In summary, our current data indicated that expression of mPRa may have a negative correlation with ER expression. Coordinately, mPRa expression was significantly higher in HER2+ subtype cancers as compared to ER+ subtype cancers. In addition, mPRa expression may also associate with EGFR + cancers and cancers with higher level of Ki67 expression. These data support our hypothesis that P4 interacts with caveolin-1 and modulates the activities of the PI3K pathways and cell proliferation through caveolar membrane bound growth factor receptors, which may include mPRa and HER2/EGFR. MPRa may emerge as a novel biomarker for breast cancer beyond the widely used ER, PR, and HER2. Acute brain ischemia is primarily caused by a disruption of cerebral blood flow through thromboembolism that leads to an oxygen and glucose deprivation, excessive glutamate release and subsequent postsynaptic overstimulation of glutamate receptors, a process known to be critical in ischemia-induced neuronal death. Over the past 10 years, a series of in vitro and in vivo studies in models of hypoxic/ischemic insults has demonstrated the neuroprotective potential of some inert gases, among which xenon has been identified as the most promising agent. However, the major obstacle to the L-Thyroxine widespread clinical use of xenon is its scarceness and excessive cost of production. Interestingly argon, which is a cost-efficient and easily available gas with no narcotic and anesthetic action at normal atmospheric pressure, has been also shown to provide organoprotection and neuroprotection against hypoxic-ischemic insults. Recent in vivo studies have further shown that intraischemic argon at 50 vol% provides both cortical and subcortical neuroprotection in rats subjected to transient middle cerebral artery occlusion. However, despite this latter study, our knowledge on the ability of argon to provide neuroprotection in acute ischemic stroke still remains limited and Trihexyphenidyl HCl should be augmented to evaluate the actual neuroprotective potential of this gas. Particularly, whether argon could provide neuroprotection when given after ischemia still remained unknown. This latter point is not trivial since previous data have shown the critical importance of the time at which inert gases are administered, during or after ischemia, to obtain neuroprotection. Therefore, in the present report, in order to assess thoroughly the neuroprotective potential of argon and to determine whether argon could be a cost-efficient alternative to xenon, we studied the neuroprotective effect of postischemic argon in vitro in brain slices exposed to ischemia in the form of oxygen and glucose deprivation and in vivo in rats subjected to transient MCAO-induced ischemia or NMDA-induced excitotoxic insult. The present study shows that argon given after an excitotoxic or ischemic insult reduces cell injury induced by OGD ex vivo, subcortical neuronal death induced by NMDA injection, and cortical brain damage induced by MCAO.