Post-stroke gastrodin treatment ameliorates ischemic injury and increases neurogenesis and restores the Wnt/β-Catenin signaling in focal cerebral ischemia in mice.

Cerebral ischemic stroke is one of the leading causes of death and disability worldwide, and the only available drug treatment is limited to a short window following the ischemic event. Gastrodin is the major bioactive constituent extracted from thetuberGastrodia elata, and is currently used to treat dizziness in the clinic. "Early" application of gastrodin (before modeling or immediately after ischemic injury) has shown antioxidative and neuroprotective effects in a transient focal brain ischemia model in rodents; however, it is not known whether the delayed administration of gastrodin after permanent focal cerebral ischemia ameliorates neural injury and increases neurogenesis.

Wip1 knockout inhibits neurogenesis by affecting the Wnt/β-catenin signaling pathway in focal cerebral ischemia in mice.

Neurogenesis correlates closely with the recovery of neural function after brain ischemia but the critical proteins and signaling pathways involved remain unclear. The phosphatase WIP1 has been shown to regulate neurogenesis in models of aging. However, it is not known if WIP1 affects neurogenesis and functional recovery after brain ischemia.

The probable metabolic relation between phosphate uptake and energy storages formations under single-stage oxic condition.

To investigate the possible biochemical metabolisms for excess phosphate uptake in a sequencing batch reactor (SBR) with single-stage oxic process, which was reported using glucose as the sole carbon source previously, glucose and acetate were fed to two SBRs as the sole carbon source, respectively. The changes of polyhydroxyalkanoates (PHAs), glycogen and the removal of phosphorus were compared between two SBRs. It was observed that the phosphorus removal efficiency was 91.