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Jia, J.

Publications and source records attributed to Jia, J..

4 recordsLinked to original sources

Fast-backward replay of sequentially memorized items in humans

Storing temporal sequences of events (i.e., sequence memory) is fundamental to many cognitive functions. However, how the sequence order information is maintained and represented in working memory and its behavioral significance, particularly in human subjects, remains unknown. Here, we recorded electroencephalography (EEG) in combination with a temporal response function (TRF) method to dissociate item-specific neuronal reactivations. We demonstrate that serially remembered items are successively reactivated during memory retention. The sequential replay displays two interesting properties compared to the actual sequence. First, the item-by-item reactivation is compressed within a 200-400 ms window, suggesting that external events are associated within a plasticity-relevant window to facilitate memory consolidation. Second, the replay is in a temporally reversed order and is strongly related to the recency effect in behavior. This fast-backward replay, previously revealed in rat hippocampus and demonstrated here in human cortical activities, might constitute a general neural mechanism for sequence memory and learning.

neuroscience

Bifunctional enzyme SpoT is involved in biofilm formation of Helicobacter pylori with multidrug resistance by upregulating efflux pump Hp1174 (gluP)

The drug resistance of Helicobacter pylori (H. pylori) is gradually becoming a serious problem. Biofilm formation is an important factor that leads to multidrug resistance in bacteria. The ability of H. pylori to form biofilms on the gastric mucosa has been known. However, there are few studies on the regulation mechanisms of H. pylori biofilm formation and multidrug resistance. Guanosine 3-diphosphate 5-triphosphate and guanosine 3,5-bispyrophosphate [(p)ppGpp] are global regulatory factors and are synthesized in H. pylori by the bifunctional enzyme SpoT. It has been reported that (p)ppGpp is involved in the biofilm formation and multidrug resistance of various bacteria. In this study, we found that SpoT also plays an important role in H. pylori biofilm formation and multidrug resistance. Therefore, it is necessary to carry out some further studies regarding its regulatory mechanism. Considering that efflux pumps are of great importance in the biofilm formation and multidrug resistance of bacteria, we tried to find if efflux pumps controlled by SpoT participate in these activities. Then, we found that Hp1174 (glucose/galactose transporter, gluP), an efflux pump of the MFS family, is highly expressed in biofilm-forming and multi-drug resistance (MDR) H. pylori and is upregulated by SpoT. Through further research, we determined that gluP involved in H. pylori biofilm formation and multidrug resistance. Furthermore, the average expression level of gluP in clinical MDR strains was considerably higher than that in clinical drug-sensitive strains. Taken together, our results revealed a novel molecular mechanism of H. pylori tolerance to multidrug.

microbiology

Post-reactivation new learning impairs and updates human episodic memory through dissociable processes

Learning of competing information after reactivation has the potential to disrupt memory reconsolidation and thus impair a consolidated memory. Yet this effect has rarely been detected in episodic memory. By introducing an additional retrieving cue to the target memory, the current study detected significant impairment on the reactivated episodic memory, in addition to an integration of new information to the old memory. However, while the integration effect followed the time window of reconsolidation disruption, the impairment effect did not. MEG measurements further revealed alpha power change during reactivation and post-reactivation learning which showed different correlation patterns with the integration and impairment effects, confirming that the two effects relied on different processes. Therefore, post-reactivation new learning disrupts episodic memory but not through reconsolidation disruption. Further findings that the impairment effect was correlated with participants voluntary inhibition ability suggest an inhibition-based memory updating process underlying post-reactivation new learning.

neuroscience

Transcriptional regulation by NR5A2 couples cell differentiation and inflammation in the pancreas

Tissue-specific differentiation and inflammatory programmes are thought to independently contribute to disease. The orphan nuclear receptor NR5A2 is a key regulator of pancreas differentiation and SNPs in or near the human gene are associated with risk of pancreatic cancer. In mice, Nr5a2 heterozygosity sensitizes the pancreas to damage, impairs regeneration, and cooperates with mutant KRas in tumor progression. Through global transcriptomic analysis, we uncover a basal pre-inflammatory state in the pancreas of Nr5a2 heterozygous mice that is reminiscent of pancreatitis-induced inflammation and is conserved in histologically normal human pancreata with reduced NR5A2 mRNA expression. In Nr5a2+/- mice, Nr5a2 undergoes a dramatic transcriptional switch relocating from tissue-specific to inflammatory loci thereby promoting AP-1-dependent gene transcription. Importantly, deletion of c-Jun in the pancreas of these mice rescues the pre-inflammatory phenotype and the defective regenerative response to damage. These findings provide compelling evidence that the same transcriptional networks supporting homeostasis in normal tissue can be subverted to foster inflammation upon genetic or environmental constraints.

cancer biology