Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Myeloid derived suppressor cells (MDSCs) are a type of immature, differentiated, heterogeneous cells derived from the bone marrow. MDSC plays a dual role in parasitic infections. On the one hand, the cells can induce helper T cell 1/2 (Th1/Th2) immune responses by inducing host secretion of interferon-γ (IFN-γ), interleukin (IL)-4, and IL-13. On the other hand, they can also secrete IL-10, IL-17 and transforming growth factor-β (TGF-β) to induce regulatory T cells (Treg)/Th17 immune responses, thereby exerting immune protection or immune escape. This article provides a review of the research progress on the immune regulation of host T cells by MDSC in parasitic infections.

Malignancies are diseases resulting from an imbalance of cell growth and proliferation， endangering human health and life. Currently， there is no clinically effective treatment for tumors. Tumor cells may alter cell adhesion and tumor cell migration and movement by degrading the extracellular matrix， generating vascular factors， affecting epithelial-mesenchymal transformation， or altering the tumor microenvironment. The mechanisms which lead to multidrug resistance （MDR） are the regulation of membrane proteins， apoptosis-regulated gene expression， enzyme-mediated multidrug resistance， DNA damage repair， and epithelial-stromal transformation， resulting in ineffective treatment of tumors. Therefore， the search for natural， safe， and effective chemosensitizers has become a critical part in tumor research. Due to the increasing use of Chinese medicine in cancer treatment， researchers have conducted more extensive studies on its monomers and compounds. In addition， the mechanisms of Chinese medicine in inhibiting tumor invasion and metastasis and reversing drug resistance are gradually unraveled. The monomers and compounds of Chinese medicine may inhibit tumor invasion， metastasis， and drug resistance by enhancing the sensitivity of chemotherapy drugs and adjuvant properties. Furthermore， they can also improve the tolerance of patients to chemotherapy drugs， relieve side effects of chemotherapy， reduce the chance of recurrence， and prolong the life of patients. The development of traditional Chinese medicine plays an important role in reducing tumor recurrence and metastasis， reversing drug resistance， prolonging the prognosis of cancer patients， improving their quality of life， and prolonging their survival time. Currently， various types of Chinese medicines have been proven to be capable of reducing tumor invasion and metastasis， and reversing drug resistance. The present article reviewed development and findings of Chinese medicine as an anti-tumor invasion， anti-metastasis， and anti-tumor resistance therapy in recent years， in order to provide ideas for future research on anti-tumor effect of active components in Chinese medicine.

High expression of Fightless I (FLII) is associated to multiple tumors. Based on our previous study that FLII might be involved in the nuclear export, we assessed the possible interaction of FLII with the nuclear envelop associating proteins Importin β and Nup88. We first constructed GST-FLII, GST-LRR recombinant plasmids and transformed them into the Rosetta strain to produce GST-FLII, GST-LRR fusion protein. After purification of these proteins, GST-pull down, as well as co-immunoprecipitation, were used to test the interaction of FLII with Importin β and Nup88. FLII interacted with Importin β and Nup88, and FLII LRR domain is responsible for these interactions. Thus, FLII may play a role in nuclear export through interaction with Importin β and Nup88.
Humans ; Microfilament Proteins ; metabolism ; Nuclear Pore Complex Proteins ; metabolism ; Receptors, Cytoplasmic and Nuclear ; metabolism ; Recombinant Fusion Proteins ; metabolism ; beta Karyopherins ; metabolism