prognosis were found in OC patients. • Circ-ITCH inhibits the cell viability and motility by CCK8, cell cycle, wound healing and invasion assay. • Circ-ITCH inhibits the tumorigenesis ability in xenograft NOD mice in vivo. • Circ-TCH acts as a ceRNA role of circ-ITCH through sponging miR-145 and up-regulation of RASA1 expression. As the leading cause of death for gynecological cancers, ovarian cancer (OC) ranks fifth overall for cancer-related death among women. Emerging evidence has indicated that circular RNA (circRNA), recognized as functional non-coding transcripts in eukaryotic cells, may be involved in many physiological or pathological processes. It was reported that circ-ITCH is downregulated in multi cancers and serves as a powerful tumor suppressor among through a competing endogenous RNA (ceRNA) pathway. However, the existence and the role of circ-ITCH in OC was not reported. Here, we found a broad down-regulation of circ-ITCH in OC tissues and cells, which correlates with a worse prognosis in OC patients. Functional studies suggest that circ-ITCH overexpression inhibits the cell viability and motility by CCK8, cell cycle, wound healing assay and invasion assay. It also inhibits the tumorigenesis ability in xenograft NOD mice in vivo. Mechanically, we demonstrated that circ-TCH acts as a ceRNA to sponge miR-145, increases the level of RASA1, and inhibits the malignant progression of OC cells via the circ-ITCH-miR-145-RASA1 axis in vitro and in vivo. Taken together, our findings provide a novel tumor suppressive role regarding circ-ITCH function in the malignant progression of OC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

CTP synthase knockdown during early development distorts the nascent vertebral column and causes fluid retention in multiple tissues in zebrafish

Highlights: • Morpholino-based knockdown of ctps during early development produces zebrafish embryos with curved spines and tissue oedema. • Knockdown of ctps1a, and not ctps1b, induces more severe, longer-lasting defects. • Phenotypes are exacerbated when morpholinos against both gene variants are supplied together at uneven ratios. • The same phenotypes were recovered from embryos treated with DON, a CTPS activity-inhibiting drug. CTP Synthase (CTPS) is a metabolic enzyme that is recognized as a catalyst for nucleotide, phospholipid and sialoglycoprotein production. Though the structural characteristics and regulatory mechanisms of CTPS are well-understood, little is known regarding the extent of its involvement during the early developmental stages of vertebrates. Zebrafish carries two CTPS genes, annotated as ctps1a and ctps1b. Phylogenetic analyses show that both genes had diverged from homologues in the ancestral Actinopterygii, Oreochromis niloticus. Conservation of common CTPS-catalytic regions further establishes that both proteins are likely to be functionally similar to hsaCTPS. Here, we show that ctps1a is more critical throughout the initial period of embryonic development than ctps1b. The effects of concurrent partial knockdown are dependent on ctps1a vs ctps1b dosage ratios. When these are equally attenuated, abnormal phenotypes acquired prior to the pharyngula period disappear in hatchlings (48hpf); however, if either gene is more attenuated than the other, these only become more pronounced in advanced stages. Generally, disruption to normal ctps1a or ctps1b expression levels by morpholinos culminates in the distortion of the early spinal column as well as multiple-tissue oedema. Other effects include slower growth rates, increased mortality rates and impaired structural formation of the young fish's extremities. Embryos grown in DON, a glutamine-analogue drug and CTPS antagonist, also exhibit similar characteristics, thus strengthening the validity of the morpholino-induced phenotypes observed. Together, our results demonstrate the importance of CTPS for the development of zebrafish embryos, as well as a disparity in activity and overall importance amongst isozymes.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Transgelin-1 (SM22α) interacts with actin stress fibers and podosomes in smooth muscle cells without using its actin binding site

Highlights: • Transgelin-1 interacts with stress fibers and podosomes via its type-3 CH-domain. • EF-hand affects the transgelin-1–actin interaction cooperatively with CLIK23. • Phosphorylation in CLIK23 does not affect the transgelin-1–actin interaction. • Increased numbers of CLIK23 do not compensate for the deletion of the CH-domain. Transgelin-1 (SM22α) has been recognized as a smooth muscle marker and a tumor suppressor, but many details of the working mechanisms remain unclear. Transgelin-1 belongs to the calponin family of actin-binding proteins with an N-terminal calponin homology domain (CH-domain) and a C-terminal calponin-like module (CLIK23). Here, we demonstrate that transgelin-1 interacts with actin stress fibers and podosomes in smooth muscle cells via its type-3 CH-domain, while CLIK23 is dispensable for the binding to the actin structures. We further suggest that the EF-hand motif in transgelin-1 contributes to proper folding of the CH-domain and in turn to the interaction with the actin structures. These results are in contrast to the ones reported in in vitro studies that demonstrated CLIK23 was necessary for the transgelin-1–actin binding, while the CH-domain was not. Besides, within cells, transgelin-1 phosphorylation at Ser181 in CLIK23 did not affect its colocalization with the actin structures, while the same phosphorylation was reported in in vitro studies to negatively regulate actin binding. Thus, our results suggest the molecular basis of intracellular interaction between transgelin-1 and actin, distinct from that in vitro. The actin binding capability intrinsic to CLIK23 may not appear within cells probably because of the weaker competition for actin binding compared to other actin binding molecules.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Role of leukotriene B4 12-hydroxydehydrogenase in α-galactosylceramide-pulsed dendritic cell therapy for non-small cell lung cancer

Highlights: • LTB4DH in CD4{sup +} T cells rescued IFN-γ production with PGE{sub 2}. • LTB4DH in CD8{sup +} T cells rescued tumoricidal activity with PGE{sub 2}. • LTB4DH in CD8{sup +} T cells increased the expression of cytotoxic molecules with PGE{sub 2}. Invariant natural killer T (iNKT) cells exhibit potent antitumor effects upon activation by recognizing a specific glycolipid antigen. We previously performed phase I–II clinical studies to utilize iNKT cells using α-galactosylceramide-pulsed dendritic cells and identified leukotriene B4 12-hydroxydehydrogenase (LTB4DH) as a biomarker highly expressed in T cells derived from non-small cell lung cancer (NSCLC) patients who showed prolonged survival in respond to the iNKT cell immunotherapy. Because LTB4DH expression correlated with prolonged survival of NSCLC patients, we considered LTB4DH to play a role in iNKT cell immunotherapy. We herein demonstrate that the overexpression of LTB4DH in CD4{sup +} or CD8{sup +} T cells increases interferon-γ production and tumoricidal activity in the presence of prostaglandin E{sub 2}. Moreover, the expression of granzyme a, granzyme b, and perforin mRNA was increased in LTB4DH-overexpressing cells.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Long noncoding RNA LSINCT5 acts as an oncogene via increasing EZH2-induced inhibition of APC expression in osteosarcoma

Long noncoding RNAs (lncRNAs) are recognized as a class of critical regulators in various tumors. Recently, lncRNA LSINCT5 has been reported to promote the progression of bladder cancer, ovarian cancer, gastric cancer, and breast cancer. However, the biological function of LSINCT5 remains elusive in osteosarcoma (OS). In our study, we found that LSINCT5 was significantly upregulated in OS tissues than in adjacent normal tissues. Additionally, the expression of LSINCT5 was inversely associated with the prognosis of patients with OS. LSINCT5 knockdown dramatically inhibited OS cell proliferation in vitro and tumor growth in vivo. Mechanistic exploration revealed that LSINCT5 interacted with EZH2 to suppress the expression of APC, a negative regulator of the Wnt/β-catenin pathway. Moreover, rescue assays suggested that LSINCT5 exerted oncogenic roles by partially inhibiting APC expression in OS. In summary, our study demonstrated that LSINCT5 was a promising candidate for OS prognosis and therapy.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Structural and biochemical insights into inhibition of human primase by citrate

Highlights: • The crystal structure of the citrate bound p49 was determined at a 2.2 Å resolution. • The crystal structure indicates that citrate inhibits primase activity. • Citrate binds to p49 with low affinity with a K{sub d} = 513 μM. • We demonstrated that citrate inhibits primase activity. The eukaryotic primase/polymerase complex synthesizes approximately 10{sup 7} primers, one per Okazaki fragment, during the replication of mammalian chromosomes, which contain 10{sup 9} base pairs. Primase catalyzes the synthesis of a short RNA segment to a single-stranded DNA template. Primase is important in DNA replication because no known replicative DNA polymerases can initiate the synthesis of a DNA strand without an initial RNA primer. The primase subcomplex is composed of a small catalytic subunit (p49), and a large accessory subunit (p58). Priming mechanisms remain poorly understood, although large numbers of structures of archaeal and eukaryotic p49 and/or p58 as well as structures of bacterial enzymes have been determined. In this study, we determined the structure of human p49 at 2.2 Å resolution with citrate in its inactive forms. Dibasic citrate was bound at the nucleotide triphosphate (NTP) β, γ-phosphate binding site through nine hydrogen bonds. We also measured the dissociation constant of citrate and NTPs. We further demonstrated that the p49 activity is regulated by pH and citrate, which was not previously recognized as a key regulator of DNA replication. We propose that the citrate inhibits the primase and regulates DNA replication at the replication fork.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Dll4-Notch1 signaling but not VEGF-A is essential for hyperoxia induced vessel regression in retina

Highlights: • Our study find that VEGF-A is not an indispensable factor in hyperoxia induced vessel regression. • Hyperoxia exposure inactivated Dll4-Notch1 signaling in vessel regression region. • Inhibition of Dll4-Notch1 signaling by short-time administration of Dll4 neutralizing antibodies or DAPT exaggerates hyperoxia induced vascular regression. It is well recognized that decreased vascular endothelial growth factor A (VEGF-A) mRNA plays an important role in retinal vessel regression induced by hyperoxia. However, this concept has been challenged by increasing new evidence. Furthermore, VEGF-A strongly enhances Dll4 expression and inhibition of Dll4-Notch signaling leads to excessive sprouting angiogenesis. Recently, it is shown that inactivation of Dll4-Notch1 signaling reduce hyperoxia induced vessel regression. It is unknown whether sprouting angiogenesis contributes to the protective effect or not and further investigations are needed. Moreover, the expression of Dll4 or Notch1 activation in the regressing plexus remains elucidated. To determine the role of VEGF-A and Dll4-Notch1 signaling in hyperoxia induced vascular regression in the retina, we used mice at postnatal day 5 (P5) - P7. Hyperoxia induced massive vascular regression in the central plexus but not in the angiogenic plexus and had no effect on sprouting angiogenesis. Immunostaining showed that VEGF-A was significantly repressed in the angiogenic front region after hyperoxia exposure but not detectable in the central area of both normoxia and hyperoxia treated retinas. In contrast, Notch ligand Delta-like 4 (Dll4) and Notch1 intracellular domain (N1-ICD) expression were inhibited in the regressing capillaries of central retina but comparable in the angiogenic plexus after high oxygen treatment. Moreover, administration of Dll4 neutralizing antibody or γ-Secretase inhibitor DAPT significantly aggravated vessel regression induced by short-time hyperoxia administration. Our data show that repressed Dll4-Notch1 signaling pathway but not downregulation of VEGF-A expression are responsible for hyperoxia induced pervasive vessel regression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Short-term administration of iso-α-acids increases transthyretin transcription in the hippocampus

Cognitive decline and dementia are currently recognized as major problems in the aging population; however, there is still no promising treatment for these conditions. Previously, our group reported that iso-α-acids (IAAs), which are hop-derived bitter components present in beer, prevent inflammation and cognitive impairment in an Alzheimer's disease model mice (5xFAD mice) and yield significant reduction in amyloid β (Αβ) in the brain. However, data on the molecular mechanisms underlying these physiological effects of IAAs remain limited. Here, we used transcriptome analysis and found that oral administration of IAAs to 5xFAD mice for 7 days induces a 58.9-fold increase in the expression of transthyretin (TTR; Ttr) in the hippocampus compared with controls. In addition, real-time quantitative PCR showed that oral administration of IAAs significantly increased Ttr transcription in the hippocampi of wild type C57BL/6J mice but not in the cerebral cortex. TTR is an Αβ protein scavenger; thus, an increase in its expression could prevent amyloid aggregate formation. These results indicate that IAAs reduce Αβ in the brain by elevating TTR levels.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

STAM-binding protein regulates melanoma metastasis through SLUG stabilization

Highlights: • STAMBP regulates melanoma migration and invasion but not survival in vitro. • STAMBP regulates SLUG stability. • STAMBP suppression inhibits melanoma metastasis in vivo. STAM-binding protein, STAMBP, is a JAMM-family deubiquitinating enzyme containing the microtubule-interacting/transport domain and STAM-binding domain. Although the biological importance of STAMBP in development has been recognized because the microcephaly-capillary malformation syndrome in human is caused by its somatic mutations, the role of STAMBP in cancer has not yet been determined. In this study, we demonstrate that STAMBP is a key molecule for regulating melanoma migration and invasion, but not survival, by knocking down STAMBP in vitro. STAMBP regulates SLUG expression through a post-transcriptional mechanism to control protein stability and further contributes to the in vivo metastatic potential of melanoma. Collectively, these results indicate the importance of STAMBP in melanoma metastasis by regulating SLUG. It is therefore a potential therapeutic target.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2019

Approaches to investigate the role of chelation in the corrosivity of biomass-derived oils

The need to provide the U.S. market with a renewable liquid fuel energy source from a non-food feedstock stream has gained considerable traction due to benefits such as improved energy efficiency, reduced environmental impacts, and enhanced national security. Practical achievement of these goals via biomass and bio-waste utilization involves production of liquid intermediates containing corrosive, reactive species like carboxylic acids, ketones, aldehydes, and hydroxyaldehydes. Such mixtures challenge materials of containment, processing, and transport. It is widely recognized that the smaller organic acids, such as acetic and formic, are corrosive and can remove protective surface oxides on alloys used in bio-oil processing infrastructure, and ketones can swell sealing polymers. However, literature shows, and findings herein confirm, larger carboxylic acids and bidentate alcohols are present. This highlights the potential for synergistic, detrimental effects of constituents in bio-oil corrosion, including direct reactivity of small acids compounded with the possibility of mobilization of protective metal oxide layers via chelation by larger acids and oxygenates. The question of whether species beyond small acids can significantly contribute to corrosion requires analytical approaches previously not applied to bio-oil corrosion studies and certainly not previously applied corroboratively. As such, this work introduces a combination of optical, mass spectral, and electrochemical impedance spectroscopies with an incubation approach to study metal mobilization, to facilitate elucidating chelation's role in bio-oil corrosive pathways. To enable systematic study of these oxygenates' material compatibility individually and in combination, a model matrix of bio-oil constituents was also developed based on identification of key components of real bio-oils.

09 BIOMASS FUELS↗
DOE OSTI2025

Enhancing biomass flowability for entrained flow Gasification: The role of densification and torrefaction

Gasification presents a key strategy in addressing future energy demands while minimizing environmental impact. This has been recognized as a promising method to convert biomass to higher value products such as biofuels or hydrogen. Among gasification technologies, high-temperature and high-pressure reactors, particularly the R-GAS® system, emerge as an advanced option boasting superior conversion efficiency. However, akin to conventional high-temperature and high-pressure gasifiers, R-GAS® necessitates small particle sizes for optimal carbon conversion, a requirement yet to be fully explored for biomass. Hence, this study investigated the effectiveness of combined mechanical and thermal preprocessing techniques in modifying the physicochemical properties of biomass to suit gasification systems. Mechanical techniques including densification and pulverization, alongside thermal techniques such as torrefaction and steam explosion, were examined. The results demonstrate that torrefaction fosters producing of uniform granular material, enhancing flowability and reducing energy requirements for pulverization compared to steam explosion. Notably, torrefied corn stover exhibited lower internal friction angles and effective cohesion (40.09 ± 0.22° and 0.56 ± 0.01 kPa, respectively) compared to steam exploded corn stover (41.87 ± 0.65° and 0.83 ± 0.06 kPa, respectively), indicative of improved flowability. Additionally, pulverization of torrefied corn stover required approximately 16 % less energy than steam exploded corn stover and 91 % less energy than raw corn stover. Furthermore, the torrefaction-induced alterations in particle size, shape, and packing densities emphasize its potential to optimize flow and handling processes for gasification. These findings underline that densification followed by torrefaction effectively addresses biomass variability, leading to more efficient and sustainable energy conversion.

09 - BIOMASS FUELS↗
DOE OSTI2017

Pickin’ Up Good Vibrations

Although conformational change has long been recognized as critical to protein function, whether the same goes for equilibrium dynamical fluctuations has been the subject of myriad squabbles. There are also those who rigidly deny any dynamical effects, those who claim fluctuations drive functional conformational change, while those who claim to have snared exquisitely evolved function-channeling vibrations.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2016

Occupancy data analytics and prediction: A case study

Occupants are a critical impact factor of building energy consumption. Numerous previous studies emphasized the role of occupants and investigated the interactions between occupants and buildings. However, a fundamental problem, how to learn occupancy patterns and predict occupancy schedule, has not been well addressed due to highly stochastic activities of occupants and insufficient data. This study proposes a data mining based approach for occupancy schedule learning and prediction in office buildings. The proposed approach first recognizes the patterns of occupant presence by cluster analysis, then learns the schedule rules by decision tree, and finally predicts the occupancy schedules based on the inducted rules. A case study was conducted in an office building in Philadelphia, U.S. Based on one-year observed data, the validation results indicate that the proposed approach significantly improves the accuracy of occupancy schedule prediction. The proposed approach only requires simple input data (i.e., the time series data of occupant number entering and exiting a building), which is available in most office buildings. Furthermore, this approach is practical to facilitate occupancy schedule prediction, building energy simulation and facility operation.

32 ENERGY CONSERVATION, CONSUMPTION, AND UTILIZATI↗