Trends in drug-resistant tuberculosis after the implementation of the DOTS strategy in Shenzhen, China, 2000-2013.

SETTING: The DOTS strategy has been regarded as the most cost-effective way to stop the spread of tuberculosis (TB) since its launch by the World Health Organization. OBJECTIVE: To estimate the effects of DOTS by tracking long-term trends in multidrug-resistant TB (MDR-TB). DESIGN: A retrospective cohort study was conducted from 2000 to 2013 to analyse trends in resistance to anti-tuberculosis drugs and the effect of DOTS-based treatment in Shenzhen, China, using the χ2 test. RESULTS: An overall MDR-TB rate of 4.2% was observed between 2000 and 2013, with an annual reduction of 0.16%. From 2000 to 2013, trends in resistance to isoniazid (INH), rifampicin (RMP) and MDR-TB declined significantly in new TB patients (P < 0.01), but not in retreatment cases. Sputum smear conversion rates after 2 months of treatment decreased significantly, in particular after 2007, in new and retreatment cases. CONCLUSION: INH and RMP resistance and MDR-TB rates declined significantly, suggesting that DOTS-based programmes were successful in reducing drug resistance in new cases but not in retreatment cases. The decreasing sputum smear conversion rates may have been due to an increase in the number of migrants. These two findings suggest that TB is unlikely to be completely eliminated by 2050 in Shenzhen.

Phosphatidylinositol 3 kinase/protein kinase B is responsible for the protection of paeoniflorin upon H2O2-induced neural progenitor cell injury.

Promoting neural stem/progenitor cell (NSC/NPC) survival in the pro-apoptotic environment is critical to stem cell replacement for neurodegenerative disease therapy. Paeoniflorin (PF), one of the principal bioactive components in Paeoniae Radix, has been used widely in central nervous system (CNS) diseases treatment and serves as an antioxidant to protect neurons against oxidative stress. The present study investigated the protective effects of PF on NPC injury induced by hydrogen peroxide (H2O2). After challenge with 200 µM H2O2 for 2h, loss of cell viability and excessive apoptotic cell death were observed in cultured NPC, PF treatment conferred protective effects against the loss of cellular viability in a concentration-dependent manner. PF pretreatment also inhibited NPC apoptosis induced by H2O2 by reversing the decreased level of Procaspase-3 and balancing Bcl-2 and Bax expression. Furthermore, PF-mediated NPC protection was associated with an increase in phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt-1) phosphorylation in a time- and concentration-dependent manner. Selective inhibition of PI3K using LY294002 abolished PF-mediated phosphorylation of Akt-1 and NPC protection upon oxidative stress. These data suggest that PF-mediated NPC protection on H2O2 injury is reliant on the activation of the PI3K/Akt-1 pathway, giving insight to an essential role of PF in NPC protection.