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Veress G.,Pathology Unit | Veress G.,Debrecen University | Meszar Z.,Debrecen University | Muszil D.,Debrecen University | And 4 more authors.
Brain Structure and Function | Year: 2013

The cannabinoid 1 (CB1) receptor is expressed by a sub-population of primary sensory neurons. However, data on the neurochemical identity of the CB1 receptor-expressing cells, and CB1 receptor expression by the peripheral and central terminals of these neurons are inconsistent and limited. We characterised CB1 receptor expression in dorsal root ganglia (DRG) and spinal cord at the lumbar 4-5 level, as well as in the urinary bladder and glabrous skin of the hindpaw. About 1/3 of DRG neurons exhibited immunopositivity for the CB1 receptor, the majority of which showed positivity for the nociceptive markers calcitonin gene-related peptide (CGRP) or/and Griffonia (bandeiraea) simplicifolia IB4 isolectin-binding. Virtually all CB1 receptor-immunostained fibres showed immunopositivity for CGRP in the skin, while very few did in the urinary bladder. No CB1 receptor-immunopositive nerve fibres were IB4 positive in either peripheral tissue. Spinal laminae I and II-outer showed the highest density of CB1 receptor-immunopositive punctae, the majority of which showed positivity for CGRP or/and IB4 binding. These data indicate that a major sub-population of nociceptive primary sensory neurons expresses CB1 receptors that are transported to both peripheral and central terminals of these cells. Therefore, the present data suggest that manipulation of endogenous CB1 receptor agonist levels in these areas may significantly reduce nociceptive input into the spinal cord. © 2012 Springer-Verlag.

Horvath A.,University of Szeged | Santha P.,University of Szeged | Horvath V.,University of Szeged | Torok N.,University of Szeged | And 4 more authors.
Acta Biologica Hungarica | Year: 2013

A new, rapid method is described which permits the genotyping of genetically modified animals from a microlitre volume of whole blood samples via one step polymerase chain reaction amplification. The major advantage of the presented method is the exclusion of a DNA preparation step, which significantly reduces the time expenditure and work load of the genetic testing. Pilot studies indicate, that this method is efficient and applicable also on tissue biopsies and larger amount of blood providing a rapid and reliable new technique over conventional genotyping approaches. © 2013 Akadémiai Kiadó, Budapest.

Wan Y.,Gongli Hospital | Xu J.,Gongli Hospital | Meng F.,Xuzhou Medical College | Bao Y.,Xuzhou Medical College | And 7 more authors.
Critical Care Medicine | Year: 2010

Objective: Elderly patients undergoing major surgery often develop cognitive dysfunction and the mechanism of this postoperative complication remains elusive. We sought to determine whether postoperative cognitive dysfunction in old mice is associated with the pathogenesis of Alzheimer's disease. Design: Prospective, randomized study. Setting: University teaching hospital-based research laboratory. SUBJECTS: One-hundred and twenty C57BL/6 14-mo-old male mice (weighing 30-40 g). InterventionS: Mice received intraperitoneal injections of either vehicle or Celastrol (a potent anti-inflammatory compound) for 3 days before undergoing sham surgery or partial hepatectomy, on the surgery day, and for a further 4 days after surgery. Cognitive function, hippocampal neuroinflammation, and pathologic markers of Alzheimer's disease were assessed 1 day after surgery day 1, 3, or 7. Measurements and Main Results: Cognitive impairment following surgery was associated with the appearance of certain pathologic hallmarks of Alzheimer's disease: microgliosis, astrogliosis, enhanced transcriptional and translational activity of β-amyloid precursor protein, β-amyloid production, and τ protein hyperphosphorylation in the hippocampus. Surgery-induced changes in cognitive dysfunction were prevented by the administration of Celastrol as were changes in β-amyloid and τ processing. Conclusions: These data suggest that surgery can provoke astrogliosis, β-amyloid accumulation, and τ phosphorylation in old subjects, which is likely to be associated with the cognitive decline seen in postoperative cognitive dysfunction. Copyright © 2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

Zhao H.,Section of Anaesthetics | Luo X.,Section of Anaesthetics | Luo X.,Hubei University of Medicine | Zhou Z.,Section of Anaesthetics | And 5 more authors.
Kidney International | Year: 2014

Chronic allograft nephropathy (CAN) is a common finding in kidney grafts with functional impairment. Prolonged hypothermic storage-induced ischemia-reperfusion injury is associated with the early onset of CAN. As the noble gas xenon is clinically used as an anesthetic and has renoprotective properties in a rodent model of ischemia-reperfusion injury, we studied whether early treatment with xenon could attenuate CAN associated with prolonged hypothermic storage. Exposure to xenon enhanced the expression of insulin growth factor-1 (IGF-1) and its receptor in human proximal tubular (HK-2) cells, which, in turn, increased cell proliferation. Xenon treatment before or after hypothermia-hypoxia decreased cell apoptosis and cell inflammation after reoxygenation. The xenon-induced HK-2 cell proliferation was abolished by blocking the IGF-1 receptor, mTOR, and HIF-1 individually. In the Fischer-To-Lewis rat allogeneic renal transplantation model, xenon exposure of donors before graft retrieval or recipients after engraftment enhanced tubular cell proliferation and decreased tubular cell death and cell inflammation associated with ischemia-reperfusion injury. Compared with control allografts, xenon treatment significantly suppressed T-cell infiltration and fibrosis, prevented the development of CAN, and improved renal function. Thus, xenon treatment promoted recovery from ischemia-reperfusion injury and reduced susceptibility to the subsequent development of CAN in allografts © 2013 International Society of Nephrology.

Luo X.,Hubei University of Medicine | Zhao H.,Section of Anaesthetics | Hennah L.,Section of Anaesthetics | Ning J.,Section of Anaesthetics | And 3 more authors.
British Journal of Anaesthesia | Year: 2015

Background: Metastatic recurrence of ovarian cancer is the foremost cause of postoperative mortality. With recent research indicating that inhalation of anaesthetics may influence cancer cell behaviour, this study investigated the effects of isoflurane on the expression of tumorigenic markers and proliferative capacity in ovarian cancer cells. Methods: Ovarian cancer (SK-OV3) cells were cultured and then exposed to 2% isoflurane for 2 h. The expression of markers involved in cell proliferation, angiogenesis, and migration were assessed up to 24 h after treatment using immunofluorescence staining, western blotting, and flow cytometry. The effects of isoflurane on in vitro angiogenesis and migration were also determined. Results: Isoflurane exposure significantly increased insulin-like growth factor (IGF)-1 and IGF-1R expression, cell cycle progression, and cell proliferation in SK-OV3 cells. Increased expression of the angiogenic markers vascular endothelial growth factor (VEGF) by 56% (P<0.05) and angiopoietin-1 by 62% (P<0.05) was also observed 24 h after isoflurane exposure together with an enhanced in vitro angiogenesis. Cell migration was significantly increased after exposure to isoflurane together with increased production of both matrix metalloproteinases 2 and 9 (both P<0.05) by almost five-fold relative to control. These effects were abolished when IGF-1R signalling was blocked either by neutralizing antibody or by small interfering RNA. Conclusions: Our data indicate that isoflurane increases the malignant potential of ovarian cancer cells through the up-regulation of markers associated with the cell cycle, proliferation, and angiogenesis. This study warrants further investigations. © The Author 2014. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.

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