Relevant bibliographies by topics / HK2

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Academic literature on the topic 'HK2'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "HK2"

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Slagter, Margrita H., Andreas Scorilas, Louis JG Gooren, et al. "Effect of Testosterone Administration on Serum and Urine Kallikrein Concentrations in Female-to-Male Transsexuals." Clinical Chemistry 52, no. 8 (2006): 1546–51. http://dx.doi.org/10.1373/clinchem.2006.067041.

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Abstract Background: Concentrations of human tissue kallikreins (hKs), a group of 15 secreted serine proteases found in many tissues, are modulated by steroid hormones in cancer cell lines. To gain insight into in vivo kallikrein regulation we measured kallikrein concentrations in serum and urinary tissue in female-to-male transsexuals before and after testosterone administration. Methods: We collected blood and urine samples before treatment and after 4 and 12 months from 28 female-to-male transsexuals who received 250 mg of testosterone esters intramuscularly every 2 weeks. We used ELISA assays to measure multiple kallikreins in serum and urine. Results: After testosterone administration, serum testosterone concentrations increased by ∼15-fold. Serum kallikrein concentrations increased dramatically for hK3 (prostate-specific antigen) and increased moderately for hK2, hK5, hK6, hK7, hK8, hK10, and hK11. In urine, we noted major increases for hK3 and hK2 only. For all other kallikrein concentrations, we observed no considerable changes. Conclusions: We conclude that, in serum and urine of female-to-male transsexuals after testosterone administration, hK3 (prostate-specific antigen) and to a lesser extent hK2 concentrations increase dramatically, but concentration of other kallikreins increase either moderately in serum (hK5, hK6, hK7, hK8, hK10, and hK11) or not at all in either serum (hK4, hK13, hK14) or urine (hK4, hK5, hK6, hK7, hK8, hK10, hK11, hK13, hK14).
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Danno, Katsunori, and Tsunenobu Kimoto. "Deep Hole Traps in As-Grown 4H-SiC Epilayers Investigated by Deep Level Transient Spectroscopy." Materials Science Forum 527-529 (October 2006): 501–4. http://dx.doi.org/10.4028/www.scientific.net/msf.527-529.501.

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Deep levels in as-grown p-type 4H-SiC epilayers have been investigated by DLTS. Three deep hole traps (HK2, HK3 and HK4) can be detected by DLTS in the temperature range from 350K to 700K. They are energetically located at 0.84 eV (HK2), 1.27 eV (HK3) and 1.44 eV (HK4) above the valence band edge. The activation energy of the traps does not show any meaningful change regardless of applied electric field, indicating that the charge state of the deep hole traps may be neutral after hole emission (donor-like). By the low-energy electron irradiation, the HK3 and HK4 concentrations are significantly increased, suggesting that the origins of the HK3 and HK4 may be related to carbon displacement. Study on the thermal stability of these hole traps has revealed that the trap concentrations of HK3 and HK4 are reduced to below the detection limit (1-2 × 1011 cm-3) by annealing at 1350°C. The HK2 is thermally more stable than HK3 and HK4, and becomes lower than the detection limit by annealing at 1550°C.
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Chee, Jessica, Jasmine Singh, Anupam Naran, Neil L. Misso, Philip J. Thompson, and Kanti D. Bhoola. "Novel expression of kallikreins, kallikrein-related peptidases and kinin receptors in human pleural mesothelioma." Biological Chemistry 388, no. 11 (2007): 1235–42. http://dx.doi.org/10.1515/bc.2007.139.

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Abstract Malignant mesothelioma is an aggressive cancer of the pleura that is causally related to exposure to asbestos fibres. The kallikrein serine proteases [tissue (hK1) and plasma (hKB1) kallikreins, and kallikrein-related peptidases (KRP/hK2–15)] and the mitogenic kinin peptides may have a role in tumourigenesis. However, it is not known whether hK1, hKB1, KRP/hK proteins or kinin receptors are expressed in pleural mesotheliomas. The expression of hK1, hKB1, KRP/hK2, 5, 6, 7, 8 and 9, and kinin B1 and B2 receptors was assessed in archived selected normal tissue and mesothelioma tumour sections by immunoperoxidase and immunofluorescence labelling. hK1, hKB1 and kinin B1 and B2 receptors were expressed in malignant cells of the epithelioid and sarcomatoid components of biphasic mesothelioma tumour cells. The percentage of cells with cytoplasmic and nuclear labelling and the intensity of labelling were similar for hK1, hKB1 and the kinin receptors. KRP/hK2, 6, 8 and 9 were also expressed in the cytoplasm and nuclei of mesothelioma cells, whereas KRP/hK5 and hK7 showed predominantly cytoplasmic localisation. This is a first report, but further studies are required to determine whether these proteins have a functional role in the pathogenesis of mesothelioma and/or may be potential biomarkers for pleural mesothelioma.
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Marshall, Aaron J., Edgard Mejia, Sen Hou, Affan Sher, Grant Hatch, and Michel Aliani. "PI3K-dependent Reprogramming of Hexokinase Isoforms Regulates B Lymphocyte Metabolism." Journal of Immunology 204, no. 1_Supplement (2020): 151.30. http://dx.doi.org/10.4049/jimmunol.204.supp.151.30.

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Abstract The PI3K signalling pathway is known to regulate B cell metabolic programming upon activation, but the mechanisms involved are not well understood. Here we find that the PI3K pathway controls reprogramming of hexokinases (HKs), the enzymes that convert glucose into glucose-6-phosphate as a key rate-limiting step of glycolysis and other metabolic pathways. In primary mouse B cells, PI3K pathway inhibition substantially impaired the activation-induced increase in extracellular acidification rates (ECAR), a measure of glycolysis. In contrast, B cells isolated from PI3Kdelta gain-of-function mutant mice exhibit elevated ECAR. We find that B cell activation substantially elevates protein levels of HK2 and HK3 isoforms, but not HK1, in a PI3K-dependant manner. PI3K or mTOR inhibition significantly reduced induction of HK2 and HK3 expression, whereas Akt inhibition did not affect HK isoform expression. In human B lymphoma cells, HK isoforms differ significantly in their degree of mitochondrial localization, with HK1 being mitochondrial, HK3 being cytoplasmic and HK2 present in both mitochondria and cytoplasm. To assess whether HK isoforms have unique non-redundant functions, HK2-deficient B lymphoma cells were generated and were found to exhibit decreased ECAR as well as significant changes in metabolomic profile, despite normal expression and localization of HK1 and HK3. Taken together, our study reveals that PI3K-dependant reprogramming of hexokinase isoforms can impact on B cell glycolysis and other metabolic pathways. Studies in progress are examining the functional importance of HK2 in antibody responses using mice with B cell-specific deletion of this enzyme.
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Bustamante, Marta F., Patricia G. Oliveira, Ricard Garcia-Carbonell, et al. "Hexokinase 2 as a novel selective metabolic target for rheumatoid arthritis." Annals of the Rheumatic Diseases 77, no. 11 (2018): 1636–43. http://dx.doi.org/10.1136/annrheumdis-2018-213103.

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ObjectivesRecent studies indicate that glucose metabolism is altered in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS). Hexokinases (HKs) catalyse the first step in glucose metabolism, and HK2 constitutes the principal HK inducible isoform. We hypothesise that HK2 contributes to the synovial lining hypertrophy and plays a critical role in bone and cartilage damage.MethodsHK1 and HK2 expression were determined in RA and osteoarthritis (OA) synovial tissue by immunohistochemistry. RA FLS were transfected with either HK1 or HK2 siRNA, or infected with either adenovirus (ad)-GFP, ad-HK1 or ad-HK2. FLS migration and invasion were assessed. To study the role of HK2 in vivo, 108 particles of ad-HK2 or ad-GFP were injected into the knee of wild-type mice. K/BxN serum transfer arthritis was induced in HK2F/F mice harbouring Col1a1-Cre (HK2Col1), to delete HK2 in non-haematopoietic cells.ResultsHK2 is particular of RA histopathology (9/9 RA; 1/8 OA) and colocalises with FLS markers. Silencing HK2 in RA FLS resulted in a less invasive and migratory phenotype. Consistently, overexpression of HK2 resulted in an increased ability to migrate and invade. It also increased extracellular lactate production. Intra-articular injection of ad-HK2 in normal knees dramatically increased synovial lining thickness, FLS activation and proliferation. HK2 was highly expressed in the synovial lining after K/BxN serum transfer arthritis. HK2Col1 mice significantly showed decreased arthritis severity, bone and cartilage damage.ConclusionHK2 is specifically expressed in RA synovial lining and regulates FLS aggressive functions. HK2 might be an attractive selective metabolic target safer than global glycolysis for RA treatment.
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Seiler, Kristina, Petra Minder, Iris Mashimo, et al. "Hexokinase Proteins Impart Distinct Functions in Myeloid Development and Cell Death." Blood 132, Supplement 1 (2018): 5088. http://dx.doi.org/10.1182/blood-2018-99-112145.

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Abstract Many key oncogenic pathways converge to adapt tumor cell metabolism to requirements of cancer cells. Aberrant proliferation that is frequently associated with cancer cells is also linked to an adjustment of metabolism in order to fuel cell growth and division. Cancer cells prefer utilizing glycolysis for energy production and providing essential building blocks for a variety of macromolecules. Hexokinases (HKs) are rate-limiting enzymes that catalyze the first and irreversible step of glycolysis, the ATP-dependent phosphorylation of glucose to glucose-6-phosphate. Four HK isoforms are expressed in mammalian cells, HK1, HK2, HK3 and HK4 (also known as glucokinase). HKs promote and sustain a concentration gradient that facilitates glucose entry, which ensures the initiation of glucose dependent pathways. In general, HKs have a cytoprotective role that was highlighted by enhanced sensitivity of cancer cells to drugs when HKs were inhibited. Previously we have reported that HK3 was transcriptionally regulated by PU.1 (SPI-1) in myeloid cells. Further, HK3 expression was significantly reduced in patient acute myeloid leukemia (AML) cells, particularly in acute promyelocytic leukemia (APL) cells expressing the PML-RARA oncofusion protein. We now report on the expression and regulatory function of HKs, particularly HK3, during myeloid differentiation and granulocyte associated cell death. First, we analyzed mRNA HK levels in human CD34+ hematopoietic progenitors cells differentiated towards granulocytes or macrophages by qPCR. Interestingly, while HK1 and HK2 levels remain stable during all stages of myeloid differentiation, HK3 mRNA levels significantly increased. The same pattern of HK mRNA expression was seen in NB4 APL and HL60 AML cell lines differentiated towards granulocytes and monocytes using all-trans retinoic acid (ATRA) and vitamin D3, respectively. To determine a specific role for HK1-3 function in myeloid cells, HK1-3 knockdowns (KD) and knockouts (KO) in NB4 and HL60 cell lines, using shRNA or gRNAs (Cas9/CRISPR technology), respectively, were generated. NB4 HK KD AML cells were tested for their differentiation upon ATRA treatment. Knockdown of HKs generally resulted in a decreased differentiation response of about 20% as assessed by the differentiation marker CD11b. We next determined energy metabolism of HK altered KD and KO cells, relative to parental cells, using a seahorse analyzer. While lowering HK1 or HK3 levels in NB4 and HL60 AML cells did not affect glycolytic capacity at steady state, HK2 inhibition significantly reduced steady state glycolytic capacity. In contrast, knocking down or knocking out HK3 resulted in a higher sensitivity to ATRA-induced cell death during differentiation, which was coupled with higher glycolytic capacity. Together, our findings suggest that HK2 has an important role in steady state metabolism of AML cells while HK3 appears to be a metabolic switch for cell survival during myeloid differentiation. Disclosures No relevant conflicts of interest to declare.
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Shrivastava, Rashmi, Ananta Kumar Ghosh, and Amit Kumar Das. "Intra- and intermolecular domain interactions among novel two-component system proteins coded by Rv0600c, Rv0601c and Rv0602c of Mycobacterium tuberculosis." Microbiology 155, no. 3 (2009): 772–79. http://dx.doi.org/10.1099/mic.0.019059-0.

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Two-component signal transduction pathways comprising a histidine kinase and its cognate response regulator play a dominant role in the adaptation of Mycobacterium tuberculosis to its host, and its virulence, pathogenicity and latency. Autophosphorylation occurs at a conserved histidine of the histidine kinase and subsequently the phosphoryl group is transferred to the conserved aspartate of its cognate response regulator. Among the twelve two-component systems of M. tuberculosis, Rv0600c (HK1), Rv0601c (HK2) and Rv0602c (TcrA) are annotated as a unique three-protein two-component system. HK1 contains an ATP-binding domain, and HK2, a novel Hpt mono-domain protein, contains the conserved phosphorylable histidine residue. HK1 and HK2 complement each other's functions. Interactions among different domains of the HK1, HK2 and TcrA proteins were studied using a yeast two-hybrid system. Self-interaction was observed for HK2 but not for HK1 or TcrA. HK2 was found to interact reasonably well with both HK1 and TcrA, but HK1 interacted weakly with TcrA. The conserved aspartate-containing receiver domain of TcrA interacted well with HK2 but not with HK1. These results suggest the existence of a novel signalling mechanism amongst HK1–HK2–TcrA, and a model for this mechanism is proposed.
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Agnihotri, S., M. Li, M. R. Wilson, et al. "PS2 - 174 Hexokinase 2 Drives Radio-Resistance through ERK Signaling and Sensitizes Cells to Azole Compounds." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, S4 (2016): S14. http://dx.doi.org/10.1017/cjn.2016.368.

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Our ongoing work has demonstrated that hexokinase 2 (HK2) but not HK1 or HK3 is a critical mediator of tumour glycolysis and mitochondrial metabolism in Glioblastoma (GB). Furthermore, HK2 is highly expressed in GB but not in normal brain making it an attractive therapeutic target. Our current findings now support that loss of HK2 alters tumor vasculature, increases sensitivity to radiation, and confers a significant survival benefit in several GB xenograft-bearing mice. Using a genome wide transcript analysis, we identified that loss of HK2 attenuates several pro-growth signaling pathways in GB including ERK signaling. Mechanistically, ERK rescue experiments in HK2 depleted cells rescues cell sensitivity to radiation and reduces DNA damage. Furthermore using a systems biology approach and a rationale drug screen we identified several antifungal agents in the azole class as to inhibit tumor metabolism and growth in HK2 expressing GB cells. Loss of HK2 in GB cells dampened the effect of several azoles suggesting that the mechanism of action is mediated in part through HK2. Furthermore, we tested several azole compounds known to cross the blood brain barrier in vivo. Clinically achievable doses of azoles as single agents increased survival in several orthotopic xenograft GB mouse models. In summary, HK2 drives several oncogenic pathways associated with GB including ERK signaling and sensitizes tumour cells to the azole class of antifungals. Future work will determine whether azoles work synergistically with radiation and temozolomide and elucidate the mechanisms by which they inhibit GB growth in HK2 expressing cells.
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Wolf, Amparo, Sameer Agnihotri, Johann Micallef, et al. "Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme." Journal of Experimental Medicine 208, no. 2 (2011): 313–26. http://dx.doi.org/10.1084/jem.20101470.

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Proliferating embryonic and cancer cells preferentially use aerobic glycolysis to support growth, a metabolic alteration commonly referred to as the “Warburg effect.” Here, we show that the glycolytic enzyme hexokinase 2 (HK2) is crucial for the Warburg effect in human glioblastoma multiforme (GBM), the most common malignant brain tumor. In contrast to normal brain and low-grade gliomas, which express predominantly HK1, GBMs show increased HK2 expression. HK2 expression correlates with worse overall survival of GBM patients. Depletion of HK2, but neither HK1 nor pyruvate kinase M2, in GBM cells restored oxidative glucose metabolism and increased sensitivity to cell death inducers such as radiation and temozolomide. Intracranial xenografts of HK2-depleted GBM cells showed decreased proliferation and angiogenesis, but increased invasion, as well as diminished expression of hypoxia inducible factor 1α and vascular endothelial growth factor. In contrast, exogenous HK2 expression in GBM cells led to increased proliferation, therapeutic resistance, and intracranial growth. Growth was dependent on both glucose phosphorylation and mitochondrial translocation mediated by AKT signaling, which is often aberrantly activated in GBMs. Collectively, these findings suggest that therapeutic strategies to modulate the Warburg effect, such as targeting of HK2, may interfere with growth and therapeutic sensitivity of some GBMs.
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Federzoni, Elena A., Peter Valk, Bob Löwenberg, Martin F. Fey, and Mario P. Tschan. "Linking the Glycolytic Enzyme HK3 to Neutrophil Differentiation of APL Cells Via PU.1." Blood 118, no. 21 (2011): 2425. http://dx.doi.org/10.1182/blood.v118.21.2425.2425.

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Abstract Abstract 2425 Objectives: Identification and characterization of hexokinase 3 (HK3), as novel transcriptional target of the myeloid master regulator PU.1, with a role in APL cell differentiation and survival. Materials: HK3 and PU.1 quantitative RT-PCR in primary AML patient samples (n=170) and granulocytes isolated from healthy donors (n=20). Gene expression profiling in PU.1-knockout and PU.1-restored myeloid cell lines. Generation of NB4 and HT93 PU.1 as well as HK3 knockdown cell lines. ATRA-induced differentiation of these cell lines was assessed by CD11b and CEBPE expression. In vivo binding of PU.1 and PML-RARA to the HK3 promoter was shown by ChIP assays. Viability of NB4 cell lines was assessed by Alamar Blue staining. Results: We identified HK3 as putative transcriptional target of PU.1 by gene expression profiling in PU.1-knockout and PU.1-restored myeloid cell lines. Unlike the other three hexokinase family members (HK1, HK2 and HK4), HK3 expression is limited to hematopoietic cells, where it is mainly expressed in the myeloid lineage. We found 50-times lower HK3 mRNA levels in primary non-APL patients as compared to granulocytes from healthy donors. Most interestingly, we found that HK3 expression in APL patients with the t(15;17) translocation was 400-times lower (p<0.0001) than compared to granulocytes. Given the particularly low HK3 and PU.1 expression in APL patients, we decided to investigate the role of HK3 and its possible regulation by PU.1 during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of NB4 and HT93 APL cell lines. Firstly, we observed a 5500- and 1100-fold increase of HK3 mRNA levels during neutrophil differentiation of NB4 and HT93, respectively. This was paralleled by markedly increased HK3 protein levels. No increased HK3 levels were observed in ATRA-resistant NB4-R2 cell lines. HK1 and HK2 mRNA expression was not markedly increased during neutrophil differentiation pointing to a particular role for HK3 in neutrophil differentiation. Regulation of the liver specific HK4 was not investigated. Next, we observed significantly decreased HK3 expression, both at the mRNA and protein levels, in all PU.1 knockdown cell lines upon ATRA-induced differentiation. In vivo PU.1 binding to three different regions of the HK3 promoter was found. Given our findings in primary APL patients, we decided to test if PML-RARa binds to the HK3 promoter, and indeed, PML-RARA binds to the same promoter regions as PU.1. Knocking down HK3 in APL cell lines resulted in significantly reduced neutrophil differentiation as measured by CD11b and CEBPE expression. Also, we observed that NB4 HK3 knockdown cell lines treated with ATRA were less viable compared to control cells. Conclusions: Our results strongly suggest that HK3 is a novel PU.1 transcriptional target functionally involved in neutrophil differentiation and cell viability of APL cells. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "HK2"

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Réhault-Godbert, Sophie. "Etude fonctionnelle des kallicréines prostatiques humaines hK2 et hK3." Tours, 2001. http://www.theses.fr/2001TOUR4012.

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Les kallicréines humaines hK2 et hK3 sont deux protéases à sérine exprimées essentiellement dans la prostate. HK3 participerait à la liquéfaction du plasma séminal en dégradant les séménogélines, les protéines majeures du coagulum formé immédiatement après éjaculation. Le rôle physiologique des kallicréines hK2 et hK3 n'est cependant pas clairement établi. Chez les patients atteints de cancer de la prostate, les concentrations sériques en hK2 et hK3 augmentent fortement suggérant que ces protéases pourraient jouer un rôle dans la croissance tumorale. Afin de faciliter la détection de hK3 enzymatiquement active dans les fluides biologiques, nous avons dans un premier temps conçu des substrats fluorogéniques peptidiques pour hK3. Ces substrats, dérivés de la séquence des séménogélines, se sont avérés beaucoup plus sensibles à l'hydrolyse par hK3 que ceux actuellement utilisés pour mesurer l'activité de cette protéase. Nous avons montré dans un deuxième temps que hK2 et hK3 pourraient participer à la progression cancéreuse selon deux voies au moins. Ces kallicréines sont capables de dégrader les protéines de liaison des facteurs de croissance de type insuline (IGFBPs), ce qui contribuerait à augmenter la biodisponibilité des IGFs dont l'action mitogénique favoriserait la croissance tumorale. D'autre part, nous avons mis en évidence que hK2 et hK3 pourraient en inactivant les inhibiteurs physiologiques de l'urokinase et de la plasmine (PAI-1, inhibiteur de l'activateur du plasminogène-1 et alpha2-antiplasmine), augmenter indirectement l'activité protéolytique de ces deux protéases sur les protéines de la matrice extracellulaire et faciliter ainsi la dissémination des cellules cancéreuses<br>HK2 and hK3 are two serine proteases mainly expressed in the prostate gland. HK3 is thought to be responsible for the liquefaction of seminal plasma through proteolysis of the semenogelins, the major proteins forming coagulum immediately after ejaculation. Nevertheless, the physiological function of kallikreins hK2 and hK3 is still unclear. Men suffering from prostate cancer have high plasma concentrations of both kallikreins hK2 and hK3 which suggests that these two kallikreins could be involved in tumor growth. .
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Gingras, Alexandre. "Hormonodépendance et activité des kallicréines hK2 et hK3 dans les cellules LNCaP." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ33658.pdf.

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Gravel, Caroline. "Effet d'un milieu conditionné fibroblastique sur l'activité des kallicréines prostatiques hK2 et hK3." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0019/MQ49021.pdf.

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Cavalcante, Isadora Pontes. "Correlação da expressão de GLUT1, HK1, HK2 e HK3 com alta captação de 18/F-FDG em hiperplasia macronodular adrenal primária." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-12012015-125308/.

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Introdução: Hiperplasia Macronodular Adrenal Primária (PMAH) é uma causa rara de Síndrome de Cushing (SC), caracterizada por macronódulos funcionantes geralmente acometendo ambas as glândulas adrenais. Recentemente, o exame 18F-FDG PET/CT detectou três pacientes com PMAH apresentando captação aumentada de 18F-FDG. No entanto, ainda não foi elucidado o mecanismo pelo qual a PMAH apresentaria uma alta captação de 18F-FDG. Objetivos: Os objetivos deste estudo foram investigar se a expressão de GLUT1, HK1, HK2 e/ou HK3 estão relacionados à alta captação de 18F-FDG na PMAH e comparar estas expressões com tecidos adrenais provenientes de pacientes com AAC e CAA. Métodos: 12 pacientes com PMAH que realizaram 18F-FDG-PET/CT, previamente à adrenalectomia. A captação de 18F-FDG foi quantificada como maximum standardized uptake value (SUVmax). Expressão do RNAm foi investigada através de RT-PCR e a expressão proteica através de técnicas de imunoistoquímica. Expressão gênica e proteica dos pacientes com PMAH foi comparada com 15 pacientes com AAC e 10 pacientes com CAA. As correlações foram realizadas através do teste de coeficiente de correlação de Pearson e as comparações, através do teste Kruskal-Wallis, seguido do ajuste de Dunn. Significância estatística foi considerada quando p < 0.05. Resultados: Todos os pacientes com PMAH apresentaram alta captação de 18F-FDG, cujo SUVmáx variou de 3.3 a 8.9 e o tamanho do maior nódulo variou de 3.5 a 15cm. Foi observada forte correlação positiva entre o tamanho do maior nódulo e o SUVmáx nos pacientes com PMAH. No entanto, não foi estabelecida correlação entre a expressão de GLUT1, HK1, HK2 e HK3 e o SUVmáx nos pacientes com PMAH. A expressão do SLC2A1 e HK2 foi significativamente maior nos pacientes com CAA do que nos pacientes com AAC e PMAH. Conclusões: A captação aumentada de 18F-FDG na PMAH não está relacionada ao aumento da expressão de GLUT1, HK1, HK2 e HK3. Estudos futuros serão necessários para elucidar a via glicolítica que é responsável pelo metabolismo da glicose na PMAH<br>Introduction: Primary macronodular adrenal hyperplasia (PMAH) is a rare cause of Cushing\'s syndrome, characterized by functioning adrenal macronodules and increased cortisol production. Recently, integrated 18F-FDG-PET/CT examination revealed an increased 18F-FDG uptake in patients with PMAH. However, it is still unclear the mechanism by which PMAH would present with a high 18F-FDG uptake in PET/CT. Objectives: The aim of this study was to investigate whether GLUT1, HK1, HK2 and/or HK3 expression would account for the high18F-FDG uptake in PMAH and compare these expressions with ACA and ACC adrenal tisuue. Methods: 12 patients undergoing adrenalectomy for PMAH with previous 18F-FDG-PET/CT. 18F-FDG uptake was quantified as the maximum standardized uptake value (maxSUV). mRNA expression was investigated through quantitative RT-PCR and protein expression was investigated using immunohistochemical studies. PMAH gene and protein expression were compared to 15 patients with ACA and 10 with ACC. Correlations were performed through Pearson\'s correlation coefficient test and comparisons through Kruskal-Wallis test, followed by Dunn adjust. Statistical significance was considered when p < 0.05. Results: All patients with PMAH presented with high 18F-FDG uptake, the range of SUVmax in these patients varied from 3.3 to 8.9 and the nodule sizes varied from 3.5 to 15 cm. There was a strong positive correlation between the nodule size and 18F-FDG uptake. However, no correlation could be established between gene and protein expression of GLUT1, HK1, HK2 and HK3 and 18F-FDG uptake. SLC2A1 and HK2 expression was significantly higher in patients with CCA than in patients with AAC and PMAH. Conclusions: Increased 18F-FDG uptake in PMAH does not arise from the overexpression of GLUT1, HK1, HK2 or HK3. Further investigation is required to elucidate the glycolytic pathway involved in glucose metabolism in PMAH
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Bourgeois, Luc. "Etude de la spécificité des kallicréines prostatiques humaines HK1, HK2 et HK3 à l'aide de substrats fluorescents dérivés de molécules naturelles." Tours, 1998. http://www.theses.fr/1998TOUR4020.

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Dans la prostate humaine trois gènes de kallicréines tissulaires codent les protéases HK1, HK2 et HK3, libérées dans le fluide séminal. HK2, récemment purifiée, est étudiée comme marqueur sérique des pathologies prostatiques en remplacement ou en complément du marqueur actuel HK3 (PSA, Prostate specific antigen). HK1 est connue pour son activité productrice de kinine. Dans le tractus génital et les foyers métastatiques. Le rôle de ces protéases est méconnu. L'activité enzymatique de HK1 peut être suivie avec des substrats synthétiques contrairement à celles de HK2 et HK3. Des inhibiteurs de la famille des serpines régulent leur activité ; le PCI (protein C inhibitor) inhibe les trois enzymes. L'#1-Antichymotrypsine (ACT) inhibe HK3 et la Kallistatine HK1. Ces serpines interagissent comme des substrats suicides avec leur protéase cible et sont clivées au niveau de leur boucle réactive. Les séquences entourant ces sites de clivage ont été utilisées pour élaborer des substrats peptidiques fluorogéniques. La même stratégie a été utilisée pour développer des substrats à partir des semenogelines, protéines structurales du coagulum seminal et substrats naturels de HK3. Les peptides dérivés du PCI sont clivés préférentiellement par HK1 et HK2, et après modification permettent d'obtenir des substrats spécifiques pour chacune. Aucun substrat sensible de HK3 n'a pu être développé à partir des serpines ; le clivage d'un peptide dérivé de l'act, inhibiteur physiologique de HK3, obtenu dans des conditions expérimentales optimisées, suggère un mode d'interaction particulier entre ces deux partenaires. Un substrat 100 fois plus sensible que les substrats actuels a été synthétisé pour HK3 à partir d'une séquence entourant un site de clivage post-éjaculatoire de la semenogeline. Les séquences peptidiques de cibles naturelles des Kallicréines ont permis de synthétiser des substrats sensibles et spécifiques ; leur utilisation permettra de mieux comprendre le rôle biologique des enzymes<br>No summary available
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Richardson, Susanne. "Effect of human kallikreins HK2 and HK3 on the anti-protease system of the cervical mucus of the human female." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0018/MQ38181.pdf.

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Haidar, Malak. "Rôle du facteur de croissance transformant (TGF-β2) dans la virulence des macrophages infectés par Theileria annulata". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T044.

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Les parasites Theileria (Theileria. annulata and T. parva) sont des protozoaires intracellulaires qui font partie du phylum des Apicomplexa. Theileria infecte les leucocytes bovins et les transforment en cellules cancéreuses, induisant un genre de leucémie chez le bovin et conduisant à la mort de l’animal. Les cellules infectées par Theileria démontrent certaines caractéristiques de cellules cancéreuses telles qu’une importante capacité d’invasion et de migration cellulaire. Cependant, le traitement de cellules infectées avec une drogue Theiléricide spécifique (buparvaquone) permet l'élimination du parasite et la réversion du phénotype transformé. De plus, la virulence peut être atténuée par passages répétés sur culture cellulaire. La similitude entre les cellules transformées par Theileria et la leucémie humaine fait de Theileria un modèle très important permettant l’étude des mécanismes cellulaires induits par le parasite au cours de la transformation de la cellule hôte. Mon laboratoire d’accueil a publié une augmentation significative de TGF-β2 dans les cellules virulentes et a constaté que parmi les 1158 cibles de TGF-β, 68 gènes ont été reconnus d'avoir modifié leurs niveaux de transcription concomitante avec l'atténuation. Dans ce travail de thèse, nous avons étudié les voies de signalisations impliquées dans la régulation de l’adhésion et l’invasion des cellules infectées par Theileria. Nous nous sommes particulièrement intéressés à l’étude de la voie de signalisation TGF-β2 et ses effecteurs. Nos résultats montrent que l’activation de la voie de signalisation de TGF-β2 par Theileria entraîne une augmentation de l’invasion et de l’adhérence des cellules transformées par deux mécanismes différents, soit en activant la voie de signalisation PGE2/EP4/cAMP/PKA/EPAC/CREB, soit en stimulant la voie GRB2/PI3-K/AP-1. Les macrophages atténués infectés par Theileria sont plus stressés oxydativement ce qui diminue leur adhérence et leur invasion cellulaire. Ceci nous a amené à étudier en collaboration avec un autre doctorant (Mehdi Metheni) le rôle de TGF-β2 dans la régulation du stress oxydatif dans les macrophages infectés par Theileria. Nos données montrent que les niveaux élevés de TGF-β2 stimule l’expression de la catalase, une enzyme anti-oxydante qui convertit le H2O2 en H2O et la baisse de H2O2 favorise la virulence en augmentant l’invasion et l’adhésion des cellules infectées par Theileria (résultats supplémentaires). De plus, nous avons examiné le statut de stress oxydatif et le type de glycolyse utilisé par les cellules infectées par Theileria. Les cellules transformées par Theileria agissent comme des cellules cancéreuses, elles consomment énormément de glucose. La protéine BAD joue un rôle important dans l’apoptose ainsi que dans la voie de glycolyse. Son activité est régulée par phosphorylation en réponse à des facteurs de croissance et de survie. BAD peut être phosphorylée par la PKA sur le résidu sérine 155. Durant ma thèse, nous avons examiné le rôle de la phosphorylation de BAD par la PKA dans la régulation du métabolisme cellulaire des macrophages infectés par Theileria. Nos résultats montrent que l’abolition de la phosphorylation de BAD par la PKA dissocie le complexe mitochondrial formé entre BAD et HK2, ce qui induit l’ubiquitynation et la dégradation de HK2 par le protéasome. La baisse de HK2 stimule la voie de phosphorylation oxydative en faveur de l’effet Warburg dans les cellules infectées par Theileria<br>Theileria parasites (Theileria. annulata and T. parva) are intracellular protozoa and members of the phylum Apicomplexa. Theileria parasites are the only eukaryotes that possess the property of being able to transform another eukaryote, their leukocyte host cells. Transformed leukocytes show many characteristics of tumour cells such as heightened invasive capacity; however the tumour-like phenotype can be totally reversed upon drug induced parasite death and attenuated by multiple in vitro passages. Such multiple-passaged attenuated lines are used as live vaccines against tropical theileriosis. The similarities in tumour hyper-invasiveness between Theileria-transformed leukcocytes and human lymphomas imply that observations on Theileria-induced leukocyte transformation have the potential to give generally applicable insights into the mechanisms underpinning tumour virulence. My host laboratory described higher TGF-β2 levels in virulent infected macrophages and following microarray analysis of virulent compared to attenuated macrophages found that among the 1158 TGF-β-targets, 68 genes had altered transcript levels concomitant with attenuation. In this study, we investigate the signalling pathways involved in the regulation of cellular adhesion and invasiveness of Theileria-infected cells. We were especially interested in the study of TGF-β2 signalling in Theileria-transformed virulent versus attenuated macrophages. My results indicate that following Theileria infection of macrophages, the TGF-β2 signalling pathway is activated and induces an increase in adhesion of virulent transformed macrophages through two different mechanisms: either by activating a PGE2 / EP4 / cAMP / PKA / EPAC / CREB signaling pathway, or by stimulating a GRB2 / PI3-K / AP-1 pathway. As attenuated macrophages display heightened oxidative stress, which underpins their loss of adhesion and invasiveness, in collaboration with another PhD student (Mehdi Metheni) we investigated the role of TGF-β2 in the regulation of the oxidative stress status of Theileria-infected macrophages. Our data show that high levels of TGF-β2 increase the expression of catalase, an anti-oxidant enzyme that converts H2O2 into H2O and the drop in H2O2 output results in regain of the virulence trait heightened adhesion of Theileria-transformed macrophages to fibronectin. Theileria-transformed macrophages display many features of cancer cells such as their consumption of larger quantities of glucose. The BCL-2 family protein BAD has an alternative function in glucose metabolism separate from its role in apoptosis. The activity of BAD is regulated by phosphorylation in response to growth/survival factors. BAD can be phosphorylated on Ser155 by PKA. So during my thesis studies I examined the role of PKA mediated phosphorylation of BAD in the regulation of the cellular metabolism of Theileria-transformed macrophages. My results showed that ablation of BAD S155 phosphorylation dissociates the mitochondrial complex of BAD and HK2 and cytosolic HK2 becomes ubiquitinated and degraded by the proteasome. Loss of HK2 switches the metabolism of Theileria-transformed leukocytes from Warburg-like to OXPHOS-like glycolysis
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Zhang, Rui. "Metabolic Disorder leads to Retinal degeneration: Function, morphology and metabolic pathway analysis." Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/25459.

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INTRODUCTION The retina prefers to metabolize glucose through glycolysis rather than oxidative phosphorylation (OXPHOS) to meet their energy demand even when oxygen is abundant, known as the “Warburg effect”, despite having abundant functional mitochondria. We created transgenic mice with selective knockdowns of key enzymes in glycolysis and OXPHOS including hexokinase (HK) 2, lactate dehydrogenase (LDH) A and pyruvate dehydrogenase (PDH) E1α in rods to study the importance of glycolysis and OXPHOS in retinal metabolism and the role of metabolic derangement in the pathogenesis of retinal diseases. MATERIALS AND METHODS Immunohistochemistry and Western blots were performed to study the changes in protein expression and regulation. Scotopic electroretinography and optical coherence tomography were performed to study the retinal function and structure. Gas and liquid chromatography-mass spectrometry were employed to study the changes in13C-glucose-derived metabolites in the retina. RESULTS Knockdown of HK2 in rods led to photoreceptor degeneration, with reduction in the thickness of the retina and impaired retinal function. Knockdown of HK2 decreased pyruvate production but promoted the tricarboxylic acid (TCA) cycle in the retina. Knockdown of LDHA and PDHE1α in rods also led to retinal degeneration, with thinning of the retina and impaired retinal function. Deletion of LDHA and PDHE1α suppressed glycolysis and the TCA cycle in the retina. CONCLUSION We found that HK2/LDHA-mediated glycolysis and PDHE1α mediated-OXPHOS in rods are indispensable for the maintenance of photoreceptor structure and function. Disturbance in aerobic glycolysis or OXPHOS leads to metabolic remodelling in the retina and photoreceptor degeneration.
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Cloutier, Sylvain. "Sélection et production de scFv contre la kallicréine humaine hK2 par la technologie du phage display." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ33600.pdf.

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Obiezu, Christina V. "Hormonal regulation of prostate-specific antigen and human glandular kallikrein in males and females in vivo, effects of androgens and antiandrogens on plasma and urinary PSA and hK2 levels." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ49759.pdf.

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Books on the topic "HK2"

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Setiadharma, Prayudi. Mari mengenal HKI. Goodfaith Production, 2010.

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Mari mengenal HKI. Goodfaith Production, 2010.

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Simposium, Nasional HKI (2000 Jakarta Indonesia). Prosiding Simposium Nasional HKI: Tema, strategi komersialisasi HKI, membangun jaringan pemilik HKI dengan industri, 23 Nopember 2000. Deputi Menteri Negara Riset dan Teknologi, Bidang Pendayagunaan dan Pemasyarakatan Iptek, 2000.

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Li, Pungga Ja. Ja tawng hko len. name of publisher not identified, 2010.

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Membumikan HKI di Indonesia. Nuansa Aulia, 2009.

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Nghiêm, Xuân Hy. Hky-Hsong thi tuap. The author, 2000.

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HKD "Napredak" u Zagrebu. Napredak, 1996.

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Sardjono, Agus. Membumikan HKI di Indonesia. Nuansa Aulia, 2009.

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F, Aunur Rahim. HKI, hukum Islam & fatwa MUI. Graha Ilmu, 2010.

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Domi, Etleva. Vepra të autorëve dhe studiuesve Francezë për Shqipërinë dhe Shqiptarët: (Shek. XVI-XX) : bibliografi. Biblioteka Kombëtare, 2001.

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Book chapters on the topic "HK2"

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Villars, P., K. Cenzual, J. Daams, et al. "HKS." In Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m. Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_356.

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Brown, J. M. "HO2." In Landolt-Börnstein - Group II Molecules and Radicals. Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11313410_68.

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Brown, J. M. "HS2." In Landolt-Börnstein - Group II Molecules and Radicals. Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11313410_69.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "HKS." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7557.

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Villars, P., K. Cenzual, R. Gladyshevskii, et al. "Bi4TaO8Cl ht2." In Landolt-Börnstein - Group III Condensed Matter. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22847-6_643.

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Villars, P., K. Cenzual, J. Daams, et al. "PtBi2 ht2." In Structure Types. Part 9: Space Groups (148) R-3 - (141) I41/amd. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02702-4_113.

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Villars, P., K. Cenzual, J. Daams, et al. "SrZrO3 ht2." In Structure Types. Part 10: Space Groups (140) I4/mcm – (136) P42/mnm. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19662-1_15.

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Hirota, E., K. Kuchitsu, T. Steimle, J. Vogt, and N. Vogt. "143 HN2+ Diazenylium." In Molecules Containing No Carbon Atoms and Molecules Containing One or Two Carbon Atoms. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-540-70614-4_144.

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Heesen, Bernd. "Bewertung der HKG." In Beteiligungsmanagement und Bewertung für Praktiker. Springer Fachmedien Wiesbaden, 2020. http://dx.doi.org/10.1007/978-3-658-30792-9_14.

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Heesen, Bernd. "Bewertung der HKG." In Beteiligungsmanagement und Bewertung für Praktiker. Springer Fachmedien Wiesbaden, 2016. http://dx.doi.org/10.1007/978-3-658-14260-5_14.

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Conference papers on the topic "HK2"

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Verkerk, Philippe, B. Lounis, J. Y. Courtois, Christopher E. Salomon, and Gilbert Grynberg. "Measurement of the friction coefficient in 1D corkscrew molasses by Rayleigh spectroscopy." In OSA Annual Meeting. Optica Publishing Group, 1992. http://dx.doi.org/10.1364/oam.1992.pd24.

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Probe transmission spectrum in a one-dimensional cesium corkscrew molasses displays a narrow (=30-70 kHz) Rayleigh resonance, which permits to estimate the friction coefficient of the cooling force to be a 5.8 ± 0.4 hk2 at 31.
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JIANG, Yuxin, Michelle KY Siu, Jingjing Wang, et al. "Abstract LB-270: Hexokinase II (HK2) regulates stemness of ovarian cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-270.

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Behar, V., R. Yosef, E. Dor-On, N. Amsalem, Y. Horev, and OM Becker. "PO-424 modulating hexokinase 2 (HK2) as a novel approach to target metabolic immuno-oncology." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.935.

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Braun, Katharina, David Ulmert, Christian von Bodman, et al. "Abstract 3282: Does the catalytic activity of prostate-specific antigen (PSA) or kallikrein-related peptidase 2 (hK2) secreted by novel transgenic mice models critically influence development of prostate cancer or release of PSA or hK2 in blood." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3282.

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Mathias, Rasika A., Yoonhee Kim, Margaret Taub, et al. "Exome Sequencing Identifies Rare Functional Coding Variants In HK2, MTRR And DCAF5 That Determine Lung Function Decline In COPD." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5870.

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Behar, Vered, Reut Yosef Hamo, Eyal Dor-On, and Oren M. Becker. "Abstract 1725: A bi-functional mechanism of action: Activating the NLRP3 inflammasome and triggering apoptosis in cancer via a HK2-VDAC modulator." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1725.

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Xiang, Tiancheng, Hongyan Si, and Yanru Zhao. "A Theoretical Study of the HO2 + HN2 Reaction." In 2nd International Conference on Computer Science and Electronics Engineering (ICCSEE 2013). Atlantis Press, 2013. http://dx.doi.org/10.2991/iccsee.2013.333.

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Chen, Heng-Yi, Tse-Yu Lin, Li-Yang Huang, et al. "HP2." In MUM 2018: 17th International Conference on Mobile and Ubiquitous Multimedia. ACM, 2018. http://dx.doi.org/10.1145/3282894.3289731.

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Boemer, Fabian, Anamaria Costache, Rosario Cammarota, and Casimir Wierzynski. "nGraph-HE2." In the 7th ACM Workshop. ACM Press, 2019. http://dx.doi.org/10.1145/3338469.3358944.

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Kolarevic, Branko. "CAD@HKU." In ACADIA 1998: Do Computers Make a Difference in Design Studios? ACADIA, 1998. http://dx.doi.org/10.52842/conf.acadia.1998.016.

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Reports on the topic "HK2"

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Asvapathanagul, Pitiporn, Leanne Deocampo, and Nicholas Banuelos. Biological Hydrogen Gas Production from Food Waste as a Sustainable Fuel for Future Transportation. Mineta Transportation Institute, 2022. http://dx.doi.org/10.31979/mti.2021.2141.

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In the global search for the right alternative energy sources for a more sustainable future, hydrogen production has stood out as a strong contender. Hydrogen gas (H2) is well-known as one of the cleanest and most sustainable energy sources, one that mainly yields only water vapor as a byproduct. Additionally, H2 generates triple the amount of energy compared to hydrocarbon fuels. H2 can be synthesized from several technologies, but currently only 1% of H2 production is generated from biomass. Biological H2 production generated from anaerobic digestion is a fraction of the 1%. This study aims to enhance biological H2 production from anaerobic digesters by increasing H2 forming microbial abundance using batch experiments. Carbon substrate availability and conversion in the anaerobic processes were achieved by chemical oxygen demand and volatile fatty acids analysis. The capability of the matrix to neutralize acids in the reactors was assessed using alkalinity assay, and ammonium toxicity was monitored by ammonium measurements. H2 content was also investigated throughout the study. The study's results demonstrate two critical outcomes, (i) food waste as substrate yielded the highest H2 gas fraction in biogas compared to other substrates fed (primary sludge, waste activated sludge and mixed sludge with or without food waste), and (ii) under normal operating condition of anaerobic digesters, increasing hydrogen forming bacterial populations, including Clostridium spp., Lactococcus spp. and Lactobacillus spp. did not prolong biological H2 recovery due to H2 being taken up by other bacteria for methane (CH4) formation. Our experiment was operated under the most optimal condition for CH4 formation as suggested by wastewater operational manuals. Therefore, CH4-forming bacteria possessed more advantages than other microbial populations, including H2-forming groups, and rapidly utilized H2 prior to methane synthesis. This study demonstrates H2 energy renewed from food waste anaerobic digestion systems delivers opportunities to maximize California’s cap-and-trade program through zero carbon fuel production and utilization.
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Asvapathanagul, Pitiporn, Leanne Deocampo, and Nicholas Banuelos. Biological Hydrogen Gas Production from Food Waste as a Sustainable Fuel for Future Transportation. Mineta Transportation Institute, 2022. http://dx.doi.org/10.31979/mti.2022.2141.

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In the global search for the right alternative energy sources for a more sustainable future, hydrogen production has stood out as a strong contender. Hydrogen gas (H2) is well-known as one of the cleanest and most sustainable energy sources, one that mainly yields only water vapor as a byproduct. Additionally, H2 generates triple the amount of energy compared to hydrocarbon fuels. H2 can be synthesized from several technologies, but currently only 1% of H2 production is generated from biomass. Biological H2 production generated from anaerobic digestion is a fraction of the 1%. This study aims to enhance biological H2 production from anaerobic digesters by increasing H2 forming microbial abundance using batch experiments. Carbon substrate availability and conversion in the anaerobic processes were achieved by chemical oxygen demand and volatile fatty acids analysis. The capability of the matrix to neutralize acids in the reactors was assessed using alkalinity assay, and ammonium toxicity was monitored by ammonium measurements. H2 content was also investigated throughout the study. The study's results demonstrate two critical outcomes, (i) food waste as substrate yielded the highest H2 gas fraction in biogas compared to other substrates fed (primary sludge, waste activated sludge and mixed sludge with or without food waste), and (ii) under normal operating condition of anaerobic digesters, increasing hydrogen forming bacterial populations, including Clostridium spp., Lactococcus spp. and Lactobacillus spp. did not prolong biological H2 recovery due to H2 being taken up by other bacteria for methane (CH4) formation. Our experiment was operated under the most optimal condition for CH4 formation as suggested by wastewater operational manuals. Therefore, CH4-forming bacteria possessed more advantages than other microbial populations, including H2-forming groups, and rapidly utilized H2 prior to methane synthesis. This study demonstrates H2 energy renewed from food waste anaerobic digestion systems delivers opportunities to maximize California’s cap-and-trade program through zero carbon fuel production and utilization.
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Ferragut, Pablo, Federico Goldenberg, Cecilia Correa, and Christiaan Gischler. Hidrógeno verde y el potencial para Uruguay: insumos para la elaboración de la Hoja de Ruta de Hidrógeno Verde de Uruguay. Inter-American Development Bank, 2022. http://dx.doi.org/10.18235/0004615.

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El Hidrógeno (H2) verde se presenta como una de las alternativas de descarbonización más relevantes, en particular en aquellos sectores cuyas emisiones son difíciles de abatir. Se espera que en los próximos años la demanda de H2 verde a nivel global crezca de manera acelerada. El desarrollo tecnológico y la implementación de acciones de política para avanzar en la descarbonización de las economías en el marco del Acuerdo de París serán los impulsores que marcarán el ritmo de la evolución del mercado del H2 verde y abrirán ventanas de oportunidad para aquellos países capaces de abastecer esta demanda de forma competitiva. Uruguay, por la calidad de sus recursos naturales, las características de su matriz energética, las capacidades generadas en el proceso de transición de la matriz eléctrica, la logística desarrollada y la confiabilidad del país para recibir inversiones, se perfila con un gran potencial en la economía del H2 verde. El presente documento tiene como objetivo principal resumir y poner a disposición los resultados obtenidos del análisis técnico sobre la oportunidad que el H2 verde podría representar para Uruguay. El estudio realizado permitió evaluar de forma preliminar la competitividad de Uruguay en el mercado de H2, amoníaco, metanol y jet-fuel verde, entre otros; bajo distintos escenarios de demanda, en mercados de destino seleccionados (EEUU, Reino Unido, Unión Europea, bunkers internacionales y el mercado doméstico).
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Palmer, David, and Eliot Liu. Open E-Research in the HKU Scholars Hub. The University of Hong Kong, 2016. http://dx.doi.org/10.5353/rt_233946.

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Merz, J. Water Balances, Floods and Sediment Transport in the HKH. International Centre for Integrated Mountain Development (ICIMOD), 2004. http://dx.doi.org/10.53055/icimod.425.

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Merz, J. Water Balances, Floods and Sediment Transport in the HKH. International Centre for Integrated Mountain Development (ICIMOD), 2004. http://dx.doi.org/10.53055/icimod.425.

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Kerstiens, Eron L. H2 System Presentation. Office of Scientific and Technical Information (OSTI), 2018. http://dx.doi.org/10.2172/1425750.

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Zimmerman, Jonathan, and Mattie Hensley. H2@Rail Workshop. Office of Scientific and Technical Information (OSTI), 2019. http://dx.doi.org/10.2172/1763223.

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Johnston, Mariann R. EERE-SBIR TECHNOLOGY TRANSFER OPPORTUNITY: H2 Safety Sensors for H2. Office of Scientific and Technical Information (OSTI), 2015. http://dx.doi.org/10.2172/1227251.

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Bach, M., M. Michael Serrato, and E. Eric Nelson. H02 WETLAND TREATMENT SYSTEM WATER CHEMISTRY SAMPLING AND RESULTS REPORT. Office of Scientific and Technical Information (OSTI), 2008. http://dx.doi.org/10.2172/923835.

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You might also be interested in the extended bibliographies on the topic 'HK2' for particular source types:
Journal articles Dissertations / Theses Books
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