Relevant bibliographies by topics / Heat-mediated release

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Academic literature on the topic 'Heat-mediated release'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Heat-mediated release"

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Cantet, Juan M., Zhantao Yu, and Agustín G. Ríus. "Heat Stress-Mediated Activation of Immune–Inflammatory Pathways." Antibiotics 10, no. 11 (2021): 1285. http://dx.doi.org/10.3390/antibiotics10111285.

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Physiological changes in animals exposed to elevated ambient temperature are characterized by the redistribution of blood toward the periphery to dissipate heat, with a consequent decline in blood flow and oxygen and nutrient supply to splanchnic tissues. Metabolic adaptations and gut dysfunction lead to oxidative stress, translocation of lumen contents, and release of proinflammatory mediators, activating a systemic inflammatory response. This review discusses the activation and development of the inflammatory response in heat-stressed models.
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Zhang, W., and P. J. Lachmann. "Neutrophil lactoferrin release induced by IgA immune complexes can be mediated either by Fc alpha receptors or by complement receptors through different pathways." Journal of Immunology 156, no. 7 (1996): 2599–606. http://dx.doi.org/10.4049/jimmunol.156.7.2599.

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Abstract Our previous results showed that neutrophil secondary granule release, indicated by release of lactoferrin, was a slow process when induced by IgA immune complexes (IC) formed in heat-inactivated serum, but became very fast if IgA IC were formed in normal human serum. This phenomenon did not apply to the IC of other Ab isotypes. In this paper, we demonstrate that the fast lactoferrin release is caused by complement, mainly due to the deposition of C3b and iC3b on IgA IC. Either CR1 or CR3 can mediate the response and both receptors have to be blocked to prevent it. Complement also inf
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Obi, Syotaro, Toshiaki Nakajima, Takaaki Hasegawa, et al. "Heat induces interleukin-6 in skeletal muscle cells via TRPV1/PKC/CREB pathways." Journal of Applied Physiology 122, no. 3 (2017): 683–94. http://dx.doi.org/10.1152/japplphysiol.00139.2016.

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Interleukin-6 (IL-6) is released from skeletal muscle cells and induced by exercise, heat, catecholamine, glucose, lipopolysaccharide, reactive oxygen species, and inflammation. However, the mechanism that induces release of IL-6 from skeletal muscle cells remains unknown. Thermosensitive transient receptor potential (TRP) proteins such as TRPV1–4 play vital roles in cellular functions. In this study we hypothesized that TRPV1 senses heat, transmits a signal into the nucleus, and produces IL-6. The purpose of the present study is to investigate the underlying mechanisms whereby skeletal muscle
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Saikia, Nabanita, Anupam Nath Jha, and Ramesh Ch Deka. "Dynamics of Fullerene-Mediated Heat-Driven Release of Drug Molecules from Carbon Nanotubes." Journal of Physical Chemistry Letters 4, no. 23 (2013): 4126–32. http://dx.doi.org/10.1021/jz402231p.

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Iga, Katsumi, Naoru Hamaguchi, Yasutaka Igari, Yasuaki Ogawa, Hajime Toguchi, and Tsugio Shimamoto. "Heat-specific drug release of large unilamellar vesicle as hyperthermia-mediated targeting delivery." International Journal of Pharmaceutics 57, no. 3 (1989): 241–51. http://dx.doi.org/10.1016/0378-5173(89)90214-7.

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Coaxum, Sonya D., Tina M. Griffin, Jody L. Martin та Ruben Mestril. "Influence of PKC-α overexpression on HSP70 and cardioprotection". American Journal of Physiology-Heart and Circulatory Physiology 292, № 5 (2007): H2220—H2226. http://dx.doi.org/10.1152/ajpheart.01080.2006.

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Recent research has indicated that the protein kinase C (PKC) isoforms and the heat shock proteins (HSPs) are involved in cardioprotection. We have investigated the possible interaction between these two protein families. We have found that adenoviral-mediated expression of PKC-α in neonatal rat ventricular myocytes (NRVM) not only increases the expression of HSP70 but also protects against simulated ischemia-reperfusion. In addition, Western blots of PKC-α-infected NRVM indicated that other HSPs are not induced in the same manner as HSP70. In an effort to determine the mechanism of induction
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Crane, John K., Shilpa S. Choudhari, Tonniele M. Naeher, and Michael E. Duffey. "Mutual Enhancement of Virulence by Enterotoxigenic and Enteropathogenic Escherichia coli." Infection and Immunity 74, no. 3 (2006): 1505–15. http://dx.doi.org/10.1128/iai.74.3.1505-1515.2006.

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ABSTRACT Enterotoxigenic Escherichia coli (ETEC) and enteropathogenic E. coli (EPEC) are common causes of diarrhea in children in developing countries. Dual infections with both pathogens have been noted fairly frequently in studies of diarrhea around the world. In previous laboratory work, we noted that cholera toxin and forskolin markedly potentiated EPEC-induced ATP release from the host cell, and this potentiated release was found to be mediated by the cystic fibrosis transmembrane conductance regulator. In this study, we examined whether the ETEC heat-labile toxin (LT) or the heat-stable
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Takagi, Satoshi, Yuki Sasaki, Sumie Koike, et al. "Platelet-derived lysophosphatidic acid mediated LPAR1 activation as a therapeutic target for osteosarcoma metastasis." Oncogene 40, no. 36 (2021): 5548–58. http://dx.doi.org/10.1038/s41388-021-01956-6.

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AbstractOsteosarcoma is the most common primary malignant bone cancer, with high rates of pulmonary metastasis. Osteosarcoma patients with pulmonary metastasis have worse prognosis than those with localized disease, leading to dramatically reduced survival rates. Therefore, understanding the biological characteristics of metastatic osteosarcoma and the molecular mechanisms of invasion and metastasis of osteosarcoma cells will lead to the development of innovative therapeutic intervention for advanced osteosarcoma. Here, we identified that osteosarcoma cells commonly exhibit high platelet activ
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Gupta, Sanjiv, and A. A. Knowlton. "HSP60 trafficking in adult cardiac myocytes: role of the exosomal pathway." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (2007): H3052—H3056. http://dx.doi.org/10.1152/ajpheart.01355.2006.

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The heat shock proteins (HSP) are a highly conserved family of proteins with critical functions in protein folding, protein trafficking, and cell signaling. These proteins also protect the cell against injury. HSP60 has been found in the extracellular space and has been identified in the plasma of some individuals. HSP60 is thought to be a “danger signal” to the immune system and is also highly immunogenic. Thus extracellular HSP60 is possibly toxic to the cell. The mechanism by which HSP60 is released into the extracellular space is unknown, as is whether it is released by cardiac myocytes. W
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Kelly, Ryan M., Jianmin Chen, Lauren E. Yauch, and Stuart M. Levitz. "Opsonic Requirements for Dendritic Cell-Mediated Responses to Cryptococcus neoformans." Infection and Immunity 73, no. 1 (2005): 592–98. http://dx.doi.org/10.1128/iai.73.1.592-598.2005.

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ABSTRACT The encapsulated pathogenic yeast Cryptococcus neoformans is poorly recognized by phagocytic cells in the absence of opsonins. Macrophages will bind and internalize complement- or antibody-opsonized C. neoformans; however, less is known about the role of opsonins in dendritic cell (DC)-mediated recognition of the organism. Thus, we studied the opsonic requirements for binding to C. neoformans by cultured human monocyte-derived and murine bone marrow-derived DCs and whether binding leads to antifungal activity and cytokine release. Binding of unopsonized C. neoformans to human and muri
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Book chapters on the topic "Heat-mediated release"

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Brendler Goettems Fiorin, Pauline, Mirna Stela Ludwig, Matias Nunes Frizzo, and Thiago Gomes Heck. "Environmental Particulate Air Pollution Exposure and the Oxidative Stress Responses: A Brief Review of the Impact on the Organism and Animal Models of Research." In Reactive Oxygen Species [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101394.

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Particulate matter (PM) is a mixture of solid particles and liquid droplets found in the air, and it is one of the most harmful air pollutants. When inhaled, it affects the pulmonary system, cardiovascular systems, and other tissues. The size, composition, and deposition of PM, mainly related to fine and ultrafine particulate matter, are factors that determine the harmful effects of exposure to particles. Among the main effects is the inducer of ROS production, and consequently oxidative tissue damage in target organs and other responses, mediated by inflammatory cytokines and cellular stress
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Tiwari, Mr Prabhakar Singh. "Basic Mechanism Involved in the Process of Inflammation and Repair-I." In Edited Book of Pathophysiology. Iterative International Publishers, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/nbennurebch3.

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Inflammation is a complex biological response of vascular tissues to harmful stimuli such as pathogens, damaged cells, or irritants. It serves as a protective mechanism aimed at removing the injurious stimuli and initiating the healing process. The clinical signs of inflammation, famously described by the Roman physician Celsus, include redness (rubor), heat (calor), swelling (tumor), and pain (dolor), with loss of function (functio laesa) later added by Galen. Inflammation can be classified into two main types: acute and chronic. Acute inflammation is the immediate response to injury, charact
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Conference papers on the topic "Heat-mediated release"

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Ribes, J. A., D. D. Wagner, and C. W. Francis. "FIBRIN-STIMULATED RELEASE OF VON WILLEBRAND FACTOR FROM ENDOTHELIAL CELLS IS LINKED TO FIBRINOPEPTIDE B CLEAVAGE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643772.

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von Willebrand factor (vWf) is synthesized in endothelial cells and stored in specialized organelles, the Weibel-Palade bodies. We have examined the role of fibrin as a potential physiological secretagogue of vWf from Weibel-Palade bodies using indirect immunofluorescence staining of endothelial cells to detect release. Addition of fibrinogen to endothelial cell cultures resulted in the formation of a clot, and this was temporally associated with vWf release. Addition to endothelial cells of preformed fibrin prepared by clotting fibrinogen with thrombin also stimulated release of vWf within 10
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Reports on the topic "Heat-mediated release"

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Lichter, Amnon, Joseph L. Smilanick, Dennis A. Margosan, and Susan Lurie. Ethanol for postharvest decay control of table grapes: application and mode of action. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7587217.bard.

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Original objectives: Dipping of table grapes in ethanol was determined to be an effective measure to control postharvest gray mold infection caused by Botrytis cinerea. Our objectives were to study the effects of ethanol on B.cinerea and table grapes and to conduct research that will facilitate the implementation of this treatment. Background: Botrytis cinerea is known as the major pathogen of table grapes in cold storage. To date, the only commercial technology to control it relied on sulfur dioxide (SO₂) implemented by either fumigation of storage facilities or from slow release generator pa
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