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Periodontitis is a complex disease characterized by distinct inflammatory stages, with a peak of inflammation in the early phase and less prominent inflammation in the advanced phase. The insulin-like growth factor 2-binding proteins 2 (IGF2BP2) has recently been identified as a new m 6 A reader that protects m 6 A-modified messenger RNAs (mRNAs) from decay, thus participating in multiple biological processes. However, its role in periodontitis remains unexplored. Here, we investigated the role of IGF2BP2 in inflammation and osteoclast differentiation using a ligature-induced periodontitis model. Our findings revealed that IGF2BP2 responded to bacterial-induced inflammatory stimuli and exhibited differential expression patterns in early and advanced periodontitis stages, suggesting its dual role in regulating this disease. Depletion of Igf2bp2 contributed to increased release of inflammatory cytokines, thereby exacerbating periodontitis after 3 d of ligature while suppressing osteoclast differentiation and ameliorating periodontitis after 14 d of ligature. Mechanistically, we demonstrated that IGF2BP2 directly interacted with Cd5l and Cd36 mRNA via RNA immunoprecipitation assay. Overexpression of CD36 or recombinant CD5L rescued the osteoclast differentiation ability of Igf2bp2 -null cells upon lipopolysaccharide stimulus, and thus the downregulation of Cd36 and Cd5l effectively reversed periodontitis in the advanced stage. Altogether, this study deepens our understanding of the potential mechanistic link among the dysregulated m 6 A reader IGF2BP2, immunomodulation, and osteoclastogenesis during different stages of periodontitis., Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Aims and Objectives: This study aimed to comprehensively review the research literature to provide an overview of the effects of Humanitude on people with dementia and their caregivers., Background: Humanitude is a relationship-centred and compassionate care approach that focuses on improving the communication between people with dementia and their caregivers. There is a lack of updated and comprehensive synthesis on the evidence of the effects of Humanitude in dementia care., Design and Methods: This paper adopted the scoping review framework by Arksey and O'Malley. We searched through the following databases: Pubmed, CINAHL, EMBASE, PsycINFO, ProQuest, Scopus and Web of Science from its inception to 3 September 2021. Three investigators independently screened the titles and abstracts and assessed the full-text articles for eligibility. The PRISMA-ScR checklist was included in this scoping review., Results: We retrieved 1317 articles from databases and grey sources. Eleven studies were included after the screening. The synthesised results suggest that Humanitude can reduce agitation and psychological symptoms and improve the general well-being of people with dementia. Humanitude also has positive effects in improving care communication, empathy, job satisfaction and reducing burnout among caregivers., Conclusion: Humanitude shows the potential for positive effects on people with dementia and their caregivers. However, most studies did not include a comparator group and could not provide rigorous findings as compared to randomised controlled trials. There is a need for randomised controlled studies to demonstrate the effectiveness of Humanitude on people with dementia and their caregivers., Relevance for Clinical Practice: This paper reviewed the literature on all types of publications that examine the use of Humanitude in people with dementia and their caregivers. Thus, it provided an up-to-date overview of the effects of Humanitude to inform clinical practice., (© 2022 John Wiley & Sons Ltd.)

Colorectal cancer is the third leading cancer in the world in terms of incidence and mortality. The role of differentially expressed Claudin-14 (CLDN14) in CRC has not been reported. We observed that CLDN14 was associated with the progression of CRC. Our functional studies have shown that CLDN14 promoted the proliferation of CRC cells. In addition, CLDN14 also increased the migration and invasion of CRC cells. In vivo experiments also showed that CLDN14 promoted the growth of colorectal cancer via the PI3K/AKT/mTOR. In summary, our research suggests that CLDN14 promotes the progression of colorectal cancer. Our findings may provide new strategies for clinical management and patient prognosis of CRC.

Interprofessional education (IPE) is increasingly utilized to prepare students for their future careers in the health sciences as collaborative practitioners. Although it is considered an accreditation requirement in most health science disciplines, little is known about first year student's perceptions of IPE in Canada. In September of 2018, students from dentistry, kinesiology, medicine, nursing, nutrition, pharmacy, and physiotherapy in their first year of their professional program at the University of Saskatchewan were surveyed to obtain a baseline of perspectives and attitudes toward IPE. The survey consisted of an adaptation of the Readiness for Interprofessional Learning Scale (RIPLS) and additional questions to assess students' skills and interest in IPE. Descriptive and univariate statistics were used to determine associations with demographic variables. The response rate was 88% ( n = 509). Health science students in all disciplines had positive perceptions of IPE, with overall mean RIPLS scores for domain 1 (teamwork and collaboration), 2 (professional identity), and 3 (roles and responsibilities) of 40.5/45, 33.3/40 and 6.3/10, respectively. Students in kinesiology had significantly lower RIPLS scores than other health science disciplines ( p < .05). Female gender, and having a past degree, or previous experience with interprofessional collaboration through school or work were traits that were associated with statistically significantly higher RIPLS scores ( p < .05).

Aim: Evodiamine (EVO) has been reported to play an important role in regulating gastrointestinal motility, but the evidence is insufficient, and the mechanism remains unknown. The aim of this study is to investigate the possible role of EVO in stress-induced colonic hypermotility and the potential mechanisms via both in vivo and in vitro investigations., Methods: Male Sprague-Dawley rats were exposed to water avoidance stress (WAS) for 1 h or sham WAS daily for 10 consecutive days to construct the rat model. The colonic contractile activity was studied in an organ bath system. The serum CCK-8 level was detected using an enzyme immunoassay kit, and gastrointestinal transit was detected by intragastric administration of India ink., Results: WAS induced gastrointestinal hypermotility in male rats. EVO significantly inhibited the contractile activity of colonic muscle strips; this effect was not blocked by TTX and the CCK 1 receptor antagonist devazepide. Chronic WAS induced a slight but nonsignificant increase in the serum CCK-8 level, while EVO elevated the serum CCK-8 level in the WAS rats in a dose-dependent manner. Exogenous CCK-8 significantly inhibited the contractile activity of the colonic muscle strips; this effect was not blocked by TTX but was completely blocked by devazepide. Both EVO and CCK-8 inhibited gastrointestinal transit, and the effect of EVO could be partially blocked by devazepide., Significance: EVO can reverse stress-induced gastrointestinal hypermotility. This effect may partially occur as a result of promoting the release of CCK and then activating the CCK 1 receptor instead of directly activating the CCK 1 receptor., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Increasing evidence suggests that Fusobacterium nucleatum is involved in colorectal carcinogenesis. Previous studies have explored whether F. nucleatum may trigger colonic epithelial-mesenchymal transition. The results of the present study demonstrated that F. nucleatum enhances the proliferation and invasion of NCM460 cells compared with that of normal control and DH5α cells. Furthermore, F. nucleatum significantly increased the phosphorylation of p65 (a subunit of nuclear factor-κB), as well as the expression of interleukin (IL)-6, IL-1β and matrix metalloproteinase (MMP)-13. Additionally, F. nucleatum infection did not affect the expression levels of epithelial (E-)cadherin and β-catenin. E-cadherin knockdown in NCM460 cells did not induce the activation of inflammatory responses in response to F. nucleatum infection, whereas it increased inflammation in response to β-catenin silencing. F. nucleatum infection could not increase the proportion of cells at S phase when E-cadherin was silenced. Nevertheless, F. nucleatum infection enhanced the proportion of NCM460 cells at S phase when transfected with small interfering RNAs to knock down β-catenin expression. In conclusion, the results of the present study demonstrated that F. nucleatum infection interacted with E-cadherin instead of β-catenin, which in turn enhances the malignant phenotype of colorectal cancer cells.