Journal articles: 'MODULATING RESPONSES'

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Hariri, Ahmad R., Susan Y. Bookheimer, and John C. Mazziotta. "Modulating emotional responses." NeuroReport 11, no. 1 (January 2000): 43–48. http://dx.doi.org/10.1097/00001756-200001170-00009.

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Leder, Christoph, Melanie Ziegler, and Meinrad Gawaz. "Modulating Immune Responses and Inflammation." Seminars in Thrombosis and Hemostasis 36, no. 02 (March 2010): 219–22. http://dx.doi.org/10.1055/s-0030-1251507.

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Wen, Ya-Chien, and Chen-Gia Tsai. "The effect of harmonization on cortical magnetic responses evoked by music of rapidly changing tonalities." Psychology of Music 45, no. 1 (July 7, 2016): 22–35. http://dx.doi.org/10.1177/0305735616639386.

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The act of shifting from one key to another is termed tonal modulation, which has been used to articulate emotion expressions and formal structures in Western music. The present study recorded cortical activity to examine how the auditory-evoked magnetic fields are affected by harmonizing music of rapidly changing tonalities. Participants were asked to covertly sing the pitch names of well-learned modulating melodies along with the harmonized or unharmonized melodies. In our musical stimuli, three flats were added to the key signature for every four beats. Such a rapid modulation is achieved by a chromatic inflection of the submediant tone between the third and fourth beats. Tonal modulations with such chromatic progressions are termed chromatic modulations. A major finding was that the amplitude of N1m (neuromagnetic response at approximately 110 ms after the onset of a stimulus) was significantly reduced by harmonization only when a modulation occurred. We also observed that harmonization enhanced the P2m (neuromagnetic response at approximately 200 ms after the onset of a stimulus) amplitude. The results provide evidence of the impacts of harmonization on attention efforts and pitch categorization.

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Matsuzaki, Takeshi, and James Chin. "Modulating immune responses with probiotic bacteria." Immunology and Cell Biology 78, no. 1 (February 2000): 67–73. http://dx.doi.org/10.1046/j.1440-1711.2000.00887.x.

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Batty, Matthew J., Gwladys Chabrier, Alanah Sheridan, and Matthew C. Gage. "Metabolic Hormones Modulate Macrophage Inflammatory Responses." Cancers 13, no. 18 (September 17, 2021): 4661. http://dx.doi.org/10.3390/cancers13184661.

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Macrophages are phagocytotic leukocytes that play an important role in the innate immune response and have established roles in metabolic diseases and cancer progression. Increased adiposity in obese individuals leads to dysregulation of many hormones including those whose functions are to coordinate metabolism. Recent evidence suggests additional roles of these metabolic hormones in modulating macrophage inflammatory responses. In this review, we highlight key metabolic hormones and summarise their influence on the inflammatory response of macrophages and consider how, in turn, these hormones may influence the development of different cancer types through the modulation of macrophage functions.

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Radtke, Franziska A., Gareth Chapman, Jeremy Hall, and Yasir A. Syed. "Modulating Neuroinflammation to Treat Neuropsychiatric Disorders." BioMed Research International 2017 (2017): 1–21. http://dx.doi.org/10.1155/2017/5071786.

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Neuroinflammation is recognised as one of the potential mechanisms mediating the onset of a broad range of psychiatric disorders and may contribute to nonresponsiveness to current therapies. Both preclinical and clinical studies have indicated that aberrant inflammatory responses can result in altered behavioral responses and cognitive deficits. In this review, we discuss the role of inflammation in the pathogenesis of neuropsychiatric disorders and ask the question if certain genetic copy-number variants (CNVs) associated with psychiatric disorders might play a role in modulating inflammation. Furthermore, we detail some of the potential treatment strategies for psychiatric disorders that may operate by altering inflammatory responses.

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Kasahara, S., H. Wago, and E. L. Cooper. "Dissociation of Innate and Adaptive Immunity by UVB Irradiation." International Journal of Immunopathology and Pharmacology 15, no. 1 (January 2002): 1–11. http://dx.doi.org/10.1177/039463200201500101.

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Increasing ultraviolet-B irradiation (UVB) resulting from diminution of stratospheric ozone is becoming a serious international problem. UVB irradiation exerts not only carcinogenic effects on animals but also causes them to become vulnerable to infections by modulating their immune responses. UVB irradiation suppresses innate immune functions of cells such as macrophages, neutrophils, Langerhans cells, dendritic cells, and the serum component, complement. UVB irradiation also causes changes in cytokine profiles, represented by the induction of a paradigm switch involving Th1/Th2 phenotypes. According to earlier studies, Th1 responses are suppressed, whereas Th2 activities are augmented by UVB irradiation. These immune modulations are caused by several pathways via cytokines and neuropeptides, and eventually may lead to increasing incidences of infection, allergy, and cancer. We have reviewed reports concerning UVB-irradiation induced immune modulation from the viewpoint of risks for human diseases and, in addition, for ecosystems and immunity of lower animals.

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Warren, Daniel, Christopher Simpkins, Matthew Cooper, and Robert Montgomery. "Modulating Alloimmune Responses with Plasmapheresis and IVIG." Current Drug Target -Cardiovascular & Hematological Disorders 5, no. 3 (June 1, 2005): 215–22. http://dx.doi.org/10.2174/1568006054064735.

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Ringertz, BO. "NEUTROPHIL AGGREGATION - FACTORS MODULATING STIMULUS-SPECIFIC RESPONSES." Acta Pathologica Microbiologica Scandinavica Series C: Immunology 94C, no. 1-6 (August 15, 2009): 1–9. http://dx.doi.org/10.1111/j.1699-0463.1986.tb02082.x.

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Menon, Ashwathi Puravankara, Beatriz Moreno, Daniel Meraviglia-Crivelli, Francesca Nonatelli, Helena Villanueva, Martin Barainka, Angelina Zheleva, Hisse M. van Santen, and Fernando Pastor. "Modulating T Cell Responses by Targeting CD3." Cancers 15, no. 4 (February 13, 2023): 1189. http://dx.doi.org/10.3390/cancers15041189.

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Harnessing the immune system to fight cancer has become a reality with the clinical success of immune-checkpoint blockade (ICB) antibodies against PD(L)-1 and CTLA-4. However, not all cancer patients respond to ICB. Thus, there is a need to modulate the immune system through alternative strategies for improving clinical responses to ICB. The CD3-T cell receptor (TCR) is the canonical receptor complex on T cells. It provides the “first signal” that initiates T cell activation and determines the specificity of the immune response. The TCR confers the binding specificity whilst the CD3 subunits facilitate signal transduction necessary for T cell activation. While the mechanisms through which antigen sensing and signal transduction occur in the CD3–TCR complex are still under debate, recent revelations regarding the intricate 3D structure of the CD3–TCR complex might open the possibility of modulating its activity by designing targeted drugs and tools, including aptamers. In this review, we summarize the basis of CD3–TCR complex assembly and survey the clinical and preclinical therapeutic tools available to modulate CD3–TCR function for potentiating cancer immunotherapy.

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Deepa, Chandran, and R. Shekhar. "Effect of Premedication with Intravenous Clonidine in Modulating the Haemodyanamic Responses during Laparoscopic Surgeries." Indian Journal of Anesthesia and Analgesia 5, no. 4 (2018): 545–53. http://dx.doi.org/10.21088/ijaa.2349.8471.5418.7.

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Qin, Ming, Guangsheng Du, and Xun Sun. "Biomimetic cell-derived nanocarriers for modulating immune responses." Biomaterials Science 8, no. 2 (2020): 530–43. http://dx.doi.org/10.1039/c9bm01444f.

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Tomita, Tadakimi, Rebekah B. Guevara, Lamisha M. Shah, Andrews Y. Afrifa, and Louis M. Weiss. "Secreted Effectors Modulating Immune Responses to Toxoplasma gondii." Life 11, no. 9 (September 20, 2021): 988. http://dx.doi.org/10.3390/life11090988.

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Toxoplasma gondii is an obligate intracellular parasite that chronically infects a third of humans. It can cause life-threatening encephalitis in immune-compromised individuals. Congenital infection also results in blindness and intellectual disabilities. In the intracellular milieu, parasites encounter various immunological effectors that have been shaped to limit parasite infection. Parasites not only have to suppress these anti-parasitic inflammatory responses but also ensure the host organism’s survival until their subsequent transmission. Recent advancements in T. gondii research have revealed a plethora of parasite-secreted proteins that suppress as well as activate immune responses. This mini-review will comprehensively examine each secreted immunomodulatory effector based on the location of their actions. The first section is focused on secreted effectors that localize to the parasitophorous vacuole membrane, the interface between the parasites and the host cytoplasm. Murine hosts are equipped with potent IFNγ-induced immune-related GTPases, and various parasite effectors subvert these to prevent parasite elimination. The second section examines several cytoplasmic and ER effectors, including a recently described function for matrix antigen 1 (MAG1) as a secreted effector. The third section covers the repertoire of nuclear effectors that hijack transcription factors and epigenetic repressors that alter gene expression. The last section focuses on the translocation of dense-granule effectors and effectors in the setting of T. gondii tissue cysts (the bradyzoite parasitophorous vacuole).

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La Torre, Maria Ester, Maria Antonietta Panaro, Melania Ruggiero, Rita Polito, Antonia Cianciulli, Francesca Martina Filannino, Dario Domenico Lofrumento, et al. "Extracellular Vesicles Cargo in Modulating Microglia Functional Responses." Biology 11, no. 10 (September 29, 2022): 1426. http://dx.doi.org/10.3390/biology11101426.

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Extracellular vesicles (EVs) represent a heterogeneous group of membranous structures derived from cells that are released by all cell types, including brain cells. EVs are now thought to be an additional mechanism of intercellular communication. Both under normal circumstances and following the addition of proinflammatory stimuli, microglia release EVs, but the contents of these two types of EVs are different. Microglia are considered the brain-resident immune cells that are involved in immune surveillance and inflammatory responses in the central nervous system. In this research, we have analyzed the effects of EVs isolated from microglia in response to LPS (Lipopolysaccharide) on microglia activation. The EVs produced as result of LPS stimulation, knows as EVs-LPS, were then used as stimuli on microglia BV2 resting cells in order to investigate their ability to induce microglia to polarize towards an inflammatory state. After EVs-LPS stimulation, we analyzed the change to BV2 cells’ morphology, proliferation, and migration, and investigated the expression and the release of pro-inflammatory cytokines. The encouraging findings of this study showed that EVs-LPS can activate microglia in a manner similar to that of LPS alone and that EVs derived from control cells cannot polarize microglia towards a pro-inflammatory state. This study has confirmed the critical role of EVs in communication and shown how EVs produced in an inflammatory environment can exacerbate the inflammatory process by activating microglia, which may have an impact on all brain cells.

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Rudra, Jai S., Tao Sun, Katelyn C. Bird, Melvin D. Daniels, Joshua Z. Gasiorowski, Anita S. Chong, and Joel H. Collier. "Modulating Adaptive Immune Responses to Peptide Self-Assemblies." ACS Nano 6, no. 2 (January 30, 2012): 1557–64. http://dx.doi.org/10.1021/nn204530r.

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Lewis, P. "Polynucleotide vaccines in animals: enhancing and modulating responses." Vaccine 15, no. 8 (June 1997): 861–64. http://dx.doi.org/10.1016/s0264-410x(96)00279-4.

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Nabors, G. S. "Modulating ongoing Th2-cell responses in experimental leishmaniasis." Parasitology Today 13, no. 2 (February 1997): 76–79. http://dx.doi.org/10.1016/s0169-4758(96)10078-8.

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Demirovic, Dino, Sylvianne Schnebert, Carine Nizard, and Suresh I. S. Rattan. "Cellular stress responses for monitoring and modulating ageing." Free Radical Biology and Medicine 65 (September 2013): S28. http://dx.doi.org/10.1016/j.freeradbiomed.2013.08.023.

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Cox, Eric, Frank Verdonck, Daisy Vanrompay, and Bruno Goddeeris. "Adjuvants modulating mucosal immune responses or directing systemic responses towards the mucosa." Veterinary Research 37, no. 3 (April 14, 2006): 511–39. http://dx.doi.org/10.1051/vetres:2006014.

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Uwazie, Crystal C., Tyler U. Faircloth, Rhett N. Parr, Yenamala U. Reddy, Peiman Hematti, Devi Rajan, and Raghavan Chinnadurai. "Contrariety of Human Bone Marrow Mesenchymal Stromal Cell Functionality in Modulating Circulatory Myeloid and Plasmacytoid Dendritic Cell Subsets." Biology 12, no. 5 (May 16, 2023): 725. http://dx.doi.org/10.3390/biology12050725.

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Mesenchymal Stromal Cells (MSCs) derived from bone marrow are widely tested in clinical trials as a cellular therapy for potential inflammatory disorders. The mechanism of action of MSCs in mediating immune modulation is of wide interest. In the present study, we investigated the effect of human bone-marrow-derived MSCs in modulating the circulating peripheral blood dendritic cell responses through flow cytometry and multiplex secretome technology upon their coculture ex vivo. Our results demonstrated that MSCs do not significantly modulate the responses of plasmacytoid dendritic cells. However, MSCs dose-dependently promote the maturation of myeloid dendritic cells. Mechanistic analysis showed that dendritic cell licensing cues (Lipopolysaccharide and Interferon-gamma) stimulate MSCs to secret an array of dendritic cell maturation-associated secretory factors. We also identified that MSC-mediated upregulation of myeloid dendritic cell maturation is associated with the unique predictive secretome signature. Overall, the present study demonstrated the dichotomy of MSC functionality in modulating myeloid and plasmacytoid dendritic cells. This study provides clues that clinical trials need to investigate if circulating dendritic cell subsets in MSC therapy can serve as potency biomarkers.

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Flood, Michael D., Johnnie M. Moore-Dotson, and Erika D. Eggers. "Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells." Journal of Neurophysiology 120, no. 2 (August 1, 2018): 867–79. http://dx.doi.org/10.1152/jn.00855.2017.

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Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses from rod bipolar cells, whereas D1 receptor blockade during light adaptation partially prevented this decline. To determine what mechanisms were involved in the modulation of inhibitory light responses, we measured the effect of D1 receptor activation on spontaneous currents and currents evoked from electrically stimulating amacrine cell inputs to rod bipolar cells. D1 receptor activation decreased the frequency of spontaneous inhibition with no change in event amplitudes, suggesting a presynaptic change in amacrine cell activity in agreement with previous reports that rod bipolar cells lack D1 receptors. Additionally, we found that D1 receptor activation reduced the amplitude of electrically evoked responses, showing that D1 receptors can modulate amacrine cells directly. Our results suggest that D1 receptor activation can replicate a large portion but not all of the effects of light adaptation, likely by modulating release from amacrine cells onto rod bipolar cells. NEW & NOTEWORTHY We demonstrated a new aspect of dopaminergic signaling that is involved in mediating light adaptation of retinal inhibition. This D1 receptor-dependent mechanism likely acts through receptors located directly on amacrine cells, in addition to its potential role in modulating the strength of serial inhibition between amacrine cells. Our results also suggest that another D2/D4 receptor-dependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

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Chun, Sangjun, Massoud Daheshia, Nelly A. Kuklin, and Barry T. Rouse. "Modulation of Viral Immunoinflammatory Responses with Cytokine DNA Administered by Different Routes." Journal of Virology 72, no. 7 (July 1, 1998): 5545–51. http://dx.doi.org/10.1128/jvi.72.7.5545-5551.1998.

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ABSTRACT The efficacy of plasmid DNA encoding cytokine administered by different routes, systemic or surface exposure, was evaluated and compared for their modulating effects on subsequent lesions caused by infection with herpes simplex virus (HSV). Systemic or topical administration of both interleukin-4 (IL-4) and IL-10 DNA but not IL-2 DNA caused a long-lasting suppression of HSV-specific delayed-type hypersensitivity response. IL-4 or IL-10 DNA preadministration also modulated the expression of immunoinflammatory lesions associated with corneal infection of HSV. Suppression of ocular lesions required that the DNA be administered to the nasal mucosa or ocular surfaces and was not evident after intramuscular administration. The modulating effect of IL-10 DNA was most evident after topical ocular administration, whereas the effects of IL-4 DNA given by both routes appeared to be equal. Preexposure of IL-4 DNA, but not IL-10 DNA, resulted in a significant change in Th subset balance following HSV infection. Our results indicate that the modulating effect of IL-4 or IL-10 DNA may proceed by different mechanisms. Furthermore, our results suggest that surface administration of cytokine DNA is a convenient means of modulating immunoinflammatory lesions.

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Menezes, Carla M. S., Karin Kirchgatter, Sílvia M. Di Santi, Carine Savalli, Fabíola G. Monteiro, Gilberto A. Paula, and Elizabeth I. Ferreira. "In vitro evaluation of verapamil and other modulating agents in Brazilian chloroquine-resistant Plasmodium falciparum isolates." Revista da Sociedade Brasileira de Medicina Tropical 36, no. 1 (January 2003): 5–9. http://dx.doi.org/10.1590/s0037-86822003000100002.

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Verapamil, was assayed to record its modulating effect upon Brazilian Plasmodium falciparum isolates resistant to chloroquine. Other cardiovascular drugs known to be modulating agents in resistant malaria and/or multidrug-resistant neoplasias, including nifedipine, nitrendipine, diltiazem and propranolol, were also evaluated. Concentrations similar to those for cardiovascular therapy were used in the in vitro microtechnique for antimalarial drug susceptibility. Intrinsic antiplasmodial activity was observed from the lowest concentrations without a significant modulating action. Other reported modulating agents, such as the antipsychotic drug trifluoperazine and the antidepressants desipramine and imipramine, demonstrated similar responses under the same experimental conditions. Results suggest a much higher susceptibility of Brazilian strains, as well as an indifferent behaviour in relation to modulating agents.

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Choi, Seungyeop, Kwanhwi Ko, Jongwon Lim, Sung Kim, Sung-Hun Woo, Yoon Kim, Jaehong Key, Sei Lee, In Park, and Sang Lee. "Non-Linear Cellular Dielectrophoretic Behavior Characterization Using Dielectrophoretic Tweezers-Based Force Spectroscopy inside a Microfluidic Device." Sensors 18, no. 10 (October 19, 2018): 3543. http://dx.doi.org/10.3390/s18103543.

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Characterization of cellular dielectrophoretic (DEP) behaviors, when cells are exposed to an alternating current (AC) electric field of varying frequency, is fundamentally important to many applications using dielectrophoresis. However, to date, that characterization has been performed with monotonically increasing or decreasing frequency, not with successive increases and decreases, even though cells might behave differently with those frequency modulations due to the nonlinear cellular electrodynamic responses reported in previous works. In this report, we present a method to trace the behaviors of numerous cells simultaneously at the single-cell level in a simple, robust manner using dielectrophoretic tweezers-based force spectroscopy. Using this method, the behaviors of more than 150 cells were traced in a single environment at the same time, while a modulated DEP force acted upon them, resulting in characterization of nonlinear DEP cellular behaviors and generation of different cross-over frequencies in living cells by modulating the DEP force. This study demonstrated that living cells can have non-linear di-polarized responses depending on the modulation direction of the applied frequency as well as providing a simple and reliable platform from which to measure a cellular cross-over frequency and characterize its nonlinear property.

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Domínguez-Soto, Angeles, Mateo de las Casas-Engel, Rafael Bragado, José Medina-Echeverz, Laura Aragoneses-Fenoll, Enrique Martín-Gayo, Nico van Rooijen, et al. "Intravenous Immunoglobulin Promotes Antitumor Responses by Modulating Macrophage Polarization." Journal of Immunology 193, no. 10 (October 17, 2014): 5181–89. http://dx.doi.org/10.4049/jimmunol.1303375.

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Khan, Mohammad W., Mojgan Zadeh, Praveen Bere, Elias Gounaris, Jennifer Owen, Todd Klaenhammer, and Mansour Mohamadzadeh. "Modulating intestinal immune responses by lipoteichoic acid-deficientLactobacillus acidophilus." Immunotherapy 4, no. 2 (February 2012): 151–61. http://dx.doi.org/10.2217/imt.11.163.

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Russo, Isabella, Luigi Bubacco, and Elisa Greggio. "LRRK2 as a target for modulating immune system responses." Neurobiology of Disease 169 (July 2022): 105724. http://dx.doi.org/10.1016/j.nbd.2022.105724.

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Kim, Soo-Jung, Matthew Leong, Matthew B. Amrofell, Young Je Lee, and Tae Seok Moon. "Modulating Responses of Toehold Switches by an Inhibitory Hairpin." ACS Synthetic Biology 8, no. 3 (February 5, 2019): 601–5. http://dx.doi.org/10.1021/acssynbio.8b00488.

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Trisnanto, Suko Bagus, and Yasushi Takemura. "Modulating relaxation responses of magnetic nanotracers for submillimeter imaging." Applied Physics Letters 115, no. 12 (September 16, 2019): 123101. http://dx.doi.org/10.1063/1.5102081.

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Bose, Mukulika, and Pinku Mukherjee. "Role of Microbiome in Modulating Immune Responses in Cancer." Mediators of Inflammation 2019 (June 12, 2019): 1–7. http://dx.doi.org/10.1155/2019/4107917.

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The complex interactions between genes and the environment play important roles in disease susceptibility and progression. One of the chronic diseases that is affected by this gene-environment interplay is cancer. However, our knowledge about these environmental factors remains limited. The microorganisms that inhabit our bodies have recently been acknowledged to play a crucial role as an environmental factor, to which we are constantly exposed. Studies have revealed significant differences in the relative abundance of certain microbes in cancer cases compared with controls. It has been reported that changes in the composition of normal gut microbiota can increase/decrease cancer susceptibility and progression by diverse mechanisms including, but not limited to, inflammation—a well-known hallmark of carcinogenesis. The microbiota can also affect the response to various treatments including immunotherapy. The microbiome-immune-cancer axis will continue to provide insight into the basic mechanisms of carcinogenesis. In this review, we provide a brief understanding of the mechanisms by which microbiota affects cancer development, progression, and treatment.

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Patin, Alexandra, and René Hurlemann. "Modulating amygdala responses to emotion: Evidence from pharmacological fMRI." Neuropsychologia 49, no. 4 (March 2011): 706–17. http://dx.doi.org/10.1016/j.neuropsychologia.2010.10.004.

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Scriven, James E., Mark W. Tenforde, Stuart M. Levitz, and Joseph N. Jarvis. "Modulating host immune responses to fight invasive fungal infections." Current Opinion in Microbiology 40 (December 2017): 95–103. http://dx.doi.org/10.1016/j.mib.2017.10.018.

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Nie, Ting, Robert E. Akins, and Kristi L. Kiick. "Production of heparin-containing hydrogels for modulating cell responses." Acta Biomaterialia 5, no. 3 (March 2009): 865–75. http://dx.doi.org/10.1016/j.actbio.2008.12.004.

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Goonoo, Nowsheen. "Modulating Immunological Responses of Electrospun Fibers for Tissue Engineering." Advanced Biosystems 1, no. 8 (July 17, 2017): 1700093. http://dx.doi.org/10.1002/adbi.201700093.

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Kageyama, Kazunori, and Takahiro Nemoto. "Molecular Mechanisms Underlying Stress Response and Resilience." International Journal of Molecular Sciences 23, no. 16 (August 12, 2022): 9007. http://dx.doi.org/10.3390/ijms23169007.

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Borson, D. B. "Roles of neutral endopeptidase in airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (April 1, 1991): L212—L225. http://dx.doi.org/10.1152/ajplung.1991.260.4.l212.

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In recent years, studies of the regulation of the airways have focused to an increasing degree on the roles of neuropeptides. Several peptides have been shown to be present in airways and mediate such diverse responses as ion transport, mucus secretion, bronchospasm or relaxation, edema, cough, changes in vascular permeability, and neutrophil chemotaxis. More recently, studies have described the roles of peptidases, most notably neutral endopeptidase (NEP, also known as enkephalinase, or E.C. 3.4.24.11) and kininase II (also known as angiotensin-converting enzyme, or E.C. 3.4.15.1) in modulating peptide-induced responses. The enzymes cleave a wide variety of peptides, generating metabolites that are inactive in the systems studied to date. Thus inhibitors of NEP potentiate responses to peptides that are cleaved by it. Therefore, NEP plays roles in modulating peptide-induced effects analogous to the role of acetylcholinesterase in modulating cholinergic neurotransmission. In several experimental respiratory diseases, the activity of neutral endopeptidase is decreased, resulting in increased responses to peptides. The therapeutic application of recombinant NEP protects the airways from the adverse actions of stimuli that release inflammatory peptides, and induction of the NEP gene expression by glucocorticoids suggest a possible mechanism for the action of these steroids in treating airway diseases such as asthma, chronic bronchitis, or cystic fibrosis.

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Burgess, Ellen D., Paul M. Keane, and Mamoru Watanabe. "Norepinephrine and calcium responses to altered sodium intake in modulating and non-modulating high-renin hypertension." Journal of Hypertension 6, no. 4 (December 1988): S85–87. http://dx.doi.org/10.1097/00004872-198812040-00023.

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Krol, Magdalena, and Wael El-Deredy. "Payoff Changes Sensitivity by Modulating the Processing Style." Perception 41, no. 5 (January 1, 2012): 623–25. http://dx.doi.org/10.1068/p7124.

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In a perceptual decision-making task, we compared a neutral payoff and two asymmetric payoffs: a liberal one, favouring positive responses, and a conservative one, favouring negative responses. Participants were presented with ambiguous images composed of superimposed target and non-target photographs, and asked to decide whether the target dominated in the picture. Signal-detection analysis demonstrated that the liberal payoff yielded significantly higher sensitivity than other payoffs. We argue that the liberal payoff encourages confirming the target's domination, hence making it easier to ignore non-target elements of the picture. We conclude that payoff can influence perceptual decisions by changing the approach to the perceptual task, and how attention is allocated between different elements of the sensory input.

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Solomon, Keith R. "Endocrine-Modulating Substances in the Environment: The Wildlife Connection." International Journal of Toxicology 17, no. 2 (February 1998): 159–71. http://dx.doi.org/10.1080/109158198226684.

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Historical observations, first publicized in Rachel Carson's Silent Spring, demonstrated biological effects of persistent, bioaccumulative pollutants on wildlife. These effects included disruption of reproduction and, in some situations, responses mediated through the endocrine system. The substances that caused these effects were mainly highly chlorinated halocarbon compounds, such as DDT (and metabolites), other organochlorine pesticides, polychlori-nated biphenyls, poly chlorinated dibenzo-p-dioxins, and poly chlorinated dibenzofurans. In contrast, responses of fish to industrial discharges and pulp mill effluents have implicated more water-soluble compounds. Characterizations of wildlife exposures require consideration of temporal and spatial factors that they exacerbate or ameliorate responses. Likewise, effects of endocrine-modulating substances m ay appear at subsequent stages of development, not at the time of exposure. Consistent with the declines in environmental concentrations of persistent, bioaccumulative substances, populations of several wild bird species, including bald eagles, cormorants, herring gulls, and Caspian terns, have increased, recovering from declines noted in previously polluted areas during the 1960s and 1970s.

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Tian, Sha, Susan Chyou, and Theresa Lu. "S.118. Modulating Lymph Node Vascular Growth and Function Leads to Modulation of Immune Responses." Clinical Immunology 131 (2009): S164. http://dx.doi.org/10.1016/j.clim.2009.03.486.

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Yan, Yuxi, Quan Zhao, Ya Huang, Janine Y. Yang, Jie Zou, Chunxia Ao, Xiaojuan Chai, Renhong Tang, and WenQing Yang. "Experimental Autoimmune Encephalomyelitis Animal Models Induced by Different Myelin Antigens Exhibit Differential Pharmacologic Responses to Anti-Inflammatory Drugs." Journal of Immunological Sciences 6, no. 1 (March 31, 2022): 18–24. http://dx.doi.org/10.29245/2578-3009/2022/1.1231.

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Background and objective Experimental autoimmune encephalomyelitis (EAE) is the most commonly used model for studying autoimmune-mediated myelin degradation in multiple sclerosis (MS). Here, we evaluated the pharmacologic responses of several anti-inflammatory drugs with varying mechanisms of actions (MOAs) using EAE models induced by different MOG immunogens to reveal differential pharmacologic characteristics of the disease models and provide a general guidance in animal model selection for MS research. Methods The pharmacologic responses of anti-inflammatory drugs with different mechanisms of actions (MOAs) were evaluated using EAE models induced by either myelin oligodendrocyte glycoprotein p35-55 ï¼MOG35-55ï¼or p1-128 (MOG1-128). EAE animal models were developed in mice with C57BL/6 background. The animals were treated with different anti-MS medications, including 3 B cell-mediated agents and 2 T cell-mediated agents, respectively. Clinical symptoms were monitored and scored, and pharmacodynamic markers including cytokine secretion, inflammatory cell infiltration, and demyelination in spinal cord were analyzed. Results In MOG35-55 peptide-induced EAE model, T cell modulating agents Secukinumab and Fingolimod significantly alleviated clinical symptoms, while B cell-depleting agents, BTK inhibitors PRN2246 and Telitacicept, displayed minimal therapeutic effects or even exacerbated disease progression. In contrast, both T cell-modulating agents and B cell-depleting agents ameliorated disease severity in MOG1-128-induced EAE model. T cell and B cell infiltration in spinal cord increased with disease progression in MOG1-128-induced EAE model. Conclusions Our results demonstrated that induction of EAE by different myelin antigens resulted in differential pharmacologic responses to drugs with specific MOAs. The MOG35-55 peptide-induced EAE model only responded to T cell-modulating drugs, whereas the MOG1-128 protein-induced EAE model exhibited therapeutic sensitivity to both T cell- and B cell-modulating agents. These data suggest the MOG35-55 peptide-induced EAE model is suitable for assessing T cell-modulating agents while MOG1-128 protein-induced model can be employed to evaluate both T cell- and B cell-modulating agents.

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Cao, Yuan, Liping Ding, Wenting Hu, Junxia Peng, and Yu Fang. "A surfactant-modulated fluorescent sensor with pattern recognition capability: sensing and discriminating multiple heavy metal ions in aqueous solution." J. Mater. Chem. A 2, no. 43 (2014): 18488–96. http://dx.doi.org/10.1039/c4ta03608e.

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Gao, Kan, Chun-long Mu, Aitak Farzi, and Wei-yun Zhu. "Tryptophan Metabolism: A Link Between the Gut Microbiota and Brain." Advances in Nutrition 11, no. 3 (December 11, 2019): 709–23. http://dx.doi.org/10.1093/advances/nmz127.

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ABSTRACT The gut-brain axis (GBA) is a bilateral communication network between the gastrointestinal (GI) tract and the central nervous system. The essential amino acid tryptophan contributes to the normal growth and health of both animals and humans and, importantly, exerts modulatory functions at multiple levels of the GBA. Tryptophan is the sole precursor of serotonin, which is a key monoamine neurotransmitter participating in the modulation of central neurotransmission and enteric physiological function. In addition, tryptophan can be metabolized into kynurenine, tryptamine, and indole, thereby modulating neuroendocrine and intestinal immune responses. The gut microbial influence on tryptophan metabolism emerges as an important driving force in modulating tryptophan metabolism. Here, we focus on the potential role of tryptophan metabolism in the modulation of brain function by the gut microbiota. We start by outlining existing knowledge on tryptophan metabolism, including serotonin synthesis and degradation pathways of the host, and summarize recent advances in demonstrating the influence of the gut microbiota on tryptophan metabolism. The latest evidence revealing those mechanisms by which the gut microbiota modulates tryptophan metabolism, with subsequent effects on brain function, is reviewed. Finally, the potential modulation of intestinal tryptophan metabolism as a therapeutic option for brain and GI functional disorders is also discussed.

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Polumuri, Swamy kumar, Lydia Haile, Roshni Rao, and Daniela Verthelyi. "Aggregation and innate immune response modulating impurities." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 129.2. http://dx.doi.org/10.4049/jimmunol.198.supp.129.2.

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Abstract Therapeutic proteins can induce immune responses that affect the safety and efficacy even if derived from human sequences. The factors that contribute to the immunogenicity of this therapeutics are poorly understood, but protein aggregation is thought to facilitate it. Previously, our lab showed that trace levels of product or process derived innate immune response modulating impurities (IIRMIs) can also increase product immunogenicity. In this study we hypothesized that protein aggregates and IIRMIs may synergize to facilitate product immunogenicity and explored it using clinical grade Human Serum Albumin (HSA) and Intravenous Immunoglobulin (IVIG) proteins as model. Protein aggregations formed by mechanical stress (shaking and stirring) were characterized by SDS-PAGE, turbidity, MFI and FlowCAM. Cellular responses to aggregated proteins with trace levels of IIRMs were tested in human PBMC. We show that stirring and shaking resulted in the formation of stable aggregates with size ranges of 2 – 50 μm for stirred HSA; and 2–100 μm for IVIG. Despite the similarity in size, the functional assays showed that aggregates of IVIG result in increased mRNA expression of IL-8, IL-6, IL-1β and CCL-2 whereas HSA aggregates did not. Further, we analyzed how the aggregated product changed the transcriptome using Nanostring and showed that aggregated IVIG (shaken or stirred) significantly increased the mRNA of CCL2, CCL7, CCL3, CCL24, CSF1, CXCL2, IRAK1, EGR2, CEBPβ, PPARg, TNFSF15 and whereas HSA aggregates did not. Similarly MAPKs (pp38, pERK and pJNK) and pAKT were activated when PBMC were stimulated with IVIG aggregates but not HSA aggregates. Lastly, we examined whether the effect was mediated by Toll like receptors.

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Liao, Zhencheng, Lei Dong, and Chunming Wang. "Modulating, instead of suppressing, foreign body responses for biomaterials design." Engineered Regeneration 2 (2021): 91–95. http://dx.doi.org/10.1016/j.engreg.2021.08.002.

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van Bon, L., A. Scharstuhl, B. Pennings, R. J. F. Huijbens, M. H. Wenink, K. C. M. Santegoets, M. Vonk, W. van den Berg, F. Wagener, and T. R. D. J. Radstake. "Modulating TLR responses in systemic sclerosis via heme oxygenase-1." Annals of the Rheumatic Diseases 69, Suppl 2 (March 1, 2010): A39—A40. http://dx.doi.org/10.1136/ard.2010.129627k.

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Pulendran, Bali. "Modulating vaccine responses with dendritic cells and Toll-like receptors." Immunological Reviews 199, no. 1 (June 2004): 227–50. http://dx.doi.org/10.1111/j.0105-2896.2004.00144.x.

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Zeng, Melody Y., Irina Miralda, Cortney L. Armstrong, Silvia M. Uriarte, and Juhi Bagaitkar. "The roles of NADPH oxidase in modulating neutrophil effector responses." Molecular Oral Microbiology 34, no. 2 (February 7, 2019): 27–38. http://dx.doi.org/10.1111/omi.12252.

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Gasparini, Chiara, and Marc Feldmann. "NF-κB as a Target for Modulating Inflammatory Responses." Current Pharmaceutical Design 18, no. 35 (October 8, 2012): 5735–45. http://dx.doi.org/10.2174/138161212803530763.

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Tian, Linlu, Yongxia Wu, Heejin Choi, Kaipo Yang, and Xue-Zhong Yu. "Pim2 negatively regulates T-cell immune responses through modulating autophagy." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 148.11. http://dx.doi.org/10.4049/jimmunol.210.supp.148.11.

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Abstract Pim kinases affect cell survival, cell proliferation, transcriptional activation, and protein translation by phosphorylating various target substrates. We previously showed that Pim2 plays a distinct role from Pim1 and Pim3, and negatively regulates T-cell allogeneic response and anti-tumor immunity. Pim2 was reported to promote the induction of autophagy in cancer cells, a cellular process that critically impacts T-cell effector function, survival and memory formation. We hypothesize that Pim2 constrains T-cell immune responses through modulating autophagy. Using western blot and electron microscopy, we evaluated the effect of Pim2 on autophagic flux in resting and activated T cells. Pim2 deficiency in T cells attenuated LC3 lipidation, P62 degradation as well as autophagosome formation, suggesting that Pim2 facilitates autophagy in T cells. Mechanistically, Pim2 directly bound with P62 and loss of Pim2 led to accumulation of P62 which further blocked autophagic flux in T cells. Furthermore, augmentation of autophagy via overexpressing Atg5 or metformin treatment reduced effector cytokine production in Pim2-deficient T cells in vitroand reversed the heightened ability of Pim2-deficient T cells for inducing graft-versus-host disease and for controlling breast cancer growth in vivo. Taken together, Pim2 is a key promotor of autophagy in T cells and targeting Pim2 to suppress autophagy may represent a promising strategy to improve T-cell effector function in cancer immunotherapy. The work was supported by NIH grants: R01 CA258440 and R21 CA263140.

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Journal articles on the topic 'MODULATING RESPONSES'

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