In vitro exposure to thapsigargin induced murine cardiomyocyte dysfunction reminiscent of the in vivo setting, the effects of which were ablated by the NADPH oxidase inhibitor apocynin and the mitochondrial Ca uptake inhibitor Ru360.In addition, apocynin abrogated thapsigargin-induced loss of mitochondrial membrane potential and permeability transition pore opening, similar to chronic Akt activation.
Many salespeople would tell customers that dies were the property of the customer.
In general, just about everyone (except the Trustee) agrees that  Medallic dies usually belong to Medallic (unless the customer arranged otherwise), and  NWTM dies usually belong to the customer.
The court has approved the settlement for the ownership transfer in the amount of 0.00 per die." However, I have seen nothing in court records or hearings suggesting that the Court has determined that NWTM has retained ownership of NWTM dies -- in fact, the hearing is designed to tackle that issue!
I also have seen nothing about the court approving any specific settlement at 0: it authorized the Trustee to settle, but the implication was that it was at whatever the Trustee and the customer agreed to.
Today, a law firm representing a number of creditors filed a "Motion to Enforce a Prior Court Order." From the title, it means that somebody (allegedly) didn't do what the Judge told them to in a signed order. In this case, it's pretty much what I wrote in my "NWTM False Claims" post: Calvert is allowing E-mails to be sent out claiming that the Court said things it did not, and trying to cheat (trick people into paying for dies they own, by lying and saying that the court said it was OK). There is an old expression "where there is smoke, there is fire." I interpret to mean that if you discover one bad thing happening, it is MUCH more likely that other bad things are happening there than in some other random location.
And while some have referred to allegations of wrongdoing as a "crazy colorful conspiracy theory", this is at least the second time there has been a credible court filing showing that Mr.Thapsigargin compromised echocardiographic parameters, including elevating LVESD and reducing fractional shortening; suppressed cardiomyocyte contractile function, intracellular Ca handling, and cell survival; and enhanced carbonyl formation, apoptosis, superoxide production, NADPH oxidase expression, and mitochondrial damage.Interestingly, these anomalies were attenuated or mitigated by chronic Akt activation.Given that NADPH oxidase was recently implicated in ER stress-induced tissue injury, this study was designed to examine the role of NADPH oxidase in ER stress-induced cardiac mechanical defects and the impact of Akt activation on ER stress-induced cardiac anomalies.Wild-type and transgenic mice with cardiac-specific overexpression of an active mutant of Akt (My Akt) were subjected to the ER stress inducer thapsigargin (1 and 3 mg/kg, ip, for 48 h).► The beneficial effect of Akt was mediated through NADPH oxidase and mitochondrial function.