Eighty patients with hyperthyroidism treated in PLA 903 Hospital from February 2016 to May 2017 were randomly divided into two groups with 40 cases in each group.Patients in control group received routine outpatient education and those in study group received regular formatted mobile short message during follow-up in addition to routine education.The knowledge of disease,the compliance and satisfaction of treatment were assessed.After 12 weeks of follow-up,the TSH level was higher [0.430(0.050,2.806) vs.0.210(0.003,1.098) mU/L,Z=-8.07,P＜0.01],FT3 [(3.24± 1.18) vs.(4.18±2.07)ng/L,t=-2.49,P＜ 0.05] and FT4 levels [(12.43±6.82) vs.(19.58±19.06) ng/L,t=-2.26,P＜0.05] were lower in study group than those in control group.The scores of disease knowledge (6.12± 1.77 vs.5.25±1.79,t=4.67,P＜0.05),the Morisky scores of medication compliance (3.77±0.47 vs.3.37±0.73,t=8.22,P＜0.01),the rates of compliance for returning (85％ vs.65％,x2=4.27,P＜0.05) and the satisfaction rates with treatments (93％ vs.75％,x2=3.30,P＜0.05) in the study group were significantly higher than those in the control group.The score of disease knowledge in study group increased from 4.32± 1.55 before treatment to 6.12± 1.77 after 12 weeks of follow-up (t=22.65,P＜0.01).The results indicate that the health education plus regular formatted text message during follow-up can effectively improve the disease knowledge score,the compliance and satisfaction with treatment in patients with hyperthyroidism.

Objective To investigate the protective role of Sestrin2 overexpression in hypoxia and re-oxygenation injury (H/R) injury of hippocampal neurons and its mechanism in rats.Methods Neurons were enzymatically isolated from hippocampi of newborn Sprague-Dawley rats (less than 24 h old) and culturedinvitro. These neurons were randomly assigned into 4 groups (n=20) using a random number table: control group, H/R group, vector group and Sestrin2 overexpression group. The hippocampal neurons were seeded in 6-well plates at a density of 2×104 cells/mL; neurons in the latter two groups were transfected with lentiviruses containing empty vector andSestrin2overexpressed genes, respectively; the hippocampal neurons in the later three groups were subjected to oxygen-glucose deprivation (OGD) for 6 h followed by restoration of O2 supply for 20 h. The reactive oxygen species (ROS) content was detected by Reactive Species Assay Kit, and the ATP concentration was detected by ATP Assay Kit. Cell apoptosis rates were measured by flow cytometry. The levels of Sestrin2, dynamin-related protein 1 (Drp1), Fis1, and apoptosis-related proteins Bcl-2, Bax and cytochrome C (Cyt C) were measured by Western blotting. The ratio of Bcl-2 to Bax was calculated. The ultrastructure of mitochondria was observed by transmission electron microscopy.Results As compared with control group, H/R group had significantly lower ATP concentration, Bcl-2 protein expression and ratio of Bcl-2 to Bax ([11.15±0.42] nmol/mg proteinvs. [5.30±0.39] nmol/mg protein; 2.20±0.26vs. 0.91±0.02; 6.46± 0.41vs. 1.04±0.05), statistically higher average fluorescence intensity of ROS and cell apoptosis rate (152.41±17.38vs. 1530.00±14.69; 3.77％±0.74％vs. 56.57％±1.35％), and significantly higher protein levels of Sestrin2, Drp1, Fis1, Bax and Cyt C (0.66±0.06vs. 1.11±0.20; 0.48±0.03vs. 1.16±0.07; 1.14± 0.09vs. 2.47±0.09; 0.34±0.03vs. 0.88±0.04; 0.17±0.03vs. 0.30±0.03,P<0.05); what's more, the structure of mitochondria was obviously destroyed in I/R group. As compared with H/R group, Sestrin2 overexpression group had significantly increased ATP concentration, Sestrin2 and Bcl-2 protein expressions and ratio of Bcl-2 to Bax ([8.95±0.27] nmol/mg protein; 2.67±0.07; 1.80±0.19; 3.95±0.28), significantly lower average fluorescence intensity of ROS and cell apoptosis rate (337.27±15.32; 10.33％±2.60％), and statistically lower protein levels of Drp1, Fis1, Bax and Cyt C (0.43±0.02; 1.11±0.08; 0.45± 0.02; 0.17±0.02,P<0.05); the structure of mitochondria was relatively completed in Sestrin2 overexpression group.Conclusion Sestrin2 overexpression can inhibit mitochondrial fission, reduce accumulation of reactive oxygen species, improve mitochondrial energy metabolism and block mitochondria mediated apoptosis pathway, thereby alleviating I/R injury of rat hippocampal neurons.

The disease treatment of patients with gastrointestinal cancer is accompanied by impaired bodily functions. Frailty is very common in patients with gastrointestinal cancer, and is closely related to its various adverse health outcomes, which seriously affects their prognosis. This article reviews the risk factors, correlation with adverse health outcomes and intervention methods of frailty in gastrointestinal cancer patients. It is pointed out that medical and nursing staff should identify the frailty state of patients with gastrointestinal cancer as soon as possible and make early interventions to improve the prognosis of patients.

Objective:To explore the effect of comprehensive follow-up mode in patients with chronic obstructive pulmonary disease (COPD) .Methods:From February to June 2019, a total of 80 COPD patients in The First Affiliated Hospital of Guangxi Medical University were enrolled and divided into the control group and the comprehensive follow-up group (40 cases in each group) . All patients were given home rehabilitation program guidance and health education. The control group was followed up using telephone, while the comprehensive follow-up group were followed up by telephone combined with Internet which lasted for one year. The differences of pulmonary function, motor function, compliance and recurrence between the two groups were compared.Results:One year after discharge, percentage of forced vital capacity to the predicted value (FVC%) , percentage of forced expiratory volume in one second to the predicted value (FEV1%) , 6 minutes walking distance, SF-36 quality of life and rehabilitation compliance rate in the comprehensive follow-up group were higher than those of the control group, while CAT score, mMRC score, number of patients with acute attack of COPD and recurrence rate were lower than those of the the control group, and the differences were statistically significant ( P<0.05) . Conclusions:For CPOD patients, the comprehensive follow-up mode can effectively reduce the 1-year recurrence rate, promote the recovery of respiratory and motor functions, and improve compliance and quality of life.

Objective To investigate the impact of sample typeon the detection of c-KIT exon 17 mutation in acute myeloid leukemia (AML) patients. Methods A retrospective study was conducted on 51 bone marrow samples collected from 37 AML patients [17 maleand 20 female, with a median age of 33 (range from 1 to 82)] at diagnosis or after treatment from June 2016 to August 2018. Of the 37 cases of AML, 24 were t(8; 21) AML, 11 were inv(16)/t(16;16) AML and 2 were non-CBF-AML. RNA and DNA were simultaneously extracted from every sample. PCR followed by Sanger sequencing were used to screen c-KIT exon 17 mutation, and the comparisons were made between paired cDNA and DNAsamples. Results (1) Of the 51 paired samples, 14 pairs were simultaneously detected positive for c-KITmutation in both of cDNA and DNA samples, but 17 pairs were detected negative in both, and the remaining 20 pairswere only detected positive for the mutation in cDNA but not in DNA, with an inconsistency rate of 39.2％. The positive rate of detecting c-KITmutation was significantly higher in cDNA than in DNA samples (66.7％vs 27.5％,P=0.000073). (2)Inconsistent mutation results between paired cDNA and DNA samples occurred in t(8;21)AML, inv(16)AML and non-CBF-AML patients with the inconsistency rate of 36.4％(12/33), 27.2％(3/11) and 71.4％ (5/7), respectively. (3)The inconsistency rate was significantly higher in samples collected after treatment compared with those collected at diagnosis (72.7％vs 13.8％, P=0.00003). (4) All 5 serially monitored patients with c-KITmutation had inconsistency in mutation detection between cDNA and DNA samples during follow up. Conclusion cDNA improves the detection of c-KIT exon 17 mutation in AML patients compared with DNA, which is especially common after treatment.

Objective:To explore the protective effect and mechanism of scutellarin (Scu) on sepsis associated-acute kidney injury (SA-AKI).Methods:① In vivo experiment: 36 male C57BL/6 mice were divided into normal saline (NS) control group, lipopolysaccharide (LPS) induced SA-AKI model group (LPS group), 20 mg/kg Scu control group (Scu 20 control group), and 5, 10, 20 mg/kg Scu pretreatment groups by random number table with 6 mice in each group. The SA-AKI model was reproduced by intraperitoneal injection of 10 mg/kg LPS. The NS control group was injected with NS intraperitoneally. The Scu pretreatment groups were intraperitoneally injected with different doses of Scu every day before LPS injection for 1 week. Scu 20 control group was injected with 20 mg/kg Scu for 1 week. After 24 hours of LPS treatment, mice in each group were sacrificed, kidney tissues were collected, and kidney injury was detected by hematoxylin-eosin (HE) staining. Western blotting was used to detect the protein expression levels of nuclear factor-κB (NF-κB) signaling pathway related molecules, apoptosis-related proteins and cysteine-rich protein 61-connective tissue growth factor-nephroblastoma overexpressed gene 1 (CCN1). ② In vitro experiment: human renal tubular epithelial cell line HK-2 was cultured in vitro and used for experiment when the cells fused to 80%. In the cells without LPS treatment and after 100 g/L LPS treatment, pcDNA3.1-CCN1 and small interfering RNA (siRNA) CCN1 sequence were transfected to overexpress and inhibit CCN1 expression, respectively, to observe whether CCN1 was involved in NF-κB signaling pathway activation and apoptosis. In addition, 100g/L LPS and 20 μmol/L Scu were added into HK-2 cells transfected with and without CCN1 siRNA to investigate the mechanism of protective effect of Scu on LPS-induced HK-2 cells injury. Results:① The results of in vivo experiment: the renal function of SA-AKI mice induced by LPS was significantly decreased, and had kidney histological damage and severely damaged renal tubules. Scu could alleviate renal function and histological damage in a dose-dependent manner. Western blotting results showed Scu could reduce the protein expression of NF-κB signaling pathway related molecules and CCN1 in the renal tissue, and had a significant alleviating effect on apoptosis, indicating that CCN1 was involved in NF-κB signaling pathway activation and apoptosis. ② The results of in vitro experiment: in HK-2 cells not treated with LPS, CCN1 overexpression had no effect on apoptosis related protein and pro-inflammatory factors of NF-κB signaling pathway. In HK-2 cells treated with LPS, overexpression of CCN1 significantly inhibited the mRNA expressions of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1), with significant differences as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT): 3.20±0.57 vs. 4.88±0.69, TNF-α mRNA (2 -ΔΔCT): 2.99±0.44 vs. 5.00±0.81, MCP-1 mRNA (2 -ΔΔCT): 2.81±0.50 vs. 5.41±0.75, all P < 0.05], and the apoptosis-related protein was significantly down-regulated. However, when siRNA was used to inhibit the expression of CCN1, the mRNA expressions of pro-inflammatory factors were significantly increased as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT): 6.01±1.13 vs. 4.88±0.69, TNF-α mRNA (2 -ΔΔCT): 5.15±0.86 vs. 5.00±0.81, all P < 0.05], and apoptosis-related protein was significantly up-regulated. In the LPS-induced HK-2 cells, the mRNA expressions of pro-inflammatory factors were significantly down-regulated after Scu treatment as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT) : 2.55±0.50 vs. 6.15±1.04, TNF-α mRNA (2 -ΔΔCT): 2.58±0.40 vs. 3.95±0.52, MCP-1 mRNA (2 -ΔΔCT): 2.64±0.44 vs. 6.21±0.96, all P < 0.05], and apoptosis-related protein was also significantly reduced. When the expression of CCN1 was inhibited by siRNA, the protective effect of Scu on cells was weakened, which showed that the mRNA expressions of pro-inflammatory factors in cells was significantly up-regulated compared with the cells without inhibition of CCN1 expression [IL-1β mRNA (2 -ΔΔCT): 5.34±0.76 vs. 2.55±0.50, TNF-α mRNA (2 -ΔΔCT): 3.66±0.54 vs. 2.58±0.40, MCP-1 mRNA (2 -ΔΔCT): 5.15±0.79 vs. 2.64±0.44, all P < 0.05], and the expression of apoptosis related protein was also significantly up-regulated. Conclusions:Scu could protect the renal function in SA-AKI mice, and the protective effect is associated with NF-κB signaling pathway and CCN1. Thus, Scu could alleviate LPS-induced kidney injury by regulating the NF-κB signaling pathway.

As a type of experiential psychotherapy,Satir communication model can help the individual system and the family system achieve a state from dysfunction to healthy function,which can enrich the intervention connotation of family support and provide a new direction for the realization of full-life circle care.This paper aims to introduce the concept,core elements,common treatment techniques,application and effects,current challenges and relevant suggestions of Satir communication model in the nursing field from the perspective of family support,in order to provide references for the localization development and clinical integration of Satir communication model in the field of nursing in China.

ObjectiveTo study the effect of apigenin on the proliferation and apoptosis of human colon cancer CL187 cells and the underlying mechanisms. MethodHuman colorectal cancer CL187 cells were treated with different concentrations of apigenin （0， 30， 45， 60 mg·L^-1） according to the results of the preliminary experiment. The proliferation of CL187 cells was detected by methyl thiazolyl tetrazolium （MTT） and colony formation assays， and the apoptosis was observed via Hoechst 33258 staining. Real-time fluorescence quantitative PCR was conducted to determine the mRNA levels of cysteine protease-3 （Caspase-3）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the CL187 cells treated with apigenin. Western blot was employed to measure the protein levels of Caspase-3， Bcl-2， and Bax associated with apoptosis， protein kinase B （Akt） and phosphorylated Akt （p-Akt） in phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） pathway， and extracellular signal-regulated kinases 1/2 （ERK1/2）， p-ERK1/2， c-Jun N-terminal kinase （JNK）， p-JNK， p38 mitogen-activated protein kinase （MAPK）， and p-p38 MAPK protein in MAPK pathway. ResultCompared with the blank group， the apigenin groups had low cell survival rates and high inhibition rates on cell proliferation （P<0.01）. Apigenin decreased the cell clone number and clone formation rate， and increased the inhibition rate on clone formation （P<0.01）. After CL187 cells were treated with different concentrations of apigenin for 48 h， typical apoptosis characteristics such as nuclear pyknosis， chromatin condensation， and enhanced fluorescence reaction were observed. Compared with blank group， 45， 60 mg·L^-1 apigenin treatments down-regulated the mRNA level of anti-apoptotic gene Bcl-2 （P<0.01） and all the apigenin treatments up-regulated those of the pro-apoptotic genes Bax and Caspase-3 （P<0.05， P<0.01）. Similarly， apigenin treatments down-regulated the protein level of Bcl-2 （P<0.05， P<0.01） and up-regulated those of Caspase-3 （P<0.05， P<0.01） and Bax （P<0.01， 45， 60 mg·L^-1）. The blank group had higher protein level of Akt than the 60 mg·L^-1 apigenin group （P<0.01）， higher protein levels of p-Akt， ERK1/2， and p-ERK1/2 than the 45， 60 mg·L^-1 apigenin groups （P<0.01）， and higher protein levels of JNK and p-JNK than the apigenin groups （P<0.05， P<0.01）. Compared with blank group， 60 mg·L^-1 apigenin up-regulated the protein level of p38 MAPK （P<0.05）， and all the apigenin groups up-regulated that of p-p38 MAPK （P<0.01）. Furthermore， apigenin lowered the p-Akt/Akt ratio （P<0.05， P<0.01） and p-ERK1/2/ERK1/2 ratio （P<0.01）， while it increased the p-JNK/JNK ratio （45， 60 mg·L^-1； P<0.05， P<0.01） and p-p38 MAPK/p38 MAPK ratio （P<0.05， P<0.01）. ConclusionApigenin can inhibit the proliferation and promote the apoptosis of CL187 cells by inhibiting the PI3K/Akt signaling pathway and regulating the expression of proteins in the MAPK signaling pathway.

Objective:The causes of infertility are complex and diverse, and congenital adrenal hyperplasia (CAH) is often overlooked in screening for infertility. In this study, CAH was diagnosed in women with high androgenemia who were infertile during childbearing age, and the diagnosis and treatment of CAH in pregnant women was investigated.Methods:This study included 20 women with high androgenemia and infertility in the childbearing age who were referred to the Endocrinology Department after visiting the Reproductive Medicine Center of the First Affiliated Hospital of Nanjing Medical University from December 2016 to April 2019. All patients were tested for blood hormone levels, glucose, and lipid metabolism, underwent ACTH stimulation test, uterus and bilateral ovarian B-ultrasound, adrenal computed cosmography (CT), etc. Full-length sequencing of the CYP21A2 gene was performed as necessary.Results:Among the 20 women with hyperandrogenism who were infertile, there were 7 cases of CAH (35.0%), including 6 cases of 21-hydroxylase deficiency (21-OHD) confirmed by gene sequencing; 10 cases of polycystic ovary syndrome (PCOS); 3 cases of idiopathic hyperandrogenemia (IHA). Sex hormone results showed that testosterone in CAH group was significantly higher than that in PCOS group and IHA group [(4.4±2.0 vs 2.9±0.4, 2.8±0.8) nmol/L, P<0.05]; ACTH stimulation test showed that the 17-hydroxyprogesterone (17-OHP) in CAH group was significantly higher than that in PCOS group [(101.0±100.8 vs 1.4±0.8) ng/ml, P<0.05]. There was no significant difference between CAH group and IHA group [(101.0±100.8 vs 3.0±1.8)ng/ml, P>0.05]. However, the 17-OHP (60 min) in CAH group was significantly higher than that in PCOS group and IHA group [(200.1±80.8 vs 3.1±1.2, 3.4±0.2) ng/ml, P<0.05]. Glucocorticoid therapy was given to patients with CAH, and 4 patients had successful pregnancy. No clinical symptoms of CAH and external genital malformations were found in the offspring of patients who had been delivered. Conclusions:The ACTH stimulation test is of great significance in the differential diagnosis of CAH, especially 21-OHD. Genetic testing helps to identify the type of mutation in CAH patients. On the one hand, glucocorticoid therapy may improve the pregnancy rate of CAH patients, on the other hand, it can help to reduce the status of maternal high androgen and avoid masculine manifestation of female offspring.

ObjectiveTo investigate the material basis and mechanism of Arnebia euchroma against hepatocarcinoma by network pharmacology， and to verify the potential targets of A. euchroma against hepatocarcinoma by molecular docking and experiments. MethodThe main active ingredients of A. euchroma were collected by retrieving the literature through China National Knowledge Network （CNKI） and Traditional Chinese Medicine System Pharmacology Database and Analysis Platform（TCMSP）. The active ingredients were screened out by FAFDrug4 platform according to the pharmacokinetics （ADME） properties of the drugs. The screening compounds and liver cancer targets were collected by using several databases and analyzed by drawing Venn diagrams. The protein-protein interaction （PPI） network was constructed by Cytoscape and STRING database. DAVID database was used to perform Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis of key targets. Autodock was used to perform molecular docking of targets on core pathways. Cell counting kit-8 （CCK-8） experiment was carried out to validate the activities of five naphthoquinones. Based on the predicted results in the H22 tumor-bearing mouse model， the key targets of isovalerylshikonin against hepatocarcinoma were verified by hematoxylin-eosin （HE） staining， enzyme-linked immunosorbent assay （ELISA）， and Western blot assay. ResultFifty-five active ingredients and 34 targets of active ingredients against hepatocarcinoma were screened out. The active molecules with high degree values in the “drug-active ingredient-target-disease” network were mainly naphthoquinones. PPI network obtained several core targets of A. euchroma against hepatocarcinoma. Twenty-two pathways were screened out by KEGG analysis， mainly involving phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt）， vascular endothelial growth factor （VEGF）， tumor necrosis factor （TNF）， and other signaling pathways. The results of molecular docking showed that the five naphthoquinones had a good affinity with the targets of the PI3K/Akt signaling pathway. The results of CCK-8 and animal experiments showed that the lipid-soluble component isovalerylshikonin had good anti-cancer potential， and the high-dose group reduced the serum levels of VEGF and alpha fetoprotein （AFP） levels and elevated interferon-γ （IFN-γ） level （P<0.05， P<0.01）. The high-dose group also down-regulated phosphorylate（p）-Akt （Ser473） and B-cell lymphoma （Bcl）-2 protein expressions and up-regulated Bcl-2-antagonist of cell death （Bad） protein expression （P<0.01）. ConclusionA. euchroma can inhibit hepatocarcinoma cell proliferation and tumor angiogenesis and induce cancer cell apoptosis through the PI3K/Akt signaling pathway， which provides ideas and clues for the subsequent in-depth investigation of its specific mechanism.