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Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The treatment of premenopausal patients with endometrial cancer has not yet been standardized, first of all, drug dosage, drug intake, treatment time and so on, there are no clear standards. Secondly, because of the high recurrence rate, is it unclear whether the patient needs to be removed after delivery. By reading a large number of literature and clinical prospective study, the main drug treatment is given priority to with low dose, treatment time is generally about 9-12 months. In addition to the traditional simple oral hormone therapy, in recent years, the treatment of LNG-IUS, the LNG-IUS and GnRHa combined therapy, hysteroscopic surgery and hormone combination therapy are gradually carried out. And through assisted reproductive technology, the success rate of pregnancy is increasing after treatment. Research shows that the treatment of premenopausal endometrial cancer is very promising at present, but a large number of clinical trials are needed to improve the treatment strategy. In this paper, by combining with clinical practice and the literature, we do a review about indication selection, pretreatment evaluation, treatment plan, curative effect evaluation, condition monitoring, and the problems that need to be faced after birth. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effect of Artesunate (Art) on the expression of transferrin receptor (TtR)in K562/ADM cells. Methods: The drug-resistant K562/ADM cells were cultured with 1000 ng/mL doxorubicin for two weeks followed by Artesunate treatment with different concentrations (12.5 μg/mL, 25μg/mL and 50 μg/mL) or different time (12 h, 24 h, 36 h, and 48 h). The content of transferrin receptor in K562/ADM cells was determined by flow cytometry. The effect of Artesunate on the expression of transferrin receptor protein in K562/ADM cells was measured by Westem blot. Cell counting kit-8 (CCK-8) assay was used to evaluate inhibitory effect of Art combined with doxorubicin (ADM) in K562/ADM cells.The reversal index was defined as the IC50 of the experimental group divided by the IC50 of the control group in K562/ADM cells. Results: Art effectively decreased the content of transferrin receptor and the expression of transferrin receptor protein in K562/ADM cells in a dose-dependent manner. Moreover, Art also inhibited transferrin receptor protein expression in K562/ADM cells in a time-dependent manner.The different concentrations of Art(12.5 μg/mL, 25μg/mL and 50 μg/mL) could induce reversal of drug-resistance with the reversal index being 1.38, 2.12 and 2.95 times (P＜0.05). Art inhibited cell proliferation of K562/ADM cells, and the IC50 were19.7 μmol/L. Conclusions: Art effectively down-regulated the transferrin receptor content as well as transferrin receptor protein expression in K562/ADM cells, which resulted in reversal of drug resistance of K562/ADM cells. Art also inhibited K562/ADM cells proliferation, which has great value in clinical treatment of leukemia. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To establish SRB1 gene-knockdown microglia cell line and investigate the function of microglia SRB1 receptor in the phagocytosis of Aβ during the process of Alzheimer's disease (AD). Methods: The expression of SRB1 gene in human microglia 1900 was determined by reverse transcription-PCR. three lentiviral sliRNA targeting SRB1 were designed and the best interferring sliRNA sequence was selected. The resulting lentiviral construct was used to knockdown SRB1 gene in human microglia. Intracellular Aβ42 Quantification was performed to test the phagocytosis function of the SRB1 knockdown microglia cell line. Results: The lentiviral particles were successfully prepared and showed effective infection capacity and knockdown effects. SRB1 gene silencing was performed in Human microglia 1900 with a knock-down efficiency of 83.7%. The phagocytosis function was significantly decreased to 57% in SRB1 gene-silencing microglia cell line. Conclusion: The SRB1 knock-down cell line was established. The function of SRB1 gene was confirmed by oligomer Aβ(oAβ) phagocytosis test. These findings have identified a significant role of SRB1 in Aβ clearance. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)