Plasmodium falciparum(Lab.culture FCR3 isolate) developed resistance to sodium artesunate after exposure to the drug in vitro.The drug effective concentration which resulted in 50 per cent schizont maturation inhibition (IC50) was 1.6ng/ml (4.1nmol/L) before exposure to the drug.After 130 days of discontiguous exposure to sodium artesunate in a stepwise fashion,the sensitivity of the isolate to the drug decreased,with its IC50 3-fold higher than that of the parent isolate.The resistance to artesunate decreased significantly after the resistant line was grown in drug-free medium.

Objective To identify the genotype of merozoite surface protein 1 (MSP1) of Plasmodium falciparum isolates from Hainan Province. Methods Nested PCR was applied to amplify the MSP1 of Blocks 2 and 3 Plasmodium falciparum isolates from Hainan Province. Two allelic family representitive gene fragments were sequenced.Results From 36 out of 39 blood samples from Plasmodium falciparum patients, 44 gene fragments of blocks 2 and 3 of the MSP1 were amplified, of which the MAD20 type allele was dominant(75%). followed by K1 type allele. No RO33 type allele was found. The mixed infection rate of the two different allelic type was 19 4%. Sequence analysis showed that the sequences of MAD20 and K1 type isolates from Hainan Province were highly homologous to that of the MAD20 and K1 allelic prototypes.Conclusion Two principal allelic types of MSP1 gene, MAD20 and K1 type, exist in malaria endemic areas in Hainan Province, the MAD20 type being the dominant.

Objective To analyze the incidence,bacterial spectrum and clinical features of peripherally inserted central catheter-associated bloodstream infection in neonates, and to investigate the effect of infection control strategies on the occurrence of infection,by which it is helpful in choosing effective strategies for clinical practice. Methods Clinical data, results of blood culture and culture of the catheter tip were collected from 72 infants (66 of them were very low birth weight) admitted to NICU from July, 2007 to August, 2008. The incidence of PICC-associated bloodstream infection (PICC-BSI) in the old hospital was compared with that of the new hospital. Results Bacterial colonization was not found. PICC-BSI was found in 15 cases (18. 1%), including 11 cases (13.2%) with definite sepsis and 4 cases (4. 8 %) with clinical sepsis.The incidence of PICC-BSI was 10. 2/1 000 PICC-days as a whole,with 16. 1/1 000 PICC-days in the old hospital and,7. 7/1 000 PICC-days in the new hospital respectively. Eleven organisms were isolated including Coagulase negative staphylococcus (CoNS) (4 strains), Acinetobacter baumannii (3 strains), Klebsiella pneumonia (2 strains), Enterococcus(1 strain), and Candida parapsilosis (1 strain). The incidence of PICC-BSI in the new hospital was lower compared with that of the old hospital. Conclusion Most of the isolated organisms of PICC-BSI are opportunistic and multi-drug resistant pathogen. PICC-BSI can be reduced by the effective infection control strategies in NICU.

Objective To investigate the role of nuclear transcription factor kappa B (NF-κB) -matrix metalloproteinase-9 (MMP-9) signaling pathway in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods 150 male SD rats were randomly assigned to air control group (AC group) , CO poisoning group (CO group) , pyrrolidine thiocarbamate (PDTC) + CO poisoning group (PC group). DEACMP model was reconstructed by modified intraperitoneal injections. The 1, 3, 7, 14, and 21 d after intraperitoneal injection were observed here by different approaches. Morris water maze test was used to test the learning and memory ability of rats.HE staining was used to observe the morphology of hippocampal CA3 cells. Immunofluorescence and Western Blot methods were used to detect the expression of NF-κB and MMP-9. RT-PCR was used to measure the expression of MMP-9 mRN A. Transmission electron microscopy was used to observe the ultrastructure of synapses. Results After14 days, the average intubation period of CO group was longer than that of AC group (P < 0.05) , and that of PC group was shorter than that of CO group (P < 0.05). However, average intubation period of PC group was longer than that of AC group (P< 0.05). In CO group, the expression of NF-κB in hippocampus increased (day 1). At day 3, the expression of NF-κB rapidly increased. The expression of MMP-9 gene and protein increased in the first three days and then decreased thereafter. The expression of NF-κB and MMP-9 in PC group was lower than that in CO group (P < 0.05) , while it was higher than AC group (P < 0.05). The peak value of apoptosis in CO group was delayed to 7-14 d after exposure, the apoptotic cells in PC group decreased significantly, and it was obvious on the 14 th day.Electron microscopy showed that the damage of synapses ultrastructure in CO group was significantly heavier than that in PC group on the 14 th day. Conclusions NF-κB-MMP-9 signal pathway leads to DEACMP, and PDTC could alleviate the impairment of learning and memory ability in rats with acute CO poisoning.

Objective: To investigate the effects of astaxanthin on neuronal injury in hippocampus of rats after acute carbon monoxide poisoning(ACMP) and the relationship with NF-κB inflammatory signaling pathway. Methods: Male SD rats screened by water maze were randomly divided into three group(n=50): control group (NC group), CO poisoning group (COP group), CO poisoning+ astaxanthin group (AST group) . ACMP rat model was established by static inhaled exposure method. Meanwhile, rats in AST group were further given astaxanthin twice a day by gavage.At 1 day, 7 days, 14 days, 21 days and 28 days after CO poisoning (10 rats in each group were selected), the learning and memory abilities were evaluated by Morris water maze test. The pathological changes of the neurons in hippocampal CA1 region were observed by hematoxylin-eosin(HE) staining.The expression and activation of NF-κB in hippocampus were detected by immunoblotting and immunofluorescence, and the expression of TNF-α and IL-6 protein in hippocampus were examined by ELISA. Results: Morris water maze test showed that there were no significant difference in escape latency and crossing platform times between the three groups (P>0.05). Compared with NC group, the escape latency of COP group was prolonged at 14, 21 and 28 days after CO poisoning (t=-6.04, -6.28, -8.18, all P<0.05), and the number of crossing platform was decreased (t= 5.96, 7.85, 6.51, all P<0.05). Compared with the COP group, the escape latency of the rats in AST group at the 14, 21 and 28 days was shortened (t=4.74, 4.82, 5.98, all P<0.05), and the number of crossing platform was increased (t=-3.72, -4.45, -6.53, all P<0.05). Compared with NC group, the number of NF-κ B positive cells in CA1 area of hippocampus in COP group increased at every time point (t=-8.62, -18.00, -16.67, -11.15, -6.22, all P<0.05); the number of NF-κ B positive cells in CA1 area in AST group decreased at 7 d, 14 d, 21 d and 28 d after CO poisoning, the difference was statistically significant (t= 6.55, 6.96, 4.40, 4.17; all P<0.05). Western blot showed that the changes of NF-κB protein was similar to that of immunofluorescence. After 7 days of CO poisoning, the level of NF-κB protein in hippocampus of COP group was (1.44±0.08), it was higher than that of NC group (t=-20.07, P<0.05), while that of AST group was (0.68±0.10), it was lower than that of COP group (t=10.23, P<0.05). The results of Elisa showed that TNF-α and IL-6 in the hippocampus of COP group were higher than those of NC group at every time point(all P<0.05), while compared with COP group, TNF-α and IL-6 in AST group were lower (all P<0.05). After 7 days of CO poisoning, TNF -α in COP group ((39.04±5.29) pg/ml)was higher than that in NC group ((14.13±2.12) pg/ml) (t=-7.58, P<0.05); TNF -α in AST group ((25.77±3.31) pg/ml) was lower than that in COP group (t=3.69, P<0.05). After 7 days of CO poisoning, the level of IL-6 in COP group ((181.79±9.12) pg/ml)was higher than that in NC group ((73.12±11.04) pg/ml) (t=-8.24, P<0.05), and the level of IL-6 in AST group ((121.47±9.80) pg/ml) was lower than that in COP group (t=7.80, P<0.05). Conclusion The excessive inflammatory response which mediated by NF-κB signaling pathway is involved in ACMP-induced neuronal damage in hippocampus.Astaxanthin can down-regulate the expression of NF-κB inflammatory signaling pathway related proteins, and pave a way for the treatment of ACMP brain damage and cognitive dysfunction.