Objective To investigate the effect of epidermal growth factor (EGF) on the proliferation of endometrial adenocarcinoma cells,phosphorylation of estrogen receptor α (ERα)and Ack1 in the absence of estrogen.MethodsIshikawa cell line was stimulated by EGF without estrogen settings, Cell Counting Kit-8 (CCK-8) was used to evaluate cell proliferation, Western blot was used to detect ER α phosphorylation and Ack1 phosphorylation.Giving tyrosine inhibitor dasatinib to assess the effect of EGF on cell proliferation,phosphorylation of ERα and Ack1 in Ishikawa cells.Results EGF enhanced the proliferation of endometrial adenocarcinoma cells (P<0.05).EGF induced ERα phosphorylation at Tyr-537 and phosphorylation of Ack1.Compared with untreated control, Dasatinib inhibited the proliferation of endometrial adenocarcinoma cells (P<0.05), phosphorylation of ERα Tyr-537 and Ack1.Conclusions EGF promotes Ishikawa cells proliferation in the possible way of activating ER α site-specific phosphorylation at Tyr-537 and phosphorylation Ack1, which could be blocked by dasatinib.

BACKGROUND:The production and release of a large amount of inflammatory factors caused by immune system inflammatory response mainly contributes to secondary spinal cord injury. OBJECTIVE:To investigate the effects of umbilical cord Wharton’s jely mesenchymal stem cel transplantation on repair of injured neurological function and expression of inflammatory factors monocyte chemoattractant protein 1 and interleukin 10 in rats with acute spinal cord injury. METHODS: Eighty-one healthy adult male Sprague-Dawley rats were randomly and equaly divided into sham operation, model and cel transplantation groups, with 27 rats per group. Rats in the latter two groups were subjected to hemisection of the spinal cord to establish acute spinal cord injury models. Rat models in the cel transplantation group received umbilical cord Wharton’s jely mesenchymal stem cel injection (1×106)via the tail vein. Rat neurological function was evaluated using the BBB score at different time points after spinal cord injury. The expression of monocyte chemoattractant protein 1 and interleukin 10 in injured spinal cord tissue was detected using ELISA assay at different time points after spinal cord injury. Migration and neuronal differentiation of umbilical cord Wharton’s jely mesenchymal stem cels in the injured spinal cord tissue were determined using immunohistochemical staining method. RESULTS AND CONCLUSION:Compared with the sham operation and model groups, rat neurological function was significantly recovered in the cel transplantation group (P < 0.05). Compared to the model group, monocyte chemoattractant protein 1 level in the serum and monocyte chemoattractant protein 1 mRNA and protein expression in the injured spinal cord tissue were significantly lower (P < 0.05), but interleukin 10 mRNA and protein expression in the injured spinal cord tissue was significantly higher (P < 0.05), in the cel transplantation group. In the cel transplantation group, umbilical cord Wharton’s jely mesenchymal stem cels could migrate to the injured region and express glial fibrilary acidic protein. These findings suggest that umbilical cord Wharton’s jely mesenchymal stem cels promote rat neurological function recovery by regulating the inflammatory response in the injured spinal cord tissue, which is likely to be one of mechanisms by which transplantation of umbilical cord Wharton’s jely mesenchymal stem cels treats spinal cord injury.

Objective:To investigate the clinical application value of amplitude-integrated electroencephalogram (aEEG) in evaluating the prognosis of brain function in children with disturbance of consciousness.Methods:A total of 100 children with disturbance of consciousness admitted to the pediatric intensive care unit (PICU) in the Third Affiliated Hospital of Zhengzhou University from October 2018 to September 2019 were enrolled.All patients completed aEEG and video electroencephalogram (vEEG) (monitoring hours≥ 6 h), modified Glasgow coma scale (GCS) rating, peripheral blood brain injury marker S100β protein and neuron-specific enolase (NSE) detection within 48 hours of admission.The prognosis was evaluated based on the above results.The actual prognosis of the children was recorded by telephone follow-up based on the pediatric cerebral performance category score (PCPC) until 6 months of onset or clinical death.The receiver operating characteristic curve (ROC) was used to analyze and compare the clinical efficacy of aEEG, vEEG, improved GCS, S100β protein, and NSE in evaluating the prognosis of brain function in children with disturbance of consciousness. Kappa consistency test was made to evaluate the correlation between the estimated prognosis and the actual prognosis. Results:The area under the ROC curve (AUC) of aEEG, vEEG, improved GCS, S100β protein and NSE was 0.847, 0.810, 0.729, 0.685 and 0.784, respectively, indicating the five methods had statistically significant value in evaluating the prognosis of brain function (all P<0.05). Taking the Z value as the gold standard, the clinical efficacy of aEEG in evaluating the prognosis of brain function was significantly different from that of S100β ( Z>1.96, P<0.05), but showed no significant difference with that of other 3 methods.Using the best cut-off value as the gold standard for evaluating the prognosis, aEEG had the highest sensitivity to evaluate a poor prognosis (90.5%). The Kappa consistency test showed that the prognosis predicted by aEEG was consistent with the actual prognosis ( Kappa=0.550, P<0.01). Conclusions:aEEG has a good evaluation value for the brain function prognosis of children with disturbance of consciousness.aEEG has high sensitivity, and the predicated prognosis is consistent with the actual clinical prognosis, so it can be widely used in the diagnosis and treatment of PICU.

Objective: To analyze the expression and prognostic significance of esophageal squamous cell carcinoma associated long non-coding RNA-1 (ESCCAL-1) in esophageal squamous cell carcinoma (ESCC) tissues. Methods: From August 2011 to May 2013, 73 patients with ESCC, who received radical resection in The First Affiliated Hospital of Zhengzhou University and Henan Cancer Hospital, were enrolled. The expressions of ESCCAL-1 in esophageal tumor tissues and corresponding adjacent non-tumor tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). T test, chi square test and multivariate analysis were performed for statistical analysis. Results: The expression of ESCCAL-1 was 28.03±9.37 in esophageal tumor tissues of patients with ESCC, which was higher than that in corresponding adjacent normal tissues (11.39±4.15), and the difference was statistically significant (t=2.964, P<0.01). However there were no statistically significant differences in the expressions of ESCCAL-1 among the patients with different age, gender, histological grade, classification of Union for International Cancer Control (UICC), T stage or lymph nodes metastasis (all P>0.05). The median disease-free survival (DFS) time and overall survival (OS) time of patients with low ESCCAL-1 expression were 39 months and 42 months, respectively, which were longer than those of patients with high ESCCAL-1 expression (30 months and 37 months), and the differences were statistically significant (χ²=9.049, P=0.003; χ²=10.165, P=0.001). The results of multivariate analysis showed that ESCCAL-1 expression was the independent risk factor of DFS and OS (high risk (HR)=2.45, 95% confidence interval (CI) 1.22 to 4.93, P=0.012; HR=2.29, 95%CI 1.14 to 4.59, P=0.019). Conclusions ESCCAL-1 may be involved the genesis and development of ESCC. The expression of ESCCAL-1 in esophageal tumor tissues may be a prognostic parameter for patients with ESCC receiving radical resection.

OBJECTIVE: To investigate the effect of ulinastatin pretreatment on isoflurane-induced mitochondria-dependent neuronal apoptosis in the hippocampus of rats. METHODS: Thirty-six male SD rats were randomly assigned into control group, isoflurane group and ulinastatin group. In the latter two groups, the rats were subjected to acute exposure to 0.75% isoflurane for 6 h and pretreated with 50 000 U/kg of ulinastatin before isoflurane exposure, respectively. After the treatments, apoptosis of the hippocampal neurons was detected using TUNEL assay, and the mitochondrial membrane potential (△ ψm) was measured using JC-1 mitochondrial membrane potential kit; cytochrome C release and caspase-3 activity were examined with Western blotting, and intracellular reactive oxygen species (ROS) was detected using the fluorescent probe H2DCFDA. RESULTS: Compared with those in the control group, the rats with acute exposure to isoflurane showed markedly increased TUNEL-positive cells in the hippocampus ( < 0.05), which were obviously reduced by ulinastatin pretreatment ( < 0.05). The △ψm of the hippocampal neurons was significantly reduced after isoflurane exposure ( < 0.05), and was partly recovered by ulinastatin pretreatment ( < 0.05). Acute exposure to isoflurane resulted in obviously increased cellular ROS, cytochrome C release and caspase-3 activity in the hippocampal neurons ( < 0.05), and these changes were significantly inhibited by ulinastatin pretreatment ( < 0.05). CONCLUSIONS Ulinastatin pretreatment provides neuroprotection against isoflurane-induced apoptosis of the hippocampal neurons in rats possibly by inhibiting mitochondria-dependent apoptosis pathway.
Animals ; Apoptosis ; Glycoproteins ; Hippocampus ; Isoflurane ; Male ; Rats ; Rats, Sprague-Dawley

Objective: To explore the expression of long noncoding RNA (lncRNA) HOXA11-AS in esophageal squamous cell carcinoma tissues and the relationship of HOXA11-AS level with clinical outcomes. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression level of HOXA11-AS in cell lines HET-1A, EC9706, EC109, and in tumor tissue and paired adjacent tissue samples from 73 ESCC patients who received surgical resection.The correlations of the expression level of HOXA11-AS with clinicopathological features and prognosis were also analyzed. Results: The relative expression levels of HOXA11-AS in tumor tissue and paired adjacent tissue were 0.832±0.387 and 2.486±1.087, respectively, with significant difference (P<0.001). The expression of HOXA11-AS was upregulated in 63.0%(46/73)ESCC tissues. The relative expression levels of HOXA11-AS in HET-1A, EC-9706 and EC-109 cells were 1.000, 23.553±3.221 and 17.217±1.968, respectively. The expression level of HOXA11-AS was upregulated in ESCC cell lines (P<0.001). High expression level of HOXA11-AS was correlated with histological grade and lymph node metastasis of ESCC patients (P<0.05). However, it was not associated with the age, gender, depth of infiltration and TNM staging (P>0.05). The median overall survival (OS) and median disease-free survival (DFS) of patients with low HOXA11-AS expression were 43 months and 42 months, respectively, significantly longer than 37 months and 28 months of patients with HOXA11-AS high expression (P<0.05). Cox model multivariate analysis showed that the expression of HOXA11-AS and lymph node metastasis were independent factors of poor prognosis of ESCC patients. Conclusions The expression of HOXA11-AS is upregulated in esophageal cancer cell lines and tissues. High expression of HOXA11-AS is associated with poor prognosis of ESCC patients.Therefore, LncRNA HOXA11-AS may serve as a predictive marker of postoperative ESCC patients.

Antibodies, Monoclonal, Murine-Derived ; adverse effects ; Antineoplastic Agents ; adverse effects ; Humans ; Lung Diseases, Interstitial ; chemically induced ; Rituximab ; Waldenstrom Macroglobulinemia ; drug therapy