Objective: To investigate the mechanism of matrine inhibiting the proliferation of cervical squamous cancer cells. Methods: CCK-8 method was used to detect the effect of matrine on the survival rate of SiHa and C33A cells, and flow cytometry was used to detect cell cycle. High throughput sequencing technology was used to screen the differentially expressed genes between control cells and cells being treated with matrine. qRT-PCR and Western blotting method were used to detect the expression of BDNF-AS and BDNF in cervical squamous cancer cells and allograft tumor tissue. A total of 32 cases of cervical squamous cell carcinoma tissues were collected in the Second People’s Hospital of Nanyang from March 2013 to December 2016. qRT-PCR was used to detect the expression of BDNF-AS in cervical squamous cell carcinoma tissues of these cases. Results: Matrine significantly inhibited the proliferation of cervical squamous carcinoma cells. A total of 924 differentially expressed genes were screened out from cervical squamous carcinoma cells before and after being treated with matrine, 637 (68.9%) were up-regulated while 287 (31.1%) were down-regulated. Matrine up-regulated the expression of BDNF-AS. The expression of BDNF-AS was negative correlated with the degree of pathological differentiation and clinical stage (P < 0.05). BDNF-AS expression in tissues was associated with survival of patients with cervical squamous cell carcinoma. Multivariate analyses suggested the expression of BDNF-AS was served as an independent predictor for overall survival. Conclusion: BDNF-AS may be a tumor suppressor in the tumorigenesis and tumor progression of cervical squamous cell carcinoma. Matrine may inhibit the proliferation of cervical squamous carcinoma cells by up-regulating the expression of BDNF-AS.

Humans ; Multiple Myeloma ; Leukemia, Myeloid, Acute ; Melphalan

Objective To determine the current situation of radiological health management in medical institutions in Nanyang, China, to analyze existing problems and propose improvement measures, and to improve the management level of radiological diagnosis and treatment practice in medical institutions. Methods According to the work plan of the Occupational Disease Prevention and Control Project in Henan Province, China, 66 medical institutions engaged in radiological diagnosis and treatment at different levels were selected for a questionnaire survey, in combination with on-site inspections, inquiries, and access to relevant materials. Results Of 66 medical institutions, 65 institutions held radiological diagnosis and treatment licenses, with a license holding rate of 98.5%. There were 17 “new construction, reconstruction, and expansion” projects, with an evaluation rate of 94.1%. In this survey, a total of 391 radiological diagnosis and treatment equipment were involved, and 387 units of equipment were tested for status, with a detection rate of 99.0% and a qualification rate of 94.8% (367/387); 55 units of equipment were tested for stability, with a detection rate of 14.1%; the workplace protection detection rate was 99.0%, and the qualification rate was 100%; 66 medical institutions had 1809 radiation workers, with an occupational health examination rate of 97.8%; 1262 people were trained, with a training rate of 95.7%; 1773 people were monitored for individual dose, with a monitoring rate of 98.0%. Conclusion Medical institutions should further strengthen management in licensing change, construction project evaluation, and equipment stability monitoring to improve the level of radiological health management.

OBJECTIVE To investigate the effect and mechanism of α7 nicotinic acetylcholine receptor （α7nAChR） agonists PNU-282987 on cognitive function in temporal lobe epilepsy （TLE） model rats. METHODS Sixty rats were randomly divided into control group， model group， PNU-282987 group （3 mg/kg） and methyllycaconitine （MLA）+PNU-282987 group （6 mg/kg MLA+3 mg/kg PNU-282987）， with 15 rats in each group. Except for control group， the TLE model was established in the other groups. After the model was successfully established， each group was given relevant medicine or normal saline intraperitoneally， once a day， for two consecutive weeks. The epilepsy attack of rats was observed and scored， and the duration of seizures was recorded； the cognitive function of rats was detected； pathological morphology of neurons in CA1 region was observed； the levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6） and IL-1β in the hippocampus were detected； the positive expressions of ionized calcium-binding adapter molecule-1 （IBA-1）， α7nAChR， nuclear factor-κB （NF-κB） p65， p-NF-κB p65 in the hippocampus were detected. RESULTS Compared with model group， the score and duration of seizures， the number of IBA-1 positive cells， the levels of TNF- α， IL-6 and IL-1β， the expressions of NF- κB p65 and p-NF- κB p65 protein decreased significantly in the hippocampus （P＜0.05）； the escape latency time was shortened significantly （P＜0.05）， the time spent in the original platform quadrant and times of crossing the platform increased significantly （P＜0.05）； neuronal damage in the CA1 region of the hippocampus was significantly reduced； the expression of α7nAChR protein increased significantly in hippocampus （P＜0.05）. Compared with PNU-282987 group， the above indexes of rats in MLA+PNU-282987 group were reversed significantly （P＜0.05）. CONCLUSIONS PNU-282987 could improve cognitive dysfunction in TLE model rats， and its mechanism may be associated with inhibiting microglia-mediated inflammatory response through α7nAChR/NF- κB signaling pathway， thus reducing hippocampal neuronal damage.

Objective: To study the risk factors of nosocomial infection after laparoscopic radical gastrectomy for gastric cancer in our hospital, and to explore the preventive measures. Methods: A total of 349 patients with gastric cancer who underwent laparoscopic radical gastrectomy in our hospital from April 2015 to January 2018 were selected. The incidence of nosocomial infection was observed and recorded. Pathogenic bacteria were collected and identified. The sex, age, pathological type, gastric cancer stage, preoperative hospitalization time, operation time, invasive operation, diabetes history, smoking history, drinking history and other indicators were analyzed to analyze the risk factors of infection. Results: There were 40 cases of nosocomial infection after operation in 349 cases, the infection rate was 11.5%, lung infection was the main cause, accounting for 55%, followed by abdominal infection, accounting for 30%.Forty-seven pathogenic bacteria were isolated and cultured from 40 infected patients, among which 29 were Gram-negative bacteria and 18 were Gram-positive bacteria. The main Gram-negative bacteria were Pseudomonas aeruginosa (31.9%) and Klebsiella pneumoniae (19.1%). Gram-positive bacteria were Staphylococcus aureus (19.1%) and Streptococcus hemolyticus (12.8%). Univariate analysis showed that age, gastric cancer stage, operation time, history of diabetes mellitus, smoking history and other factors were the influencing factors of postoperative nosocomial infection, the difference was statistically significant (P<0.05). Multivariate logistic regression analysis showed that age ≥65 years, gastric cancer stage ≥ Ⅲ, operation time ≥3 hours, history of diabetes mellitus and smoking were independent risk factors for postoperative nosocomial infection (P<0.05). Conclusions Nosocomial infection in patients after laparoscopic radical gastrectomy could not be ignored. Perioperative nursing and preventive measures can reduce the incidence of infection and promote the recovery of patients.

Aim To explore the role of miR-27a on the proliferation and metastasis of renal cell carcinoma (RCC) and its mechanism. Methods The expression of miR-27a in RCC cancer tissues, para-carcinoma tissues, RCC cells (Caki-1, 786-0 and ACHN) and normal renal tubular epithelial cells ( HK2) were detected by RT-qPCR. After miR-27a-inhibitor transfect-ed into 786-0 and ACHN cells, cell proliferation was measured by CCK-8 assay; cell colony formation was detected by colony formation assay; cell migration and invasion were detected by cell wound healing assay and Transwell assay, respectively; the pretein expression of P-catenin was detected by Western blot. After trans-fected miR-27a inhibitor into ACHN cells then treated with LiCl (Wnt/p-catenin signal agonist), cell proliferation , migration and invasion were detected. Results The expression of miR-27a in RCC cancer tissues was significantly higher than that in para-carcinoma tissues, and increased with stage progression. Compared with HK-2 cells, the expression levels of miR-27a in RCC cells were elevated. After transfection with miR-27a inhibitor, the cell colony formation, cell prolifera-tion, invasion and migration ability of 786-0 and ACHN cells were significantly reduced. MiR-27a in-i hibitor reduced the expression of p-catenin in ACHN cells. LiCl promoted the proliferation, invasion and migration ability of ACHN cells transfected with miR-27a inhibitor. Conclusions MiR-27a is highly expressed in RCC cancer tissues and RCC cells, and knockdown of miR-27a inhibits proliferation and metastasis in RCC cells through Wnt/p-catenin signaling pathway.

Objective: To investigate the effect of miR-135a on the malignant biological behaviors of human laryngeal carcinoma epithelial Hep-2 cells and its sensitivity to oxaliplatin. Methods: Samples of laryngeal carcinoma tissues and para-cancerous tissues were collected from 10 patients who underwent laryngectomy in Nanyang Hospital Affiliated to Zhengzhou University-Nanyang City Center Hospital from January 2018 to June 2018. The expression of miR-135a in laryngeal carcinoma tissues and Hep-2 cells was detected by qPCR.After being transfected with miR-135 inhibitor, cell proliferation viability of Hep-2 cells was measured by CCK-8 assay, cell colony formation ability was detected by colony formation assay, and cell proliferation invasion and migration abilities were detected by Transwell analysis, and the expression of SOX2 protein in Hep-2 cells was detected by WB. Hep-2 cells transfected with miR-135 inhibitor were further treated with various concentrations (0.5, 1.0, 1.5 and 2.0 μmol/L) of oxaliplatin, and the cell proliferation viability was detected by CCK-8 while cell apoptosis was detected by Annexin-V-FITC/PI double staining flow cytometry. miR-135a inhibitor plasmid, control pcDNA empty vector (SOX2-Con) plasmid, and pcDNA-SOX2 (SOX2-OE) plasmid were transfected into Hep-2 cells to construct the miR-135a inhibitor+SOX2-Con group and miR-135a inhibitor+SOX2-OE group, and the cell viability, cell colony formation ability, cell invasion and migration ability in two groups were detected. Results: Compared with para-cancerous tissues, miR135a expression in laryngeal cancer tissues was significantly increased (P<0.01). Compared with normal NHP cells, miR-135a expression in Hep-2 cells was significantly increased (P<0.01). miR-135a inhibitor significantly reduced the expression level of miR-135a in Hep-2 cells (P<0.01). miR-135a knockdown significantly reduced the cell proliferation viability, cell colony number, migration, invasion and SOX2 expression in Hep-2 cells (all P <0.01), but significantly enhanced the sensitivity of Hep-2 cells to oxaliplatin (P<0.01). Compared with miR-135a inhibitor+SOX2-Con group, the cell proliferation viability, cell colony number, migration and invasion of Hep-2 cells in miR-135a inhibitor+SOX2-OE group were significantly increased (P<0.01); Meanwhile, the cells of the 2 groups were treated with different concentrations of oxaliplatin, and the results of CCK-8 assay showed that, compared with the miR-135a inhibitor+ SOX2-Con group, the cell proliferation viability of Hep-2 cells in miR-135a inhibitor+SOX2-OE group was significantly increased (P< 0.01). Conclusion: miR-135a knockdown inhibits the malignant biological behaviors and promotes oxaliplatin-sensitivity of Hep-2 cells possibly by inhibiting the expression of the transcription factor SOX2.

OBJECTIVETo investigate the clinical significance of serum midkine (MK) in children with henoch-schnlein purpura(HSP).

METHODSOne hundred and six children with HSP admitted in our hospital from March 2013 to March 2016 were enrolled in HSP group, but then 80 healthy volunteers were used as control. MK, interleukin-2 (IL-2), IL-4, IL-6, IL-10, tumor necrosis factor (TNF), interferon γ (IFN-γ) and IL-17 in peripheral blood were measured by ELISA, biochemical indicators including white blood cell count (WBC), platelet (Plt), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), D-dimer, immunoglobulin A (IgA), IgE, IgG, IgM and other clinical data were recorded and analyzed.

RESULTSAmong 106 cases of henoch-schonlein purpura, 42 patients combined with renal failure (isolated hematuria in 4 cases, 17 cases of isolated proteinuria, hematuria and proteinuria in 21 cases). Midkine level in children with HSP was significantly higher than that in the control group [291.70(248.50-396.41) pg/ml vs 217.30(198.98-243.65) pg/ml)](P<0.05); the MK level in group of HSP with nephritis was higher than that in group of HSP without nephritis [326.58(266.58-459.25) pg/ml vs 280.72(233.67-384.36) pg/ml] (P<0.05). IL-4, IL-6, IL-17, TNF and IFN-γ levels in children with HSP were higher than those in the control group(P<0.05), but IL-10 level was lower than that in control group. IL-2 level was not significantly different between 2 groups. Cytokines levels in HSP nephritis group and HSP without renal involvement were not significantly different. Pearson correlation analysis showed that midkine level positively correlated with IL-4, IL-6, IL-17, IgA and IgE (P<0.05). By ROC curve analysis, the AUC of midkine was 0.902, 95% CI 0.841-0.963 (P<0.001), threshold 295.50 pg/ml. The sensitivity and specificity of midkine for predicting Henoch-Schonlein purpura nephritis were 80.60% and 88.30% respecitvely.

CONCLUSIONPlasma MK plays an important role in the development of Henoch-Schonlein purpura and Henoch-Schonlein purpura nephritis. Plasma MK can be used as an effective indicator for early diagnosis and prediction of HSP and renal damage.

Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer, who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells. Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.

Plumbagin (Plumbago zeylanica L.) has a wide spectrum of anticancer activity with a relatively lower toxicity. The molecular mechanisms of proliferation inhibition and apoptosis induction by plumbagin on esophageal squamous carcinoma cell lines may be important for the structure modification and clinical application of plumbagin. After treatment of KYSE-30, KYSE-70 and KYSE-140 cells with 0-20 μmol·L^-1 of plumbagin for 24, 48, 72 h, CCK8 was used to examine the proliferation, Annexin V and PI immunofluorescence staining for apoptosis, real-time PCR and Western blot for FoxM1 mRNA and protein expression, dual-luciferase reporter gene assay for the transcriptional activity of FoxM1, respectively. In addition, the relationship between anti- tumor effect of plumbagin and FoxM1 was investigated in vivo. Plumbagin significantly inhibited proliferation and induced apoptosis of esophageal squamous carcinoma cell in vitro and in vivo. Moreover, plumbagin down-regulated the expression of FoxM1 through suppression of its gene transcription. Our findings suggest that plumbagin may inhibit the proliferation of esophageal squamous carcinoma cell in vivo and in vitro through down-regulating the expression of FoxM1.