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Articoli di riviste sul tema "Peripheral inflammation"

Autore: Grafiati

Pubblicato: 31 agosto 2024

Ultima modifica: 19 luglio 2025

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1

De Kock, Marc, Sebastien Loix, and Patricia Lavand'homme. "Ketamine and Peripheral Inflammation." CNS Neuroscience & Therapeutics 19, no. 6 (2013): 403–10. http://dx.doi.org/10.1111/cns.12104.

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Träger, Ulrike, and Sarah J. Tabrizi. "Peripheral inflammation in neurodegeneration." Journal of Molecular Medicine 91, no. 6 (2013): 673–81. http://dx.doi.org/10.1007/s00109-013-1026-0.

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3

Poutler, L. W. "Central inflammation is more important than peripheral inflammation." Respiratory Medicine 91 (November 1997): 9–10. http://dx.doi.org/10.1016/s0954-6111(97)90097-4.

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4

Hamid, Q. A. "Peripheral inflammation is more important than central inflammation." Respiratory Medicine 91 (November 1997): 11–12. http://dx.doi.org/10.1016/s0954-6111(97)90098-6.

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5

Groven, N., E. A. Fors, V. C. Iversen, L. R. White, and S. K. Reitan. "Peripheral inflammation in fibromyalgia syndrome." European Neuropsychopharmacology 27 (October 2017): S634. http://dx.doi.org/10.1016/s0924-977x(17)31194-x.

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6

Lisney, S. J. W. "The development of peripheral inflammation." Pain Forum 4, no. 3 (1995): 153–54. http://dx.doi.org/10.1016/s1082-3174(11)80047-4.

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7

Brevetti, Gregorio, Giuseppe Giugliano, Linda Brevetti, and William R. Hiatt. "Inflammation in Peripheral Artery Disease." Circulation 122, no. 18 (2010): 1862–75. http://dx.doi.org/10.1161/circulationaha.109.918417.

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8

Signorelli, Salvatore, Elisa Marino, and Salvatore Scuto. "Inflammation and Peripheral Arterial Disease." J 2, no. 2 (2019): 142–51. http://dx.doi.org/10.3390/j2020012.

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Abstract (sommario):

Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) C-reactive protein (CRP), fibrinogen) have been measured in atherosclerotic diseases including PAD. This paper summarizes the data on the inflammatory biomarkers for PAD pathophysiology and highlights the most usef

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Callas, Peter, Matthew Allison, Michael Criqui, and Mary Cushman. "Inflammation and peripheral venous disease." Thrombosis and Haemostasis 112, no. 09 (2014): 566–72. http://dx.doi.org/10.1160/th13-10-0860.

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SummaryThe inflammatory response to healing in venous thrombosis might cause vein damage and post-thrombotic syndrome. Inflammation may also be involved in venous insufficiency apart from deep-vein thrombosis. We studied the association of inflammation markers with venous insufficiency in a general population sample. We characterised 2,404 men and women in a general population cohort for peripheral venous disease and its severity using physical exam, symptom assessment, and venous ultrasound. Inflammation markers, C-reactive protein (CRP), fibrinogen, interleukin 1-beta (IL-1-beta), IL-8, IL-1

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10

Schafer, M., Y. Imai, S. Mousa, I. Antonijevic, G. R. Uhl, and C. Stein. "Peripheral Opioid Analgesia in Inflammation." Anesthesiology 81, SUPPLEMENT (1994): A920. http://dx.doi.org/10.1097/00000542-199409001-00919.

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11

D'Mello, Charlotte, and Mark G. Swain. "Liver-brain inflammation axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 5 (2011): G749—G761. http://dx.doi.org/10.1152/ajpgi.00184.2011.

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It is becoming increasingly evident that peripheral organ-centered inflammatory diseases, including chronic inflammatory liver diseases, are associated with changes in central neural transmission that result in alterations in behavior. These behavioral changes include sickness behaviors, such as fatigue, cognitive dysfunction, mood disorders, and sleep disturbances. While such behaviors have a significant impact on quality of life, the changes within the brain and the communication pathways between the liver and the brain that give rise to changes in central neural activity are not fully under

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12

Krumrych, Wiesław, and Janusz Danek. "Chemiluminescence of Peripheral Blood Neutrophils in Mares with Endometritis." Bulletin of the Veterinary Institute in Pulawy 56, no. 1 (2012): 51–56. http://dx.doi.org/10.2478/v10213-012-0010-8.

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Abstract The aim of the study was to evaluate the oxygen metabolism of neutrophils in peripheral blood of mares in relation to intensity of endometrium inflammations. The study involved 36 half-breed mares, aged 4-22 years, showing fertility disturbances. In 26 mares neutrophils were found in uteral smears, which indicated endometritis (15 - moderate inflammation and 11 - severe inflammation). In the rest mares, cytological examination excluded inflammation. Blood samples were evaluated in terms of neutrophils chemiluminescence without stimulation (CL-WS) and with stimulation by opsonised zymo

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13

Blomqvist, Anders, and David Engblom. "Neural Mechanisms of Inflammation-Induced Fever." Neuroscientist 24, no. 4 (2018): 381–99. http://dx.doi.org/10.1177/1073858418760481.

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Fever is a common symptom of infectious and inflammatory disease. It is well-established that prostaglandin E2 is the final mediator of fever, which by binding to its EP3 receptor subtype in the preoptic hypothalamus initiates thermogenesis. Here, we review the different hypotheses on how the presence of peripherally released pyrogenic substances can be signaled to the brain to elicit fever. We conclude that there is unequivocal evidence for a humoral signaling pathway by which proinflammatory cytokines, through their binding to receptors on brain endothelial cells, evoke fever by eliciting pr

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14

Ferrari, Carina C., and Rodolfo Tarelli. "Parkinson's Disease and Systemic Inflammation." Parkinson's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/436813.

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Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in thesubstantia nigra(SN). Peripheral inflammation can transform the “primed” microglia into an “active” state, which can trigger stronger responses dealing wi

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15

Santo Signorelli, Salvatore, Massimiliano Anzaldi, and Valerio Fiore. "Inflammation in Peripheral Arterial Disease (PAD)." Current Pharmaceutical Design 18, no. 28 (2012): 4350–57. http://dx.doi.org/10.2174/138161212802481273.

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16

Machado, A., A. J. Herrera, J. L. Venero, et al. "Peripheral Inflammation Increases the Damage in Animal Models of Nigrostriatal Dopaminergic Neurodegeneration: Possible Implication in Parkinson's Disease Incidence." Parkinson's Disease 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/393769.

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Inflammatory processes described in Parkinson’s disease (PD) and its animal models appear to be important in the progression of the pathogenesis, or even a triggering factor. Here we review that peripheral inflammation enhances the degeneration of the nigrostriatal dopaminergic system induced by different insults; different peripheral inflammations have been used, such as IL-1β and the ulcerative colitis model, as well as insults to the dopaminergic system such as 6-hydroxydopamine or lipopolysaccharide. In all cases, an increased loss of dopaminergic neurons was described; inflammation in the

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17

Djaldetti, Meir. "Piperine – An Immunomodulator and Inflammation Mitigator." Journal of Clinical and Laboratory Research 2, no. 5 (2021): 01–04. http://dx.doi.org/10.31579/2768-0487/027.

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Black pepper, one of the most widespread spices, gained the entitlement “King of spices” founded on its peculiar pungent test and therapeutic properties, both owed to its active alkaloid - piperine. Mounting evidence indicates that piperine possesses immunomodulatory and therapeutic activities. The aim of this mini review was to summarize the role of piperine in abolishing inflammation, its part in the immune activity of peripheral blood mononuclear- and a number of other cells, its capacity to elicit production of inflammatory cytokines and its function as a synergist endorsing the beneficial

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18

Denes, A., P. Thornton, N. J. Rothwell, and S. M. Allan. "Inflammation and brain injury: Acute cerebral ischaemia, peripheral and central inflammation." Brain, Behavior, and Immunity 24, no. 5 (2010): 708–23. http://dx.doi.org/10.1016/j.bbi.2009.09.010.

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19

Dural, İbrahim Etem, Zafer Yalım, Uğur Aksu, Mehmet Özgeyik, Serkan Gökaslan, and Ömer Faruk Yılmaz. "EFFECT OF SYSTEMIC IMMUNE-INFLAMMATION INDEX ON MORTALITY IN PATIENTS WITH PERIPHERAL ARTERY DISEASE." Kocatepe Tıp Dergisi 26, no. 1 (2025): 28–32. https://doi.org/10.18229/kocatepetip.1442806.

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OBJECTIVE: Peripheral artery disease ranks as the third leading cause of death and illness following coronary artery disease and cerebrovascular disease among atherosclerotic conditions, representing a significant health concern worldwide. Our study aims to explore the association between the systemic immune- inflammation index a combined marker of inflammation and aggregation and survival in patients with peripheral artery disease. MATERIAL AND METHODS: In this retrospective cohort study, we examined the medical records of 432 individuals diagnosed with peripheral artery disease between the y

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20

Mietto, Bruno Siqueira, Klauss Mostacada, and Ana Maria Blanco Martinez. "Neurotrauma and Inflammation: CNS and PNS Responses." Mediators of Inflammation 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/251204.

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Traumatic injury to the central nervous system (CNS) or the peripheral nervous system (PNS) triggers a cascade of events which culminate in a robust inflammatory reaction. The role played by inflammation in the course of degeneration and regeneration is not completely elucidated. While, in peripheral nerves, the inflammatory response is assumed to be essential for normal progression of Wallerian degeneration and regeneration, CNS trauma inflammation is often associated with poor recovery. In this review, we discuss key mechanisms that trigger the inflammatory reaction after nervous system trau

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21

Rittner, Heike L., Christian Lux, Dominika Labuz, et al. "Neurokinin-1 Receptor Antagonists Inhibit the Recruitment of Opioid-containing Leukocytes and Impair Peripheral Antinociception." Anesthesiology 107, no. 6 (2007): 1009–17. http://dx.doi.org/10.1097/01.anes.0000291454.90754.de.

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Background Neurokinins (e.g., substance P) contribute to pain transmission in the central nervous system, peripheral neurogenic inflammation, and leukocyte recruitment in inflammation. Leukocyte recruitment involves (1) up-regulation of adhesion molecule expression through neurokinin-1 (NK1) receptors on endothelial cells, (2) augmented chemokine production, or (3) chemotaxis through NK1 receptors on leukocytes. In inflammation, leukocytes can trigger endogenous antinociception through release of opioid peptides and activation of opioid receptors on peripheral sensory neurons. The authors hypo

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22

Su, Xiaomin, and Howard J. Federoff. "Immune Responses in Parkinson’s Disease: Interplay between Central and Peripheral Immune Systems." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/275178.

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The etiology of Parkinson’s disease (PD) is complex and most likely involves numerous environmental and heritable risk factors. Recent studies establish that central and peripheral inflammation occurs in the prodromal stage of the disease and sustains disease progression. Aging, heritable risk factors, or environmental exposures may contribute to the initiation of central or peripheral inflammation. One emerging hypothesis is that inflammation plays a critical role in PD neuropathology. Increasing evidence suggest that activation of the peripheral immune system exacerbates the discordant centr

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23

Pol, Olga, and Margarita M. Puig. "Expression of Opioid Receptors During Peripheral Inflammation." Current Topics in Medicinal Chemistry 4, no. 1 (2004): 51–61. http://dx.doi.org/10.2174/1568026043451519.

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24

Stein, C., A. Herz, and K. Peter. "PERIPHERAL OPIOID RECEPTORS MEDIATING ANALGESIA IN INFLAMMATION." Anesthesiology 71, Supplement (1989): A762. http://dx.doi.org/10.1097/00000542-198909001-00762.

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25

Rees, Huw, Kathleen A. Sluka, Karin N. Westlund, and William D. Willis. "Do dorsal root reflexes augment peripheral inflammation?" NeuroReport 5, no. 7 (1994): 821–24. http://dx.doi.org/10.1097/00001756-199403000-00021.

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26

Stettner, Mark, Sandra Labus, Jan-philipp Weinberger, et al. "Schwann cell locomotion during peripheral nerve inflammation." Journal of Neuroimmunology 275, no. 1-2 (2014): 72. http://dx.doi.org/10.1016/j.jneuroim.2014.08.189.

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27

Omote, Keiichi, Koji Hazama, Tomoyuki Kawamata, et al. "Peripheral nitric oxide in carrageenan-induced inflammation." Brain Research 912, no. 2 (2001): 171–75. http://dx.doi.org/10.1016/s0006-8993(01)02733-0.

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28

Chesnokova, Vera, Robert N. Pechnick, and Kolja Wawrowsky. "Chronic peripheral inflammation, hippocampal neurogenesis, and behavior." Brain, Behavior, and Immunity 58 (November 2016): 1–8. http://dx.doi.org/10.1016/j.bbi.2016.01.017.

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29

Azhari, Hassan, and Mark G. Swain. "Role of Peripheral Inflammation in Hepatic Encephalopathy." Journal of Clinical and Experimental Hepatology 8, no. 3 (2018): 281–85. http://dx.doi.org/10.1016/j.jceh.2018.06.008.

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30

Gray, Marcus, and Gerald Holtmann. "Gut Inflammation: More Than a Peripheral Annoyance." Digestive Diseases and Sciences 62, no. 9 (2017): 2205–7. http://dx.doi.org/10.1007/s10620-017-4587-x.

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31

Marottoli, Felecia M., Yuriko Katsumata, Kevin P. Koster, Riya Thomas, David W. Fardo та Leon M. Tai. "Peripheral Inflammation, Apolipoprotein E4, and Amyloid-β Interact to Induce Cognitive and Cerebrovascular Dysfunction". ASN Neuro 9, № 4 (2017): 175909141771920. http://dx.doi.org/10.1177/1759091417719201.

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Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer’s disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. The goal of this study was to determine the interactive effect of APOE4, Aβ, and chronic repeated peripheral inflammation on cerebrovascular and cognitive dysfunction in vivo. EFAD mice are a well-characterized mouse model that e

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32

Sehgal, Nalini. "Peripherally Acting Opioids and Clinical Implications for Pain Control." Pain Physician 3;14, no. 3;5 (2011): 249–58. http://dx.doi.org/10.36076/ppj.2011/14/249.

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Opioid receptors are widely expressed in the central and peripheral nervous system and in the non-neuronal tissues. Data from animal and human clinical studies support the involvement of peripheral opioid receptors in analgesia, especially in the presence of inflammation. Inflammation has been shown to increase the synthesis of opioid receptors in the dorsal root ganglion neurons and enhance transport and accumulation of opioid receptors in the peripheral terminals of sensory neurons. Under the influence of chemokines and adhesion molecules, opioid peptide-containing immune cells extravasate a

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33

Aries, Michelle, Makayla Cook, and Tiffany Hensley-McBain. "A Pilot Study to Investigate Peripheral Low-Level Chronic LPS Injection as a Model of Neutrophil Activation in the Periphery and Brain in Mice." International Journal of Molecular Sciences 25, no. 10 (2024): 5357. http://dx.doi.org/10.3390/ijms25105357.

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Lipopolysaccharide-induced (LPS) inflammation is used as model to understand the role of inflammation in brain diseases. However, no studies have assessed the ability of peripheral low-level chronic LPS to induce neutrophil activation in the periphery and brain. Subclinical levels of LPS were injected intraperitoneally into mice to investigate its impacts on neutrophil frequency and activation. Neutrophil activation, as measured by CD11b expression, was higher in LPS-injected mice compared to saline-injected mice after 4 weeks but not 8 weeks of injections. Neutrophil frequency and activation

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34

Long, Campbell, Arianne Fritts, Jessica Broadway, Olga Brawman-Mintzer, and Jacobo Mintzer. "Neuroinflammation: A Driving Force in the Onset and Progression of Alzheimer’s Disease." Journal of Clinical Medicine 14, no. 2 (2025): 331. https://doi.org/10.3390/jcm14020331.

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Background/Objectives: The goal of this commentary is to highlight several key components of the inflammatory process as it relates to amyloid toxicity in Alzheimer’s disease (AD), including the role of neuroinflammatory factors and peripheral inflammatory events. Methods: Google Scholar and PubMed were used to find articles with the following keywords: Alzheimer’s disease, amyloids, neuroinflammation, peripheral inflammation, microglia, cytokines, and treatments. Sources that were case reports, not peer-reviewed, or older than 30 years were excluded. Abstracts were reviewed first for their re

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35

Mengr, Anna, Veronika Strnadová, Štěpán Strnad, et al. "Feeding High-Fat Diet Accelerates Development of Peripheral and Central Insulin Resistance and Inflammation and Worsens AD-like Pathology in APP/PS1 Mice." Nutrients 15, no. 17 (2023): 3690. http://dx.doi.org/10.3390/nu15173690.

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Alzheimer’s disease (AD) is a progressive brain disorder characterized by extracellular amyloid-β (Aβ) plaques, intracellular neurofibrillary tangles formed by hyperphosphorylated Tau protein and neuroinflammation. Previous research has shown that obesity and type 2 diabetes mellitus, underlined by insulin resistance (IR), are risk factors for neurodegenerative disorders. In this study, obesity-induced peripheral and central IR and inflammation were studied in relation to AD-like pathology in the brains and periphery of APP/PS1 mice, a model of Aβ pathology, fed a high-fat diet (HFD). APP/PS1

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36

Weaver, Lehn K., Niansheng Chu, and Edward M. Behrens. "TLR9-mediated inflammation drives a Ccr2-independent peripheral monocytosis through enhanced extramedullary monocytopoiesis." Proceedings of the National Academy of Sciences 113, no. 39 (2016): 10944–49. http://dx.doi.org/10.1073/pnas.1524487113.

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Monocytes are innate immune cells that interact with their environment through the expression of pattern recognition receptors, including Toll-like receptors (TLRs). Both monocytes and TLRs are implicated in driving persistent inflammation in autoimmune diseases. However, cell-intrinsic mechanisms to control inflammation, including TLR tolerance, are thought to limit inflammatory responses in the face of repeated TLR activation, leaving it unclear how chronic TLR-mediated inflammation is maintained in vivo. Herein, we used a well-characterized model of systemic inflammation to determine the me

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Muralinath, E., Naidu K. Mohan, Prasad Ch. Srinivas, et al. "Exploring Drugs Targeting Peripheral Nerve Paralysis." Advanced Research and Reviews in Geriatric Nursing & Health Sciences 1, no. 2 (2024): 7–14. https://doi.org/10.5281/zenodo.12624315.

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<em>Peripheral nerve paralysis, condition manifested by the impaired fucation of nerves outside the central nervous system, poses more challenges to patients and health care professionals. Corticosteroids , namely prednisone, are generally prescribed to decrease inflammation and mitigate the immune response that may result in nerve damage. These drugs assist alleviate symptoms and increase the recovery particularly of Peripheral nerves, especially CYP in cases of acute paralysis because of inflammatory conditions. Nonsteroidal anti_ inflammatory drugs (NSAIDs), like ibuprofen, perform by reduc

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Brack, Alexander, Dominika Labuz, Anu Schiltz, et al. "Tissue Monocytes/Macrophages in Inflammation." Anesthesiology 101, no. 1 (2004): 204–11. http://dx.doi.org/10.1097/00000542-200407000-00031.

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Background Opioid-containing leukocytes migrate to peripheral sites of inflammation. On exposure to stress, opioid peptides are released, bind to opioid receptors on peripheral sensory neurons, and induce endogenous antinociception. In later stages of Freund's complete adjuvant-induced local inflammation, monocytes/macrophages are a major opioid-containing leukocyte subpopulation, but these cells also produce proalgesic cytokines. In this study, the role of tissue monocytes/macrophages in hyperalgesia and in peripheral opioid-mediated antinociception was investigated. Methods After intraplanta

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Paouri, Evi, and Spiros Georgopoulos. "Systemic and CNS Inflammation Crosstalk: Implications for Alzheimer’s Disease." Current Alzheimer Research 16, no. 6 (2019): 559–74. http://dx.doi.org/10.2174/1567205016666190321154618.

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After years of failed therapeutic attempts targeting beta-amyloid (A&#946;) in AD, there is now increasing evidence suggesting that inflammation holds a pivotal role in AD pathogenesis and immune pathways can possibly comprise primary therapeutic targets. Inflammation is a key characteristic of numerous diseases including neurodegenerative disorders and thus not surprisingly suppression of inflammation frequently constitutes a major therapeutic strategy for a wide spectrum of disorders. Several brain-resident and peripherally-derived immune populations and inflammatory mediators are involv

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Lopez, CM, Sciullo MP Di, Casas FN Claveles, et al. "Therapeutic targets to reduce the contribution of pulmonary neutrophilic inflammation towards obesity-associated co-morbidities: a mini-review." Open Journal of Pharmaceutical Science and Research 1, no. 1 (2019): 123–33. https://doi.org/10.36811/ojpsr.2019.110006.

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Epidemiology and experimental models have shown a close link between adipose tissue inflammation, systemic inflammation and pulmonary neutrophilic inflammation, which predispose obese patients to pulmonary diseases, obesity-associated co-morbidities and cancer. Increased content and activation of neutrophils in the lung microvasculature, resulting from peripheral activation of neutrophils, and increased adhesion of neutrophils to the lung microvasculature are important factors explaining the increased susceptibility of obese patients towards respiratory diseases and loss of insulin sensitivity

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Gu, Dandan, Yiming Xia, Zihan Ding, et al. "Inflammation in the Peripheral Nervous System after Injury." Biomedicines 12, no. 6 (2024): 1256. http://dx.doi.org/10.3390/biomedicines12061256.

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Nerve injury is a common condition that occurs as a result of trauma, iatrogenic injury, or long-lasting stimulation. Unlike the central nervous system (CNS), the peripheral nervous system (PNS) has a strong capacity for self-repair and regeneration. Peripheral nerve injury results in the degeneration of distal axons and myelin sheaths. Macrophages and Schwann cells (SCs) can phagocytose damaged cells. Wallerian degeneration (WD) makes the whole axon structure degenerate, creating a favorable regenerative environment for new axons. After nerve injury, macrophages, neutrophils and other cells a

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Vorobyeva, O. V., A. A. Pilipovich, and V. V. Fateeva. "Impact of endothelial inflammation on depression in patients with cerebral microangiopathy: a prospective study." Neurology, Neuropsychiatry, Psychosomatics 14, no. 1 (2022): 32–37. http://dx.doi.org/10.14412/2074-2711-2022-1-32-37.

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Epidemiological studies demonstrate a strong relationship between depression and cerebral microangiopathy (CM) associated with arterial hypertension (AH) and cerebral atherosclerosis, but the pathogenetic mechanisms underlying this relationship are not fully understood.Objective: to evaluate the relationship between the level of peripheral markers of endothelial inflammation and depression severity in patients with CM.Patients and methods. The level of peripheral markers of endothelial inflammation was assessed by enzyme immunoassay, and the severity of depression was assessed using the HADS s

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Chieppa, Marcello. "Role of Dendritic Cells in Inflammation." International Journal of Molecular Sciences 21, no. 12 (2020): 4432. http://dx.doi.org/10.3390/ijms21124432.

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Gamache, Daniel A., John T. Povlishock, and Earl F. Ellis. "Carrageenan-induced brain inflammation." Journal of Neurosurgery 65, no. 5 (1986): 679–85. http://dx.doi.org/10.3171/jns.1986.65.5.0679.

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✓ Administration of the mucopolysaccharide, carrageenan (CAR), into the hind paw of the rat or mouse induces a local inflammation characterized by increased arachidonic acid metabolism, increased vascular permeability, edema, and neutrophil extravasation. Carrageenan-induced hind-paw inflammation is inhibited by prostaglandin synthesis inhibitors, and this assay predicts the clinical success of anti-inflammatory agents in reducing peripheral inflammation. The purpose of this study was to determine if intraventricular injection of CAR would induce brain inflammation similar to that evoked by CA

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Xie, Jiaqiang, Zhenxi Guo, Yijing Zhu, Mingde Ma, and Guangwei Jia. "Peripheral blood inflammatory indexes in breast cancer: A review." Medicine 102, no. 48 (2023): e36315. http://dx.doi.org/10.1097/md.0000000000036315.

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Immune and inflammatory responses play an important role in tumorigenesis and metastasis. Inflammation is an important component of the tumor microenvironment, and the changes in inflammatory cells may affect the occurrence and development of tumors. Complete blood count at the time of diagnosis and treatment can reflect the inflammatory status within the tumor. Studies have shown that the number of certain inflammatory cells in peripheral blood and their ratios are important prognostic factors for many malignancies, including neutrophil, lymphocyte, monocyte, and platelet counts, as well as n

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Mallard, Carina. "Central and peripheral inflammation in developmental brain injury." Reproductive Toxicology 56 (August 2015): 4–5. http://dx.doi.org/10.1016/j.reprotox.2015.07.010.

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Kim, Ryul, Han-Joon Kim, Aryun Kim, et al. "Does peripheral inflammation contribute to multiple system atrophy?" Parkinsonism & Related Disorders 64 (July 2019): 340–41. http://dx.doi.org/10.1016/j.parkreldis.2019.03.020.

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Depino, Amaicha Mara. "Peripheral and central inflammation in autism spectrum disorders." Molecular and Cellular Neuroscience 53 (March 2013): 69–76. http://dx.doi.org/10.1016/j.mcn.2012.10.003.

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Gentle, M. J., and V. L. Tilston. "Reduction in Peripheral Inflammation by Changes in Attention." Physiology & Behavior 66, no. 2 (1999): 289–92. http://dx.doi.org/10.1016/s0031-9384(98)00297-2.

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