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The damaging effect of threat on creativity has been confirmed by many studies. However, the neural mechanism underlying this effect has not been clarified. We designed an experiment to explore changes in brain activation when creativity is threatened. Specifically, participants performed the Chinese Remote Associates Test (RAT) under three conditions. The control condition was accompanied by no sound, the neutral condition was accompanied by unpredictable neutral sounds, and the threat condition was manipulated through unpredictable aversive sounds. We used functional near-infrared spectroscopy measurements to collect cognitive neurological data. The results showed that the threat condition reduced the accuracy and response time of the RAT and led to individual negative emotions. Participants' prefrontal cortex and supramarginal gyrus activation decreased under threat. These results provide a reference for clarifying the negative impact of threat on creativity and highlight its cognitive neural mechanisms.

Using nucleotide variation in the first internal transcribed spacer of nuclear ribosomal DNA, five different genotypes (designated G1–G5) have been identified and the preponderance of genotype G1 in humans and of genotype G3 in pigs led to the proposal that parasites bearing the two genotypes have an affinity for a particular host species. A subsequent study using eggs of genotype G1 from humans and G3 from pigs to infect pigs and mice indicated that there is a significant difference in the ability to infect and establish as larvae in mice and as adults in pigs between the two genotypes. Extending previous investigations, the present study investigated whether there are differences in development as designated by egg hatching, larvae migration and distribution in the mice between the Ascaris strains with known genotypes. Ascaris eggs of genotypes G1 (predominating in human-derived worms) and G3 (predominating in pig-derived worms) were used to infect C57BL/6 mice orally. Eggs/larvae were examined from the small and large intestines, thoracic and abdominal cavities, peripheral blood, livers and lungs at intervals of 2 h until 12 h post-infection, then periodically until 34 days of infection. Results showed distinct differences in egg hatching (the timing and location of hatching, and the numbers hatched), and in larvae migration and distribution (the means and constituent ratios, the time of peak recovery, and larvae reappearing in intestines) between the two strains. The results can explain the findings of significantly higher larval recovery of genotype G1 than G3 in the mice, and may shed some enlightenment to understand the difference in host affiliation of Ascaris of different genotypes.

To investigate the effect of crude antigens of Ascaris lumbricoides on the secretion of IL-6 and TGF-β of human lung adenocarcinoma cells (A549 cells), and the apoptosis of A549 cells.Crude antigens of A. lumbricoides were prepared. A549 cells were co-cultured with 25, 125, and 500 µg/ml crude antigens of A. lumbricoides for 1, 18, and 24 h, named as low concentration group, medium concentration group, and high concentration group, respectively. Meanwhile, A549 cells were co-cultured with culture medium (negative control) and 12.5 µg/ml adriamycin (positive control). The apoptosis rate was detected by using Annexin V-FITC apoptosis detection kit. The cell changes were determined by flow cytometry. The levels of mRNA expression of IL-6 and TGF-β were detected by ELISA and real time PCR, respectively.The apoptosis rate of A549 cells induced by crude antigens for 1, 18, and 24 h was significantly higher than that of negative control (P0.01). The apoptosis rate in medium concentration group (treated for 18 h) was highest [(47.10 ± 3.68)%]. After co-culture with 125 µg/ml crude antigens for 18 h, the proportion of G0/G1 phase cells increased and that of S phase cells decreased, and there was a significant difference between medium concentration group and negative control group. At the same time, the level of IL-6 increased with the increasing concentration of crude antigens. However, no significant difference was found in the level of TGF-β among the groups. In the medium concentration group, mRNA expression levels of IL-6 (5.95 ± 0.31) and TGF-β (3.43 ± 0.35) of A549 cells reached peak on the 18th hour, and were significantly higher than that of the control (P0.01).The cell cycle of A549 cells is blocked in G0/G1 phase induced by crude antigens of A. lumbricoides. And the apoptosis may be related to the changes in the level of TGF-β and IL-6.

Lanthanum is one of rare earth with extremely active chemical property and has been evidenced to possess antibacterial effect as well as the function of blocking calcium flux and regulating cellular immunity. Our previous studies showed that lanthanum could affect the biological activity of LPS and inhibit the activity in vitro. In this study, we explored the anti-LPS effects of lanthanum chloride in vivo so as to provide evidence in searching for new anti-endotoxic agents for the prevention and treatment of endotoxemia.(1) 96 BALB/c mice were divided into 2 groups: experimental group including 84 mice injected intraperitoneally with 17.5 mg/kg, LD(50) dose, of LPS mixed with lanthanum chloride of the dosages of 1 mg/kg, 2 mg/kg, 5 mg/kg, 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg respectively; and control group including 12 mice injected intraperitoneally with 17.5 mg/kg of LPS. The mortality rates of different mice within 7 days were observed so as to observe the protective effect of lanthanum chloride. (2) 40 BALB/c mice were randomly divided into 2 group 2: experimental group injected intraperitoneally with lanthanum chloride of the dosages 10 mg/kg for 3 days and then injected with 1 LD(50) dosage of LPS 30 minutes after the last injection of lanthanum chloride of the dosages 10 mg/kg; and control group injected intraperitoneally with normal saline for 3 days and then with 1 LD(50) dosage of LPS 30 minutes after the last injection of normal saline. The mortality rates of different mice within 7 days were observed. (3) 40 BALB/c mice were randomly divided into 4 groups: LPS group, injected intraperitoneally with LPS of sublethal dosage (12.5 mg/kg), lanthanum chloride treatment group, injected intraperitoneally with LPS of sublethal dosage 1 hour after the venous injection of 10 mg/kg lanthanum chloride, lanthanum chloride control group, injected intravenously with 10 mg/kg lanthanum chloride, and NS control group, injected intraperitoneally with NS. Four hours after the intraperitoneal injection blood sample were collected to detect the plasma tumor necrosis factor-alpha (TNFalpha) and liver and thymus tissues were collected to examine the expression of TNFalpha mRNA and apoptosis of thymocytes by Rt-PCR and flow cytometry so as to observe the effects of lanthanum chloride on LPS-induced reaction in vivo.The mortality rates of the mice administrated with LD(50) dosage of LPS combined with 5, 10, and 20 mg/kg lanthanum chloride were 0, 0, and 8% respectively, all significantly lower than that of the control group (67%, all P0.01). The mortality rate of the LPS-challenged mice that were pretreated with 10 mg/kg of lanthanum chloride was 20%, significantly lower than that of the control group (55%, P0.05). (2) In the mice with endotoxemia that were pretreated with lanthanum chloride the plasma TNFalpha level was 0.44 +/- 0.22 ng/ml and the TNFalpha mRNA expression in liver was (3.93 +/- 0.62) x 10(5) copies/ micro g RNA, both significantly lower than those of the mice with endotoxemia without pretreatment of lanthanum chloride, 0.99 +/- 0.24 ng/ml and (1.9 +/- 0.33) x 10(7) copies/ micro g RNA (both P0.001). The percentage of DNA fragmentation of thymocytes in the mice challenged with LPS and pretreated with lanthanum chloride was 14.77% +/- 1.0%, significantly lower than that of the untreated mice (55.38% +/- 3.88%, P0.001), the percentage of hypodiploidy in thymocytes of the mice challenged with LPS was 15.56% +/- 0.59%, significantly higher than that of the lanthanum chloride treated mice (6.05% +/- 0.71%, P0.001). (3) Morphologic observation showed that pathological changes of the thymocytes and liver and lung tissues were remarkably milder in the lanthanum chloride-treated mice than in the mice challenged only by LPS.(1) Lanthanum chloride can bind LPS and reduce its toxicity, which shows protective effects on mice challenged by lethal dose LPS. (2) Lanthanum chloride can greatly decrease the secretion of TNFalpha and TNFalpha mRNA expression in the mice the secretion of TNFalpha and TNFalpha mRNA expression in the mice challenged with LPS. Furthermore, LPS-induced apoptosis of thymocyte and damage of liver and lungs are inhibited by lanthanum chloride.