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81.
HSS Journal ® - 相似文献
82.
HSS Journal ® - Spinal fusion surgery is performed all over the world to help patients with cervical and thoracolumbar pathology. As outcomes continue to improve in patients with spine-related... 相似文献
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Jianfeng Liang Dongman Chao Harleen K Sandhu Yanbing Yu Li Zhang Gianfranco Balboni Dong H Kim Ying Xia 《British journal of pharmacology》2014,171(23):5417-5430
Background and Purpose
Astrocytic excitatory amino acid transporters (EAATs) regulate extracellular glutamate concentrations and play a role in preventing neuroexcitotoxicity. As the δ-opioid receptor (DOP receptor) is neuroprotective against excitotoxic injury, we determined whether DOP receptor activation up-regulates EAAT expression and function.Experimental Approach
We measured mRNA and protein expression of EAAT1, EAAT2 and EAAT3 in cultured mouse astrocytes exposed to a specific DOP receptor agonist (UFP-512) with or without a DOP receptor antagonist, DOP receptor siRNA or inhibitors of PKC, PKA, PI3K, p38, MAPK, MEK and ERK, and evaluated the function of EAATs by measuring glutamate uptake.Key Results
Astrocytic DOP receptor mRNA and protein were suppressed by DOP receptor siRNA knockdown. DOP receptor activation increased mRNA and protein expression of EAAT1 and EAAT2, but not EAAT3, thereby enhancing glutamate uptake of astrocytes. DOP receptor-induced EAAT1 and EAAT2 expression was largely reversed by DOP receptor antagonist naltrindole or by DOP receptor siRNA knockdown, and suppressed by inhibitors of MEK, ERK and p38. DOP receptor-accelerated glutamate uptake was inhibited by EAAT blockers, DOP receptor siRNA knockdown or inhibitors of MEK, ERK or p38. In contrast, inhibitors of PKA, PKC or PI3K had no significant effect on DOP receptor-induced EAAT expression.Conclusions and Implications
DOP receptor activation up-regulates astrocytic EAATs via MEK-ERK-p38 signalling, suggesting a critical role for DOP receptors in the regulation of astrocytic EAATs and protection against neuroexcitotoxicity. As decreased EAAT expression contributes to pathophysiology in many neurological diseases, including amyotrophic lateral sclerosis, our findings present a new platform for potential treatments of these diseases.Table of LinksTARGETS | LIGANDS |
---|---|
δ receptor (DOP receptor) | Calphostin C |
μ receptor (MOP receptor) | DPDPE |
EAAT1 | DL-TBOA |
EAAT2 | FR180204 |
EAAT3 | L-glutamate |
ERK | Naltrindole |
MEK | SB203580 |
p38MAPK (p38) | UCPH-101 |
PI3K | U0126 |
PKA | |
PKC |
86.
Amneet Sandhu Joseph L. Schuller Wendy S. Tzou Alexis Z. Tumolo William H. Sauer Duy T. Nguyen 《Pacing and clinical electrophysiology : PACE》2019,42(3):301-305
A 62‐year‐old man was referred to our institution for high‐density, symptomatic premature ventricular contractions (PVCs) with resultant decrease in left ventricular (LV) function having failed prior ablation attempts. Successful, durable ablation of the patient's mid‐myocardial PVC arising from the LV summit region was achieved through the proximal great cardiac vein with ablation depth augmented by use of half‐normal saline irrigant. Though standard ablation of ventricular arrhythmias using normal saline irrigation from the coronary venous system has been well‐reported, this may be of limited value in addressing mid‐myocardial sites of origin. This novel case describes the safe use of cooled radiofrequency ablation with use of half‐normal saline irrigant from the distal coronary sinus as an option to address complex sites of PVC origin such as the LV summit. 相似文献
87.
We tested the hypothesis that loss of mitochondrial adenine nucleotides during myocardial ischemia is induced by the accumulation of inorganic phosphate (Pi) and a decrease in cytosolic ATP. In the isolated perfused rat heart, loss of mitochondrial adenine nucleotides (ATP + ADP + AMP) was preceded by the rise in tissue Pi and the loss of tissue ATP. After 30 min ischemia, the average rate of loss of mitochondrial adenine nucleotides was c. 1.5% of the initial pool/min. In isolated heart mitochondria, there are two pathways for adenine nucleotide release: a 'fast', phosphate-dependent pathway, which is inhibited by atractyloside; and a 'slow', phosphate-independent pathway, which is insensitive to atractyloside. Decreasing the pH from 7.4 to 6.5 significantly decreased the rate of release by the phosphate-dependent pathway (but not the phosphate-independent pathway). Analysis of release rates indicated that HPO4-2 is responsible for the phosphate-induced release; Vmax = 53.8% of the pool/per minute, Km = 7.5 mM. In vitro, extramitochondrial ATP inhibited adenine nucleotide release in the presence of Pi such that the rate of release was inversely proportional to the extramitochondrial [ATP]; extrapolation to zero ATP indicated a release rate of 2 to 3% of the pool/per minute, which is approximately equal to the rate of the 'slow' phosphate-independent pathway. Moreover, increasing the Pi concentration did not increase the rate of adenine nucleotide release in the presence of extramitochondrial ATP. Accumulation of mitochondrial adenine nucleotides was observed when the mitochondria were incubated in the presence of 4 mM or greater ATP. The results suggest that the rise in intracellular Pi during myocardial ischemia does not induce the loss of adenine nucleotides from the mitochondrial compartment, but rather that degradation of cytosolic ATP results in a slowing of ATP influx such that the rate of efflux (phosphate-independent) exceeds the rate of influx. 相似文献
88.
Baumgartner C; Morell A; Hirt A; Bucher U; Forster HK; Doran JE; Matter L; Brun del Re G; Wagner HP 《Blood》1988,71(5):1211-1217
Elimination of neoplastic B cell populations from autologous bone marrow grafts also removes normal B lymphocytes. This is potentially hazardous for the reconstitution of the immune system in patients undergoing high-dose chemotherapy and total body irradiation followed by autologous marrow rescue. Five pediatric patients with B cell non- Hodgkin's lymphoma in first remission undergoing such a regimen were studied. They received bone marrow pretreated with anti-Y 29/55 monoclonal antibody and complement. B and T lymphocyte subpopulations reached normal levels within 6 months after autologous bone marrow transplantation (ABMT), and serum immunoglobulin levels became normal within 4 to 9 months. Vaccination with diphtheria and tetanus toxoid, trivalent poliomyelitis vaccine of the Salk type, and pneumococcal capsular antigens (38 to 54 months after transplantation) gave rise to specific antibody production. ABO isoagglutinins could be demonstrated in all patients. The response pattern was similar to that of patients who received unmanipulated autologous bone marrow. It is concluded that ex vivo anti-Y 29/55 depletion of the marrow graft does not induce relevant disturbances of humoral immune functions. 相似文献
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