Objective To evaluate the hemodynamic responses of esmolol to nasotracheal intubation with fiberbronchoscope(FOB). Methods Thirty-five ASAⅠorⅡpatients undergone stomatology and otorhinolaryngology surgery were randomly divided into fiberoptic nasotracheal intubation esmolol group (esmolol group) and fiberoptic nasotracheal intubation group (control group). The intravenous administration of esmolol 1mg?kg-1 was performed 2 min before tracheal intubation in esmolol group. Noninvasive SBP,DBP,MBP,HR and SpO2 were recorded before and after anesthetic induction,at intubation and 1,2,3,4,5 min after intubation. Results The SBP,DBP and MBP 1 min after intubation in esmolol group were significantly lower than those in control group(P

With the universal two-child policy implementation, the birth rate increased, posing challenges to pediatrician allocation. Based on the birth rate, we calculated pediatrician demands and gaps during the period from 2016 to 2020 by the method of health service demand. The results showed that except Beijing and Shanghai, the ped-iatrician supply and demand ratios are less than 0 . 80 and additional numbers of pediatricians ranging from 191 981 to 198 287 are needed to meet the service demands. We recommend increasing the number of pediatricians taking both national supply-demand ratios and gaps by rationally using reasonable enrolment quota and improving the treatment and other reasonable ways to increase pediatricians. In addition, we should enhance information disclosure and guid-ance, and improve the hierarchical hospital visit system to alleviate the pressure of big cities.

With the universal two-child policy implementation, the birth rate increased, posing challenges to the maternity beds resource allocation. Based on the birth rate and the method of health service demand, we calculat-ed the maternity beds demands and gaps during the period from 2016 to 2020 . Results showed that numbers between 73 478 and 99 004 of maternity beds are needed annually and mainly allocated to eastern and central areas as well. In addition, the maternity beds of different delivery institutions should be adjusted and the hierarchical diagnosis system should be improved in order to alleviate the pressure of the obstestric acceepts in big cities like Beijing and Shanghai.

Objective To explore the effect of miR-23b-3p regulation on osteogenic differentiation of renal intersti-tial fibroblasts(hRIFs)on the formation of Randall plaque and its possible mechanism.Methods qRT-PCR was used to detect the expression levels of miR-23b-3p and osteogenic marker:myocyte enhancer factor 2C(MEF2C),osteocalcin(OCN),osteopontin(OPN),runt-related transcription factor 2(Runx2)mRNA in Randall plaque tis-sue of CaOx stone patients(RP)and normal papillary tissue of kidney tumor patients undergoing nephrectomy(nRP).Isolation and culture of human normal hRIFs were isolated and cultured in vitro.The miR-23b-3p overex-pression plasmid pSi-miR-23b-3p and its negative no-load plasmid pSi-NC,the MEF2C lentivirus overexpression plasmid Lv-MEF2C and the no-load plasmid Lv-NC were transfected into hRIFs cells,and the cells were induced to osteogenic differentiation for 14 days.The activity of alkaline phosphatase(ALP)was determined by ELISA.Aliz-arin red staining was used to observe the formation of mineralized nodules.The expression levels of miR-23b-3p and MEF2C,OCN,OPN,Runx2 mRNA were detected by qRT-PCR.The expression level of MEF2C protein was de-tected by Western blot.Dual luciferase reporter gene assay verified the targeting relationship between miR-23b-3p and MEF2C.Results ① Compared with the nRP group,miR-23b-3p was low expressed and MEF2C,OCN,OPN,and Runx2 were highly expressed in the RP group.② 14 days after osteogenic induction of hRIFs cells,the activity of ALP in cells significantly increased,the ability of cells to form mineralized nodules was enhanced,the expression level of miR-23b-3p significantly decreased,the mRNA expression levels of MEF2C,OCN,OPN,and Runx2 significantly increased,and the expression level of MEF2C protein significantly increased.③ Overexpres-sion of miR-23b-3p decreased the activity of ALP in hRIFs cells after osteogenic induction,inhibited the formation of mineralized nodules in cells,and down-regulated the mRNA expression levels of OCN,OPN,and Runx2 in cells.④ Overexpression of MEF2C reversed the inhibitory effect of miR-23b-3p overexpression on osteoblast differ-entiation of hRIFs cells.⑤ MEF2C was the downstream target gene of miR-23b-3p.Conclusion miR-23b-3p is underexpressed in RP tissues and during osteoblastic differentiation of hRIFs cells.Up-regulation of miR-23b-3p in-hibits osteogenic differentiation of hRIFs cells,and its mechanism may be related to targeted silencing MEF2C.

Since there is a lack of obvious clinical symptoms in the early stage of hepatocellular carcinoma (HCC), most patients have progressed to the advanced stage at the time of confirmed diagnosis. There are limited treatment options for HCC patients who miss the opportunity for surgery, so it is of great importance to find new therapeutic targets. Tumor-associated macrophages (TAMs) are a group of macrophages existing in the tumor immune microenvironment and affect the malignant behaviors of HCC cells and the state of immune escape within the tumor. This article introduces the origin and classification of TAM, summarizes the role and mechanism of TAMs in vascular proliferation, invasion and metastasis, formation and maintenance of stemness, and anti-tumor immunity in HCC, and briefly describes the current research advances in therapeutic targets for TAM, and it is pointed out that targeting TAM may be a promising direction for clinical treatment.

ObjectiveTo investigate the effect of kinesin family member 15 （KIF15） on the proliferation of hepatocellular carcinoma （HCC） cells and its mechanism of action. MethodsTCGA and GEPIA datasets were analyzed to determine the expression of KIF15 in HCC and its effect on tumor stage and survival. Quantitative real-time PCR and Western blot were used to measure the expression level of KIF15 in human-derived HCC cell lines （HepG2， Hep3B， MHCC-97H， and LM3） and human normal liver cell line L02 cultured in vitro， and Hep3B and HepG2 were selected for subsequent studies. CCK-8 assay， plate colony formation assay， and EdU staining were performed for Hep3B cells transfected with shRNA-NC or shRNA-KIF15 and HepG2 cells transfected with LV-vector or LV-KIF15 to evaluate the viability and proliferative capacity of these cells. GSEA was used to analyze the potential signaling pathways associated with KIF15 in HCC， and Western blot was used for detection. The independent-samples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsThe analysis of TCGA and GEPIA datasets showed that in HCC patients， the expression of KIF15 in HCC tissue was significantly higher than that in normal tissue， and the HCC patients with high KIF15 expression tended to have a poorer prognosis. Compared with sh-NC-Hep3B， sh3-Hep3B showed significant reductions in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Compared with vector-HepG2， LV-KIF15-HepG2 showed significant increases in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Subcutaneous tumor assay showed that compared with sh-NC-Hep3B， sh3-Hep3B showed reductions in tumor volume and tumor weight， as well as a significant reduction in the immunohistochemical score of Ki67 and a significant increase in the immunohistochemical score of TUNEL （P<0.05）. GSEA analysis showed that the PI3K/AKT/mTOR pathway was positively correlated with KIF15 in HCC （NES=1.59， P<0.001）. Western blot showed that LY294002 could inhibit the PI3K/AKT/mTOR pathway upregulated in LV-KIF15-HepG2， and compared with LV-KIF15-HepG2， LY294002+LV-KIF15-HepG2 showed significant reductions in cell viability， clone formation number， and EdU positive rate （all P<0.05）. ConclusionKIF15 enhances the viability and proliferative capacity of HCC cells by upregulating the PI3K/AKT/mTOR signaling pathway.

Allografts ; COVID-19 ; China/epidemiology* ; Disease Outbreaks ; Humans ; Kidney Transplantation/adverse effects* ; SARS-CoV-2