Chronic wasting disease (CWD), a prion disease affecting free-ranging and captive cervids (deer and elk), is widespread in the United States and parts of Canada. The large cervid population, the popularity of venison consumption, and the apparent spread of the CWD epidemic are likely resulting in increased human exposure to CWD in the United States. Whether CWD is transmissible to humans, as has been shown for bovine spongiform encephalopathy (the prion disease of cattle), is unknown. We generated transgenic mice expressing the elk or human prion protein (PrP) in a PrP-null background. After intracerebral inoculation with elk CWD prion, two lines of "humanized" transgenic mice that are susceptible to human prions failed to develop the hallmarks of prion diseases after Ͼ657 and Ͼ756 d, respectively, whereas the "cervidized" transgenic mice became infected after 118 -142 d. These data indicate that there is a substantial species barrier for transmission of elk CWD to humans.

Background: Increasing evidences have documented that microRNAs (miRNAs) act as oncogenes or tumor suppressors in gastric cancer (GC). In this study, we aimed to investigate the expression of miR-133b in a large number of GC samples and elucidate its role in GC carcinogenesis and the detailed mechanism. Methods: We used Taqman probe stem-loop real-time PCR to accurately measure the levels of miR-133b in 100 pairs of gastric cancer tissues and the adjacent non-neoplastic tissues. miR-133b mimics were overexpressed in GC cell lines, miR-133b inhibitors were also introduced in GES cells to investigate its role on regulating cell proliferation, cell migration and cell invasion. The target of miR-133b was identified by luciferase reporter assay and western blot. Fascin actin-bundling protein 1 (FSCN1) siRNA was used to achieve the knockdown of FSCN1 in GC cells and to investigate its role on modulating GC cell proliferation and invasion. Results: miR-133b was significantly down-regulated in GC cell lines and in GC tissues compared with adjacent normal tissues. Moreover, lower-level of miR-133b was also associated with venous invasion and a more aggressive tumor phenotype. Re-introduction of miR-133b in GC cells can inhibit cell proliferation, cell migration and invasion. In contrary, knockdown of miR-133b in GES cells can promote cell proliferation and invasion. Further investigation indicated that miR-133b targeted FSCN1 in GC cells and knockdown of FSCN1 can also inhibit GC cell growth and invasion. Conclusion: Our findings demonstrated that miR-133b was significantly down-regulated in GC tissues and exerted its tumor suppressor role in GC cells. The investigation of the detailed mechanism showed that miR-133b directly targeted FSCN1 which functioned as an oncogenic gene in GC cells. These results suggested that miR-133b can be developed as a new diagnostic marker or therapeutic target for GC.

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Although forgetting was once regarded as a passive decline in memory and an occasional source of embarrassment, recent research suggests that it is an active biological process of removing outdated or irrelevant memories via activation of specific genes and signal transduction pathways. Rho family G proteins are known to have a role in synaptic plasticity mediated by the actin cytoskeleton. However, the current study reveals that another Rho guanosine triphosphate enzyme (GTPase), RAC‐2, facilitates the occurrence of forgetting in Caenorhabditis elegans independent of actin dynamics. Functioning downstream of RAC‐2 in the same signalling pathway, JNK‐1 and its phosphorylated protein are required to positively regulate forgetting. The pan‐neuronal rescue of RAC‐2 or JNK‐1, instead of AWC neuron‐specific expression, reverses the delayed forgetting caused by the rac‐2 mutation, which indicates that the involvement of RAC‐2/JNK‐1 in more than AWCs must be required. In summary, our work elucidates the action of the Rho GTPase RAC‐2 and downstream JNK‐1 as a potential novel pathway in forgetting in C. elegans.

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Strong light inhibits germination of Artemisia sphaerocephala and A. ordosica at low temperature and its relevance to revegetation in sandy lands of Inner Abstract Artemisia sphaerocephala and A. ordosica are two dominant shrub species in Mu Us sandy land (Inner Mongolia, China) and are widely used for vegetation restoration. However, there are two different conclusions about the effect of light on their germination: light promotes germination versus light inhibits germination. The aim of this study was to evaluate these two conclusions and relate the results to instances of failure of these two species to germinate well when air-dispersed in revegetation projects. The effects of fluctuating temperature, light/dark, source (population), position on mother plant, storage condition, and storage time were tested on germination of achenes of these two species. At low temperature, final percent germination (FPG) of achenes in dark and nearly dark conditions was significantly higher than those in light. At 10:20°C, achenes of both A. sphaerocephala and A. ordosica had higher FPG in dark than in light regardless of source, position on mother plants or storage condition. At suboptimum (5:15°C) and supraoptimal (25:35°C) temperatures, germination of A. sphaerocephala and A. ordosica achenes was inhibited in both light and darkness. It was concluded that light inhibits germination of A. sphaerocephala and A. ordosica achenes at low (10:20°C) temperature but not at high (15:25°C) temperature. Since the temperature in Mu Us sandy land is around 10:20°C in early June, when air sowing is done, achenes should germinate best when they are covered by a thin layer of sand.

Recent studies have suggested that innate immune responses exhibit characteristics associated with memory linked to modulations in both vertebrates and invertebrates. However, the diverse evolutionary paths taken, particularly within the invertebrate taxa, as should lead to similarly diverse innate immunity memory processes. Our understanding of innate immune memory in invertebrates primarily comes from studies of the fruit fly Drosophila melanogaster, the generality of which is unclear. Caenorhabditis elegans typically inhabits soil harboring a variety of fatal microbial pathogens; for this invertebrate, the innate immune system and aversive behavior are the major defensive strategies against microbial infection. However, their characteristics of immunological memory remains infantile. Here we discovered an immunological memory that promoted avoidance and suppressed innate immunity during reinfection with bacteria, which we revealed to be specific to the previously-exposed pathogens. During this trade-off switch of avoidance and innate immunity, the chemosensory neurons AWB and ADF modulated production of serotonin and dopamine, which in turn decreased expression of the innate immunity-associated genes and led to enhanced avoidance via the downstream insulin-like pathway. So our current study profiles the immune memories during C. elegans reinfected by pathogenic bacteria, and further reveal the chemosensory neurons, neurotransmitter(s), and their associated molecular signaling pathways are responsible for a trade-off switch between the two immunological memories.