Stated Boasting Of AG-221

Матеріал з HistoryPedia
Перейти до: навігація, пошук

, 2015)] are the intravenous administration of recombinant tissue plasminogen activator (rtPA) to enzymatically digest the thrombi, endovascular therapy to mechanically remove the large proximal clots, or a combination of both treatment regimes, with the aim to restore blood flow to the hypoperfused area. However, the proportion of stroke patients that satisfy the criteria to undergo treatment is low. Approximately 94% of patients are ineligible for treatment with rtPA (de Los Rios la Rosa et al., 2012; Madsen et al., 2015), due to diminishing benefit and increased risk when administrating Succimer rtPA more than 4.5 h after the ischemic event, in addition to exclusion criteria which includes those patients >80 years, taking anticoagulants, with a history of previous strokes in the last 3 months, those with severe or mild strokes, or lacking a penumbral region (de Los Rios la Rosa et al., 2012; Emberson et al., 2014; Saver et al., 2015). Moreover, the effectiveness of rtPA is limited; only ?10% of patients have a better outcome with treatment, with the site and nature of the occlusion appearing to be a factor RSL3 concentration in efficacy (Paciaroni et al., 2012; Emberson et al., 2014). Hence this approach addresses AG-221 datasheet low eligibility rate to receive treatment following acute ischemic stroke, reperfusion may result in ischemia�Creperfusion injury or subsequent hemorrhage (Paciaroni et al., 2012; Emberson et al., 2014). To date, there are no therapeutic interventions available to inhibit neuronal cell death, or to facilitate regeneration or neurogenesis following a neuronal injury. Research into the cellular and molecular events following an ischemic event in the brain provide a key resource for evaluation of putative therapeutics (Dirnagl et al., 1999; Moskowitz et al., 2010). Of particular interest is a range of endogenous proteins whose expression is up-regulated by stroke-induced brain ischemia, where manipulation of expression may contribute to neuroprotection, neuroregeneration, or neurogenesis.