(J Vase Surg 2010;51:203-6 )”
“Epidemiological studies have

(J Vase Surg 2010;51:203-6.)”
“Epidemiological studies have raised the possibility of caffeine serving as a neuroprotective agent in Parkinson’s disease (PD). This possibility has gained support from findings that dopaminergic neuron toxicity induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or other neurotoxins is attenuated by co-administration

of caffeine in mice. Here we examined the time window of caffeine’s neuroprotection as well as the effects of caffeine’s metabolites (theophylline PRN1371 supplier and paraxanthine) in the MPTP mouse model of PD. In the first experiment, caffeine pre-treatment (30 mg/kg ip) significantly attenuated MPTP-induced striatal dopamine depletion when it was given 10 min, 30 min, 1 h, or 2 h but not 6 h before MPTP (40 mg/kg ip) treatment. Meanwhile, caffeine post-treatment Tideglusib molecular weight also significantly attenuated striatal dopamine loss when it was given 10 min, 30 min, 1 h or 2 h but not 4 h, 8 h or 24 h after MPTP injection. In the second experiment, both theophylline (10 or 20 mg/kg) and paraxanthine

(10 or 30 mg/kg) administration (10 min before MPTP) significantly attenuated MPTP-induced dopamine depletion in mice, as did caffeine (10 mg/kg) treatment. Thus the metabolites of caffeine also provide neuroprotective effects in this mouse model of PD. The data suggest that if caffeine protects against putative toxin-induced dopaminergic neuron injury in humans, then precise temporal pairing between caffeine and toxin exposures may not be critical because the duration of neuroprotection by caffeine may be extended by protective effects of its major metabolites. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“A Y-27632 in vitro 52-year-old man presented 33 months after thoracic aortic endovascular repair with hemoptysis and was found to have an aortobronchial fistula secondary to a mycotic aneurysm. The endograft infection was managed in a two-stage

fashion. During the initial stage, the patient underwent an ascending-to-descending thoracic aortic bypass. Neither cardiopulmonary bypass, hypothermic circulatory arrest, nor aortic cross-clamping were used. During the same hospitalization, the patient underwent successful endograft explantation through a left thoracotomy. Imaging at 6 months demonstrated no anastomotic concerns and resolution of residual pulmonary inflammation. Thoracic aortic endograft infections necessitating endograft removal can potentially be successfully and safely managed without the need for cardiopulmonary bypass, hypothermic circulatory arrest, or interruption of aortic blood flow. (J Vase Surg 2010;51:207-9.)”
“In this study we investigate on the effect of amyloid-beta1-40 (A beta 1-40) on the oxotremorine (OXO)-induced release of [(3)H] dopamine (DA), [(3)H]GABA and [(3)H]acetylcholine (ACh) from synaptosomes in the rat nucleus accumbens (NAc). OXO in presence of himbacine (HIMBA) was able to increase the basal release of [(3)H]GABA.

Comments are closed.