Objective To explore the treatment of kala-azar with antimonial resistance in children. Method The clinical data of antimony resistant Kala Azar in a child was analyzed retrospectively, and the related literature were reviewed. Results A 2-year- and 5-month-old boy, suffered from fever, pancytopenia and hepatosplenomegaly. He was diagnosed with kala-azar by bone marrow examination, and improved after the treatment of adequate antimonial. Later, he relapsed twice and the treatment of adequate was effective.. This was the third relapse, and was considered as antimonial resistance. Liposomal amphotericin B (1 mg/kg on day 1, 2 mg/kg on day 2, 3mg/kg on day 3~7 and day 10, with accumulated dose of 21 mg/kg) was used and effective. The child improved and no relapse in one-year follow-up. Conclusion Liposomal amphotericin B can be used in the treatment of kala-azar with antimonial resistance in children.

Optic nerve is composed by the axonal of retinal ganglion cells,there are no Schwann cells around it,and optic nerve belongs to the central nervous,so it cannot regenerate when injuried. In 1985 So and Aguayo have made a success in peripheral nerve retinal transplant,which completely changes the concept that optic nerve injury cannot regenarate. Currently nerve injury recovry has following several methods: use of neurotrophic factor,such as nerve growth factor,ciliary neurotrophic factor and brain-derived neurotrophic factor,etc. These factors could promote the regeneration and repair of retinal ganglion cells; treatment of gene correction and gene regulation,by changing the expression of host gene,reduce the effect due to the disease,slow the progress of the disease course or provide protection against the disease; neural stem cell transplantatin and tissue-engineered Schwann cell transplantion. But these treatments are still at the stage of animal experiment,how timely and effctively reduce the apoptosis and increase the survival rate of ganglion cells,even further promote nerve regeneration and recovery,there is still not a perfect method so far.

Arthritis, Juvenile ; therapy ; Child ; Humans ; Macrophage Activation Syndrome ; therapy ; Plasmapheresis

AIM: To investigate the effect of deoxycholic acid (DCA) on the energy metabolism in human normal colon epithelial NCM460 cells.METHODS: NCM460 cells was treated with DCA at 10, 30 and 100 μmol/L for 5 d, or DCA at 100 μmol/L for 3, 5 and 7 d.After treated with DCA at 100 μmol/L for 3 d, the cells were treated with resveratrol, the activator of sirtuin 3 (SIRT3), for the next 4 d.Adenosine triphosphate (ATP) production in the mitochondria and lactate acid level were detected.The protein expression of SIRT3 was determined by Western blot.RESULTS: DCA inhibited the ATP production, increased lactate acid level, and downregulated the protein expression of SIRT3 in a dose-and time-dependent manner.Resveratrol at 10 μmol/L reversed the effects of DCA on the NCM460 cells.CONCLUSION: DCA induces the dysfunction of energy metabolism in NCM460 cells, and the mechanism may be related with SIRT3.