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Journal articles on the topic 'HDMO'

Author: Grafiati

Published: 11 September 2021

Last updated: 15 February 2022

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1

Medina-Medina, Ixaura, Paola García-Beltrán, Ignacio de la Mora-de la Mora, Jesús Oria-Hernández, Guy Millot, Robin Fahraeus, Horacio Reyes-Vivas, José G. Sampedro, and Vanesa Olivares-Illana. "Allosteric Interactions byp53mRNA Govern HDM2 E3 Ubiquitin Ligase Specificity under Different Conditions." Molecular and Cellular Biology 36, no. 16 (May 23, 2016): 2195–205. http://dx.doi.org/10.1128/mcb.00113-16.

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HDM2 and HDMX are key negative regulatory factors of the p53 tumor suppressor under normal conditions by promoting its degradation or preventing itstransactivity, respectively. It has more recently been shown that both proteins can also act as positive regulators of p53 after DNA damage. This involves phosphorylation by ATM on serine residues HDM2(S395) and HDMX(S403), promoting their respective interaction with thep53mRNA. However, the underlying molecular mechanisms of how these phosphorylation events switch HDM2 and HDMX from negative to positive regulators of p53 is not known. Our results show that these phosphorylation events reside within intrinsically disordered domains and change the conformation of the proteins. The modifications promote the exposition of N-terminal interfaces that support the formation of a new HDMX-HDM2 heterodimer independent of the C-terminal RING-RING interaction. The E3 ubiquitin ligase activity of this complex toward p53 is prevented by thep53mRNA ligand but, interestingly, does not affect the capacity to ubiquitinate HDMX and HDM2. These results show how ATM-mediated modifications of HDMX and HDM2 switch HDM2 E3 ubiquitin ligase activity away from p53 but toward HDMX and itself and illustrate how the substrate specificity of HDM2 E3 ligase activity is regulated.

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2

Bernal, Federico, Mark Wade, Amy M. Silverstein, Gregory L. Verdine, Geoffrey M. Wahl, and Loren D. Walensky. "A Stapled p53 Helix Targets HDMX to Overcome Nutlin-3 Resistance and Reactivate the p53 Tumor Suppressor Pathway in Cancer." Blood 112, no. 11 (November 16, 2008): 2645. http://dx.doi.org/10.1182/blood.v112.11.2645.2645.

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Abstract p53 is a transcription factor that induces cell cycle arrest or apoptosis in response to DNA damage and cellular stress, and thereby plays a critical role in protecting cells from malignant transformation. The E3 ubiquitin ligase HDM2 controls p53 levels through a direct binding interaction that neutralizes the transactivation activity of p53 and targets it for degradation via the ubiquitylation-proteasomal pathway. Whereas the HDM2-homologue HDMX lacks ubiquitin ligase function, it participates in regulating the p53 axis by heterodimerizing with HDM2 and sequestering p53 through protein interaction. Loss of p53 activity, either by deletion, mutation, or HDM2/HDMX overexpression, is the most common defect in human cancer. Tumors expressing wild type p53 are rendered vulnerable by pharmacologic approaches that stabilize and upregulate p53. In this context, HDM2 and HDMX have emerged as independent therapeutic targets for restoring p53 activity and resensitizing cancer cells to apoptosis in vitro and in vivo. The small molecule nutlin-3 is an effective antagonist of the p53-HDM2 interaction. However, several studies have demonstrated the inability of nutlin-3 to disrupt the p53-HDMX complex, rendering tumor cells that overexpress HDMX nutlin-3-resistant. We have previously described the synthesis and characterization of a hydrocarbon-stapled alpha-helical p53 peptide (SAH-p53-8) that binds HDM2 with low nanomolar affinity, targets HDM2 in situ, and reactivates the p53 tumor suppressor pathway in HDM2-overexpressing osteosarcoma cells. We now report that SAH-p53-8 binds HDMX with even higher affinity, co-immunoprecipitates with endogenous HDMX, and induces apoptosis and cell cycle arrest in nutlin-3-resistant cancer cells that overexpress HDMX. Thus, by inserting a chemical staple into a peptide fragment of the p53 transactivation domain, we have generated the first bifunctional inhibitor of HDM2 and HDMX, enabling the investigation and pharmacologic modulation of both targets in human cancer.

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3

Pereg, Yaron, Suzanne Lam, Amina Teunisse, Sharon Biton, Erik Meulmeester, Leonid Mittelman, Giacomo Buscemi, et al. "Differential Roles of ATM- and Chk2-Mediated Phosphorylations of Hdmx in Response to DNA Damage." Molecular and Cellular Biology 26, no. 18 (September 15, 2006): 6819–31. http://dx.doi.org/10.1128/mcb.00562-06.

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ABSTRACT The p53 tumor suppressor plays a major role in maintaining genomic stability. Its activation and stabilization in response to double strand breaks (DSBs) in DNA are regulated primarily by the ATM protein kinase. ATM mediates several posttranslational modifications on p53 itself, as well as phosphorylation of p53's essential inhibitors, Hdm2 and Hdmx. Recently we showed that ATM- and Hdm2-dependent ubiquitination and subsequent degradation of Hdmx following DSB induction are mediated by phosphorylation of Hdmx on S403, S367, and S342, with S403 being targeted directly by ATM. Here we show that S367 phosphorylation is mediated by the Chk2 protein kinase, a downstream kinase of ATM. This phosphorylation, which is important for subsequent Hdmx ubiquitination and degradation, creates a binding site for 14-3-3 proteins which controls nuclear accumulation of Hdmx following DSBs. Phosphorylation of S342 also contributed to optimal 14-3-3 interaction and nuclear accumulation of Hdmx, but phosphorylation of S403 did not. Our data indicate that binding of a 14-3-3 dimer and subsequent nuclear accumulation are essential steps toward degradation of p53's inhibitor, Hdmx, in response to DNA damage. These results demonstrate a sophisticated control by ATM of a target protein, Hdmx, which itself is one of several ATM targets in the ATM-p53 axis of the DNA damage response.

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4

Juckett, Lisa. "MENTAL HEALTH AND HUNGER: RISK FACTORS FOR HOSPITALIZATION AMONG HOME-DELIVERED MEAL PARTICIPANTS." Innovation in Aging 3, Supplement_1 (November 2019): S227. http://dx.doi.org/10.1093/geroni/igz038.837.

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Abstract Home-delivered meals (HDMs) provided through the Older Americans Act (OAA) are intended to reduce hunger, promote socialization, and maximize wellness. However, HDM recipients are at increased likelihood of being hospitalized due to their complex health needs and risk for social isolation and depression. Drawing data from the OAA-HDM National Survey, we evaluated the predictors of hospitalization among HDM recipients in 2017. From our sample (n = 578), we conducted random forest classification analyses to identify the most important risk factors related to HDM recipient hospitalization. Our random forest model yielded an accuracy rate of 66.3% with risk factors most indicative of hospitalization being attributed to number of co-morbidities, depressive symptoms, and feelings of social isolation. These findings indicate that although HDMs may help alleviate hunger among older adults, innovate strategies are warranted to address the unmet mental health needs of HDM recipients.

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5

Linares, L. K., A. Hengstermann, A. Ciechanover, S. Muller, and M. Scheffner. "HdmX stimulates Hdm2-mediated ubiquitination and degradation of p53." Proceedings of the National Academy of Sciences 100, no. 21 (September 24, 2003): 12009–14. http://dx.doi.org/10.1073/pnas.2030930100.

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6

Harker, Elizabeth A., Douglas S. Daniels, Danielle A. Guarracino, and Alanna Schepartz. "β-Peptides with improved affinity for hDM2 and hDMX." Bioorganic & Medicinal Chemistry 17, no. 5 (March 2009): 2038–46. http://dx.doi.org/10.1016/j.bmc.2009.01.039.

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7

Beekman, Andrew M., Marco M. D. Cominetti, Samuel J. Walpole, Saurabh Prabhu, Maria A. O'Connell, Jesus Angulo, and Mark Searcey. "Identification of selective protein–protein interaction inhibitors using efficient in silico peptide-directed ligand design." Chemical Science 10, no. 16 (2019): 4502–8. http://dx.doi.org/10.1039/c9sc00059c.

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8

Carvajal, Luis, Daniela Ben-Neriah, Adrien Senecal, Lumie Benard, Swathi-Rao Narayanagari, Charles Kenworhty, Victor Thiruthuvanathan, et al. "Dual inhibition of HDMX and HDM2 in acute myeloid leukemia." Experimental Hematology 53 (September 2017): S46. http://dx.doi.org/10.1016/j.exphem.2017.06.058.

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9

Hayashi, Ryo, Deyun Wang, Toshiaki Hara, Jaclyn A. Iera, Stewart R. Durell, and Daniel H. Appella. "N-Acylpolyamine inhibitors of HDM2 and HDMX binding to p53." Bioorganic & Medicinal Chemistry 17, no. 23 (December 2009): 7884–93. http://dx.doi.org/10.1016/j.bmc.2009.10.032.

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10

Yasuda, Yuichiro, Tatsuya Nagano, Kazuyuki Kobayashi, and Yoshihiro Nishimura. "Group 2 Innate Lymphoid Cells and the House Dust Mite-Induced Asthma Mouse Model." Cells 9, no. 5 (May 9, 2020): 1178. http://dx.doi.org/10.3390/cells9051178.

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Asthma is an important issue not only in health but also in economics worldwide. Therefore, asthma animal models have been frequently used to understand the pathogenesis of asthma. Recently, in addition to acquired immunity, innate immunity has also been thought to be involved in asthma. Among innate immune cells, group 2 innate lymphoid cells (ILC2s) have been considered to be crucial for eosinophilic airway inflammation by releasing T helper 2 cytokines. Moreover, house dust mites (HDMs) belonging to group 1 act on airway epithelial cells not only as allergens but also as cysteine proteases. The production of interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP) from airway epithelial cells was induced by the protease activity of HDMs. These cytokines activate ILC2s, and activated ILC2s produce IL-5, IL-9, IL-13, and amphiregulin. Hence, the HDM-induced asthma mouse model greatly contributes to understanding asthma pathogenesis. In this review, we highlight the relationship between ILC2s and the HDM in the asthma mouse model to help researchers and clinicians not only choose a proper asthma mouse model but also to understand the molecular mechanisms underlying HDM-induced asthma.

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11

Lee, Dahae, Yejin Kim, Hyejung Jo, Cheolhyeon Go, Yoojin Jeong, Yoojin Jang, Dongmin Kang, Kwanjin Park, Yoon-Seong Kim, and Jae Seung Kang. "The Anti-Inflammatory Effect of Aptamin C on House Dust Mite Extract-Induced Inflammation in Keratinocytes via Regulation of IL-22 and GDNF Production." Antioxidants 10, no. 6 (June 11, 2021): 945. http://dx.doi.org/10.3390/antiox10060945.

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Atopic dermatitis (AD), a chronic inflammatory skin disease, is characterized by eczemous lesions on the skin that manifest as severe itching and last a long time. AD is thought to be a response to local allergens, including house dust mites (HDMs). Aptamin C is a modified form of vitamin C comprised of aptamers (DNA fragments) that bind specifically to vitamin C and inhibit its oxidation, thereby increasing its stability and antioxidant effects. It is already known that vitamin C shows an anti-inflammatory effect on skin inflammation. Oxidative stress is one of the major causes of inflammatory diseases, including HDM-induced skin inflammation, suggesting that the antioxidant activity of Aptamin C could regulate inflammatory responses to HDMs in the skin keratinocyte cell line HaCaT and primary skin keratinocytes. Aptamin C not only inhibited HDM-induced proliferation of both type of cells, but suppressed HDM-induced increases in interleukin (IL)-1α and IL-6 production by these cells. In addition, Aptamin C suppressed the production of IL-17 and IL-22 by T cells, which are closely associated with AD pathogenesis, as well as HDM-induced IL-22Rα expression. Aptamin C also reduced the production of thymus and activation-regulated chemokine (TARC) by suppressing the interaction between IL-22 and IL-22Rα, as well as reducing T cell migration. Although HDM treatment markedly increased the expression of glial cell line-derived neurotrophic factor (GDNF), which is associated with itching in AD skin lesions, this increase was reduced by Aptamin C treatment. Taken together, these results suggest that Aptamin C can effectively regulate inflammatory lesions, such as AD, by regulating the production of inflammatory cytokines and GDNF induced by HDM.

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12

Medina-Medina, Ixaura, Mayra Martínez-Sánchez, Jesús Hernández-Monge, Robin Fahraeus, Petr Muller, and Vanesa Olivares-Illana. "p53 promotes its own polyubiquitination by enhancing the HDM2 and HDMX interaction." Protein Science 27, no. 5 (March 25, 2018): 976–86. http://dx.doi.org/10.1002/pro.3405.

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13

Zhang, Jihui, Jie Chen, and Clive Robinson. "Cellular and Molecular Events in the Airway Epithelium Defining the Interaction Between House Dust Mite Group 1 Allergens and Innate Defences." International Journal of Molecular Sciences 19, no. 11 (November 10, 2018): 3549. http://dx.doi.org/10.3390/ijms19113549.

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Serodominant group 1 allergens of house dust mites (HDMs) are cysteine protease digestive enzymes. By increasing the detection of any allergen by dendritic antigen presenting cells, upregulating inflammatory signalling molecules, and activating cells crucial to the transition from innate to acquired immune responses, the proteolytic activity of these HDM allergens also underlies their behaviour as inhalant allergens. The significance of this property is underlined by the attenuation of allergic responses to HDMs by novel inhibitors in experimental models. The group 1 HDM allergens act as prothrombinases, enabling them to operate the canonical stimulation of protease activated receptors 1 and 4. This leads to the ligation of Toll-like receptor 4, which is an indispensable component in HDM allergy development, and reactive oxidant-regulated gene expression. Intermediate steps involve epidermal growth factor receptor ligation, activation of a disintegrin and metalloproteases, and the opening of pannexons. Elements of this transduction pathway are shared with downstream signalling from biosensors which bind viral RNA, suggesting a mechanistic linkage between allergens and respiratory viruses in disease exacerbations. This review describes recent progress in the characterisation of an arterial route which links innate responses to inhaled allergens to events underpinning the progression of allergy to unrelated allergens.

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14

Berberich, Steven. "RNAi knock of HdmX or Hdm2 leads to new insights into p53 signaling." Cell Cycle 9, no. 18 (September 15, 2010): 3640–41. http://dx.doi.org/10.4161/cc.9.18.13255.

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15

Michel, Julien, Elizabeth A. Harker, Julian Tirado-Rives, William L. Jorgensen, and Alanna Schepartz. "In Silico Improvement of β3-Peptide Inhibitors of p53•hDM2 and p53•hDMX." Journal of the American Chemical Society 131, no. 18 (May 13, 2009): 6356–57. http://dx.doi.org/10.1021/ja901478e.

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16

Eguiluz-Gracia, Ibon, Francisca Palomares, Maria Salas, Almudena Testera-Montes, Adriana Ariza, Ignacio Davila, Joan Bartra, Cristobalina Mayorga, Maria Jose Torres, and Carmen Rondon. "Precision Medicine in House Dust Mite-Driven Allergic Asthma." Journal of Clinical Medicine 9, no. 12 (November 26, 2020): 3827. http://dx.doi.org/10.3390/jcm9123827.

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House dust mites (HDMs) are the allergenic sources most frequently involved in airway allergy. Nevertheless, not every sensitized patient develops respiratory symptoms upon exposure to HDM, and there is a clinical need to differentiate allergic asthmatics (AAs) from atopic non-allergic asthmatics with HDM sensitization. This differentiation sometimes requires in vivo provocations like the bronchial allergen challenge (BAC). Interestingly, recent data demonstrate that non-atopic patients with asthma can also develop positive BAC results. This novel phenotype has been termed local allergic asthma (LAA). The interest in identifying the allergic triggers of asthma resides in the possibility of administering allergen immunotherapy (AIT). AIT is a disease-modifying intervention, the clinical benefit of which persists after therapy discontinuation. Recently, new modalities of sublingual tablets of HDM immunotherapy registered as pharmaceutical products (HDM-SLIT tablets) have become commercially available. HDM-SLIT tablets have demonstrated a robust effect over critical asthma parameters (dose of inhaled corticosteroids, exacerbations, and safety), thus being recommended by international guidelines for patients with HDM-driven AA. In this review, we will summarize the current knowledge on the phenotype and endotype of HDM-driven AA, and LAA, address the difficulties for BAC implementation in the clinic, and discuss the effects of AIT in AA and LAA.

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17

Di Renzo, Laura, Luigi Tonino Marsella, Alberto Carraro, Roberto Valente, Paola Gualtieri, Santo Gratteri, Diego Tomasi, Federica Gaiotti, and Antonino De Lorenzo. "Changes in LDL Oxidative Status and Oxidative and Inflammatory Gene Expression after Red Wine Intake in Healthy People: A Randomized Trial." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/317348.

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Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate immune system and exert a protective action by reducing low density lipoproteins (LDL) oxidation via induction of antioxidant enzymes. We evaluated the gene expression of oxidative stress (HOSp), inflammasome (HIp), and human drug metabolism pathways (HDM) and ox-LDL level at baseline and after the intake of red wine naturally enriched with resveratrol (NPVRW), in association with or without a McDonald’s meal (McDM). The ox-LDL levels significantly increase comparing baseline (B)versusMcDM and decreased comparing McDMversusMcDM + NPVRW (P≤0.05). Percentages of significant genes expressed after each nutritional intervention were the following: (1) BversusMcDM, 2.88% HOSp, 2.40% of HIp, and 3.37% of HDMp; (2) BversusMcDM + NPVRW, 1.44% of HOSp, 4.81% of HIp, and 0.96% of HDMp; (3) McDMversusMcDM + NPVRW, 2.40% of HOSp, 2.40% of HIp, and 5.77% of HDMp; (4) BversusNPVRW, 4.80% HOSp, 3.85% HIp, and 3.85% HDMp. NPVRW intake reduced postprandial ox-LDL and the expression of inflammation and oxidative stress related genes. Chronic studies on larger population are necessary before definitive conclusions.

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Luo, Minmin, Can Hu, Yayun Zhuang, Wufan Chen, Feng Liu, and Sherman Xuegang Xin. "Numerical assessment of the reduction of specific absorption rate by adding high dielectric materials for fetus MRI at 3 T." Biomedical Engineering / Biomedizinische Technik 61, no. 4 (August 1, 2016): 455–61. http://dx.doi.org/10.1515/bmt-2015-0171.

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Abstract The specific absorption rate (SAR) is an important issue to be considered in fetus MRI at 3 T due to the high radiofrequency energy deposited inside the body of pregnant woman. The high dielectric material (HDM) has shown its potential for enhancing B1 field and reducing SAR in MRI. The aim of this study is to assess the feasibility of SAR reduction by adding an HDM to the fetus MRI. The feasibility of SAR reduction is numerically assessed in this study, using a birdcage coil in transmission loaded with an electromagnetic pregnant woman model in the SEMCAD-EM solver. The HDMs with different geometric arrangements and dielectric constants are manually optimized. The ${B_1}^ + $ homogeneity is also considered while calculating the optimized fetus 10 g local SAR among different strategies in the application of HDM. The optimum maximum fetus 10 g local SAR was obtained as 2.25 W/kg, by using two conformal pads placed left and right with the dielectric constant to be 400, reduced by 24.75% compared to that without the HDM. It indicated that the SAR can be significantly reduced with strategic placement of the HDM and the use of HDM may provide a simple, effective and low-cost method for reducing the SAR for the fetus MRI at 3 T.

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19

Pereg, Y., D. Shkedy, P. de Graaf, E. Meulmeester, M. Edelson-Averbukh, M. Salek, S. Biton, et al. "Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage." Proceedings of the National Academy of Sciences 102, no. 14 (March 23, 2005): 5056–61. http://dx.doi.org/10.1073/pnas.0408595102.

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20

Meulmeester, Erik, Madelon M. Maurice, Chris Boutell, Amina F. A. S. Teunisse, Huib Ovaa, Tsion E. Abraham, Roeland W. Dirks, and Aart G. Jochemsen. "Loss of HAUSP-Mediated Deubiquitination Contributes to DNA Damage-Induced Destabilization of Hdmx and Hdm2." Molecular Cell 18, no. 5 (May 2005): 565–76. http://dx.doi.org/10.1016/j.molcel.2005.04.024.

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21

Meulmeester, Erik, Madelon M. Maurice, Chris Boutell, Amina F. A. S. Teunisse, Huib Ovaa, Tsion E. Abraham, Roeland W. Dirks, and Aart G. Jochemsen. "Loss of HAUSP-Mediated Deubiquitination Contributes to DNA Damage-Induced Destabilization of Hdmx and Hdm2." Molecular Cell 19, no. 1 (July 2005): 143–44. http://dx.doi.org/10.1016/j.molcel.2005.06.002.

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22

Datta, Shreya, Megan E. Bucks, Dipankar Koley, Pei Xin Lim, and Sergey N. Savinov. "Functional profiling of p53-binding sites in Hdm2 and Hdmx using a genetic selection system." Bioorganic & Medicinal Chemistry 18, no. 16 (August 2010): 6099–108. http://dx.doi.org/10.1016/j.bmc.2010.06.053.

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23

d’Alessandro, Miriana, Laura Bergantini, Anna Perrone, Paolo Cameli, Valerio Beltrami, Lorenzo Alderighi, Laura Pini, Elena Bargagli, and Marco Saletti. "House Dust Mite Allergy and the Der p1 Conundrum: A Literature Review and Case Series." Allergies 1, no. 2 (April 15, 2021): 108–14. http://dx.doi.org/10.3390/allergies1020008.

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The house dust mite (HDM) is globally ubiquitous in human habitats. Thirty-two allergens for Dermatophagoides farinae and 21 for Dermatophagoides pteronyssinus have been detected so far. The present minireview summarizes information about the role of Der p 1 as a key coordinator of the HDM-induced allergic response and reports on a series of Italian patients who are allergic to HDMs. We studied the specific IgE profiles in a population of patients with allergic asthma and rhinitis screened for specific immunotherapy (SIT) for HDM allergies, with the aim of obtaining insights into the pathogenic role of Der p1. Patients co-sensitized to other airborne allergens showed a higher prevalence of asthma (9/12 (75%) vs. 2/7 (29%); p < 0.05) than did HDM mono-sensitized patients. The latter group showed higher Der p1 concentrations than that of the co-sensitized group (p = 0.0360), and a direct correlation between Der p1 and Der p2 (r = 0.93; p = 0.0003) was observed. In conclusion, our study offers insights into the role of Der p1 in a population of patients with allergic rhinitis and asthma who were candidates for SIT. Interestingly, Der p1 positivity was associated with bronchial asthma and co-sensitization.

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K., Mounika, and K. N. Shivaswamy. "Skin prick test positivity to house dust mites (HDM) in patients with chronic urticaria." International Journal of Research in Dermatology 3, no. 1 (February 23, 2017): 7. http://dx.doi.org/10.18203/issn.2455-4529.intjresdermatol20170611.

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<p class="abstract"><strong>Background:</strong> The urticaria lasting for more than 6 weeks is termed chronic urticaria. The etiology of chronic urticaria and angioedema remains uncertain in most of the patients. Aeroallergens can induce or exacerbates chronic urticaria. The common aeroallergens are house dust mites (HDM), pollens, moulds, etc. House dust mites can trigger immunological process through ingestion, inhalation or inoculation. These mite allergens are resistant to high temperatures, and do not lose their antigenic property even on cooking. HDMs can also cause worsening of existing atopic dermatitis. Skin test with HDMs is well known to cause irritation due to their proteolytic enzymes.The study was undertaken with the objective to study the skin prick test positivity to house dust mites in patients with chronic urticaria<span lang="EN-IN">.</span></p><p class="abstract"><strong>Methods:</strong> The study was done on 56 consecutive patients of clinically diagnosed cases of chronic urticaria attending the OPD. The skin prick test was done according to the standard protocol.<strong></strong></p><p class="abstract"><strong>Results:</strong> We had a total of 56 patients with chronic urticaria, of which males were 30 and females were 26 with a male to female ratio of 1:0.8. Of the 56 patients with chronic urticaria skin prick test to HDM was seen in 8 (14.2%) patients. <em>D. pteronysinnus</em> 6 (10.7%) constituted the majority among the HDM positivity followed by <em>D. farinae</em> 2(3.5%). We also found skin prick test positivity to pollens, moulds and animal dander in 5, 4 and 2 patients respectively<span lang="EN-IN">. </span></p><p class="abstract"><strong>Conclusions:</strong> House dust mites can cause or trigger the urticarial symptoms and one should consider to do skin prick test to HDM in identifying the cause and thereby reliving the symptoms of urticaria on its avoidance<span lang="EN-IN">.</span></p>

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Dolan, Margaret F. J., Rebecca E. Ross, Jon Albretsen, Jofrid Skarðhamar, Genoveva Gonzalez-Mirelis, Valérie K. Bellec, Pål Buhl-Mortensen, and Lilja R. Bjarnadóttir. "Using Spatial Validity and Uncertainty Metrics to Determine the Relative Suitability of Alternative Suites of Oceanographic Data for Seabed Biotope Prediction. A Case Study from the Barents Sea, Norway." Geosciences 11, no. 2 (January 26, 2021): 48. http://dx.doi.org/10.3390/geosciences11020048.

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The use of habitat distribution models (HDMs) has become common in benthic habitat mapping for combining limited seabed observations with full-coverage environmental data to produce classified maps showing predicted habitat distribution for an entire study area. However, relatively few HDMs include oceanographic predictors, or present spatial validity or uncertainty analyses to support the classified predictions. Without reference studies it can be challenging to assess which type of oceanographic model data should be used, or developed, for this purpose. In this study, we compare biotope maps built using predictor variable suites from three different oceanographic models with differing levels of detail on near-bottom conditions. These results are compared with a baseline model without oceanographic predictors. We use associated spatial validity and uncertainty analyses to assess which oceanographic data may be best suited to biotope mapping. Our results show how spatial validity and uncertainty metrics capture differences between HDM outputs which are otherwise not apparent from standard non-spatial accuracy assessments or the classified maps themselves. We conclude that biotope HDMs incorporating high-resolution, preferably bottom-optimised, oceanography data can best minimise spatial uncertainty and maximise spatial validity. Furthermore, our results suggest that incorporating coarser oceanographic data may lead to more uncertainty than omitting such data.

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Giglio, Simona, Francesca Mancini, Francesca Gentiletti, Giorgia Sparaco, Lara Felicioni, Fabio Barassi, Carla Martella, et al. "Identification of an Aberrantly Spliced Form of HDMX in Human Tumors: A New Mechanism for HDM2 Stabilization." Cancer Research 65, no. 21 (November 1, 2005): 9687–94. http://dx.doi.org/10.1158/0008-5472.can-05-0450.

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27

Wachter, F., A. M. Morgan, M. Godes, R. Mourtada, G. H. Bird, and L. D. Walensky. "Mechanistic validation of a clinical lead stapled peptide that reactivates p53 by dual HDM2 and HDMX targeting." Oncogene 36, no. 15 (October 10, 2016): 2184–90. http://dx.doi.org/10.1038/onc.2016.361.

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28

Ishida, Mariko, Shoji Matsune, Nozomu Wakayama, Ryuji Ohashi, and Kimihiro Okubo. "Possibility of Local Allergic Rhinitis in Japan." American Journal of Rhinology & Allergy 34, no. 1 (August 14, 2019): 26–34. http://dx.doi.org/10.1177/1945892419868441.

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Background The concept of local allergic rhinitis (LAR) has been advocated recently. Allergic rhinitis in Japan is characterized by house dust mites (HDMs) and Japanese cedar pollen (JCP). To investigate LAR in Japan, total IgE and antigen-specific IgE (sIgE) were measured in inferior turbinate mucosa and their relationships with skin test (ST) and nasal allergen provocation test (NAPT) and as well as serum IgE levels were examined. Methods Subjects were 50 rhinosinusitis patients for surgery. ST was performed and serum total IgE and sIgE levels were measured preoperatively. Patients with class-0 serum anti-HDM or anti-JCP sIgE levels were subjected to NAPT with HDM or JCP, respectively, or both. In all patients, inferior turbinate mucosa was weighed and mashed, and total IgE and sIgE levels were then measured as local mucosal date per gram and per milligram. Because there is no clinical consensus how to evaluate nasal sIgE yet, both positive NAPT and detectable sIgE in obtained nasal mucosa were adopted as the diagnostic criteria of LAR in order to strictly elucidate the possibility of presence of LAR in Japan. Results JCP LAR was definitely diagnosed in 2 of 14 patients (14.3%) and HDM LAR in 5 of 21 (23.8%) in cases with rhinosinusitis symptoms in the absence of positive ST nor serum sIgE. Conclusion The present results positively support LAR by HDM or JCP being present in Japan.

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Wafer, Lucas N., Werner W. Streicher, Scott A. McCallum, and George I. Makhatadze. "Thermodynamic and Kinetic Analysis of Peptides Derived from CapZ, NDR, p53, HDM2, and HDM4 Binding to Human S100B." Biochemistry 51, no. 36 (August 29, 2012): 7189–201. http://dx.doi.org/10.1021/bi300865g.

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Migliorini, Domenico, Davide Danovi, Emanuela Colombo, Roberta Carbone, Pier Giuseppe Pelicci, and Jean-Christophe Marine. "Hdmx Recruitment into the Nucleus by Hdm2 Is Essential for Its Ability to Regulate p53 Stability and Transactivation." Journal of Biological Chemistry 277, no. 9 (December 13, 2001): 7318–23. http://dx.doi.org/10.1074/jbc.m108795200.

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Han, Xin, Guillermo Garcia-Manero, Timothy J. McDonnell, Guillermina Lozano, L. Jeffrey Medeiros, Lianchun Xiao, Gary Rosner, et al. "HDM4 (HDMX) is widely expressed in adult pre-B acute lymphoblastic leukemia and is a potential therapeutic target." Modern Pathology 20, no. 1 (November 24, 2006): 54–62. http://dx.doi.org/10.1038/modpathol.3800727.

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Yang, Yongshi, Rongfei Zhu, Nan Huang, Wenjing Li, Wei Zhang, Yin Wang, and Lin Yang. "The Dermatophagoides pteronyssinus Molecular Sensitization Profile of Allergic Rhinitis Patients in Central China." American Journal of Rhinology & Allergy 32, no. 5 (July 13, 2018): 397–403. http://dx.doi.org/10.1177/1945892418787116.

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Background House dust mites (HDMs) are the major aeroallergens in patients with rhinitis and/or asthma in China. However, the molecular sensitization of HDM is varied in different regions. Objective To investigate the Dermatophagoides pteronyssinus ( Der p) molecular sensitization profile of allergic rhinitis (AR) patients in Central China. Methods AR patients with positive skin prick tests to Der p were enrolled in our study. Specific immunoglobulin E (sIgE) for Der p, Dermatophagoides farinae ( Der f), Acarus siro ( Aca s), Blomia tropicalis ( Blo t), and Der p components Der p1, Der p2, and Der p10 were measured in all patients. Results A total of 130 patients were included. The overall prevalence of positive serum sIgE was 99.2% for Der p, 98.5% for Der f, 81.5% for Aca s, 83.1% for Blo t, 71.5% for Der p1, 64.6% for Der p2, and 11.5% for Der p10. HDM-AR patients with asthma displayed significantly higher concentrations of sIgE to Der p, Der f, Der p1, and Der p2 than did those without asthma ( P < .001). The prevalence of asthma in HDM-AR patients was higher among the patients sensitized to both Der p1 and Der p2 (62.8%) than those sensitized to only 1 allergen ( Der p1 26.7% or Der p2 16.7%; P < .05) or nonsensitized to Der p1 and Der p2 (19.4%; P < .001). Conclusion Der p has high cross-reactivity with other mite species. Der p1 and Der p2 are the major components to induce Der p sensitization among AR patients in Central China. Sensitization to both Der p1 and Der p2 may be a risk factor for developing asthma in HDM-AR patients.

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Boyde, Alan. "The Bone Cartilage Interface and Osteoarthritis." Calcified Tissue International 109, no. 3 (June 4, 2021): 303–28. http://dx.doi.org/10.1007/s00223-021-00866-9.

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AbstractThis review describes results obtained with tissue from prior studies of equine and human osteoarthritis (OA). The main methods considered are scanning electron microscopy, novel methods in light microscopy and X-ray Micro-tomography. The same samples have been re-utilised in several ways. The tissues described are hyaline articular cartilage (HAC; or substitutes), with its deep layer, articular calcified cartilage (ACC), whose deep surface is resorbed in cutting cone events to allow the deposition of subchondral bone (SCB). Multiple tidemarks are normal. Turnover at the osteochondral (ACC-HAC-SCB) junction is downregulated by overload exercise, conversely, during rest periods. Consequent lack of support predisposes to microfracture of the ACC-SCB plate, in the resorption-related repair phase of which the plate is further undermined to form sink holes. The following characteristics contribute to the OA scenario: penetrating resorption canals and local loss of ACC; cracking of ACC and SCB; sealing of cracks with High-Density Mineral Infill (HDMI); extrusion of HDMI into HAC to form High-Density Mineral Protrusions (HDMP) in HAC which may fragment and contribute to its destruction; SCB marrow space infilling and densification with (at first) woven bone; disruption, fibrillation and loss of HAC; eburnation; repair with abnormal tissues including fibrocartilage and woven bone; attachment of Sharpey fibres to SCB trabeculae and adipocyte-moulded extensions to trabeculae (excrescences).

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Jha, Manoj K., and Paul Schonfeld. "Geographic Information System–Based Analysis of Right-of-Way Cost for Highway Optimization." Transportation Research Record: Journal of the Transportation Research Board 1719, no. 1 (January 2000): 241–49. http://dx.doi.org/10.3141/1719-32.

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At the planning stages of a highway project, various location alternatives must be explored, subject to a set of design constraints. A computerized tool with which to compare alignment alternatives would significantly reduce the time and resources spent as well as help find a minimum cost (or maximum net benefit) solution. Highway design optimization (HDO) is a computerized process that minimizes an objective function composed of significant highway costs, subject to a set of design constraints, including curvature, gradient, and sight distance. Several costs of alignments, such as right-of-way, earthwork, and environment costs, are sensitive to geography. A geographic information system (GIS) may be exploited to compute such costs for use in HDO models (HDOMs). Most known HDOMs focus only on refining the optimization approach and do not provide a comprehensive formulation for all costs sensitive to alignment. Provided is a comprehensive formulation for right-of-way cost computation. A GIS-based algorithm is developed to compute the right-of-way cost, which is integrated with an HDOM based on genetic algorithms. Two examples are used to demonstrate the effectiveness of the proposed approach.

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Kallen, Joerg, Aude Izaac, Suzanne Chau, Emmanuelle Wirth, Joseph Schoepfer, Robert Mah, Achim Schlapbach, et al. "Structural States of Hdm2 and HdmX: X‐ray Elucidation of Adaptations and Binding Interactions for Different Chemical Compound Classes." ChemMedChem 14, no. 14 (May 27, 2019): 1305–14. http://dx.doi.org/10.1002/cmdc.201900201.

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Sarkari, Feroz, Anthony La Delfa, Cheryl H. Arrowsmith, Lori Frappier, Yi Sheng, and Vivian Saridakis. "Further Insight into Substrate Recognition by USP7: Structural and Biochemical Analysis of the HdmX and Hdm2 Interactions with USP7." Journal of Molecular Biology 402, no. 5 (October 2010): 825–37. http://dx.doi.org/10.1016/j.jmb.2010.08.017.

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Sonneveld, Pieter, Ingo Schmidt-Wolf, Bronno van der Holt, Laila el Jarari, Uta Bertsch, Hans Salwender, Sonja Zweegman, et al. "HOVON-65/GMMG-HD4 Randomized Phase III Trial Comparing Bortezomib, Doxorubicin, Dexamethasone (PAD) Vs VAD Followed by High-Dose Melphalan (HDM) and Maintenance with Bortezomib or Thalidomide In Patients with Newly Diagnosed Multiple Myeloma (MM)." Blood 116, no. 21 (November 19, 2010): 40. http://dx.doi.org/10.1182/blood.v116.21.40.40.

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Abstract Abstract 40 Introduction: This independent trial was designed to evaluate the efficacy of bortezomib (B) during induction and maintenance on progression-free survival (PFS) in patients with newly diagnosed symptomatic MM, who were candidates for high-dose therapy. Patients were randomly assigned to 3 cycles of standard VAD (arm A) or PAD (Arm B); PAD was dosed as B 1.3 mg/m2, days 1,4,8,11, doxorubicin 9 mg/m2, days 1–4, dexamethasone 40 mg, days 1–4, 9–12, 17–20). Patients received one (HOVON) or two (GMMG) high-dose melphalan (HDM) 200 mg/m2 with ASCT. Maintenance consisted of thalidomide (T) 50 mg daily (arm A) or B 1.3 mg/m2, 2-weekly (arm B) for 2 years. Primary endpoint was PFS, other endpoints were complete response (CR) (EBMT), immunofixation positive CR (nCR), VGPR pre-and post HDM and survival (OS). The protocol specified analysis was intention-to-treat and censored for patients who received allo-SCT after HDM1 (n=46). We report the analysis of the first 626 randomized patients. The final analysis of all patients will be presented at the meeting. Results: 13 patients were excluded (7 not eligible, 6 not evaluable). The two arms (A:n=305;B:n=308) were well balanced for age, Salmon/Durie stage II/III, renal failure (11%), and serum B2M. Medium follow-up is 40 months. 89% of patients completed induction and HDM1. In GMMG after HDM1 80% of patients received 2nd HDM. Full dose B could be administered in 82% of patients. Polyneuropathy (PNP) WHO gr 3+4 occurred in 7% (arm A) and 16% (arm B). 204 (67%, arm A) and 174 (57%, arm B) patients started maintenance. 64% of patients tolerated full dose B and 27% reduced dose. 47% of patients on B maintenance went off protocol because of toxicity (9%), progression (29%) or other (9%). In contrast 64 % on T maintenance went off protocol because of toxicity (31%), progression (31%) or other (2%). nCR/CR rates were 7/9% (arm A) vs 9/21% (arm B) at 3 months after HDM-1 and 12/26% (arm A) vs 12/38% (arm B) on protocol. ≥VGPR in arm-A vs arm-B were 40% vs 60% after HDM-1 and 61% vs 75% on protocol. PFS was superior in arm B (HR 0.81, p=0.047; adjusted for ISS: HR 0.81, p=0.056). PFS at 36 months was 42% (arm A) vs 46% (arm B). Multivariate Cox regression showed treatment arm (p=0.037), IgA (p=0.007), ISS stage (p=0.007), WHO Performance Status (p<0.0001), del13/13q- (p=0.015) and study group (2nd HDM) (p=0.015) as significant PFS variables. Patients treated with bortezomib had a better OS (HR 0.74, p=0.048), with study arm, WHO, IgA, ISS stage and del13/13q- as significant variables. Subgroup analysis of response at 12 months showed no impact on PFS and an impact of VGPR/nCR/CR on OS only in arm A. Adverse cytogenetic markers (p<0.05) in the combined group were 13q14, 17p-, t(4;14) for PFS and OS. Detailed FISH data are reported separately. The response and survival data of the subgroup analysis are given below. We conclude that B achieves high nCR/CR during induction, that B maintenance is well tolerated and is associated with additional responses. Bortezomib achieves superior PFS and results in an improvement of survival. This trial (EudraCT no. 2004-000944-26) was supported by the Dutch Cancer Foundation, the German Federal Ministry of Education and Research and a grant from Janssen-Cilag. Disclosures: Sonneveld: celgene: Membership on an entity's Board of Directors or advisory committees; janssen-Cilag: Membership on an entity's Board of Directors or advisory committees; millennium: Membership on an entity's Board of Directors or advisory committees. Off Label Use: bortezomib, induction treatment prior to high dose therapy. Schmidt-Wolf:celgene: Membership on an entity's Board of Directors or advisory committees; janssen-Cilag: Research Funding. van de Velde:Johnson & Johnson: Employment, Equity Ownership. Delforge:celgene: Membership on an entity's Board of Directors or advisory committees; janssen-cilag: Membership on an entity's Board of Directors or advisory committees. Weisel:orthobiotech: Consultancy, Membership on an entity's Board of Directors or advisory committees; celgene: Membership on an entity's Board of Directors or advisory committees. Scheid:orthobiotech: Honoraria. Goldschmidt:celgene: Honoraria, Research Funding; amgen: Honoraria, Research Funding; novartis: Honoraria, Research Funding; orthobiotech: Honoraria, Research Funding; roche: Honoraria, Research Funding.

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González-Pérez, Ruperto, Paloma Poza-Guedes, Fernando Pineda, Peter Forstenlechner, Miriam Castillo, Elena Mederos-Luís, Martina Aumayr, Víctor Matheu, Cristina Alava-Cruz, and Inmaculada Sánchez-Machín. "Mite Molecular Profile in the Th2-Polarized Moderate-to-Severe Persistent Asthma Endotype Subjected to High Allergen Exposure." International Archives of Allergy and Immunology 182, no. 1 (September 14, 2020): 21–31. http://dx.doi.org/10.1159/000510118.

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<b><i>Background:</i></b> The association among the IgE responses to prevailing groups of house dust mite (HDM) allergens in the concurrent asthma phenotypes has not been determined. <b><i>Objective:</i></b> The aim of the present study lays on a component-resolved diagnosis (CRD) model to investigate the mite molecular signature in subjects with type-2 inflammation asthma. <b><i>Methods:</i></b> We selected patients showing a clinically relevant sensitization to HDMs with moderate-to-severe persistent asthma. Skin prick test (SPT) with standardized mite extracts, a broad customized CRD serum sIgE panel including 9 <i>Dermatophagoides pteronyssinus</i> allergens and the related protein allergenic characterization, was investigated in all serum samples. <b><i>Results:</i></b> Ninety out of 93 (96.77%) patients with a positive SPT to HDM showed a concordant sIgE (≥0.35 kU<sub>A</sub>/L) to the crude extract of <i>D. pteronyssinus</i>. Major allergens (Der p 2, Der p 23, and Der p 1) were present in >70% of all subjects, with mid-tier allergens (Der p 5, Der p 7, and Der p 21) reaching up to 51% in the present cohort. A complex pleomorphic repertoire of HDM molecules recognized by IgE was depicted, including 38 distinct profiles. <b><i>Conclusions and Clinical Relevance:</i></b> The proposed CRD panel approach, containing the most prevalent HDM allergens, appeared to be sufficient to obtain a precise <i>D. pteronyssinus</i> molecular diagnosis in asthmatics with a climate-dependent high-mite allergen exposure and coexisting sensitization. A dominant role of both major and mid-tier allergens has been confirmed in moderate and severe persistent asthmatics with the preponderant Th2-high endotype.

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Ledder, Ruth G., Prem K. Sreenivasan, William DeVizio, and Andrew J. McBain. "Evaluation of the specificity and effectiveness of selected oral hygiene actives in salivary biofilm microcosms." Journal of Medical Microbiology 59, no. 12 (December 1, 2010): 1462–68. http://dx.doi.org/10.1099/jmm.0.024372-0.

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The microbiological effects of biocidal products used for the enhancement of oral hygiene relate to the active compound(s) as well as other formulation components. Here, we test the specificities of selected actives in the absence of multiple excipients. Salivary ecosystems were maintained in tissue culture plate-based hydroxyapatite disc models (HDMs) and modified drip-flow biofilm reactors (MDFRs). Test compounds stannous fluoride (SF), SDS, triclosan (TCS), zinc lactate (ZL) and ZL with SF in combination (ZLSF) were delivered to the HDMs once and four times daily for 6 days to MDFRs. Plaques were characterized by differential viable counting and PCR–denaturing gradient gel electrophoresis (DGGE). TCS and SDS were the most effective compounds against HDM plaques, significantly reducing total viable counts (P<0.05), whilst SF, ZL and ZLSF were comparatively ineffective. TCS exhibited specificity for streptococci (P<0.01) and Gram-negative anaerobes (P<0.01) following a single dosing and also on repeated dosing in MDFRs. In contrast to single exposures, multiple dosing with ZLSF also significantly reduced all bacterial groups, whilst SF and ZL caused significant but transient reductions. According to PCR–DGGE analyses, significant (P<0.05) reductions in eubacterial diversity occurred following 6 day dosing with both TCS and ZLSF. Concordance of MDFR eubacterial profiles with salivary inocula ranged between 58 and 97 %. TCS and ZL(SF) exhibited similar specificities to those reported for formulations. TCS was the most potent antibacterial, after single and multiple dosage regimens.

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Heminger, Katherine, Michael Markey, Meldrick Mpagi, and Steven J. Berberich. "Alterations in gene expression and sensitivity to genotoxic stress following HdmX or Hdm2 knockdown in human tumor cells harboring wild-type p53." Aging 1, no. 1 (January 7, 2009): 89–108. http://dx.doi.org/10.18632/aging.100008.

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Yoon, Hyun-Jae, and Hyun-Seo Kang. "Optical Design of an Integrated Two-Channel Optical Transmitter for an HDMI interface." Korean Journal of Optics and Photonics 26, no. 5 (October 25, 2015): 269–74. http://dx.doi.org/10.3807/kjop.2015.26.5.269.

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Saorín, Jose Luis, Vicente Lopez-Chao, Jorge de la Torre-Cantero, and Manuel Drago Díaz-Alemán. "Computer Aided Design to Produce High-Detail Models through Low Cost Digital Fabrication for the Conservation of Aerospace Heritage." Applied Sciences 9, no. 11 (June 6, 2019): 2338. http://dx.doi.org/10.3390/app9112338.

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Aerospace heritage requires tools that allow its transfer and conservation beyond photographs and texts. The complexity of these engineering projects can be collected through digital graphic representation. Nevertheless, physical scale models provide additional information of high value when they involve full detailed information, for which the model in engineering was normally one more product of the manufacturing process, which entails a high cost. However, the standardization of digital fabrication allows the manufacture of high-detail models at low cost. For this reason, in this paper a case study of the graphic reengineering and planning stages for digital fabrication of a full-scale high-detail model (HDM) of the spatial instrument of the European Space Agency, named the Solar Orbiter mission Polarimetric and Helioseismic Imager (SO/PHI), is presented. After the analysis of this experience, seven stages of planning and graphic reengineering are proposed through collaborative work for the low cost digital manufacture of HDMs.

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Nguyen, Hai Dang, and Anja-Katrin Bielinsky. "HDM2 ERKs PCNA." Journal of Cell Biology 190, no. 4 (August 23, 2010): 487–89. http://dx.doi.org/10.1083/jcb.201007096.

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In this issue, a study by Groehler and Lannigan (2010. J. Cell Biol. doi:10.1083/jcb.201002124) sheds light on the regulation of proliferating cell nuclear antigen (PCNA) turnover and how it is counteracted by the small chromatin-bound kinase ERK8 (extracellular signal-regulated kinase 8). Importantly, inactivation of ERK8 results in genome instability and is associated with cell transformation.

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Baek, Seung Yeb. "Fatigue Life Evaluation on Compressive & Tensional Residual Stress Induced Materials and Residual Stress Measurement using Hole Drilling Method." Journal of the Korean Welding and Joining Society 31, no. 2 (April 30, 2013): 43–48. http://dx.doi.org/10.5781/kwjs.2013.31.2.43.

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Wergeland, Line, Kevin B. Spurgers, Eystein Oveland, Torill Høiby, Manel Cascallo, Tsuyoshi Honda, James B. Lorens, Guillermina Lozano, Timothy J. McDonnell, and Bjorn T. Gjertsen. "Bcl-2 Protects against p53-Induced Apoptosis through Hdm2." Blood 112, no. 11 (November 16, 2008): 5333. http://dx.doi.org/10.1182/blood.v112.11.5333.5333.

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Abstract Hdm2 is up-regulated in several malignancies including sarcomas and acute myeloid leukemia, where it counteracts the anti-proliferative and pro-apoptotic effect of wild type p53. The anti-apoptotic protein Bcl-2 is often elevated in many tumors with wild type p53 and serves to block p53-induced apoptosis. We demonstrate that the protein level of Hdm2 positively correlates with the level of Bcl-2 and follows the Bcl-2 level in different cell systems. Over-expression of Bcl-2 protects Hdm2 from DNA-damage induced degradation in a dose dependant manner. In addition, modulation of Bcl-2 by shRNA knockdown reduced the Hdm2 protein level in parallel. Consequently, treatment of AML cells with the Bcl-2 small inhibitory molecule HA14-1 attenuated the level of Hdm2. The Bcl-2 level, but not the DNA damage induced Hdm2 degradation, was affected by disruption of the E3 ubiquitin ligase activity of Hdm2. In addition, the DNA-damage induced Hdm2 down-regulation was blocked by disrupted E1 ubiquitin-activation, defect polyubiquitination and by proteasome inhibitors. Finally, we show that Bcl-2 protection from p53-induced cell death requires co-expression of Hdm2 in double null p53/mdm2 mouse embryonic fibroblasts. Our results indicate that Bcl-2 regulates the Hdm2 level and that Hdm2 is a key mediator in Bcl-2 inhibition of p53-induced apoptosis. This is of particular therapeutic interest for cancers displaying elevated Hdm2 and Bcl-2, like sarcoma and acute myeloid leukemia.

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Gama, Vivian, Jose A. Gomez, Lindsey D. Mayo, Arthur L. Haas, and Shigemi Matsuyama. "Hdm2 Is an Ubiquitin Ligase for the Anti-Apoptotic Protein Ku70." Blood 110, no. 11 (November 16, 2007): 3347. http://dx.doi.org/10.1182/blood.v110.11.3347.3347.

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Abstract Protection of endothelial cells (ECs) from inappropriate apoptosis induced by various stresses (e.g. drugs, parasites, and reactive oxygen species) is necessary to maintain homeostasis. On the other hand, blockade of angiogenesis in malignant tissue is a promising strategy to fight against cancer. However, the molecular mechanism of survival control of ECs is not well understood. Bax is a key mediator of apoptosis in various cell types including ECs. Ku70 is a subunit of the Ku complex involved in DNA repair and is ubiquitously expressed. Recently, we found that the cytosolic form of Ku70 binds Bax and inhibits Bax-mediated apoptosis, and that the decrease of cytosolic Ku70 is necessary to activate Bax. Furthermore, we reported that ubiquitin-dependent Ku70 proteolysis is involved in Ku70 decrease in ECs treated by genotoxic stresses. The remaining important problem was the identification of Ku70 ubiquitin ligase decreasing Ku70 to activate Bax in ECs. Here we report evidences showing that Hdm2 is an ubiquitin ligase of Ku70. It is known that Hdm2 ubiquitinylates p53, a tumor suppressor protein, and that Hdm2 level increases in response to DNA damage. Using purified recombinant proteins, we confirmed that Hdm2 conjugates ubiquitin chains to Ku70. Hdm2 overexpression in human umbilical vein endothelial cells (HUVECs) induced Ku70 decrease. Genotoxic stress (i.e. etoposide treatment) induced Ku70 decrease in Mdm2 (mouse version of Hdm2)-proficient mouse embryonic fibroblasts (MEFs) whereas Ku70 decrease was significantly suppressed in Mdm2-deficient MEFs. We verified Ku70-Hdm2 association by immunoprecipitation and GST pull-downs. Nutlin-3, a well-characterized inhibitor of Hdm2-p53 interaction, effectively disrupted Hdm2-Ku70 interaction, suggesting that Hdm2 uses the same domain to bind both p53 and Ku70. In cancer cells, it has been reported that the survival kinase Akt phosphorylates Hdm2, and that this phosphorylation stimulates nuclear translocation of Hdm2 to ubiquitinylate and inactivate p53 in the nucleus. We investigated whether Akt-dependent phosphorylation of Hdm2 influences its activity to regulate Ku70 level in HUVECs. Vascular endothelial growth factor (VEGF) is known to increase ECs survival through Akt activation. Thus, VEGF was employed as a physiological activator of Akt. VEGF inhibited etoposide-induced Ku70 degradation in HUVECs. Importantly, VEGF stimulated nuclear localization of Hdm2. Constitutively active AKT, which has been reported to induce Hdm2 nuclear translocation, but not the dominant negative AKT, efficiently inhibited Ku70 degradation. Moreover, an Akt phosphorylation resistant mutant of Hdm2 was able to down-regulate Ku70 but not p53 in HUVECs, suggesting a differential mechanism of regulation for these two substrates. In addition, Hdm2 mutant without ubiquitin ligase activity did not decrease Ku70 or p53, supporting the hypothesis that Hdm2 directly modulates these proteins. Taken together, we propose that Hdm2 acts as a Ku70 ubiquitin ligase, and that VEGF-mediated activation of Akt prevents cytosolic Ku70 ubiquitinylation by Hdm2 probably by inducing Hdm2 translocation into the nucleus. Our results suggest that Ku70 level in ECs is controlled by the balance of DNA damage-induced factor (Hdm2 and p53) and survival kinase (Akt), and that Ku70 plays an important role in the decision making process of apoptosis induction in ECs.

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Evans, Susan C., Meena Viswanathan, Jason D. Grier, Meera Narayana, Adel K. El-Naggar, and Guillermina Lozano. "An alternatively spliced HDM2 product increases p53 activity by inhibiting HDM2." Oncogene 20, no. 30 (July 2001): 4041–49. http://dx.doi.org/10.1038/sj.onc.1204533.

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Wergeland, Line, Eystein Oveland, Gry Sjoholt, Siv Lise Bedringaas, Randi T. Hovland, Oystein Bruserud, and Bjorn T. Gjertsen. "Flt3 Mutations in Proximity to an Ubiquitin Dependent Endocytosis Motif Suspend Its Hdm2 Modulation." Blood 110, no. 11 (November 16, 2007): 4320. http://dx.doi.org/10.1182/blood.v110.11.4320.4320.

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Abstract Acute myeloid leukemia (AML) frequently features mutations in the receptor tyrosine kinase Flt3 and elevated expression of the oncogenic E3 ubiquitin ligase Hdm2. Additional to the p53 inhibitory effect of Hdm2, Hdm2 appears involved in endocytosis of cell surface receptors. In this study we explore the possibility of Flt3 modulation by Hdm2 in primary AML cells and cell lines (NB4 and MV4–11) with wild type Flt3 (Flt3-wt) or mutated Flt3 (Flt3-ITD). Flt3 ligand (FL), small molecular inhibitors and small interfering RNA (siRNA) were used to elucidate the relation between Flt3 and Hdm2 on protein level, mRNA expression and modulation of apoptosis. The basal level of Flt3 is higher in AML patients with Flt3-ITD than in patients with Flt3-wt. Flt3-ITD affects a ubiquitin endocytosis motif that in some patients are duplicated, possibly resulting in enhanced receptor cycling. Down-regulation of Flt3-wt by FL, small interfering RNA or PKC412 resulted in elevated level of Hdm2. Similarly, Hdm2 attenuation resulted in increased Flt3 protein expression. Flt3-ITD responded less to Flt3 down-regulation, and was only weakly responding to Hdm2 modulation. We demonstrate that modulation of Flt3 or Hdm2 results in reciprocal regulation, and that Flt3 with internal tandem duplications may suspend its Hdm2 modulation. Together, Flt3-ITD results in dysregulated receptor turnover and elevated Hdm2 thus interconnecting the two pathways of Flt3 and p53, both related to chemoresistance in AML.

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Kallen, Joerg, Aude Izaac, Suzanne Chau, Emmanuelle Wirth, Joseph Schoepfer, Robert Mah, Achim Schlapbach, et al. "Front Cover: Structural States of Hdm2 and HdmX: X‐ray Elucidation of Adaptations and Binding Interactions for Different Chemical Compound Classes (ChemMedChem 14/2019)." ChemMedChem 14, no. 14 (July 17, 2019): 1304. http://dx.doi.org/10.1002/cmdc.201900400.

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Sehdev, Vikas, Abbes Belkhiri, Mohammed Soutto, Ahmed M. Katsha, and Wael El-Rifai. "Regulation of HDM2 E3-ubiquitin ligase in esophageal adenocarcinoma cells by AURKA." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 35. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.35.

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Abstract:

35 Background: Esophageal adenocarcinomas (EAC) exhibit intrinsic resistance against chemotherapy. AURKA regulates cell cycle progression and its overexpression is associated with oncogenic transformation. We have recently reported that AURKA is significantly overexpressed in about 70% of human EAC tissue samples and EAC cell lines. We have previously shown that AURKA inhibits p53- and p73-mediated apoptotic pathways in GI adenocarcinomas. HDM2 is an E3-ubiquitin ligase which is closely involved in regulating p53 and p73 protein stability and activity. In this study we demonstrate that AURKA directly interacts with HDM2 and regulates HDM2 protein expression and phosphorylation in both FLO-1 and OE33 EAC cells. Methods and Results: Western blot analyses were done following AURKA overexpression with adenovirus, knockdown with si-RNA or inhibition with MLN 8237 (0.5µM) in FLO-1 and OE33 EAC cell lines. The data indicated that overexpression of AURKA induced both total and phospho-HDM2-(Ser166) protein levels. Knockdown or inhibition of AURKA significantly decreased expression of both total and phospho-HDM2-(Ser166) protein levels in FLO-1 and OE33 EAC cells. Additionally, following adenovirus mediated overexpression of AURKA, co-immunoprecipitaion (Co-IP) was done for AURKA and HDM2 in FLO-1 and OE33 EAC cells. The two-way Co-IP data indicated the presence of HDM2 in a complex associated with AURKA and vice-versa. The data from in vitro protein kinase assay indicated that recombinant AURKA directly phosphorylates recombinant HDM2 at Ser166 site. To confirm direct interaction between recombinant AURKA and HDM2 proteins we performed IP following the in vitro kinase assay. The in vitro kinase IP data indicates that kinase intact recombinant AURKA directly interacts and phosphorylates recombinant HDM2 protein. Conclusions: Our data indicate that AURKA regulates HDM2 expression and phosphorylation in both FLO-1 and OE33 EAC cells. Additionally, we also report for the first time that AURKA directly interacts with HDM2 and phosphorylates it at Ser166 site. Therefore, our study suggests that AURKA-mediated regulation of HDM2 could be the major underlying mechanism for induction of apoptosis in p53-negative EAC.

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