Objective To study the effects of mosapride and domperidone on the pulmonary infection of acute stroke patients lying in bed and with nasal feeding. Methods Eighty-nine acute stroke patients lying in bed and with nasal feeding were divided randomly into the treatment group (47 cases) and the control group (42 cases). The control group was treated routinely,and the treatment group was treated with mosapride 5 mg and domporidone 20 mg thrice a day for 4 weeks, besides routine therapy. The incidence rate of pulmonary infection, gastric residual volume (GRV) and the number of cases with gastric contents remaining after 3 hours of nasal feeding were studied. All data were analyzed statistically. Results In the treatment group, 13 cases had pulmonary infection,and the incidence rate was 27.66%(13/47). In the control group,25 cases had pulmonary infection,and the incidence rate was 59.52% (25/42). There was significant difference between the two groups (P < 0.01 ). Three hours after nasal feeding,24 cases with gastric contents remaining were discovered in the treatment group,and GRV was (50.80±15.38) ml. Two hundred and thirty-seven cases with gastric contents remaining were discovered in the control group, and GRV was (112.17±32.54) ml. Significance differences were also detected between the two groups (P<0.01). Conclusion As for the acute stroke patients lying in bed and with nasal feeding,mosapride and domperidone can remarkably cut down the pulmonary infection upon common treatment.

Objective To observe the effects of hyperbaric oxygen (HBO) exposure on the expression of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) in rats with simulated high-altitude pulmonary edema (HAPE).Methods Fifty-six rats were randomly divided into five groups:control (normal),HAPE (high altitude pulmonary edema model),1 HBOT (HAPE model and HBO therapy for 1 time),2 HBOT (HAPE model and HBO therapy twice) and NOT (normal pressure oxygen therapy) groups,and was intervened accordingly.Western blotting and real-time PCR techniques were used to analyze the expression of AQP1 and AQP5 in their lungs.The wet-todry (W/D) weight ratio and morphology of the lungs was also examined.Results The protein and gene expression of AQP1 and AQP5 in the HAPE group decreased significantly compared with the control group.There were obvious differences in the protein and mRNA expression of AQP1 and AQP5 between the 2 HBOT group and the HAPE group and between the 2 HBOT group and the 1 HBOT group.Compared with the control group and the 1 HBOT group,marked lung injury could be seen in the HAPE group.Compared with the NOT group and the 1 HBOT group,lung injury in the 2 HBOT group was relieved significantly.Conclusions HAPE in rats is associated with down-regulation of the expression of AQP1 and AQP5 in the lungs.This down-regulation can be attenuated and lung injury can be alleviated by HBOT.Two sessions of HBOT could be more helpful than one for promoting this improvement.

Objective:To explore the effects of miR-181a-5p on the occurrence and development of gastrointestinal stromal tumors (GIST) through targeting CTDSPL mediating TGF-β signaling pathway.Methods:Surgical treatment of GIST patients in the First People’s Hospital of Shangqiu City from Jan. 2016 to Dec. 2019 were selected as research objects, and tumor tissue and adjacent normal tissue were collected intraoperatively. The clinicopathological data of the patients were analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression of CTDSPL gene and miR-181a-5p expression. Western blot was used to detect the protein level of CTDSPL and TGF-β signaling pathway related factors. Human gastrointestinal stromal tumor cell lines (GIST-T1) were transfected with miR-181a-5p mimic, miR-181a-5p inhibitor, or CTDSPL overexpression vector. MTT was used to detect cell proliferation activity, Transwell assay was utilized to detect cell invasion, flow cytometry was used to determine cell apoptosis in each group.Results:Compared with adjacent tissues, expression of miR-181a-5p and TGF-β signaling pathway related factors was activated while CTDSPL expression was inhibited. Tumor size, invasion depth and modified NIH grading were related to the mRNA expression level of CTDSPL gene in GIST tumor tissues (All P<0.05) . Compared with Blank group, inhibition of miR-181a-5p or CTDSPL overexpression had the ability to inhibit the cell viability and invasion, induce apoptosis. The effects of miR-181a-5p mimic on GIST-T1 can be saved by CTDSPL overexpression. Conclusion:miR-181a-5p can promote the occurrence and development of GIST by down-regulating the CTDSPL gene level and activating TGF-β signaling pathway.

To explore the effects of long-term treatment of different dietary energy levels on ovarian expression of mRNAs for LHR and FSHR,the present study was performed in nine growth-matched littermate crossbred (Land-race×Large White X Duroc) prepubertal gilts. At approximately 30 kg of body weight and 50 day of age,gilts were housed with individual feeding stalls and placed on a normal level of feeding for 90 days (dl-90) with free ac-cess to water and food throughout the whole research. From d91 ,littermates were divided and randomly assigned to one of the following three treatment lines for 3 weeks till d112:Group H,Group M, and Group L, fed the high energy level diet (n = 3, digestible energy 14.87 MJ/kg), moderate energy level diet (n = 3, digestible energy 12.39 MJ/ kg), and low energy level diet (n = 3, digestible energy 9.98 MJ/kg), respectively. When gilts were slaughtered on d112 after 3 weeks energy treatment, both ovaries of every gilts were collected,snap frozen in liquid nitrogen and re-tained at -80℃ for use to determine and analysis the relative amount of ovarian LHR and FSHR mRNAs using semi-quantitative RT-PCR. Results showed that the effect of dietary energy treatment was notable: the ovarian ex-pression of mRNAs for LHR and FSHR was significantly higher (P<0.05) in gilts treated with high energy diet compared to gilts treated with moderate and low energy diets, while gilts treated with low energy diet had a signifi-cantly lower (P<0.05) ovarian LHR and FSHR expression compared with gilts treated with moderate and high en-ergy diets. These results revealed that ovarian expression of I.HR and FSHR in prepubertal gilts increased as the lev-el of dietary energy intake elevated,i, e. , high energy diet can markedly enhance ovarian expression of mRNAs for LHR and FSHR,whereas energy deficit markedly suppress the expression.

Objective To explore the effects of hyperbaric oxygen preconditioning on ischemia-reperfusion inflammatory reaction of rats after skin flap transplantation.Methods Fifty-six Sprague-Dawley rats were randomly divided into 3 groups:a sham ischemia-reperfusion (SH) group,an ischemia-reperfusion (IR) group and a hyperbaric oxygen reconditioning (HBO) group.Both IR group and HBO group were further divided into 3 subgroups,respectively,according to the time points of serum sampling for test post establishment of the IR model of the abdominal pedicle skin flap transplantation.The IR model of the abdominal pedicle skin flap transplantation was established in all the animals except those in the SH group,with those in the HBO group were preconditioned with HBO twice daily for 3 days before the operation.The blood was sampled at 1,3 and 5 day post-operation to test the level of IL-23 using enzyme-linked immunosorbeut assay (ELISA).The survival skin flaps were sampled from all the animals at 3 and 5 days after the operation for histological observation and evaluation.Results The average IL-23 level of HBO 3 d subgroup (17.80 ± 14.78) was significantly lower than that of the IR 3 d subgroup (38.91 ± 12.26).The average histological scores of the IR 3 d and 5 d subgroups,as well as HBO 3 d and 5 d subgroups were (2.66 ±0.44)and (3.2 ±0.53),(1.85 ±0.31) and (2.29 ±0.32),significantly higher than SH group (0.38 ±0.10).Moreover,the average histological score of the HBO 3 d and 5 d subgroups was significantly lower than IR 3 d and 5 d subgroups respectively.Conclusion Hyperbaric oxygen preconditioning can relieve the ischemia-reperfusion inflammatory reaction through reducing the serum level of IL-23 in rats after skin flap transplantation.

OBJECTIVETo investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.

METHODSAfter 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.

RESULTSMean arterial pressure (MAP), coronary perfusion pressure (CPP) and cardiac troponin I (CTNI) showed significant differences between eventual survival animals and non-survival animals at 4 h after ROSC (109.2 ± 10.7 mmHg vs. 94.8 ± 12.3 mmHg, P=0.048; 100.8 ± 6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60 ± 0.13 ug/L vs. 1.75 ± 0.10 ug/L, P=0.046). Mitral valve early-to-late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC.

CONCLUSIONCardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long-term survival after CPR.

Animals ; Blood Pressure ; Cardiopulmonary Resuscitation ; Coronary Circulation ; Heart Arrest ; Hemodynamics ; Male ; Myocardial Contraction ; physiology ; Myocardial Stunning ; Swine ; Time Factors ; Ventricular Fibrillation

Objective To investigate the effects of enteral nutrition added with glutamine on the incidences of gastrointestinal complications,intestinal mucosal barrier function and inflammatory responses in patients with acute severe traumatic brain injury (sTBI).Methods A prospective case control study was made on 107 patients with sTBI hospitalized from January 2016 to June 2017.The patients were divided into experimental group added with glutamine (n =54) and control group without glutamine (n =53) according to the random number table.The general data of the patients were recorded.After treatment,the incidences of gastrointestinal complications in both groups were compared.The serum levels of intestinal mucosal barrier function indices,namely,diamine oxidase (DAO),Dlactate acid,and intestinal fat acid binding protein (I-FABP) were evaluated by enzymology spectrophotometer method.Meanwhile,the serum levels of C-reactive protein (CRP),tumor necrosis factor-α (TNF-α),and interleukin-6 (IL-6) were also tested with enzyme-linked immunosorbent assay (ELISA).Glasgow coma scale (GCS),acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ),and hospital stay in both groups were compared.Results The two group were comparable with respect to gender,age,injury reasons,body mass index,preoperative GCS,preoperative APACHE Ⅱ,injury type and injury time (P ＞ 0.05).The experimental group had lower incidences of stress ulcer,gastric retention and diarrhea compared with the control group 14 days after treatment (P ＜ 0.05).Within 14 days after treatment,the serum levels of DAO,D-lactate acid and I-FABP were significantly decreased in the experimental group at days 7 and 14 after treatment (P ＜ 0.05).The serum levels of CRP,TNF-α and IL-6 in the experimental group were significantly decreased after treatment (P ＜ 0.05).The experimental group had better prognosis compared with the control group (P ＜ 0.05),with higher GCS scores [(9.3 ± 0.7) points vs.(8.2 ± 0.7) points],lower APACHE Ⅱ scores [(15.3 ± 1.1) points vs.(17.7 ± 1.2) points] at day 14,and shorter hospital stay [(19.1 ± 2.2) days vs.(25.3 ± 2.4) days] (P ＜ 0.01).Conclusions Enteral nutrition added with glutamine can effectively reduce the incidence of gastrointestinal complications,as well as alleviate the intestinal mucosal barrier function damage and the inflammatory responses at early stage after sTBI,which possibly improves prognosis.

OBJECTIVE: To analyze the correlation of methylation status of dachshund homolog 1 (DACH1) gene in tumor tissues with clinicopathological characteristics and prognosis of patients of esophageal cancer. METHODS: Tumor tissue, paracancerous tissue and normal esophageal mucosal specimens of 104 patients with esophageal cancer were collected. Methylation-specific PCR was used to determine the methylation status of the DACH1 gene. Univariate analysis and multivariate Logistic regression model were used to analyze the correlation between DACH1 methylation status and clinical pathological characteristics of the patients. Kaplan-Meier survival curve was used to analyze the relationship between DACH1 methylation status and prognostic survival of patients. RESULTS: The methylation rate of the DACH1 gene in esophageal cancer tumor tissue was 30.77% (32/104), which was higher than those in adjacent tissues (1.92%) and normal esophageal mucosa (0%) (P< 0.05). The methylation status of the DACH1gene in tumor tissues of patients did not correlate with the patient's age, gender, and pathological type (P> 0.05) but tumor differentiation, TNM staging, and lymph node metastasis(P< 0.05). The degree of tumor differentiation, TNM stage, and lymph node metastasis of patients are independent risk factors for the methylation status of the DACH1 gene. By March 2020, 89 of the 104 patients had died. Among them, the median survival foresophageal cancer patients with DACH1 gene methylation was 22 months, which was lower than 34 months of those without DACH1 methylation (P< 0.05). CONCLUSION Methylation of the DACH1 gene may be involved in the occurrence and progress of esophageal cancer. The degree of tumor differentiation, TNM stage, and lymph node metastasis of patients are independent risk factors for the methylation status of the DACH1 gene. Patients with esophageal cancer but unmethylated DACH1 gene have a longer prognostic survival.
Esophageal Neoplasms/pathology* ; Eye Proteins/genetics* ; Humans ; Lymphatic Metastasis ; Methylation ; Neoplasm Staging ; Prognosis ; Transcription Factors

Objective To comprehensively evaluate the clinical efficacy,safety and economic benefits of atorvastatin and fluvastatin in regulating dyslipidemia.Methods The clinical randomized controlled trials (RCTs) for comparing clinical efficacy of atorvastatin and fluvastatin on regulating dyslipidemia were retrieved from databases,including Cochrane Library,PubMed,Medline,Embase,Wiley,Springer,CNKI,Wanfang and VIP,till June 2016.Data were evaluated by two reviewers independently according to the Jadad standard.The changes of low density lipoprotein cholesterol (LDL-C),high density lipoprotein cholesterol (HDL-C),total cholesterol (TC) and triglyceride (TG) before and after treatment were extracted to perform Meta-analysis by using RevMan5.0 software.The economic evaluation was carried out,as well.Results A total of 7 RCTs were included,including 684 cases of patients treated with fluvastatin and 2 208 cases of patients treated with atorvastatin.The patients were spitted into two subgroups according to the same or different maximum dose of atorvastatin and fluvastatin.The results indicated that the effects of atorvastatin on down-regulating LDL-C,TC and TG levels were significantly better than those of fluvastatin,the differences were statistically significant (Z=23.63、23.32、5.50,P＜0.000 01).No significant difference was found in regulating HDL-C level between atorvastatin and fluvastatin.Conclusion Compared with fluvastatin,atorvastatin is more effective to regulate levels of LDL-C,TC and TG,but there is no significant difference in up-regulating HDL-C level.Additionally,application of atorvastatin is more economicallv effective.

Objective:To investigate the relationship between the expression level of lymphocyte enhancer-binding factor 1(LEF1) and CTNNB1 and the cycle arrest, apoptosis and radiation resistance of esophageal cancer cells and unravel the related mechanisms.Methods:Recombinantplasmids and empty plasmids expressing LEF1 and CTNNB1were constructed and transfected into esophageal cancer cells. RT-PCR assay was used to detect the transfection efficiency of the plasmids. Clone formation assay, CCK8 assay, cell cycle test by flow cytometry, apoptosis test by flow cytometry and Western blot were performed to detect the differences in theradioresistance, proliferation, cell cycle and apoptosis of esophageal cancer cells before and after transfection.Results:The survival rate of clonal colony cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly better than those in other groups ( P<0.05). The proliferation of clonal colony cellsat 72 h, 96 h and 120 h in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly better than those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The percentage of G 2 phase arrest cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly higher than those in the other groups (all P<0.05). The apoptosis rate of esophageal cancer cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly lower compared with those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The expression levels of Bax and Caspase 3 proteins in the pGEX-LEF1+ pCMV6-CTNNB1 group were significantly lower than those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The expression level of Bcl-2 protein in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly higher compared with those in the other groups (all P<0.05). Conclusion:LEF1 and CTNNB1 can regulate the proliferation and G 2 phase arrest of esophageal cancer cells after radiation intervention by mediating the Wnt signaling pathway, and improve the radiation resistance of esophageal cancer cells by inhibiting cell apoptosis.