Recent studies have shown that tumor microenvironment (TME) is significantly different from normal tissues, such as the change of abnormal enzyme expression, hypoxia, pH and so on. TME is closely related to the induced proliferation of tumor cells, angiogenesis, immune escape and the production of multidrug resistance. Cancer associated fibroblasts (CAFs) are the main stromal cell types in the TME. A variety of cytokines secreted by CAFs play an important role in tumor growth, invasion and metastasis. Understanding the role and mechanism of CAFs in the development of breast cancer is expected to provide a new target for improving the prognosis of breast cancer patients.

Lateral position is a common surgical position in neurosurgery, it is also a susceptible position for pressure ulcers. The reasons not only consist of the common causes of general surgery, but also consist of unique factors due to its special position. The technique and rationality of body position placement is significant for the prevention of pressure ulcers. This article reviews the causes and preventive measures of pressure ulcers with lateral position in neurosurgery operation after consulting extensive literature. We will expound and analyze the way of body position placement, placement techniques of every part, selection of material for various body positions, and precautions of position nursing in perioperative period of lateral position surgery, etc. We hope to provide references for the prevention and management of pressure ulcers in neurosurgery operation with lateral position.

Objective? To explore the effects of new orthopedic high-waist shoes on preventing foot drop deformity among spinal cord injury patients with lower limb paralysis. Methods? From April 2016 to January 2018, we selected a total of 44 spinal cord injury patients with paralysis. All of the patients were divided into experimental group and control group according to the order of admission and random number sampling approaches. Patients of experimental group wore new orthopedic high-waist shoes from the first day after admission, while patients of control group used the square soft pillow in foot. We compared the incidence of foot drop deformity among patients two weeks after admission. Results? The incidences of foot drop deformity, pressure injury on foot as well as strephenopodia of patients in experimental group and control group were 18.2% vs. 40.9%, 4.5% vs. 18.2% as well as 27.3% vs. 59.1% respectively with statistical differences (P＜0.05). Conclusions? Early use of new orthopedic high-waist shoes can effectively prevent foot drop, protect function of ankle joint and promote the rehabilitation of neuromuscular function in limb among spinal cord injury patients with paralysis.

Objective:To observe the effects of salvianolic acid B on migration and tube formation of the retinal vascular endothelial cell (RVEC) in high glucose, and explore its mechanism with network pharmacology.Methods:The cells were divided into normal group, model group and 1.0, 0.5, 0.1 μg/ml salvianolic acid B group according to the random number table method. The cells of each group were added with 5.5 mmol/L glucose for intervention, and the salvianolic acid B group was added with 1.0, 0.5, and 0.1 μg/ml salvianolic acid B for intervention. After 72 h, the cell viability of each group was detected by the CCK-8 method. The cells were divided into normal group, model group and low-, medium-, and high-dose salvianolic acid B group according to the random number table method. Then the cells of the normal group were added with 5.5 mmol/L glucose; the model group was added with 25 mmol/L glucose; the low-, medium-, and high-dose salvianolic acid B group was added with 25 mmol/L glucose and 0.062 5, 0.1250, 0.250 0 μg/ml salvianolic acid B. Then by taking Transwell test to detect the number of cell migration, and Matrigel test to analyze the total length of cells tubes. The active targets of Salvianolic acid B were screened by SuperTarget and Swiss TargetPrediction. Then, the targets of diabetic retinopathy were obtained by searching the GAD database, pharmGkb database, TTD database, DiGSeE database and OMIM database. The effective targets of drug-disease interaction were screened, and the component-target-disease interaction network was constructed by Cytoscape. Finally, the effective targets were analyzed by DAVID for GO analysis and KEGG pathway enrichment analysis. Molecular docking was performed by using Accelrys Discovery Studio Client 2.5 software.Results:The CCK-8 method showed that the cell absorbance values of 0.5 and 0.1 μg/ml salvianolic acid B group were not significantly different from those of the normal group ( P>0.05). The results of Transwell experiment and Matrigel experiment showed that compared with the model group, the relative number of migrating cells and the total length of tubule formation in each dose group of salvianolic acid B decreased ( P<0.05 or P<0.01). The interaction network revealed that salvianolic acid B acted on 46 targets and 8 signaling pathways. Conclusions:Salvianolic acid B could inhibit the migrating and tube forming ability of RVEC cultivated by high glucose. The results suggest that salvianolic acid B may play roles in preventing diabetic retinopathy.

Background: N-Alkylamides(NAAs),derived from Anacyclus pyrethrum(L.)DC,have potential anti-tumor effects.To explore the molecular mechanism and chemo-preventive capacity of NAAs,we synthesized an NAA(H-10)and evaluated whether it could inhibit the proliferation of B16,HepG2,HeLa,and HCT116 cancer cells in 2D culture.Methods: To evaluate the antiproliferative activity of H-10 in 2D and 3D culture of BD,HepG2,HeLa,and HCT116 cells,multicellular tumor spheroids were constructed to more accurately reflect the cell tumor environment.To visualize nuclear changes related to apoptosis,Hoechst 33258 staining and propidium iodide-Annexin V double staining were performed.Results: Compound H-10 strongly inhibited the growth of all tested cell lines.Hoechst 33258 staining and propidium iodide-Annexin V double staining revealed that H-10 did not cause morphological al-terations in the nuclei and moderately induced late apoptosis only when treated at 180μM.The strongest inhibitory effect was observed in HCT116 cells.Flow cytometry analysis indicated that treatment of HCT116 cells with compound H-10 resulted in robust cell growth arrest in G2 phase in 2D and 3D cell culture;in 3D-cultured HCT116 cells,growth arrest occurred in G1 phase.Treatment with compound H-10 also significantly suppressed angiogenesis of chick chorioallantoic membrane in vivo.Conclusion: Treatment with compound H-10 strongly affected clonogenic survival(in the long-term)and migration of HCT116 cells.Therefore,H-10,a compound of NAAs may be useful for treating cancer because of its anti-neoplastic effect and easy synthesis.

Objective:To explore the psychological experience and demand of parents of children with delayed recovery after congenital heart disease surgery.Methods:This study adopted phenomenological research methods from qualitative research. Using the purposive sampling method, parents of postoperative delayed recovery children with congenital heart disease who met the inclusion criteria were selected as the research objects from October to November 2019 at Fuwai Hospital, Chinese Academy of Medical Sciences. Semi-structured interviews were conducted with the parents of the children, and the data were analyzed by Colaizzi 7-step analysis method.Results:Finally, 13 parents of children with delayed recovery after congenital heart disease surgery were included. According to the interview results, four themes were extracted, which were negative psychological experience of parents of children with delayed recovery, positive psychological experience and expectation change of parents, heavy economic burden of parents and diversified needs of parents.Conclusions:During the delayed recovery period, psychological experience of parents is complex and their needs are diverse. The nursing staff should identify and pay attention to the causes of the negative psychological experience of the parents of the children, timely channel their negative emotions and strengthen the positive psychological experience in many aspects. They can assist parents to seek social help to reduce physical and mental pressure and meet the diverse needs of parents by providing high-quality nursing services and multi-channel information support.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Objective To investigate the molecular mechanism through which calenduloside E inhibits hepatocellular carcinoma(HCC)cell proliferation and migration.Methods HCC cell lines HepG2 and Huh7 treated with calenduloside E were examined for changes in cell viability using CCK-8 assay and expressions of GPX4,SLC7A11,LC3,P62 and phosphorylation of Akt/mTOR using Western blotting.The effects LY294002 and Rapamycin(the inhibitor and activator of autophagy,respectively)on proliferation and migration of calenduloside E-treated HCC cells were evaluated using EdU and Transwell assays.The TCGA database was used to explore the expression levels of GPX4 and SLC7A11 in HCC and normal liver tissues and their correlation with the patients'survival outcomes.GPX4 and SLC7A11 expressions were also detected in HCC cells and normal hepatocytes using RT-qPCR and Western blotting.Results Calenduloside E obviously inhibited the viability of HCC cells.GPX4 and SLC7A11 were highly expressed in HCC tissues and cell lines,and their expression levels were negatively correlated with the patients'survival.In HCC cell lines,calenduloside E significantly inhibited the expressions of GPX4 and SLC7A11 proteins,activated the Akt-mTOR pathway,and enhanced the expression of LC3 II.The inhibitory effect of calenduloside E on GPX4 and SLC7A11 expressions was significantly enhanced by rapamycin but attenuated by LY294002.Inhibiting the autophagy pathway obviously diminished the inhibitory effect of calenduloside E on proliferation and migration of HCC cells,while activating this pathway produced the opposite effect.Conclusion Calenduside E inhibits the proliferation and migration of HCC cells by down-regulating GPX4 and SLC7A11 expression via the autophagy pathway.

Objective To investigate the molecular mechanism through which calenduloside E inhibits hepatocellular carcinoma(HCC)cell proliferation and migration.Methods HCC cell lines HepG2 and Huh7 treated with calenduloside E were examined for changes in cell viability using CCK-8 assay and expressions of GPX4,SLC7A11,LC3,P62 and phosphorylation of Akt/mTOR using Western blotting.The effects LY294002 and Rapamycin(the inhibitor and activator of autophagy,respectively)on proliferation and migration of calenduloside E-treated HCC cells were evaluated using EdU and Transwell assays.The TCGA database was used to explore the expression levels of GPX4 and SLC7A11 in HCC and normal liver tissues and their correlation with the patients'survival outcomes.GPX4 and SLC7A11 expressions were also detected in HCC cells and normal hepatocytes using RT-qPCR and Western blotting.Results Calenduloside E obviously inhibited the viability of HCC cells.GPX4 and SLC7A11 were highly expressed in HCC tissues and cell lines,and their expression levels were negatively correlated with the patients'survival.In HCC cell lines,calenduloside E significantly inhibited the expressions of GPX4 and SLC7A11 proteins,activated the Akt-mTOR pathway,and enhanced the expression of LC3 II.The inhibitory effect of calenduloside E on GPX4 and SLC7A11 expressions was significantly enhanced by rapamycin but attenuated by LY294002.Inhibiting the autophagy pathway obviously diminished the inhibitory effect of calenduloside E on proliferation and migration of HCC cells,while activating this pathway produced the opposite effect.Conclusion Calenduside E inhibits the proliferation and migration of HCC cells by down-regulating GPX4 and SLC7A11 expression via the autophagy pathway.