Objective To study the prognostic value of procalcitonin (PCT) level in the outcome of patients with paraquat poisoning (PQ).Methods The clinical data of 128 patients with acute PQ admitted to emergency department were collected from March 2013 through March 2014.The patients were divided into two groups:the death group and the survival group (survival of 28 days).Poisoning doses,urine concentration of PQ,time elapsed from poisoning to admission,and time elapsed from poisoning to gastrolavage were documented.And on the 1 st day,the 3rd day and the 7th day after poisoning,serum PCT were detected.The level of PCT was used to investigate the prognostic values in patients with acute PQ in the death group and survival group.Results Of 128 cases,72 (56.3％) survived and 56 died in 28 days.Among them,the level of PCT increased to some extent in the first day in 90 cases,and 48 patients died.According to trend analysis,the levels of PCT in death group on the 1st day,the 3rd day and the 7th day after PQ were significantly higher than those in survival group [ld:(0.96 ±0.13) vs.(0.08 ±0.01),3d:(1.12 ±0.14) vs.(0.28 ±0.05),7d:(1.22 ±0.14) vs.(0.20 ±0.03),P ＜0.01].There was a trend of escalating PCT levels in death group,whereas the PCT level reached the peak on the 3st day and decreased gradually in the following days in survival group.The early PCT level was obviously related to poisoning doses,urine concentration,CRP,WBC,ALT,CR (the coefficient of association were 0.794,0.723,0.724,0.332,0.700,0.414,respectively,P＜0.01).Conclusions The serum level of PCT increased in patients with acute PQ was significantly positively correlated with the oral dose and urine concentration of paraquat,and it can be used as an indicator for PQ severity.There is important clinical significance in detecting the change of serum level of PCT for estimating the condition of patients and evaluating the prognosis.

Objective To explore the therapeutic effect of olmesartan (OLM) on acute lung injury induced by paraquat (PQ) in rats in order to study its action mechanism.Methods A total of 70 Wister rats wererandomly (random number) divided into 5 groups,namely control group (C group,n =10),poisoning group (PQ group,n =15),rats treated by OLM with low dose (LD group,n =15),moderate dose (MD group,n=15) and high dose (HD group,n =15).PQ (80 mg/kg) was administered by gavage route in PQ group and in OLM groups for paraquat poisoning modelling,while in C group,equivalent normal saline was given instead.The OLM was administered by gastric instillation in OLM treatment groups (LD group:5 mg/kg; MD group:10 ng/kg; HD group:15 mg/kg) 6 hours after paraquat gavage and once a day for 7 days,while in C group and PQ group,normal saline was used instead.All rats were sacrificed 12 hours after the last dose treatment.The levels of glutathione peroxidase (GSH-Px,energy units),superoxide dismutase (SOD,U/mg pro),malondialdehyde (MDA,nmol/mg pro) in lung tissue,and the levels of serum transforming growth factor beta-1 (TGF-β1,pg/mL) and pH,oxygen partial pressure (PaO2) and bicarbonate ions concentration (HCO3-) were determined.Further,the lung coefficient and lung fibrous tissue hyperplasia grading were calculated.Correlation analysis was carried out to explore the correlation among GSH-Px,SOD,MDA,lung coefficient,lung hyperplasia of fibrous tissue and TGF-β1.The lung tissue were prepared for microscopy observation after Hematoxylin-eosin staining method (HE staining) as well.The difference between groups was compared by one-way analysis of variance,and correlation analysis carried out by using Pearson and Spearman rank correlation coefficient.Results The levels of GSH-Px and SOD in lung tissue of PQ and OLM treatment groups were significantly lower than those in C group,while in OLM treatment groups,those were higher than those of PQ group,and the HD group showed most obvious (all P ＜ 0.05).The level of MDA in lung tissue in PQ and OLM treatment groups were significantly highcr than that in C group while in OLM treatment groups,that was lower than that in PQ group,and the HD group showed most obvious (all P ＜ 0.05),and there were no differences between the LD group and MD group (all P ＞ 0.05).The lung coefficient and lung fibrous tissue hyperplasia grading in PQ and OLM treatment groups were significantly higher than those in C group,while in OLM treatment groups,those were lower than those in PQ group,and the HD group showed most obvious (all P ＜ 0.05).The level of serum TGF-β1 in PQ and OLM treatment groups were significantly higher than that inC group,while in OLM treatment groups,that was lower than that in PQ group,and the HD group showed most evident (all P ＜ 0.05),and there were no differences between the LD group and MD group (all P ＞0.05).The pH,PaO2 and HCO3-in PQ and OLM treatment groups were significantly lower than those in C group,while difference between LD and HD groups was also statistical significance (all P ＜ 0.05),while there were no differences between the PQ group and LD group as well as the LD group and MD group (all P ＞ 0.05).The correlation analysis showed GSH-Px and SOD had negative correlation with TGF-β1 [the correlation coefficient (r) were respectively-0.860 and-0.856,all P＜0.05],while MDA,lung coefficient and lung fibrous tissue hyperplasia grading had positive correlation with TGF-β1 (r were respectively 0.800,0.830 and 0.656,all P ＜ 0.05).Lung tissue section showed the degree of alveolar septa widened,alveolar collapse and inflammatory cells infiltration in OLM treatment groups were milder than those in PQ group,and the mildest in HD group.Conclusions OLM can attenuate the pulmonary edema and pulmonary fibrosis caused by paraquat poisoning and maybe it is associated with reducing the expression of TGF-β1 and inhibiting oxidative stress reaction.

Objective:To explore the effect of microRNA (miRNA)-3126-5p on the proliferation and migration of colorectal cancer cells by inhibiting the expression of LIM and SH3 protein 1 ( LASP1). Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-3126-5p in colorectal cancer cell lines (HT-29, HCT116, LoVo, SW480) and normal intestinal mucosal epithelial cells (HIEC). The cell line with the lowest expression level was selected as the experimental object. The experiment was divided into 2 groups: the negative control group (transfected with miR-NC) and the miR-3126-5p group (transfected with miR-3126-5p). Cells of each group were collected 48h after transfection. qRT-PCR method was used to detect the expression level of miR-3126-5p in each group. The MTS method and the scratch healing experiment were used to detect the proliferation level and migration ability of the cells in each group. The bioinformatics software microRNA.org and the dual-luciferase reporter gene experiment were used to predict and verify the target genes of miR-3126-5p, respectively. qRT-PCR and Western blot were used to detect the expression levels of target genes in each group of cells. Measurement data were expressed as mean±standard deviation ( Mean± SD), t test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:Compared with normal intestinal mucosal epithelial cells (HIEC), the expression level of colorectal cancer cell line miR-3126-5p was significantly reduced ( P<0.05), and the cell line with the lowest expression level was HCT116 cells ( P<0.01). The expression of miR-3126-5p in HCT116 cells in the negative control group and miR-3126-5p group were (1.05±0.16) and (7.91±1.26) respectively, and the difference was statistically significant ( t=5.40, P<0.01). Compared with the negative control group, the proliferation ability of HCT116 cells in the miR-3126-5p group was significantly reduced ( t=4.52, P<0.05), and the migration ability was significantly reduced ( P<0.01). microRNA.org shows that miR-3126-5p has complementary binding sites with LIM and SH3 protein 1 ( LASP1) gene mRNA. miR-3126-5p can target LASP1 mRNA ( P<0.01). Compared with the negative control group, the expression of LASP1 gene in HCT116 cells of the miR-3126-5p group was significantly reduced ( t=4.56, P<0.01). Conclusion:The expression of miR-3126-5p in colorectal cancer cell lines is low, and miR-3126-5p can reduce the proliferation and migration ability of colorectal cancer HCT116 cells by inhibiting the expression of the target gene LASP1.

Objective:To investigate the effect of long non-coding RNA (lncRNA) HAGLR on the proliferation and migration of gastric cancer cells by inhibiting the expression of microRNA (miRNA, miR)-93-5p.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of HAGLR in gastric cancer cell lines (HS-746T, BGC823, SGC7901, MGC803) and normal gastric mucosal epithelial cells (GES-1). Selected the cell line with the lowest HAGLR expression and transfected with the negative control plasmid (negative control group) or HAGLR-high-expression plasmid (HAGLR group) respectively. The MTS method and the scratch healing test were used to detect the proliferation and migration ability of the cells after transfection. The bioinformatics software miRcode database was used to predict the target gene of HAGLR, and the dual luciferase reporter gene experiment was used to verify the binding of HAGLR to the target gene. qRT-PCR was used to detect the expression of the target gene. Western blot was used to detect the expression of Hippo signaling pathway. The software SPSS 21.0 was used to conduct statistical analysis. The t test was used for comparison between two groups, and the one-way analysis of variance was used for comparison between multiple groups. Results:Compared with GES-1 cells, the expression level of HAGLR in gastric cancer cell lines was lower (all P<0.05), and the cell line with the lowest HAGLR expression was SGC7901 cells ( P<0.01). The HAGLR expression in SGC7901 cells in the HAGLR group and the negative control group were 1.03±0.13 and 9.75±1.10, respectively. The expression level of HAGLR in the negative control group was significantly lower than that in the HAGLR group ( t=7.87, P<0.01). Compared with the negative control group, the absorbance of SGC7901 cells in the HAGLR group was significantly reduced ( P<0.05), and the scratch healing rate was significantly reduced ( P<0.01). The miRcode database showd that HAGLR and miR-93-5p have complementary binding sites. The dual luciferase reporter gene experiment showed that HAGLR can complement miR-93-5p ( P<0.01). Compared with the negative control group, the expression of miR-93-5p in SGC7901 cells in the HAGLR group was significantly reduced ( P<0.01), and the expression of Hippo signaling pathway protein was significantly reduced (all P<0.01). Conclusions:HAGLR is low expressed in gastric cancer cell lines. HAGLR inhibits the proliferation and migration of gastric cancer SGC7901 cells by negatively regulating miR-93-5p.

The clinical practice teaching reform of pediatrics based on TBL combined with medical simulation teaching model was carried out. TBL teaching plan writing under the model of medical simulation teaching was researched. The principles, requirements, contents and procedures of compiling teaching plans were formed. Emphasis should be placed on medical simulation teaching, team cooperation, humanistic quality education and humanistic skills training. The purposes of the reform were to achieve standardized operation skills, improve clinical ability, ensure medical safety, and improve the quality of medical purposes, but still the reform need further improvement in the teaching practice.

OBJECTIVETo explore the expression of CD133 and CD44 in the primary gastric adenocarcinoma (GAC) and their relationship with the expression of E-cadherin.

METHODSThe expressions of CD133, CD44, and E-cadherin was examined by immunohistochemistry in 145 specimens of GAC tissues and 30 specimens of normal gastric tissues.

RESULTSThe positivity rates of CD133, CD44, and E-cadherin in normal gastric tissues were 10.0%, 0%, and 100%, respectively, showing significant differences from the rates in GAC tissues (46.9%, 47.6%, and 42.8%, respectively) (P<0.05). The expressions of CD133, CD44, and E-cadherin were significantly related with the tumor volume, differentiation, lymph node metastasis, invasive depth, pathologic-tumor-node-metastasis (pTNM) stages, and postoperative-survival time (all P<0.05); a positive correlation was found between the expression of CD133 and CD44, and they were both negatively correlated with E-cadherin expression (P<0.005). Kaplan-Meier analysis showed a significant difference in the survival rate between CD133-positive and CD133-negative patients (P<0.001) and between CD44-positive and CD44-negative patients; the patients with positive expression of E-cadherin had a significantly longer survival than those negative for E-cadherin. Cox regression analysis indicated that CD133, CD44, and E-cadherin expressions were all independent prognostic factors of GAC (all P<0.05).

CONCLUSIONThe expressions of CD133, CD44, and E-cadherin are related to the tumor volume, differentiation, pTNM stages, invasive depth, lymph node metastasis, and prognosis of GAC, and their combined detection can be of important value in predicting the prognosis of GAC.

AC133 Antigen ; Adenocarcinoma ; metabolism ; pathology ; Antigens, CD ; metabolism ; Cadherins ; metabolism ; Cell Differentiation ; Female ; Glycoproteins ; metabolism ; Humans ; Hyaluronan Receptors ; metabolism ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Staging ; Peptides ; metabolism ; Proportional Hazards Models ; Retrospective Studies ; Stomach Neoplasms ; metabolism ; pathology ; Survival Rate ; Tumor Burden

Objective:To explore the effect of down-regulation of long non-coding RNA (lncRNA) CTB-191K22.5 on the proliferation and invasion of colorectal cancer SW480 cells and the molecular mechanism.Methods:The TCGA database was used to analyze the expression differences of CTB-191K22.5 in colorectal cancer tissues and normal tissues. The CTB-191K22.5 inhibitor (Anti-CTB-191K22.5) and negative inhibitor (Control) were transfected into colorectal cancer SW480 cells, denoted as Observation group and Control group, real-time quantitative polymerase chain reaction (qRT) -PCR) was used to evaluate the inhibitory effect. MTT method and Transwell chamber method were used to evaluate the proliferation and invasion of SW480 cells. Western blot was used to evaluate the protein levels of PI 3K/AKT/mTOR signaling pathway in SW480 cells. The bioinformatics software starBase v2.0 was used to predict the target genes of CTB-191K22.5. qRT-PCR was used to evaluate the expression of CTB-191K22.5 target gene in SW480 cells. Measurement data were expressed as Mean±SD, and t-test was used for comparison between two groups. Results:Compared with normal tissues, the expression of CTB-191K22.5 in colorectal cancer tissues was significantly increased ( P<0.01). The expression of CTB-191K22.5 in SW480 cells of the Control group and Observation group were 6.60±0.85 and 1.08±0.21, respectively. The expression level of CTB-191K22.5 decreased after transfection with Anti-CTB-191K22.5 ( P<0.01). Compared with the Control group, the SW480 cell proliferation ability of the Observation group decreased ( P<0.01). The invasion numbers of SW480 cells in the Control group and Observation group were (135.4 ± 16.29) and (42.24±14.59), respectively. The invasion ability of SW480 cells decreased after transfection with Anti-CTB-191K22.5 ( P<0.01). Compared with the Control group, the expression levels of PI 3K/AKT/mTOR signaling pathway protein in SW480 cells in the Observation group decreased. miR-326 may be the target gene of CTB-191K22.5. Compared with the Control group, transfection with Anti-CTB-191K22.5 significantly increased the expression level of miR-326 in SW480 cells ( P<0.01). Conclusion:CTB-191K22.5 is highly expressed in colorectal cancer tissues, and down-regulation of CTB-191K22.5 may inhibit the proliferation and invasion of colorectal cancer SW480 cells by targeting miR-326.

Objective:To explore the effect and mechanism of microRNA (miRNA)-4320 on the proliferation and migration of gastric cancer MGC803 cells.Methods:Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-4320 in four gastric cancer cell lines(MGC803, HS-746T, SGC7901, BGC823) MGC803 cells were infected with recombinant lentivirus carrying miR-4320 interference fragments or blank lentivirus, and set as si-miR-4320 group and NC group. Thiazole blue colorimetry and Transwell small box experiment were used to detect the proliferation and migration of MGC803 cells after miR-4320 was down-regulated. The bioinformatics software RNAhybrid was used to predict the target gene of miR-4320. The targeting relationship between miR-4320 and target gene was verified by dual-luciferase reporter gene experiment. qRT-PCR and Western blot were used to detect the expression of miR-4320 target gene. Measurement data were expressed as mean ± standard deviation ( ± s), and t-test or one-way ANOVA was used for comparison between groups. Results:The expression of miR-4320 in the four gastric cancer cell lines was significantly higher than that of normal gastric mucosal epithelial cells ( P<0.01). The expression of miR-4320 in MGC803 cells in the NC group and the si-miR-4320 group were 8.19±1.00 and 1.09±0.31, respectively. The miR-4320 interference fragment significantly reduced the expression of miR-4320 ( P<0.01). The absorbance of MGC803 cells in the si-miR-4320 group was significantly lower than that of the NC group ( P<0.05), and the migration ability was significantly lower than that of the NC group ( P<0.01). Suppressor of cytokine signaling1 ( SOCSI) is the target gene of miR-4320. Compared with the NC group, the SOCS1 gene expression in the si-miR-4320 group was significantly up-regulated ( P<0.01). Conclusions:The expression of miR-4320 is increased in gastric cancer cell lines. Down-regulating the expression of miR-4320 can inhibit the proliferation and migration of gastric cancer MGC803 cells by inducing the expression of SOCS1 gene.