ObjectiveTo explore the suitability of four qualitative research methods in the development of TCM scale. MethodsTaking the development of "Seven Emotions Scale" as an example， we conducted semi-structured interviews with 31 patients of emotional disorders and 10 healthy people by objective sampling， and collected psychological feelings and emotional cognition data related to seven emotions according to the interview outline. Two qualitative methods， descriptive qualitative research and descriptive phenomenology， were used to analyze the data and construct the item library of the scale. The conceptual framework of the scale was constructed by using commonly used grounded theory and frame analysis. ResultsDuring data analysis， it is found that the themes extracted from descriptive phenomenology were not easily understood by the interviewees， and it is difficult for the researchers to truly achieve the "suspension" required by phenomenology. Considering the feasibility and convenience of the researchers' actual operation， as well as whether the initial purpose of the scale research can be intuitively included in the interviewees' views and feelings， descriptive phenomenology is not suitable for the formation of scale items. Using descriptive qualitative research method to analyze the interview data of healthy people and patients with emotional disorders， 306 and 476 scale items were obtained respectively. Through grounded theory， five selective codes were obtained： physical symptoms， external manifestations， psychological feelings， behaviors and emotional control. Using frame analysis， four themes including physical symptoms， psychological feelings， behavior and emotional cognition were constructed. Both methods can be used to construct the conceptual frame of scale， but the framework analysis is more convenient and can better ensure the transparency of the research. ConclusionDescriptive qualitative research methods can be used to form the item library of TCM scales. Framework analysis is more suitable for the construction of the conceptual framework of the scale than grounded theory， while descriptive phenomenology is not suitable for the development of TCM scales.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective:To gain a deep understanding of the current cognition and training needs of nursing undergraduates regarding their emergency response teamwork skills, and to provide reference for the development of courses on emergency response teamwork among nursing undergraduates.Methods:From September to October 2023, purposive sampling was used to select 15 senior nursing undergraduates from Peking Union Medical College, Beijing University of Chinese Medicine, and Beijing City University as subjects for semi-structured interviews. Colazizzi 7-step analysis method was used to summarize and extract themes.Results:Three themes were extracted, including insufficient cognition and skill in emergency response, lack of emergency response teamwork cultivation, and the need for systematic and comprehensive training courses.Conclusions:Universities, hospitals, and other training institutions should work together to develop a systematic emergency response teamwork training course for nursing undergraduates, to cultivate the skills of nursing undergraduates and reserve talents for high-quality emergency response nursing teams.

Objective To investigate the effects of pterostilbene on human colon cancer LoVo cells and study the regulatory mechanism of nuclear factor E2-related factor 2(Nrf2)in the process of pterostilbene acting on LoVo cells.Methods LoVo cells were treated with different concentrations(5,10,20,40,60,80,100 panol/L)of pterostilbene.Cell viability,migration,invasion,and apoptosis were examined by CCK-8,scratch,Tran-swell,and TUNEL assays,respectively.The mitochondrial membrane potential was measured by the mitochon-drial membrane potential assay kit with JC-1.The reactive oxygen species level was measured by 2',7'-dichlo-rofluorescein diacetate.The protein levels of Nrf2,phosphorylated Nrf2,heme oxygenase 1,and apoptotic pro-teins(Bcl2 and Bax)were determined by Western blotting.In addition,cell viability,Nrf2 expression,and ap-optosis rate were determined after co-application of the Nrf2-specific agonist sulforaphane.Results Compared with the control group,40,60,80,100 μmol/L pterostilbene reduced the viability of LoVo cells(P=0.014,P＜0.001,P＜0.001,P＜0.001).Pterostilbene at 5,10,20 μmol/L did not show effects on cell viability but inhibited cell migration(P=0.008,P＜0.001,P＜0.001)and invasion(all P＜0.001).Pterostilbene at 40,60,80 μmol/L increased apoptosis(P=0.014,P＜0.001,P＜0.001),promoted mitochondrial membrane potential depolarization(P=0.026,P＜0.001,P＜0.001)and reactive oxygen species accumula-tion(all P＜0.001),and down-regulated the expression of phosphorylated Nrf2(P=0.030,P＜0.001,P＜0.001),heme oxygenase 1(P=0.015,P＜0.001,P＜0.001),and Bc12(P=0.039,P＜0.001,P＜0.001)in LoVo cells.Pterostilbene at 60,80 μmol/L down-regulated Nrf2 expression(P=0.001,P＜0.001)and up-regulated Bax expression(both P＜0.001).The application of sulforaphane reversed the effects of pterostilbene on cell viability(P＜0.001),apoptosis(P＜0.001),and Nrf2 expression(P=0.022).Conclusion Pterostilbene is a compound that can effectively inhibit colon cancer cells by inhibiting the Nrf2 pathway.

Objective:To analyze the trend of liver cancer mortality in rural key areas of Jiangsu Province, Anhui Province, Shandong Province, and Henan Province (4 provinces) from 2009 to 2019 and to explore the influence of behavioral risk factors on liver cancer mortality and its lagging effect, and provide a reference for the prevention and treatment of liver cancer in China.Methods:Based on the 2009-2019 National Cause of Death Surveillance Database of the Chinese Center for Disease Control and Prevention, and the survey data of tumor and risk factor behavior of residents in key areas of 4 provinces, Joinpoint 4.2 software was used to calculate the average annual percentage change (AAPC) for assessing the temporal trend of standardized mortality of liver cancer; Chi-square test and trend Chi-square test were used to analyze the regional distribution difference and temporal change trend of behavioral habit factors. Stata 16 was used to establish a panel model to analyze the correlation and lagging effect of behavioral risk factors with liver cancer.Results:The standardized mortality rate of liver cancer in Jinhu County, Sheyang County, Lingbi County, Shou County, Mengcheng County, Wenshang County, Juye County, Luoshan County, Shenqiu County, and Xiping County showed a downward trend (AAPC<0, P<0.05) from 2009 to 2019. The consumption frequency of pickles/salted fish, red meat, and aquatic products showed a downward trend. The consumption frequency of healthy foods such as fresh vegetables, fresh fruits, and dairy products in all counties and districts showed an upward trend, and the consumption frequency of fried foods, kimchi, smoked foods, moldy foods, coffee, and soy products remained at a low level ( P<0.05); but the consumption frequency of soy products and dairy products was still <20.00%. Fried food, pickles/salted fish, current smoking rate, alcohol consumption rate, and unvaccinated hepatitis B vaccine rate were positively correlated with liver cancer death, and there was a lag effect, and the lag period was 4, 1, 6, 5, 4 years respectively. Conclusions:From 2009 to 2019, the mortality rate of liver cancer in rural key areas of 4 provinces shows a downward trend. There is a correlation and lagging effect between behavioral risk factors such as fried food, smoking, and alcohol consumption and liver cancer death.

Objective:To explore KRAS, NRAS, BRAF gene mutations and microsatellite instability(MSI) in colorectal cancer tissues as well as their correlation with the clinicopathological characteristics of patients.Methods:The clinicopathological data of 473 colorectal cancer patients in Shanxi Province Cancer Hospital from October 2020 to May 2021 were retrospectively analyzed. The mutation status of KRAS, NRAS and BRAF gene in the paraffin tissues were detected by using amplification refractory mutation system (ARMS) method. Polymerase chain reaction (PCR)-capillary electrophoresis was used to analyze MSI status, and the correlation of the clinicopathological characteristics of patients with gene mutations and MSI status was analyzed.Results:The mutation rates of KRAS, NRAS and BRAF were 45.03% (213/473), 2.96% (14/473) and 5.50% (26/473), respectively in 473 patients with colorectal cancer. No case harbored both 2 gene mutations was detected. The mutation rate of KRAS gene in well differentiated adenocarcinoma was higher than that in poorly differentiated adenocarcinoma [47.4% (175/369) vs. 36.5% (38/104), χ2 = 3.89, P = 0.049]. NRAS mutation rate in female was higher than that in male [5.0% (10/202) vs. 1.5% (4/271), χ2 = 4.86, P = 0.027], and the NRAS mutation rate in patients with tumor diameter ≤ 3 cm was higher than that in those with tumor diameter >3 cm [7.1% (7/98) vs. 1.9% (7/375), P = 0.013]. BRAF mutation rate of tumors located in colon was higher than that in rectum [11.7% (20/171) vs.2.0% (6/302), χ2 = 19.81, P < 0.001]; BRAF mutation rate in poorly differentiated tumor was higher than that in well differentiated tumor [10.6% (11/104) vs. 4.1% (15/369), χ2 = 6.62, P = 0.010]; BRAF mutation rate in patients with mucus was higher than that in those without mucus [10.9% (11/101) vs. 4.0% (15/372), χ2 = 7.19, P = 0.007]; BRAF mutation rate in patients with lymphatic metastasis was higher than that in patients without lymphatic metastasis [8.2% (15/182) vs.3.8% (11/291), χ2 = 4.29, P = 0.038]. The incidence of high frequency MSI (MSI-H) in 473 colorectal cancer tissues was 7.19% (34/473). The incidence of MSI-H in colon was higher than that in rectum [14.0% (24/171) vs. 3.3% (10/302), χ2 = 18.82, P < 0.001]; the incidence of MSI-H in patient with poor differentiated tumor was higher than that in those with well differentiated tumor [17.3% (18/104) vs. 4.3% (16/369), χ2 = 20.46, P < 0.001]; the incidence of MSI-H in patients with mucus was higher than that in those without mucus [11.9% (12/101) vs. 5.9% (22/372), χ2 = 4.24, P = 0.039]; and the incidence of MSI-H in patients without lymphatic metastasis was higher than that in patients with lymphatic metastasis [10.0% (29/291) vs. 2.7% (5/182), χ2 = 8.75, P = 0.003]. In addition, the incidence of MSI-H was on the rise in patients with BRAF mutation ( P < 0.001). Conclusions:KRAS, NRAS, BRAF gene mutations and MSI status are correlated with the clinicopathological characteristics of patients with colorectal cancer; there is a close relationship between MSI-H and BRAF mutation.

Purpose: C5α receptor 1 (C5ΑR1) is associated with the development of various human cancers. However, whether it is involved in the development of hepatitis B virus (HBV)–related hepatocellular carcinoma (HCC) is poorly understood. We explored the expression, biological role, and associated mechanisms of C5AR1 in HBV-related hepatoma cells. Materials and Methods: The expression of C5ΑR1 mediated by HBV and HBV core protein (HBc) was detected in hepatoma cells. The function of nuclear factor кB (NF-κB) pathway in HBc-induced C5AR1 expression was assessed. The roles of C5ΑR1 in the activation of intracellular signal pathways, the upregulation of inflammatory cytokines, and the growth and migration of hepatoma cells mediated by HBc, were investigated. The effect of C5α in the development of HCC mediated by C5AR1 was also measured. Results: C5ΑR1 expression was increased in HBV-positive hepatoma cells. Dependent on HBc, HBV enhanced the expression of C5ΑR1 at the mRNA and protein levels. Besides, HBc could promote C5ΑR1 expression via the NF-κB pathway. Based on the C5ΑR1, HBc facilitated the activation of JNK and ERK pathways and the expression and secretion of interleukin-6 in hepatoma cells. Furthermore, C5ΑR1 was responsible for enhancing the growth and migration of hepatoma cells mediated by HBc. Except these, C5α could promote the malignant development of HBc-positive HCC via C5AR1. Conclusion We provide new insight into the mechanisms of hepatocarcinogenesis mediated by HBc. C5ΑR1 has a significant role in the functional abnormality of hepatoma cells mediated by HBc, and might be utilized as a potential therapeutic target for HBV-related HCC.

Purpose: C5α receptor 1 (C5ΑR1) is associated with the development of various human cancers. However, whether it is involved in the development of hepatitis B virus (HBV)–related hepatocellular carcinoma (HCC) is poorly understood. We explored the expression, biological role, and associated mechanisms of C5AR1 in HBV-related hepatoma cells. Materials and Methods: The expression of C5ΑR1 mediated by HBV and HBV core protein (HBc) was detected in hepatoma cells. The function of nuclear factor кB (NF-κB) pathway in HBc-induced C5AR1 expression was assessed. The roles of C5ΑR1 in the activation of intracellular signal pathways, the upregulation of inflammatory cytokines, and the growth and migration of hepatoma cells mediated by HBc, were investigated. The effect of C5α in the development of HCC mediated by C5AR1 was also measured. Results: C5ΑR1 expression was increased in HBV-positive hepatoma cells. Dependent on HBc, HBV enhanced the expression of C5ΑR1 at the mRNA and protein levels. Besides, HBc could promote C5ΑR1 expression via the NF-κB pathway. Based on the C5ΑR1, HBc facilitated the activation of JNK and ERK pathways and the expression and secretion of interleukin-6 in hepatoma cells. Furthermore, C5ΑR1 was responsible for enhancing the growth and migration of hepatoma cells mediated by HBc. Except these, C5α could promote the malignant development of HBc-positive HCC via C5AR1. Conclusion We provide new insight into the mechanisms of hepatocarcinogenesis mediated by HBc. C5ΑR1 has a significant role in the functional abnormality of hepatoma cells mediated by HBc, and might be utilized as a potential therapeutic target for HBV-related HCC.

The cause of immune recurrent abortion is closely related to immune abnormalities. At present, the Traditional Chinese Medicine (TCM) syndrome types of immune recurrent abortion mainly include kidney deficiency and blood stasis syndrome, spleen and kidney deficiency syndrome, blood heat syndrome, spleen deficiency syndrome and lung and kidney qi deficiency syndrome; The commonly used TCM compound for treating this disease usually could replenish kidney qi and take effect, so it is considered that the pathogenesis of this disease is mainly kidney deficiency. The mechanism of action of the TCM compound is mainly related to regulating hormone secretion, immune balance and improving local microcirculation.