The Goal Commitment/Institutional Attachment category included themes of academic and social adaptation as well as the student' communication with education management. Conclusions This study identifies to light critical issues in supporting international students with adaptation problems to university life in Turkey. It is clear that revising the content of education programs to enable international exchange is not sufficient enough by itself to meet the needs of international students.BACKGROUND Colorectal cancer (CRC) has a high incidence and mortality rate worldwide. Colitis-associated CRC (CAC) is used for describing the relationship between inflammation and CRC. No chemopreventive agents have been found to be both effective and safe in CRC. Therefore, the prevention and treatment of CAC are extremely urgent. Wu Mei Wan (WMW) has been used for the clinical treatment of enteritis with a remarkable efficacy. Here, we aim to investigate the underlying mechanism of WMW in the prevention of CAC. METHODS The AOM/DSS-induced CAC mouse model was used, and the mice were divided into normal control (NC), AOM/DSS model control (MC), and AOM/DSS plus WMW (WMW). The weight of mice, the score of DAI, survival rate, number of tumors and sample collection were performed at the end of the 14th week. Histopathological examination was performed using Hematoxylin-Eosin (HE) staining.  https://www.selleckchem.com/products/takinib.html  Tumor cell proliferation was indicated by the expression of PCNA, and p65 and p-STAT3 were detected by immunohistochemistry.ventive drug but further clinical evidence is necessary. Disruption of nucleocytoplasmic transport is increasingly implicated in the pathogenesis of neurodegenerative diseases, including ALS caused by a C9orf72 hexanucleotide repeat expansion. However, the mechanism(s) remain unclear. Karyopherins, including importin β and its cargo adaptors, have been shown to co-precipitate with the C9orf72 arginine-containing dipeptide repeat proteins (R-DPRs), poly-glycine arginine (GR) and poly-proline arginine (PR), and are protective in genetic modifier screens. Here, we show that R-DPRs interact with importin β, disrupt its cargo loading, and inhibit nuclear import of importin β, importin α/β, and transportin cargoes in permeabilized mouse neurons and HeLa cells, in a manner that can be rescued by RNA. Although R-DPRs induce widespread protein aggregation in this in vitro system, transport disruption is not due to nucleocytoplasmic transport protein sequestration, nor blockade of the phenylalanine-glycine (FG)-rich nuclear pore complex. Our results support a model in which R-DPRs interfere with cargo loading on karyopherins. © 2020, Hayes et al.HIV-1 Vpr is necessary for maximal HIV infection and spread in macrophages. Evolutionary conservation of Vpr suggests an important yet poorly understood role for macrophages in HIV pathogenesis. Vpr counteracts a previously unknown macrophage-specific restriction factor that targets and reduces the expression of HIV Env. Here, we report that the macrophage mannose receptor (MR), is a restriction factor targeting Env in primary human monocyte-derived macrophages. Vpr acts synergistically with HIV Nef to target distinct stages of the MR biosynthetic pathway and dramatically reduce MR expression. Silencing MR or deleting mannose residues on Env rescues Env expression in HIV-1-infected macrophages lacking Vpr. However, we also show that disrupting interactions between Env and MR reduces initial infection of macrophages by cell-free virus. Together these results reveal a Vpr-Nef-Env axis that hijacks a host mannose-MR response system to facilitate infection while evading MR's normal role, which is to trap and destNow, Lubow et al. reveal that the unknown restriction factor in macrophages is a protein called the mannose receptor. This protein binds and destroys proteins containing mannose, a type of sugar found on bacteria and some viruses. The experiments revealed that the mannose receptor grabs mannose on the HIV protein Env. This causes Env to be broken down and stops HIV from spreading. Lubow et al. also find that Vpr works with another protein produced by HIV called Nef to reduce the number of mannose receptors on macrophages. The two proteins do this by targeting different steps in the assembly of mannose receptors, allowing the virus to multiply and spread more efficiently. The experiments suggest that drugs that simultaneously block Vpr and Nef might prevent or suppress HIV infections. More studies are needed to develop and test potential HIV-treatments targeting Vpr and Nef. © 2020, Lubow et al.OBJECTIVES To summarize evidence relating cannabis smoking and oral disease and highlight any potential influence of cannabis smoking on clinical care and dental public health. METHODS Using rapid evidence review, a librarian facilitated a systematic search of 5 electronic databases in August and September 2018 and updated it in March 2019, yielding 581 publications. Two researchers screened the documents using pre-established inclusion criteria article was based on primary or secondary data; cannabis smoking was an exposure; at least 1 cannabis-related oral health outcome was reported; participants were humans; and the article was available in English or French. Data from retained articles were analyzed for themes without meta-analysis. RESULTS We synthesized and summarized 23 articles in 2 broad categories cannabis and oral disease; and cannabis, clinical care and dental public health. Current evidence shows that smoking cannabis is harmful to the health of the periodontium. The association between smoking cannabis and other oral disease (dental caries, soft tissue lesions and oral cancers) is sparse and inconsistent, although studies suggest that cannabis smoking is an underlying risk factor. Cannabis smoking can lead to an altered mental state that can delay dental treatment of the patient. Further, interactions between smoked cannabis and adrenaline-containing local anesthetics can result in life-threatening consequences. CONCLUSIONS Cannabis smoking is harmful to the periodontium. Further research is needed to fully understand how cannabis smoking affects oral disease and how dental professionals should integrate this knowledge into clinical care and dental public health.