Institution
Southern Illinois University School of Medicine
Education•Springfield, Illinois, United States•
About: Southern Illinois University School of Medicine is a education organization based out in Springfield, Illinois, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 3747 authors who have published 5977 publications receiving 209115 citations. The organization is also known as: SIU School of Medicine.
Topics: Population, Cancer, Ototoxicity, Receptor, Health care
Papers published on a yearly basis
Papers
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TL;DR: Data demonstrate that in the absence of endogenous IL-10, spontaneous SWS is increased and the impact of LPS on vigilance states is altered and provide further evidence for the involvement of cytokines in the regulation of sleep.
Abstract: Interleukin (IL)-1 and tumor necrosis factor (TNF) promote slow-wave sleep (SWS), whereas IL-10 inhibits the synthesis of IL-1 and TNF and promotes waking. We evaluated the impact of endogenous IL-10 on sleep-wake behavior by studying mice that lack a functional IL-10 gene. Under baseline conditions, C57BL/6-IL-10 knockout (KO) mice spent more time in SWS during the dark phase of the light-dark cycle than did genetically intact C57BL/6 mice. The two strains of mice showed generally comparable responses to treatment with IL-1, IL-10, or influenza virus, but differed in their responses to lipopolysaccharide (LPS). In IL-10 KO mice, LPS induced an initial transient increase and a subsequent prolonged decrease in SWS, as well as profound hypothermia. These responses were not observed in LPS-treated C57BL/6 mice. These data demonstrate that in the absence of endogenous IL-10, spontaneous SWS is increased and the impact of LPS on vigilance states is altered. Collectively, these observations support a role for IL-10 in sleep regulation and provide further evidence for the involvement of cytokines in the regulation of sleep.
69 citations
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TL;DR: Results indicate that NADA is a potent agonist of VR when the receptor is in the PKC-mediated phosphorylation state and exposure of NADA to the intracellular surface of the membrane-induced larger currents suggesting inaccessibility to the intrusion site might contribute to its weaker action.
Abstract: The search for an endogenous ligand for the vanilloid receptor (VR or TRPV1) has led to the identification of N-arachidonyl dopamine (NADA). This study investigates the role of protein kinase C (PK...
69 citations
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TL;DR: The data suggest that the combination of severe hearing loss and old age results in deficits in one or more inhibitory glycinergic circuits in the cochlear nucleus in the CN.
Abstract: Glycinergic neurons in the cochlear nucleus (CN) of C57BL/6J (C57) and CBA/CaJ (CBA) mice were studied by using immunocytochemical and receptor-binding techniques. Adult C57 mice exhibit progressive cochlear pathology as they age, whereas aging CBA mice retain good hearing. In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactive neurons decreased significantly. The number (Bmax) of strychnine-sensitive glycine receptors (GlyR) decreased significantly in the dorsal CN of old C57 mice. Significant effects were not observed in the CN of middle-aged C57 mice (with less-severe hearing loss) or in very old CBA mice (which do not exhibit severe hearing loss). The data suggest that the combination of severe hearing loss and old age results in deficits in one or more inhibitory glycinergic circuits in the CN.
69 citations
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TL;DR: A significant alteration in interaction between the GABA and picrotoxin binding sites was observed in the inferior colliculus of aged rats when compared to 3-month-old young adults, which appears to reflect an increased sensitivity of the receptor to GABA modulation in aged rats and, thus, may serve as a compensatory mechanism to enhance GABAA receptor function in response to a presynaptic loss of inhibition.
69 citations
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TL;DR: The early microcirculatory observations seen after rewarming suggest progressive and severe perturbations in platelet function and fibrin formation that are significantly different from ischemia/reperfusion injury.
Abstract: Frostbite represents a spectrum of injury ranging from irreversible cellular destruction to reversible changes seen after rewarming. These changes include increases in tissue edema, circulatory stasis, and progressive thrombosis leading to further tissue necrosis. For this reason, it is often difficult at the time of surgical debridement to determine the extent of frostbite injury. This delayed tissue injury is similar to that seen in muscle during ischemia/reperfusion injury. Muscle that initially appears viable on reperfusion may subsequently necrose due to collapse of the microcirculation. Adherent neutrophils have been specifically cited as important components in ischemia/reperfusion injury and have also been suggested to play a role in frostbite injury. We have used an intravital microscopic muscle preparation to study microcirculatory changes carefully in frostbite injury during rewarming. The right gracilis muscle of male Wistar rats is dissected free from its primary vascular pedicle and the rat is positioned on a specially constructed microsurgical stage. Temperature changes of the muscle are recorded. The prepared axial pattern flap is transilluminated with a microscope and projected on a video screen, allowing measurement of arteriolar diameters and changes in the numbers of stuck and rolling neutrophils before frostbite, during rewarming, and for several hours later. Cold silicone oil is used to freeze the muscle to -5 ± 2°C in 2 to 3 minutes and to hold this temperature for 5 minutes. The muscle is rewarmed with 42°C normal saline placed directly on the muscle surface. Baseline vessel diameter and leukocyte counts in 100-mm segments of the microvasculature are recorded as well as at 5, 15, and 30 minutes, and at 1, 2, and 3 hours postrewarming of frozen muscle. Observations from our initial 11 animals show that reperfusion of the muscle following freezing is varied temporally and spatially , with circulation to most vascular segments restored 5 to 10 minutes after rewarming. In 9 of 11 animals we observed the shedding of white clots in small arterioles and venules occurring as soon as 5 minutes after thawing. In some instances shedding continued for as long as 1 hour after rewarming. Microvascular hemorrhage was widespread 1 hour following the thaw, but there was no significant increase in neutrophil adherence observed until 3 hours following rewarming. The exact nature of the vascular injury and the composition of the white clots are now being determined from ultrastructural studies. Blood flow in microcirculation stops during freezing, but small-vessel perfusion returns immediately on thawing. This suggests that the vascular architecture is maintained during the freezing and thawing. Unlike ischemia/reperfusion injury, neutrophil adhesion plays a smaller role in the early response to frostbite injury. The early microcirculatory observations seen after rewarming suggest progressive and severe perturbations in platelet function and fibrin formation that are significantly different from ischemia/reperfusion injury.
69 citations
Authors
Showing all 3778 results
Name | H-index | Papers | Citations |
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Jatin P. Shah | 119 | 725 | 45680 |
Harold G. Koenig | 99 | 678 | 46742 |
Chawnshang Chang | 97 | 534 | 35629 |
Richard J. K. Taylor | 91 | 1543 | 43893 |
Martin R. Farlow | 82 | 381 | 26820 |
David A. D'Alessio | 80 | 272 | 22955 |
Dirk R. Larson | 79 | 271 | 24067 |
Andrzej Bartke | 78 | 516 | 22865 |
Michael Brenner | 76 | 564 | 22010 |
Arnulf Stenzl | 73 | 791 | 23285 |
Wolfgang H. Dillmann | 72 | 200 | 17595 |
Michael Bonkowski | 66 | 279 | 13851 |
Jacob E. Friedman | 65 | 191 | 12485 |
Richard Salvi | 65 | 447 | 16289 |
Russell Noyes | 63 | 229 | 12790 |