Greater use of appropriate specimen collection and confirmatory laboratory testing is needed.

BackgroundAlthough cryptococcal meningitis (CM) is an emerging disease worldwide, there have been few studies of the characteristics and risk factors of CM in children.MethodsWe used data collected from May 2007 through April 2012 in the Acute Meningitis-Encephalitis Syndrome Surveillance project in Shi Jiazhuang, China to describe the epidemiologic, clinical, and laboratory findings in children with CM. Furthermore, a matched case–control study was used to determine risk factors of CM.ResultsOverall 23 HIV-negative children with CM (median age: 10.91 years; range: 5 months-17 years) were enrolled in our study. The average annual incidence of CM was 0.43/100,000 with a fatality rate of 1.7%. Most patients were males (60.87%) and rural children (73.91%). Common clinical symptoms included increased intracranial pressure, such as headaches (78.3%), nausea (60.9%), altered mental status (56.5%), vomiting (52.2%), and seizures (43.5%), and frequent laboratory findings consisted of blood leukocytosis (87.0%), decreased CSF glucose (87.0%), pleocytosis (82.6%), increased intracranial pressure (73.9%) and elevated CSF proteins (65.2%). Epidemiologic, clinical, and laboratory findings were similar between patients with and without underlying diseases. Multivariate logistic regression analysis showed that children who had contact with birds/bird droppings or saprophytes were more likely to be infected than those without such contact (odds ratio(OR) =11.82; 95% confidence interval (CI), 2.21-62.24; P = 0.004). Patients with an interval of ≥20 days from onset to admission were at high risk for CM (OR= 5.31; 95%CI, 1.58-17.89; P = 0.007).ConclusionsOur findings show that CM is an uncommon disease with a high mortality rate in children. Although additional studies are needed to find effective prevention and treatments for CM, clinicians should consider CM as a potential cause for pediatric meningitis in children, particularly boys from rural areas, who had contact with birds/bird droppings or saprophytes and in children who did not receive prompt medical attention.

IntroductionOncogenic activation of the K-ras gene occurs in >90% of pancreatic ductal carcinoma and plays a critical role in the pathogenesis of this malignancy. Increase of reactive oxygen species (ROS) has also been observed in a wide spectrum of cancers. This study aimed to investigate the mechanistic association between K-ras–induced transformation and increased ROS stress and its therapeutic implications in pancreatic cancer.MethodsROS level, NADPH oxidase (NOX) activity and expression, and cell invasion were examined in human pancreatic duct epithelial E6E7 cells transfected with K-rasG12V compared with parental E6E7 cells. The cytotoxic effect and antitumor effect of capsaicin, a NOX inhibitor, were also tested in vitro and in vivo.ResultsK-ras transfection caused activation of the membrane-associated redox enzyme NOX and elevated ROS generation through the phosphatidylinositol 3′-kinase (PI3K) pathway. Importantly, capsaicin preferentially inhibited the enzyme activity of NOX and induced severe ROS accumulation in K-ras–transformed cells compared with parental E6E7 cells. Furthermore, capsaicin effectively inhibited cell proliferation, prevented invasiveness of K-ras–transformed pancreatic cancer cells, and caused minimum toxicity to parental E6E7 cells. In vivo, capsaicin exhibited antitumor activity against pancreatic cancer and showed oxidative damage to the xenograft tumor cells.ConclusionsK-ras oncogenic signaling causes increased ROS stress through NOX, and abnormal ROS stress can selectively kill tumor cells by using NOX inhibitors. Our study provides a basis for developing a novel therapeutic strategy to effectively kill K-ras–transformed cells through a redox-mediated mechanism.

General anesthesia in patients with or at risk for neuronal injury remains challenging due to the neurotoxic effects of volatile anesthetics. One inhalation anesthetic, sevoflurane, induces neuronal damage, including neuroapoptosis, and learning and memory impairment. Panax Notoginseng Saponins (PNS) is the active ingredient of Sanqui and has been reported to exert neuroprotective effects. In the current study, the protective effect of PNS on sevoflurane‑induced nerve cell injury was explored. Cell proliferation was significantly reduced in a dose‑dependent manner following stimulation with sevoflurane. Furthermore, cell apoptosis and the protein expression of caspase‑3, caspase‑9 and Bax were significantly increased, while the expression of Bcl‑2 was decreased in the sevoflurane group compared with normal control. Furthermore, the protein level of Bace‑1, APP and Aβ were elevated in the sevoflurane group compared with the control group. By contrast, PNS treatment significantly reduced the neurotoxicity induced by sevoflurane. Additionally, sevoflurane reduced activation of the AKT signaling pathway, which was activated by PNS treatment. In conclusion, the results suggested that PNS attenuates sevoflurane‑induced neurotoxicity through by stimulating cell proliferation and inhibiting cell apoptosis. These effects were mediated, at least in part, by activating the AKT signaling pathway.

No abstract