Pancreatitis in hand-foot-and-mouth disease caused by enterovirus 71.

Some viruses, including certain members of the enterovirus genus, have been reported to cause pancreatitis, especially Coxsackie virus. However, no case of human enterovirus 71 (EV71) associated with pancreatitis has been reported so far. We here report a case of EV71-induced hand-foot-and-mouth disease (HFMD) presenting with pancreatitis in a 2-year-old girl. This is the first report of a patient with acute pancreatitis in HFMD caused by EV71. We treated the patient conservatively with nasogastric suction, intravenous fluid and antivirals. The patient's symptoms improved after 8 d, and recovered without complications. We conclude that EV71 can cause acute pancreatitis in HFMD, which should be considered in differential diagnosis, especially in cases of idiopathic pancreatitis.

Caspase activity and oxidative stress of granulosa cells are associated with the viability and developmental potential of vitrified immature oocytes.

OBJECTIVE: The aim of this study is to determine whether caspase activity and oxidative stress of granulosa cells are associated with the viability and developmental potential of vitrified immature oocytes. STUDY DESIGN: Oocytes from mice were exposed to genistein or/and Z-VAD-FMK with or without vitrification. Ultrastructural alterations of granulosa cells in vitrified immature oocytes were observed. Moreover, the level of superoxide dismutase (SOD) in granulosa cells, incidence of apoptotic follicles, the viability of vitrified-warmed oocytes and their subsequent developmental competence were measured. RESULTS: Ultrastructural alterations of granulosa cells vitrified in the presence of genistein or Z-VAD-FMK were slighter than that of granulosa cells vitrified in the absence of genistein or Z-VAD-FMK. The incidence of apoptotic follicles vitrified in the presence of genistein or Z-VAD-FMK was significantly lower than that of immature oocytes vitrified in the absence of genistein or Z-VAD-FMK, whereas, the level of SOD in granulosa cells, the viability and developmental competence of immature oocytes vitrified in the presence of genistein or Z-VAD-FMK were significantly higher than that of immature oocytes vitrified in the absence of genistein or Z-VAD-FMK. CONCLUSION: Both antioxidant (genistein) and caspase inhibition (Z-VAD-FMK) improve the viability and developmental competence of vitrified immature oocytes. Genistein is superior to Z-VAD-FMK in improving the efficacy of immature oocyte vitrification.

Attenuation of brain edema and spatial learning deficits by the inhibition of NADPH oxidase activity using apocynin following diffuse traumatic brain injury in rats.

Diffuse brain injury (DBI) is a leading cause of mortality and disability among young individuals and adults worldwide. In specific cases, DBI is associated with permanent spatial learning dysfunction and motor deficits due to primary and secondary brain damage. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) is a major complex that produces reactive oxygen species (ROS) during the ischemic period. The complex aggravates brain damage and cell death following ischemia/reperfusion injury; however, its role in DBI remains unclear. The present study aimed to investigate the hypothesis that levels of NOX2 (a catalytic subunit of NOX) protein expression and the activation of NOX are enhanced following DBI induction in rats and are involved in aggravating secondary brain damage. A rat model of DBI was created using a modified weight-drop device. Our results demonstrated that NOX2 protein expression and NOX activity were enhanced in the CA1 subfield of the hippocampus at 48 and 72 h following DBI induction. Treatment with apocynin (50 mg/kg body weight), a specific inhibitor of NOX, injected intraperitoneally 30 min prior to DBI significantly attenuated NOX2 protein expression and NOX activation. Moreover, treatment with apocynin reduced brain edema and improved spatial learning function assessed using the Morris water maze. These results reveal that treatment with apocynin may provide a new neuroprotective therapeutic strategy against DBI by diminishing the upregulation of NOX2 protein and NOX activity.