How Is Learning Motivation Shaped Under Different Contexts: An Ethnographic Study in the Changes of Adult Learner’s Motivational Beliefs and Behaviors Within a Foreign Language Course

There has been a burgeoning interest of students’ motivational beliefs in determining their motivational behaviors in classroom activities: choice of task and persistence of task. Previous research mostly used quantitative methods to understand students’ general motivation, without taking contextual factors into consideration. To fill in this gap, the present study examined the influence of changing contexts on students’ motivational beliefs in a Chinese language classroom, and how those changes in motivational beliefs shaped their motivational behaviors in class activities. An ethnographic multiple-case study approach was adopted, and six adult learners were chosen from a Chinese language course in a Hong Kong university. On-going semi-structured interviews, class observations, stimulated recall and document reviews were conducted to understand student development across time. Findings show that the more proficient students were showing relatively stable motivational beliefs as well as behaviors throughout the foreign language course. In contrast, the less proficient students were demonstrating obvious changes in their motivational beliefs and hence behaviors, due to the different contexts of non-exam and high-stake exam. The study suggested students’ learning motivation in class was context-dependent, and could fluctuate substantially on a weekly basis. Those dynamic within-course changes at different learning stages and the reasons shaping the changes could give pedagogical insights to the teacher with adult learners

Learning with Free Object Segments for Long-Tailed Instance Segmentation

One fundamental challenge in building an instance segmentation model for a large number of classes in complex scenes is the lack of training examples, especially for rare objects. In this paper, we explore the possibility to increase the training examples without laborious data collection and annotation. We find that an abundance of instance segments can potentially be obtained freely from object-centric images, according to two insights: (i) an object-centric image usually contains one salient object in a simple background; (ii) objects from the same class often share similar appearances or similar contrasts to the background. Motivated by these insights, we propose a simple and scalable framework FreeSeg for extracting and leveraging these "free" object foreground segments to facilitate model training in long-tailed instance segmentation. Concretely, we investigate the similarity among object-centric images of the same class to propose candidate segments of foreground instances, followed by a novel ranking of segment quality. The resulting high-quality object segments can then be used to augment the existing long-tailed datasets, e.g., by copying and pasting the segments onto the original training images. Extensive experiments show that FreeSeg yields substantial improvements on top of strong baselines and achieves state-of-the-art accuracy for segmenting rare object categories

Evidence for the contribution of COMT gene Val158/108Met polymorphism (rs4680) to working memory training-related prefrontal plasticity.

BackgroundGenetic factors have been suggested to affect the efficacy of working memory training. However, few studies have attempted to identify the relevant genes.MethodsIn this study, we first performed a randomized controlled trial (RCT) to identify brain regions that were specifically affected by working memory training. Sixty undergraduate students were randomly assigned to either the adaptive training group (N = 30) or the active control group (N = 30). Both groups were trained for 20 sessions during 4 weeks and received fMRI scans before and after the training. Afterward, we combined the data from the 30 participants in the RCT study who received adaptive training with data from 71 additional participants who also received the same adaptive training but were not part of the RCT study (total N = 101) to test the contribution of the COMT Val158/108Met polymorphism to the interindividual difference in the training effect within the identified brain regions.ResultsIn the RCT study, we found that the adaptive training significantly decreased brain activation in the left prefrontal cortex (TFCE-FWE corrected p = .030). In the genetic study, we found that compared with the Val allele homozygotes, the Met allele carriers' brain activation decreased more after the training at the left prefrontal cortex (TFCE-FWE corrected p = .025).ConclusionsThis study provided evidence for the neural effect of a visual-spatial span training and suggested that genetic factors such as the COMT Val158/108Met polymorphism may have to be considered in future studies of such training

Licochalcone A Protects the Blood–Milk Barrier Integrity and Relieves the Inflammatory Response in LPS-Induced Mastitis

Background/Aims: Mastitis is an acute clinical inflammatory response. The occurrence and development of mastitis seriously disturb women's physical and mental health. Licochalcone A, a phenolic compound in Glycyrrhiza uralensis, has anti-inflammatory properties. Here, we examined the effect of licochalcone A on blood-milk barrier and inflammatory response in LPS-induced mice mastitis.Methods:In vivo, we firstly established mice models of mastitis by canal injection of LPS to mammary gland, and then detected the effect of licochalcone A on pathological indexes, inflammatory responses and blood-milk barrier in this model. In vivo, Mouse mammary epithelial cells (mMECs) were treated with licochalcone A prior to the incubation of LPS, and then the inflammatory responses, tight junction which is the basic structure of blood-milk barrier were analyzed. Last, we elucidated the anti-inflammatory mechanism by examining the activation of mitogen-activated protein kinase (MAPK) and AKT/NF-κB signaling pathways in vivo and in vitro.Result: The in vivo results showed that licochalcone A significantly decreased the histopathological impairment and the inflammatory responses, and improved integrity of blood-milk barrier. The in vitro results demonstrated that licochalcone A inhibited LPS-induced inflammatory responses and increase the protein levels of ZO-1, occludin, and claudin3 in mMECs. The in vivo and in vitro mechanistic study found that the anti-inflammatory effect of licochalcone A in LPS-induced mice mastitis was mediated by MAPK and AKT/NF-κB signaling pathways.Conclusions and Implications: Our experiments collectively indicate that licochalcone A protected against LPS-induced mice mastitis via improving the blood–milk barrier integrity and inhibits the inflammatory response by MAPK and AKT/NF-κB signaling pathways

Global Infectious Diseases in June 2023: Monthly Analysis

Infectious diseases are a class of diseases caused by various pathogens that can be transmitted between humans and animals or between humans and animals, thus seriously affecting the development of human society. To control the spread of infectious diseases worldwide and ensure the safety of people’s lives, it is essential to regularly analyze global infectious disease cases. This review is based on data from the World Health Organization, the Centers for Disease Control in countries around the world, Outbreak News Today and many other epidemiological websites to predict the global infectious disease outbreak trend. In addition, using the Shuci Technology global epidemic information monitoring system, we analyzed the distribution of infectious diseases that occurred around the world from 24 May 2023 to 23 June 2023

Polydatin Prevents Lipopolysaccharide (LPS)-Induced Parkinson's Disease via Regulation of the AKT/GSK3β-Nrf2/NF-κB Signaling Axis

Parkinson's disease (PD) is a common neurodegenerative disease characterized by selective loss of dopaminergic neurons in the substantia nigra (SN). Neuroinflammation induced by over-activation of microglia leads to the death of dopaminergic neurons in the pathogenesis of PD. Therefore, downregulation of microglial activation may aid in the treatment of PD. Polydatin (PLD) has been reported to pass through the blood-brain barrier and protect against motor degeneration in the SN. However, the molecular mechanisms underlying the effects of PLD in the treatment of PD remain unclear. The present study aimed to determine whether PLD protects against dopaminergic neurodegeneration by inhibiting the activation of microglia in a rat model of lipopolysaccharide (LPS)-induced PD. Our findings indicated that PLD treatment protected dopaminergic neurons and ameliorated motor dysfunction by inhibiting microglial activation and the release of pro-inflammatory mediators. Furthermore, PLD treatment significantly increased levels of p-AKT, p-GSK-3βSer9, and Nrf2, and suppressed the activation of NF-κB in the SN of rats with LPS-induced PD. To further explore the neuroprotective mechanism of PLD, we investigated the effect of PLD on activated microglial BV-2 cells. Our findings indicated that PLD inhibited the production of pro-inflammatory mediators and the activation of NF-κB pathways in LPS-induced BV-2 cells. Moreover, our results indicated that PLD enhanced levels of p-AKT, p-GSK-3βSer9, and Nrf2 in BV-2 cells. After BV-2 cells were pretreated with MK2206 (an inhibitor of AKT), NP-12 (an inhibitor of GSK-3β), or Brusatol (BT; an inhibitor of Nrf2), treatment with PLD suppressed the activation of NF-κB signaling pathways and the release of pro-inflammatory mediators in activated BV-2 cells via activation of the AKT/GSK3β-Nrf2 signaling axis. Taken together, our results are the first to demonstrate that PLD prevents dopaminergic neurodegeneration due to microglial activation via regulation of the AKT/GSK3β-Nrf2/NF-κB signaling axis

PgtE Enzyme of Salmonella enterica Shares the Similar Biological Roles to Plasminogen Activator (Pla) in Interacting With DEC-205 (CD205), and Enhancing Host Dissemination and Infectivity by Yersinia pestis

Yersinia pestis, the cause of plague, is a newly evolved Gram-negative bacterium. Through the acquisition of the plasminogen activator (Pla), Y. pestis gained the means to rapidly disseminate throughout its mammalian hosts. It was suggested that Y. pestis utilizes Pla to interact with the DEC-205 (CD205) receptor on antigen-presenting cells (APCs) to initiate host dissemination and infection. However, the evolutionary origin of Pla has not been fully elucidated. The PgtE enzyme of Salmonella enterica, involved in host dissemination, shows sequence similarity with the Y. pestis Pla. In this study, we demonstrated that both Escherichia coli K-12 and Y. pestis bacteria expressing the PgtE-protein were able to interact with primary alveolar macrophages and DEC-205-transfected CHO cells. The interaction between PgtE-expressing bacteria and DEC-205-expressing transfectants could be inhibited by the application of an anti-DEC-205 antibody. Moreover, PgtE-expressing Y. pestis partially re-gained the ability to promote host dissemination and infection. In conclusion, the DEC-205-PgtE interaction plays a role in promoting the dissemination and infection of Y. pestis, suggesting that Pla and the PgtE of S. enterica might share a common evolutionary origin.Peer reviewe

Mutation-Specific RAS Oncogenicity Explains NRAS Codon 61 Selection in Melanoma

N-RAS mutation at codon 12, 13 or 61 is associated with transformation; yet, in melanoma, such alterations are nearly exclusive to codon 61. Here, we compared the melanoma susceptibility of an N-RasQ61R knock-in allele to similarly designed K-RasG12D and N-RasG12D alleles. With concomitant p16INK4a inactivation, K-RasG12D or N-RasQ61R expression efficiently promoted melanoma in vivo, whereas N-RasG12D did not. Additionally, N-RasQ61R mutation potently cooperated with Lkb1/Stk11 loss to induce highly metastatic disease. Functional comparisons of N-RasQ61R and N-RasG12D revealed little difference in the ability of these proteins to engage PI3K or RAF. Instead, N-RasQ61R showed enhanced nucleotide binding, decreased intrinsic GTPase activity and increased stability when compared to N-RasG12D. This work identifies a faithful model of human N-RAS mutant melanoma, and suggests that the increased melanomagenecity of N-RasQ61R over N-RasG12D is due to heightened abundance of the active, GTP-bound form rather than differences in the engagement of downstream effector pathways