Objective:To analyze the current situation and requirements of education for health technicians in maternal and child health care institutions, and put forward feasible strategies and measures to improve the comprehensive quality and professional level of the talent team of maternal and child health care institutions.Methods:Questionnaire survey was carried out on education needs of health technical staff of 11 maternal and child health care hospitals in 4 provinces (regions), and provincial, municipal and district-level medical institutions. The survey results were recorded by Epidata 3.1. SPSS 22.0 software was used for statistical analysis.Results:A total of 1 678 questionnaires were included in the analysis. A total of 1 313 people received training, accounting for 78.2%. The main reason for not receiving training was that the unit didn't arrange (180 people), accounting for 49.3%(180/365). There were 779 people who had more than 3 days of training, accounting for 59.3%. There were 384 people who were trained in superior general hospitals, accounting for 29.2%, and 268 people were trained in superior maternal and child health institutions, accounting for 20.4%. There were 837 people who learned the content of new professional progress, accounting for 50.8%(837/1 648). According to the interview, there were still some requirements for thematic training, further education, online learning, continuing education and standardized training.Conclusion:Maternal and child health care institutions have accelerated the construction of professional personnel, intensified training, and thoroughly implemented health personnel training programs, established a long-term mechanism, increased funding, improved training content, ensured the quality of training, and made a good job in hierarchical training to meet the learning needs of personnel at all levels. This is of great significance for strengthening the technical personnel of maternal and child health care institutions and improving their service capacity.

ObjectiveTo observe the effect of the serum containing Puerariae Lobatae Radix on tumor necrosis factor-α （TNF-α）， endoplasmic reticulum stress signaling pathway protein endoplasmic reticulum stress protein glucose-regulated protein 78 （GRP78）， activated transcription factor 4 （ATF4）， protein kinase R-like endoplasmic reticulum kinase （PERK）， and eukaryotic translation initiation factors （eIF2α） and on inflammatory injury of macrophages induced by high glucose， and explore its possible mechanism. MethodThe control serum and serum containing Puerariae Lobatae Radix were prepared by serum pharmacology. The RAW264.7 macrophages were cultured in vitro， and 62.5 mmol·L^-1 glucose was used to induce macrophages to establish a model of severe endoplasmic reticulum （ER） stress （ERS） in vitro. Different volume fractions of serum containing Puerariae Lobatae Radix and ERS inhibitor （4-PBA） were used to interfere with the cells. Different glucose concentrations （22.5， 23.5， 25.0， 27.5， 32.5， 47.5， 72.5， 122.5 mmol·L^-1） and the effect of different volume fractions of serum containing Puerariae Lobatae Radix （0%， 2.5%， 5%， 7.5%， 10%， 15%， 20%） on the survival rate of RAW264.7 macrophages were detected by cell proliferation and cell counting kit-8 （CCK-8） assay. Based on the results of the effect of glucose concentrations on macrophage survival rate by CCK-8， Western blot （WB） was used to determine the protein expression levels of GRP78， the signature protein of ERS， by different concentrations of glucose （22.5， 32.5， 42.5， 52.5， 62.5， 72.5 mmol·L^-1） at different time periods （6， 12， 24， 36， 48 h）， and the optimal concentration and time for establishing the model of severe ERS were screened out. Based on the above experimental results， the cells were divided into blank group， 62.5 mmol·L^-1 glucose model group， 2 mmol·L^-1 4-PBA group， and high， medium， and low-dose （15%， 10%， 5%） serum containing Puerariae Lobatae Radix groups for subsequent experiments. The expression of TNF-α in the supernatant of RAW264.7 macrophages in the model of severe ERS was determined by enzyme-linked immunosorbent assay （ELISA）. The expressions of related pathway proteins in the model of severe ERS were determined by WB. ResultThe results of CCK-8 assay showed that the survival rate of macrophages reached the highest under the stimulation of glucose concentration of 27.5 mmol·L^-1 （P<0.01）， while the survival rate of macrophages increased with the concentration increasing from 22.5 mmol·L^-1 to 27.5 mmol·L^-1. When the glucose concentration was 25.0 mmol·L^-1， there was a significant difference （P<0.01）， and when the glucose concentration was 37.5 mmol·L^-1 to 122.5 mmol·L^-1， there was a downward trend. The serum containing Puerariae Lobatae Radix showed significant differences in the volume of 1% to 15% （P<0.05， P<0.01）. The results of WB found that the GRP78 protein expression was the most significant at 24 h （P<0.01）， and the GRP78 protein expression was the most significant when the glucose concentration was 62.5 mmol·L^-1 （P<0.01）. Therefore， 62.5 mmol·L^-1 of glucose was the optimal concentration to induce the model of severe ERS. As compared with the blank group， the protein expression levels of TNF-α， GRP78， ATF4， phosphorylation（p）-PERK/PERK， p-eIF2α/eIF2α in the model group were significantly increased （P<0.05， P<0.01）， and as compared with the model group， the protein expression levels of TNF-α， GRP78， ATF4， p-PERK/PERK， p-eIF2α/eIF2α in each administration group were significantly decreased （P<0.05， P<0.01）. ConclusionThe results of in vitro experiments show that Puerariae Lobatae Radix can alleviate the inflammatory injury of macrophages induced by high glucose to a certain extent and restore cell homeostasis by inhibiting the expression of GRP78， ATF4， PERK， and eIF2α in the ERS signaling pathway.

ObjectiveTo explore the mechanism of Buyang Huanwutang in regulating macrophage polarization based on the Toll-like receptor 4 （TLR4） / nuclear factor-κB （NF-κB） / nucleotide-binding oligomerization domain-like receptor 3 （NLRP3） pathway. MethodRAW264.7 macrophages were intervened with lipopolysaccharide （LPS） of different concentrations （0， 1.25， 2.5， 5， 10， 20， 40， and 80 mg·L^-1） for 24 hours. Cell Counting Kit-8 （CCK-8） assay was used to determine the cell viability of RAW264.7 macrophages. The optimal concentration was chosen to establish an in vitro inflammation model induced by LPS. Cells were divided into a blank group （20% blank serum）， a model group （20% blank serum + 10 mg·L^-1 LPS）， a model control group （20% FBS + 10 mg·L^-1 LPS）， low-， medium-， and high-dose （5%， 10%， and 20%） Buyang Huanwutang-containing serum groups， a high-dose （20%） Buyang Huanwutang combined with NLRP3 inhibitor MCC950 （50 μmol·L^-1） group， a high-dose （20%） Buyang Huanwutang combined with reactive oxygen species （ROS） inhibitor NAC （10 μmol·L^-1） group， and a high-dose （20%） Buyang Huanwutang combined with NF-κB inhibitor PDTC （10 μmol·L^-1） group. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression of interleukin-1β （IL-1β）， interleukin-18 （IL-18）， and tumor necrosis factor-α （TNF-α） in RAW264.7 macrophages. Flow cytometry was employed to measure ROS levels in macrophages. Western blot was used to determine the protein expression of M1-type macrophage-related factors inducible nitric oxide synthase （iNOS） and TNF-α， M2-type macrophage-related factors arginase-1 （Arg-1） and interleukin-10 （IL-10）， as well as the proteins in the TLR4/NF-κB/NLRP3 pathway. ResultCCK-8 results indicated that under 10 mg·L^-1 LPS stimulation， RAW264.7 macrophages exhibited the highest cell viability （P<0.01）. Compared with the blank group， the model group showed significantly increased levels of IL-1β， IL-18， and TNF-α （P<0.05，P<0.01）， increased ROS expression （P<0.05，P<0.01）， increased protein expression of M1-type macrophage factors iNOS and TNF-α （P<0.01）， decreased protein expression of M2-type macrophage factors Arg-1 and IL-10 （P<0.05，P<0.01）， and upregulated expression levels of TLR4， myeloid differentiation factor 88 （MyD88）， phosphorylated inhibitor of NF-κB （p-IκB）/NF-κB inhibitor （IκB）， phosphorylated NF-κB （p-NF-κB） p65/NF-κB p65， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， and pro-Caspase-1 （P<0.05， P<0.01）. Compared with the model group， all Buyang Huanwutang-treated groups and inhibitor groups significantly reduced levels of IL-1β， IL-18， and TNF-α （P<0.01）， suppressed the expression of inflammatory factors in RAW264.7 macrophages， decreased cellular ROS expression levels （P<0.01）， downregulated M1-type macrophages iNOS and TNF-α protein expression （P<0.01）， upregulated M2-type macrophages Arg-1 and IL-10 protein expression （P<0.01）， and lowered protein expression levels of TLR4， MyD88， p-IκB/IκB， p-NF-κB p65/NF-κB p65， NLRP3， ASC， and pro-Caspase-1 （P<0.05， P<0.01）. ConclusionBuyang Huanwutang can improve macrophage inflammation， potentially by reducing macrophage ROS levels， inhibiting RAW264.7 macrophage polarization， and downregulating the protein expression levels of the TLR4/NF-κB/NLRP3 pathway.