The Non-Anhydrous, Minimally Basic Synthesis of the Dopamine D Agonist [18F]MCL-524.

The dopamine D agonist MCL-524 is selective for the D receptor in the high-affinity state (D), and, therefore, the PET analogue, [F]MCL-524, may facilitate the elucidation of the role of D in disorders such as schizophrenia. However, the previously reported synthesis of [F]MCL-524 proved difficult to replicate and was lacking experimental details. We therefore developed a new synthesis of [F]MCL-524 using a "non-anhydrous, minimally basic" (NAMB) approach.

Mitochondrial transplantation by intra-arterial injection for acute kidney injury.

Acute kidney injury is a common clinical disorder and one of the major causes of morbidity and mortality in the postoperative period. In this study, the safety and efficacy of autologous mitochondrial transplantation by intra-arterial injection for renal protection in a swine model of bilateral renal ischemia-reperfusion injury were investigated. Female Yorkshire pigs underwent percutaneous bilateral temporary occlusion of the renal arteries with balloon catheters.

A non-anhydrous, minimally basic protocol for the simplification of nucleophilic F-fluorination chemistry.

Fluorine-18 radiolabeling typically includes several conserved steps including elution of the [F]fluoride from an anion exchange cartridge with a basic solution of KCO or KHCO and Kryptofix 2.2.2.

A Novel Biological Strategy for Myocardial Protection by Intracoronary Delivery of Mitochondria: Safety and Efficacy.

Mitochondrial dysfunction is the determinant insult of ischemia-reperfusion injury. Autologous mitochondrial transplantation involves supplying one's healthy mitochondria to the ischemic region harboring damaged mitochondria. The authors used in vivo swine to show that mitochondrial transplantation in the heart by intracoronary delivery is safe, with specific distribution to the heart, and results in significant increase in coronary blood flow, which requires intact mitochondrial viability, adenosine triphosphate production, and, in part, the activation of vascular K channels.

Mitochondrial transplantation enhances murine lung viability and recovery after ischemia-reperfusion injury.

The most common cause of acute lung injury is ischemia-reperfusion injury (IRI), during which mitochondrial damage occurs. We have previously demonstrated that mitochondrial transplantation is an efficacious therapy to replace or augment mitochondria damaged by IRI, allowing for enhanced muscle viability and function in cardiac tissue. Here, we investigate the efficacy of mitochondrial transplantation in a murine lung IRI model using male C57BL/6J mice.