Journal articles: 'Intrinsic homeostasis'

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D’Angelo, Egidio. "Homeostasis of intrinsic excitability: making the point." Journal of Physiology 588, no. 6 (March 12, 2010): 901–2. http://dx.doi.org/10.1113/jphysiol.2010.187559.

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Butler, Colin, Martin Birchall, and Adam Giangreco. "Interventional and Intrinsic Airway Homeostasis and Repair." Physiology 27, no. 3 (June 2012): 140–47. http://dx.doi.org/10.1152/physiol.00001.2012.

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Human airways are a paragon of intrinsic engineering. They experience 7,000–10,000 liters of airflow/day, have a 70-m2 surface area, and undergo complete renewal every 100–400 days. Despite this, airways are susceptible to aging, injury, and diseases that are major causes of mortality. Current airway regeneration research is focused both on understanding the cells and strategies responsible for maintaining intrinsic tissue homeostasis as well as on establishing clinical interventions for improving repair.

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Gainey, Melanie A., and Daniel E. Feldman. "Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1715 (March 5, 2017): 20160157. http://dx.doi.org/10.1098/rstb.2016.0157.

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We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Hoyes, Thomas W., Neville A. Stanton, and R. G. Taylor. "Risk homeostasis theory: A study of intrinsic compensation." Safety Science 22, no. 1-3 (February 1996): 77–86. http://dx.doi.org/10.1016/0925-7535(96)00007-0.

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Wu, Yue Kris, Keith B. Hengen, Gina G. Turrigiano, and Julijana Gjorgjieva. "Homeostatic mechanisms regulate distinct aspects of cortical circuit dynamics." Proceedings of the National Academy of Sciences 117, no. 39 (September 11, 2020): 24514–25. http://dx.doi.org/10.1073/pnas.1918368117.

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Homeostasis is indispensable to counteract the destabilizing effects of Hebbian plasticity. Although it is commonly assumed that homeostasis modulates synaptic strength, membrane excitability, and firing rates, its role at the neural circuit and network level is unknown. Here, we identify changes in higher-order network properties of freely behaving rodents during prolonged visual deprivation. Strikingly, our data reveal that functional pairwise correlations and their structure are subject to homeostatic regulation. Using a computational model, we demonstrate that the interplay of different plasticity and homeostatic mechanisms can capture the initial drop and delayed recovery of firing rates and correlations observed experimentally. Moreover, our model indicates that synaptic scaling is crucial for the recovery of correlations and network structure, while intrinsic plasticity is essential for the rebound of firing rates, suggesting that synaptic scaling and intrinsic plasticity can serve distinct functions in homeostatically regulating network dynamics.

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Cannon, Jonathan, and Paul Miller. "Synaptic and intrinsic homeostasis cooperate to optimize single neuron response properties and tune integrator circuits." Journal of Neurophysiology 116, no. 5 (November 1, 2016): 2004–22. http://dx.doi.org/10.1152/jn.00253.2016.

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Homeostatic processes that provide negative feedback to regulate neuronal firing rate are essential for normal brain function, and observations suggest that multiple such processes may operate simultaneously in the same network. We pose two questions: why might a diversity of homeostatic pathways be necessary, and how can they operate in concert without opposing and undermining each other? To address these questions, we perform a computational and analytical study of cell-intrinsic homeostasis and synaptic homeostasis in single-neuron and recurrent circuit models. We demonstrate analytically and in simulation that when two such mechanisms are controlled on a long time scale by firing rate via simple and general feedback rules, they can robustly operate in tandem to tune the mean and variance of single neuron's firing rate to desired goals. This property allows the system to recover desired behavior after chronic changes in input statistics. We illustrate the power of this homeostatic tuning scheme by using it to regain high mutual information between neuronal input and output after major changes in input statistics. We then show that such dual homeostasis can be applied to tune the behavior of a neural integrator, a system that is notoriously sensitive to variation in parameters. These results are robust to variation in goals and model parameters. We argue that a set of homeostatic processes that appear to redundantly regulate mean firing rate may work together to control firing rate mean and variance and thus maintain performance in a parameter-sensitive task such as integration.

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Ge, Rongjing, Na Chen, and Jin-Hui Wang. "Real-time neuronal homeostasis by coordinating VGSC intrinsic properties." Biochemical and Biophysical Research Communications 387, no. 3 (September 2009): 585–89. http://dx.doi.org/10.1016/j.bbrc.2009.07.066.

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Niemeyer, Nelson, Jan-Hendrik Schleimer, and Susanne Schreiber. "Biophysical models of intrinsic homeostasis: Firing rates and beyond." Current Opinion in Neurobiology 70 (October 2021): 81–88. http://dx.doi.org/10.1016/j.conb.2021.07.011.

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Ferri, Francesca, Fabio Olivieri, Roberto Cannataro, Maria Cristina Caroleo, and Erika Cione. "Phytomelatonin Regulates Keratinocytes Homeostasis Counteracting Aging Process." Cosmetics 6, no. 2 (April 18, 2019): 27. http://dx.doi.org/10.3390/cosmetics6020027.

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Phytomelatonin (PM) gained the greatest interest for its application in agriculture and its use to improve human health conditions. PM based supplement has been shown to possess antioxidant capabilities because it functions as a free radical scavenger. Reactive Oxygen Species (ROS), induced by both intrinsic (peroxide production) and extrinsic (UV-radiation) factors are biochemical mediators crucial in skin aging. Skin aging is also regulated by specific microRNAs (miRs). Herein we have shown the effect of PM free radical scavengers on the human keratinocyte cell line HaCat and on ROS formation induced by both extrinsic and intrinsic factors as well as their capability to positively modulate a member of the hsa-miR-29 family linked to aging. Our result highlights the regulatory role of PM for the keratinocytes homeostasis.

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Verheijden, Simon, and Guy E. Boeckxstaens. "Neuroimmune interaction and the regulation of intestinal immune homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 1 (January 1, 2018): G75—G80. http://dx.doi.org/10.1152/ajpgi.00425.2016.

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Many essential gastrointestinal functions, including motility, secretion, and blood flow, are regulated by the autonomic nervous system (ANS), both through intrinsic enteric neurons and extrinsic (sympathetic and parasympathetic) innervation. Recently identified neuroimmune mechanisms, in particular the interplay between enteric neurons and muscularis macrophages, are now considered to be essential for fine-tuning peristalsis. These findings shed new light on how intestinal immune cells can support enteric nervous function. In addition, both intrinsic and extrinsic neural mechanisms control intestinal immune homeostasis in different layers of the intestine, mainly by affecting macrophage activation through neurotransmitter release. In this mini-review, we discuss recent insights on immunomodulation by intrinsic enteric neurons and extrinsic innervation, with a particular focus on intestinal macrophages. In addition, we discuss the relevance of these novel mechanisms for intestinal immune homeostasis in physiological and pathological conditions, mainly focusing on motility disorders (gastroparesis and postoperative ileus) and inflammatory disorders (colitis).

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Showkatbakhsh, Milad, and Mohammed Makki. "Application of homeostatic principles within evolutionary design processes: adaptive urban tissues." Journal of Computational Design and Engineering 7, no. 1 (February 1, 2020): 1–17. http://dx.doi.org/10.1093/jcde/qwaa002.

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Abstract Nature is a repository of dynamic and intertwined processes ready to be analyzed and simulated. Homeostasis, as a scale-free and universal biological process across all species, ensures adaptability to perturbations caused by intrinsic and extrinsic stimuli. Homeostatic processes by which species maintain their stability are strongly present through ontogenetic and phylogenetic histories of living beings. Forms and behaviors of species are imperative to their homeostatic conditions. Although biomimicry has been established for many decades, and has made significant contributions to engineering and architecture, homeostasis has rarely been part of this field of research. The experiments presented in this paper aim to examine the applicability of biological principles of homeostasis into generative design processes in order to evolve urban superblocks with a degree of morphological and behavioral adaptation to environmental changes; the objective is to eventually develop a modus operandi for the design and development of cities with embedded dynamic adaptation attributes.

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Pozzi, Davide, Gabriele Lignani, Enrico Ferrea, Andrea Contestabile, Francesco Paonessa, Rosalba D'Alessandro, Pellegrino Lippiello, et al. "REST/NRSF-mediated intrinsic homeostasis protects neuronal networks from hyperexcitability." EMBO Journal 32, no. 22 (October 22, 2013): 2994–3007. http://dx.doi.org/10.1038/emboj.2013.231.

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Zaph, Colby, Amy E. Troy, Betsy C. Taylor, Lisa D. Berman-Booty, Katherine J. Guild, Yurong Du, Evan A. Yost, et al. "Epithelial-cell-intrinsic IKK-β expression regulates intestinal immune homeostasis." Nature 446, no. 7135 (February 25, 2007): 552–56. http://dx.doi.org/10.1038/nature05590.

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Tabib, Yaara, Nora S. Jaber, Maria Nassar, Tal Capucha, Gabriel Mizraji, Tsipora Nir, Noam Koren, et al. "Cell-intrinsic regulation of murine epidermal Langerhans cells by protein S." Proceedings of the National Academy of Sciences 115, no. 25 (June 5, 2018): E5736—E5745. http://dx.doi.org/10.1073/pnas.1800303115.

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AXL, a member of the TYRO3, AXL, and MERTK (TAM) receptor tyrosine kinase family, has been shown to play a role in the differentiation and activation of epidermal Langerhans cells (LCs). Here, we demonstrate that growth arrest-specific 6 (GAS6) protein, the predominant ligand of AXL, has no impact on LC differentiation and homeostasis. We thus examined the role of protein S (PROS1), the other TAM ligand acting primarily via TYRO3 and MERTK, in LC function. Genetic ablation of PROS1 in keratinocytes resulted in a typical postnatal differentiation of LCs; however, a significant reduction in LC frequencies was observed in adult mice due to increased apoptosis. This was attributed to altered expression of cytokines involved in LC development and tissue homeostasis within keratinocytes. PROS1 was then excised in LysM+ cells to target LCs at early embryonic developmental stages, as well as in adult monocytes that also give rise to LCs. Differentiation and homeostasis of LCs derived from embryonic precursors was not affected following Pros1 ablation. However, differentiation of LCs from bone marrow (BM) precursors in vitro was accelerated, as was their capability to reconstitute epidermal LCs in vivo. These reveal an inhibitory role for PROS1 on BM-derived LCs. Collectively, this study highlights a cell-specific regulation of LC differentiation and homeostasis by TAM signaling.

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Burian, Ján, Santiago Ramón-García, Gaye Sweet, Anaximandro Gómez-Velasco, Yossef Av-Gay, and Charles J. Thompson. "The Mycobacterial Transcriptional RegulatorwhiB7Gene Links Redox Homeostasis and Intrinsic Antibiotic Resistance." Journal of Biological Chemistry 287, no. 1 (November 8, 2011): 299–310. http://dx.doi.org/10.1074/jbc.m111.302588.

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Choi, Diana, Stephanie A. Schroer, Shun Yan Lu, Erica P. Cai, Zhenyue Hao, and Minna Woo. "Redundant role of the cytochrome c-mediated intrinsic apoptotic pathway in pancreatic β-cells." Journal of Endocrinology 210, no. 3 (June 30, 2011): 285–92. http://dx.doi.org/10.1530/joe-11-0073.

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Cytochrome c is one of the central mediators of the mitochondrial or the intrinsic apoptotic pathway. Mice harboring a ‘knock-in’ mutation of cytochrome c, impairing only its apoptotic function, have permitted studies on the essential role of cytochrome c-mediated apoptosis in various tissue homeostasis. To this end, we examined the role of cytochrome c in pancreatic β-cells under homeostatic conditions and in diabetes models, including those induced by streptozotocin (STZ) and c-Myc. Previous studies have shown that both STZ- and c-Myc-induced β-cell apoptosis is mediated through caspase-3 activation; however, the precise mechanism in these modes of cell death was not characterized. The results of our study show that lack of functional cytochrome c does not affect glucose homeostasis or pancreatic β-cell mass under basal conditions. Moreover, the cytochrome c-mediated intrinsic apoptotic pathway is required for neither STZ- nor c-Myc-induced β-cell death. We also observed that the extrinsic apoptotic pathway mediated through caspase-8 was not essential in c-Myc-induced β-cell destruction. These findings suggest that cytochrome c is not required for STZ-induced β-cell apoptosis and, together with the caspase-8-mediated extrinsic pathway, plays a redundant role in c-Myc-induced β-cell apoptosis.

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Yoshida, Naoto. "Homeostatic Agent for General Environment." Journal of Artificial General Intelligence 8, no. 1 (March 7, 2018): 1–22. http://dx.doi.org/10.1515/jagi-2017-0001.

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AbstractOne of the essential aspect in biological agents is dynamic stability. This aspect, called homeostasis, is widely discussed in ethology, neuroscience and during the early stages of artificial intelligence. Ashby’s homeostats are general-purpose learning machines for stabilizing essential variables of the agent in the face of general environments. However, despite their generality, the original homeostats couldn’t be scaled because they searched their parameters randomly. In this paper, first we re-define the objective of homeostats as the maximization of a multi-step survival probability from the view point of sequential decision theory and probabilistic theory. Then we show that this optimization problem can be treated by using reinforcement learning algorithms with special agent architectures and theoretically-derived intrinsic reward functions. Finally we empirically demonstrate that agents with our architecture automatically learn to survive in a given environment, including environments with visual stimuli. Our survival agents can learn to eat food, avoid poison and stabilize essential variables through theoretically-derived single intrinsic reward formulations.

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Woo, Tai-Ting, Chi-Ning Chuang, and Ting-Fang Wang. "Correction to: Budding yeast Rad51: a paradigm for how phosphorylation and intrinsic structural disorder regulate homologous recombination and protein homeostasis." Current Genetics 67, no. 3 (March 14, 2021): 397–98. http://dx.doi.org/10.1007/s00294-021-01161-8.

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Goodwin, Bryan, and Steven A. Kliewer. "I. Nuclear receptors and bile acid homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 6 (June 1, 2002): G926—G931. http://dx.doi.org/10.1152/ajpgi.00044.2002.

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Bile acids are required for the absorption of lipids and fat-soluble vitamins. The hepatic biosynthesis of bile acids is a major pathway for the catabolism and removal of cholesterol from the body. Because of their intrinsic toxicity, bile acid synthesis, transport, and metabolism must be tightly regulated. It is now apparent that members of the nuclear receptor family of lipid-activated transcription factors are key regulators of these physiological processes. A greater understanding of these receptors should afford novel opportunities for therapeutic intervention in chronic diseases such as cholestasis and dyslipidemia.

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Poovathumkadavil, Preethi, and Krzysztof Jagla. "Genetic Control of Muscle Diversification and Homeostasis: Insights from Drosophila." Cells 9, no. 6 (June 25, 2020): 1543. http://dx.doi.org/10.3390/cells9061543.

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In the fruit fly, Drosophila melanogaster, the larval somatic muscles or the adult thoracic flight and leg muscles are the major voluntary locomotory organs. They share several developmental and structural similarities with vertebrate skeletal muscles. To ensure appropriate activity levels for their functions such as hatching in the embryo, crawling in the larva, and jumping and flying in adult flies all muscle components need to be maintained in a functionally stable or homeostatic state despite constant strain. This requires that the muscles develop in a coordinated manner with appropriate connections to other cell types they communicate with. Various signaling pathways as well as extrinsic and intrinsic factors are known to play a role during Drosophila muscle development, diversification, and homeostasis. In this review, we discuss genetic control mechanisms of muscle contraction, development, and homeostasis with particular emphasis on the contractile unit of the muscle, the sarcomere.

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Kile, Benjamin. "The intrinsic apoptosis caspase cascade regulates hematopoietic stem cell homeostasis and function." Experimental Hematology 41, no. 8 (August 2013): S4. http://dx.doi.org/10.1016/j.exphem.2013.05.015.

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Kabashima, Kenji, Theresa A. Banks, K. Mark Ansel, Theresa T. Lu, Carl F. Ware, and Jason G. Cyster. "Intrinsic Lymphotoxin-β Receptor Requirement for Homeostasis of Lymphoid Tissue Dendritic Cells." Immunity 22, no. 4 (April 2005): 439–50. http://dx.doi.org/10.1016/j.immuni.2005.02.007.

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Nutt, Stephen L., Axel Kallies, and Gabrielle T. Belz. "Blimp-1 Connects the Intrinsic and Extrinsic Regulation of T Cell Homeostasis." Journal of Clinical Immunology 28, no. 2 (December 11, 2007): 97–106. http://dx.doi.org/10.1007/s10875-007-9151-6.

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Oliva, Laura, Ugo Orfanelli, Massimo Resnati, Andrea Raimondi, Andrea Orsi, Enrico Milan, Giovanni Palladini, et al. "The amyloidogenic light chain is a stressor that sensitizes plasma cells to proteasome inhibitor toxicity." Blood 129, no. 15 (April 13, 2017): 2132–42. http://dx.doi.org/10.1182/blood-2016-08-730978.

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Key PointsAmyloidogenic PCs show unique PI susceptibility and altered organelle homeostasis, consistent with defective autophagy. Amyloidogenic LC production is an intrinsic cellular stressor that sensitizes to PI toxicity.

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Doupé, David P., Owen J. Marshall, Hannah Dayton, Andrea H. Brand, and Norbert Perrimon. "Drosophila intestinal stem and progenitor cells are major sources and regulators of homeostatic niche signals." Proceedings of the National Academy of Sciences 115, no. 48 (November 7, 2018): 12218–23. http://dx.doi.org/10.1073/pnas.1719169115.

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Epithelial homeostasis requires the precise balance of epithelial stem/progenitor proliferation and differentiation. While many signaling pathways that regulate epithelial stem cells have been identified, it is probable that other regulators remain unidentified. Here, we use gene-expression profiling by targeted DamID to identify the stem/progenitor-specific transcription and signaling factors in the Drosophila midgut. Many signaling pathway components, including ligands of most major pathways, exhibit stem/progenitor-specific expression and have regulatory regions bound by both intrinsic and extrinsic transcription factors. In addition to previously identified stem/progenitor-derived ligands, we show that both the insulin-like factor Ilp6 and TNF ligand eiger are specifically expressed in the stem/progenitors and regulate normal tissue homeostasis. We propose that intestinal stem cells not only integrate multiple signals but also contribute to and regulate the homeostatic signaling microenvironmental niche through the expression of autocrine and paracrine factors.

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Rodrigues, Pedro M., Ana R. Ribeiro, Chiara Perrod, Jonathan J. M. Landry, Leonor Araújo, Isabel Pereira-Castro, Vladimir Benes, et al. "Thymic epithelial cells require p53 to support their long-term function in thymopoiesis in mice." Blood 130, no. 4 (July 27, 2017): 478–88. http://dx.doi.org/10.1182/blood-2016-12-758961.

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Key Points TEC-intrinsic ablation of p53 predominantly affects medullary TECs, altering their RANK-driven differentiation and transcriptome. Loss of p53 in TECs couples disrupted thymopoiesis to altered T-cell homeostasis and tolerance.

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Glazewski, Stanislaw, Stuart Greenhill, and Kevin Fox. "Time-course and mechanisms of homeostatic plasticity in layers 2/3 and 5 of the barrel cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1715 (March 5, 2017): 20160150. http://dx.doi.org/10.1098/rstb.2016.0150.

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Recent studies have shown that ocular dominance plasticity in layer 2/3 of the visual cortex exhibits a form of homeostatic plasticity that is related to synaptic scaling and depends on TNFα. In this study, we tested whether a similar form of plasticity was present in layer 2/3 of the barrel cortex and, therefore, whether the mechanism was likely to be a general property of cortical neurons. We found that whisker deprivation could induce homeostatic plasticity in layer 2/3 of barrel cortex, but not in a mouse strain lacking synaptic scaling. The time-course of homeostatic plasticity in layer 2/3 was similar to that of L5 regular spiking (RS) neurons (L5RS), but slower than that of L5 intrinsic bursting (IB) neurons (L5IB). In layer 5, the strength of evoked whisker responses and ex vivo miniature excitatory post-synaptic currents (mEPSCs) amplitudes showed an identical time-course for homeostatic plasticity, implying that plasticity at excitatory synapses contacting layer 5 neurons is sufficient to explain the changes in evoked responses. Spontaneous firing rate also showed homeostatic behaviour for L5IB cells, but was absent for L5RS cells over the time-course studied. Spontaneous firing rate homeostasis was found to be independent of evoked response homeostasis suggesting that the two depend on different mechanisms. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Fall, Lewis, Karl J. New, Kevin A. Evans, and Damian M. Bailey. "Arterial hypoxaemia and its impact on coagulation: significance of altered redox homeostasis." Journal of Clinical Pathology 68, no. 9 (June 4, 2015): 752–54. http://dx.doi.org/10.1136/jclinpath-2015-202952.

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AimsArterial hypoxaemia stimulates free radical formation. Cellular studies suggest this may be implicated in coagulation activation though human evidence is lacking. To examine this, an observational study was designed to explore relationships between systemic oxidative stress and haemostatic responses in healthy participants exposed to inspiratory hypoxia.ResultsActivated partial thromboplastin time and international normalised ratio were measured as routine clinical biomarkers of coagulation and ascorbate free radical (A•−) as a direct global biomarker of free radical flux. Six hours of hypoxia activated coagulation, and increased formation of A•−, with inverse correlations observed against oxyhaemoglobin saturation.ConclusionsThis is the first study to address the link between free radical formation and coagulation in vivo. This ‘proof-of-concept’ study demonstrated functional associations between hypoxaemia and coagulation that may be subject to redox activation of the intrinsic pathway. Further studies are required to identify precisely which intrinsic factors are subject to redox activation.

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Mori, Jun, Zoltan Nagy, Giada Di Nunzio, Christopher W. Smith, Mitchell J. Geer, Rashid Al Ghaithi, Johanna P. van Geffen, et al. "Maintenance of murine platelet homeostasis by the kinase Csk and phosphatase CD148." Blood 131, no. 10 (March 8, 2018): 1122–44. http://dx.doi.org/10.1182/blood-2017-02-768077.

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Key Points Csk and CD148 are nonredundant regulators of SFKs in platelets, and deletion of either induces cell-intrinsic negative feedback mechanisms. Csk is a negative regulator of SFK activity, whereas CD148 is a dual positive and negative regulator of SFK activity in platelets.

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Kim, Eugene Z., Julie Vienne, Michael Rosbash, and Leslie C. Griffith. "Nonreciprocal homeostatic compensation in Drosophila potassium channel mutants." Journal of Neurophysiology 117, no. 6 (June 1, 2017): 2125–36. http://dx.doi.org/10.1152/jn.00002.2017.

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Homeostatic control of intrinsic excitability is important for long-term regulation of neuronal activity. In conjunction with many other forms of plasticity, intrinsic homeostasis helps neurons maintain stable activity regimes in the face of external input variability and destabilizing genetic mutations. In this study, we report a mechanism by which Drosophila melanogaster larval motor neurons stabilize hyperactivity induced by the loss of the delayed rectifying K+ channel Shaker cognate B ( Shab), by upregulating the Ca2+-dependent K+ channel encoded by the slowpoke ( slo) gene. We also show that loss of SLO does not trigger a reciprocal compensatory upregulation of SHAB, implying that homeostatic signaling pathways utilize compensatory pathways unique to the channel that was mutated. SLO upregulation due to loss of SHAB involves nuclear Ca2+ signaling and dCREB, suggesting that the slo homeostatic response is transcriptionally mediated. Examination of the changes in gene expression induced by these mutations suggests that there is not a generic transcriptional response to increased excitability in motor neurons, but that homeostatic compensations are influenced by the identity of the lost conductance. NEW & NOTEWORTHY The idea that activity-dependent homeostatic plasticity is driven solely by firing has wide credence. In this report we show that homeostatic compensation after loss of an ion channel conductance is tailored to identity of the channel lost, not its properties.

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Haynes, Laura, and Susan L. Swain. "Aged-related shifts in T cell homeostasis lead to intrinsic T cell defects." Seminars in Immunology 24, no. 5 (October 2012): 350–55. http://dx.doi.org/10.1016/j.smim.2012.04.001.

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Marichal, Thomas, Nicolas Gaudenzio, Sophie El Abbas, Riccardo Sibilano, Oliwia Zurek, Philipp Starkl, Laurent L. Reber, et al. "Guanine nucleotide exchange factor RABGEF1 regulates keratinocyte-intrinsic signaling to maintain skin homeostasis." Journal of Clinical Investigation 126, no. 12 (November 7, 2016): 4497–515. http://dx.doi.org/10.1172/jci86359.

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Nakato, Gaku, Koji Hase, Takao Sato, Shunsuke Kimura, Sayuri Sakakibara, Machiko Sugiyama, Yuuki Obata, Misaho Hanazato, Toshihiko Iwanaga, and Hiroshi Ohno. "Epithelium-Intrinsic MicroRNAs Contribute to Mucosal Immune Homeostasis by Promoting M-Cell Maturation." PLOS ONE 11, no. 3 (March 1, 2016): e0150379. http://dx.doi.org/10.1371/journal.pone.0150379.

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Hu, Deqing, Han Yan, Xi C. He, and Linheng Li. "Recent advances in understanding intestinal stem cell regulation." F1000Research 8 (January 18, 2019): 72. http://dx.doi.org/10.12688/f1000research.16793.1.

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Intestinal homeostasis and regeneration are driven by intestinal stem cells (ISCs) lying in the crypt. In addition to the actively cycling ISCs that maintain daily homeostasis, accumulating evidence supports the existence of other pools of stem/progenitor cells with the capacity to repair damaged tissue and facilitate rapid restoration of intestinal integrity after injuries. Appropriate control of ISCs and other populations of intestinal epithelial cells with stem cell activity is essential for intestinal homeostasis and regeneration while their deregulation is implicated in colorectal tumorigenesis. In this review, we will summarize the recent findings about ISC identity and cellular plasticity in intestine, discuss regulatory mechanisms that control ISCs for intestinal homeostasis and regeneration, and put a particular emphasis on extrinsic niche-derived signaling and intrinsic epigenetic regulation. Moreover, we highlight several fundamental questions about the precise mechanisms conferring robust capacity for intestine to maintain physiological homeostasis and repair injuries.

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Yoo, Yoon Seon, Hye Gyeong Han, and Young Joo Jeon. "Unfolded Protein Response of the Endoplasmic Reticulum in Tumor Progression and Immunogenicity." Oxidative Medicine and Cellular Longevity 2017 (December 21, 2017): 1–18. http://dx.doi.org/10.1155/2017/2969271.

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The endoplasmic reticulum (ER) is a pivotal regulator of folding, quality control, trafficking, and targeting of secreted and transmembrane proteins, and accordingly, eukaryotic cells have evolved specialized machinery to ensure that the ER enables these proteins to acquire adequate folding and maturation in the presence of intrinsic and extrinsic insults. This adaptive capacity of the ER to intrinsic and extrinsic perturbations is important for maintaining protein homeostasis, which is termed proteostasis. Failure in adaptation to these perturbations leads to accumulation of misfolded or unassembled proteins in the ER, which is termed ER stress, resulting in the activation of unfolded protein response (UPR) of the ER and the execution of ER-associated degradation (ERAD) to restore homeostasis. Furthermore, both of the two axes play key roles in the control of tumor progression, inflammation, immunity, and aging. Therefore, understanding UPR of the ER and subsequent ERAD will provide new insights into the pathogenesis of many human diseases and contribute to therapeutic intervention in these diseases.

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Takeshima, Mika, Mari H. Ogihara, and Hiroshi Kataoka. "Sterol Characteristics in Silkworm Brain and Various Tissues Characterized by Precise Sterol Profiling Using LC-MS/MS." International Journal of Molecular Sciences 20, no. 19 (September 29, 2019): 4840. http://dx.doi.org/10.3390/ijms20194840.

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Sterols, especially cholesterol (Chl), are fundamental for animal survival. Insects lacking the ability to synthesize Chl are sterol auxotrophic animals and utilize dietary Chl and phytosterols to survive. The sterols obtained from a diet are distributed to the tissues; however, sterol homeostasis in insect tissues remains to be elucidated. This study sought to understand the sterol characteristics of insect tissues through detailed sterol quantification and statistics. The combination of sterol quantification using liquid chromatography tandem mass spectrometry (LC-MS/MS) and principal component analysis (PCA) revealed tissue-specific sterol characteristics in the silkworm, Bombyx mori, a phytophagous insect. We found that insect tissues have tissue-intrinsic sterol profiles. The brain has a unique sterol composition as compared to other tissues—high concentration of Chl and less accumulation of phytosterols. Other tissues also have intrinsic sterol characteristics, which when defined by dietary sterols or Chl metabolites, indicate preference for a sterol and consistently manage their own sterol homeostasis. Though most tissues never change sterol profiles during development, the brain drastically changes its sterol profile at the wandering stage, indicating that it could alter sterol composition in preparation for metamorphosis. These results suggest the existence of tissue- and sterol-specific systems for sterol homeostasis in insects.

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Bruneel, Kenneth, Jeroen Verstappe, Niels Vandamme, and Geert Berx. "Intrinsic Balance between ZEB Family Members Is Important for Melanocyte Homeostasis and Melanoma Progression." Cancers 12, no. 8 (August 11, 2020): 2248. http://dx.doi.org/10.3390/cancers12082248.

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It has become clear that cellular plasticity is a main driver of cancer therapy resistance. Consequently, there is a need to mechanistically identify the factors driving this process. The transcription factors of the zinc-finger E-box-binding homeobox family, consisting of ZEB1 and ZEB2, are notorious for their roles in epithelial-to-mesenchymal transition (EMT). However, in melanoma, an intrinsic balance between ZEB1 and ZEB2 seems to determine the cellular state by modulating the expression of the master regulator of melanocyte homeostasis, microphthalmia-associated transcription factor (MITF). ZEB2 drives MITF expression and is associated with a differentiated/proliferative melanoma cell state. On the other hand, ZEB1 is correlated with low MITF expression and a more invasive, stem cell-like and therapy-resistant cell state. This intrinsic balance between ZEB1 and ZEB2 could prove to be a promising therapeutic target for melanoma patients. In this review, we will summarise what is known on the functional mechanisms of these transcription factors. Moreover, we will look specifically at their roles during melanocyte-lineage development and homeostasis. Finally, we will overview the current literature on ZEB1 and ZEB2 in the melanoma context and link this to the ‘phenotype-switching’ model of melanoma cellular plasticity.

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Schulz, P. "Biological uniqueness and the definition of normality. Part 1—The concept of ‘intrinsic’ homeostasis." Medical Hypotheses 42, no. 1 (January 1994): 57–62. http://dx.doi.org/10.1016/0306-9877(94)90037-x.

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Biswas, Amlan, Dror S. Shouval, Jeremy A. Goettel, and Scott B. Snapper. "123 A Macrophage Intrinsic Role of WASP Is Critical for Maintenance of Mucosal Homeostasis." Gastroenterology 148, no. 4 (April 2015): S—32. http://dx.doi.org/10.1016/s0016-5085(15)30112-8.

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Gogishvili, Tea, Fred Lühder, Sandra Goebbels, Sandra Beer-Hammer, Klaus Pfeffer, and Thomas Hünig. "Cell-intrinsic and -extrinsic control of Treg-cell homeostasis and function revealed by inducedCD28deletion." European Journal of Immunology 43, no. 1 (November 17, 2012): 188–93. http://dx.doi.org/10.1002/eji.201242824.

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Wilson, David F. "Regulation of cellular metabolism: programming and maintaining metabolic homeostasis." Journal of Applied Physiology 115, no. 11 (December 1, 2013): 1583–88. http://dx.doi.org/10.1152/japplphysiol.00894.2013.

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Mitochondrial oxidative phosphorylation is programmed to set and maintain metabolic homeostasis. This is accomplished through an intrinsic program that determines the metabolic [ATP]/[ADP]/[Pi], where [Pi] is the concentration of inorganic phosphate (energy state) and maintains it through a bidirectional sensory/signaling control network that reaches every aspect of cellular metabolism. The program sets the energy state with high precision (to better than one part in 109) and can respond to transient changes in energy demand (ATP use) to more than 100 times the resting rate. Epigenetic and environmental factors are able to “fine tune” the programmed set point over a narrow range to meet the special needs associated with cell differentiation and chronic changes in metabolic requirements. The result is robust, across platform control of metabolism, essential to cellular differentiation and the evolution of complex organisms.

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Breathnach, CS. "Neural integration of the hormonal contribution to homeostasis." Irish Journal of Psychological Medicine 7, no. 2 (September 1990): 154–58. http://dx.doi.org/10.1017/s0790966700016797.

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AbstractApart from well known areas of overlap between endocrinology and psychiatry (e.g. studies, in psychiatric disorders, of neurohormones and of the response to manipulations of hypothalamic-pituitary-target gland axis, and analysis of behavioural and psychological disturbances in endocrinological disorders) there is a more intimate intrinsic relationship between the brain and the endocrine system which is less well known or studied. Many of the extracranial endocrine glands have autonomic innervation. Like the pituitary gland which is under direct neural (as well as humoral) diencephalic control, the extracranial endocrine glands are under direct neural control, integrated by the hypothalamus and “head ganglion of the autonomic nervous system”. Yet it is only in the case of the pancreatic islets that this integration has been clearly defined. It is postulated that by this innervation the somatic endocrine glands can respond to homeostatic needs with a rapid initial secretion before the more sustained outpouring of humoral agents typically regulated by blood-borne constituents including pituitary hormones. This is a vast area awaiting further investigation.

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Pohl, Kerstin, Elaine Hayes, Joanne Keenan, Michael Henry, Paula Meleady, Kevin Molloy, Bakr Jundi, et al. "A neutrophil intrinsic impairment affecting Rab27a and degranulation in cystic fibrosis is corrected by CFTR potentiator therapy." Blood 124, no. 7 (August 14, 2014): 999–1009. http://dx.doi.org/10.1182/blood-2014-02-555268.

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Key Points In people with cystic fibrosis, defective CFTR function alters neutrophil cytosolic ion homeostasis leading to impaired degranulation. By normalizing CFTR function, ivacaftor treatment corrects neutrophil degranulation resulting in normalized killing of bacteria.

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Muralidharan, Charanya, and Amelia K. Linnemann. "β-Cell autophagy in the pathogenesis of type 1 diabetes." American Journal of Physiology-Endocrinology and Metabolism 321, no. 3 (September 1, 2021): E410—E416. http://dx.doi.org/10.1152/ajpendo.00151.2021.

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Type 1 diabetes is an insulin-dependent, autoimmune disease where the pancreatic β cells are destroyed resulting in hyperglycemia. This multifactorial disease involves multiple environmental and genetic factors, and has no clear etiology. Accumulating evidence suggests that early signaling defects within the β cells may promote a change in the local immune milieu leading to autoimmunity. Therefore, many studies have been focused on intrinsic β-cell mechanisms that aid in the restoration of cellular homeostasis under environmental conditions that cause dysfunction. One of these intrinsic mechanisms to promote homeostasis is autophagy, defects which are clearly linked with β-cell dysfunction in the context of type 2 diabetes. Recent studies have now also pointed towards β-cell autophagy defects in the context of type 1 diabetes. In this perspectives review, we will discuss the evidence supporting a role for β-cell autophagy in the pathogenesis of type 1 diabetes, including a potential role for unconventional secretion of autophagosomes/lysosomes in the changing dialogue between the β cell and immune cells.

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Volman, Vladislav, Terrence J. Sejnowski, and Maxim Bazhenov. "Topological basis of epileptogenesis in a model of severe cortical trauma." Journal of Neurophysiology 106, no. 4 (October 2011): 1933–42. http://dx.doi.org/10.1152/jn.00458.2011.

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Epileptic activity often arises after a latent period following traumatic brain injury. Several factors contribute to the emergence of post-traumatic epilepsy, including disturbances to ionic homeostasis, pathological action of intrinsic and synaptic homeostatic plasticity, and remodeling of anatomical network synaptic connectivity. We simulated a large-scale, biophysically realistic computational model of cortical tissue to study the mechanisms underlying the genesis of post-traumatic paroxysmal epileptic-like activity in the deafferentation model of a severely traumatized cortical network. Post-traumatic generation of paroxysmal events did not require changes of the structural connectivity. Rather, network bursts were induced following the action of homeostatic synaptic plasticity, which selectively influenced functionally dominant groups of intact neurons with preserved inputs. This effect critically depended on the spatial density of intact neurons. Thus in the deafferentation model of post-traumatic epilepsy, a trauma-induced change in functional (rather than anatomical) connectivity might be sufficient for epileptogenesis.

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Krieg, Carsten, Onur Boyman, Yang-Xin Fu, and Jonathan Kaye. "B and T lymphocyte attenuator regulates CD8+ T cell–intrinsic homeostasis and memory cell generation." Nature Immunology 8, no. 2 (January 7, 2007): 162–71. http://dx.doi.org/10.1038/ni1418.

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King, Carolyn G., Takashi Kobayashi, Pedro J. Cejas, Taesoo Kim, Kwiyeom Yoon, Gregory K. Kim, Elise Chiffoleau, et al. "TRAF6 is a T cell–intrinsic negative regulator required for the maintenance of immune homeostasis." Nature Medicine 12, no. 9 (July 20, 2006): 1088–92. http://dx.doi.org/10.1038/nm1449.

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Stakenborg, Nathalie, and Guy E. Boeckxstaens. "Bioelectronics in the brain–gut axis: focus on inflammatory bowel disease (IBD)." International Immunology 33, no. 6 (March 31, 2021): 337–48. http://dx.doi.org/10.1093/intimm/dxab014.

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Abstract Accumulating evidence shows that intestinal homeostasis is mediated by cross-talk between the nervous system, enteric neurons and immune cells, together forming specialized neuroimmune units at distinct anatomical locations within the gut. In this review, we will particularly discuss how the intrinsic and extrinsic neuronal circuitry regulates macrophage function and phenotype in the gut during homeostasis and aberrant inflammation, such as observed in inflammatory bowel disease (IBD). Furthermore, we will provide an overview of basic and translational IBD research using these neuronal circuits as a novel therapeutic tool. Finally, we will highlight the different challenges ahead to make bioelectronic neuromodulation a standard treatment for intestinal immune-mediated diseases.

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Whitsett, Jeffrey A. "Review: The intersection of surfactant homeostasis and innate host defense of the lung: lessons from newborn infants." Innate Immunity 16, no. 3 (March 29, 2010): 138–42. http://dx.doi.org/10.1177/1753425910366879.

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The study of pulmonary surfactant, directed towards prevention and treatment of respiratory distress syndrome in preterm infants, led to the identification of novel proteins/genes that determine the synthesis, packaging, secretion, function, and catabolism of alveolar surfactant. The surfactant proteins, SP-A, SP-B, SP-C, and SP-D, and the surfactant lipid associated transporter, ABCA3, play critical roles in surfactant homeostasis. The study of their structure and function provided insight into a system that integrates the biophysical need to reduce surface tension in the alveoli and the innate host defenses required to maintain pulmonary structure and function after birth. Alveolar homeostasis depends on the intrinsic, multifunctional structures of the surfactant-associated proteins and the shared transcriptional regulatory modules that determine both the expression of genes involved in surfactant production as well as those critical for host defense. Identification of the surfactant proteins and the elucidation of the genetic networks regulating alveolar homeostasis have provided the basis for understanding and diagnosing rare and common pulmonary disorders, including respiratory distress syndrome, inherited disorders of surfactant homeostasis, and pulmonary alveolar proteinosis.

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Hughes, Jing W., Jung Hoon Cho, Hannah E. Conway, Michael R. DiGruccio, Xue Wen Ng, Henry F. Roseman, Damien Abreu, Fumihiko Urano, and David W. Piston. "Primary cilia control glucose homeostasis via islet paracrine interactions." Proceedings of the National Academy of Sciences 117, no. 16 (April 6, 2020): 8912–23. http://dx.doi.org/10.1073/pnas.2001936117.

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Pancreatic islets regulate glucose homeostasis through coordinated actions of hormone-secreting cells. What underlies the function of the islet as a unit is the close approximation and communication among heterogeneous cell populations, but the structural mediators of islet cellular cross talk remain incompletely characterized. We generated mice specifically lacking β-cell primary cilia, a cellular organelle that has been implicated in regulating insulin secretion, and found that the β-cell cilia are required for glucose sensing, calcium influx, insulin secretion, and cross regulation of α- and δ-cells. Protein expression profiling in islets confirms perturbation in these cellular processes and reveals additional targets of cilia-dependent signaling. At the organism level, the deletion of β-cell cilia disrupts circulating hormone levels, impairs glucose homeostasis and fuel usage, and leads to the development of diabetes. Together, these findings demonstrate that primary cilia not only orchestrate β-cell–intrinsic activity but also mediate cross talk both within the islet and from islets to other metabolic tissues, thus providing a unique role of cilia in nutrient metabolism and insight into the pathophysiology of diabetes.

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Journal articles on the topic 'Intrinsic homeostasis'

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