The Zhumadian City Center Hospital

Nomhon, China

The Zhumadian City Center Hospital

Nomhon, China
SEARCH FILTERS
Time filter
Source Type

Xu H.,The Zhumadian City Center Hospital | Feng Y.,The Zhumadian City Center Hospital | Jia Z.,Zhengzhou University | Yang J.,Zhengzhou University | And 6 more authors.
Oncology Letters | Year: 2017

Axis inhibition protein 1 (AXIN1) is character-ized as a tumor suppressor in numerous types of cancer. However, the functional role of AXIN1 in the testicular germ cell tumors (TGCTs) remains unclear. The human embryonal carcinoma-derived cell line NTera2 was transfected with a recombinant AXIN1 expression vector (pcDNA3.1-AXIN1) and/or a small interfering RNA (siRNA) directed against AXIN1 (siAXIN). Following transfection, the mRNA and protein levels of AXIN1 were determined via reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. In addition, cell viability, apoptosis and the expression of apoptosis-associated proteins [apoptosis regulator Bax (Bax) and B-cell lymphoma (Bcl)-2] and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins [phosphorylated (p)-mTOR, mTOR, p-AKT, AKT, P-70S ribosomal protein S6 (S6) and S6] were assessed. AXIN1 mRNA and protein levels were increased following transfection with pcDNA3.1-AXIN1 and decreased following transfection with siAXIN1 compared with their respective control groups. After overexpression of AXIN1, NTera2 cell viability and expression of Bcl-2, p-mTOR p-AKT and p-S6 protein was decreased, while apoptosis and Bax protein levels were increased, compared with the control group. However, there was no significant difference in AXIN1 mRNA expression, apoptosis or Bax/Bcl-2 protein expres-sion when NTera2 cells were simultaneously transfected with pcDNA3.1-AXIN1+siAXIN1. In conclusion, the results of the present study indicate that overexpression of AXIN1 protects against TGCTs via inhibiting the PI3K/AKT/mTOR signaling pathway, suggesting that AXIN1 may be a potential target for gene therapy in TGCTs. © 2017, Spandidos Publications. All rights reserved.


Guo L.,The Zhumadian City Center Hospital | Wang P.-P.,The Zhumadian City Center Hospital | Li Q.-Q.,The Zhumadian City Center Hospital
Latin American Journal of Pharmacy | Year: 2016

The purpose of the present study was to develop a novel transdermal drug-delivery system comprising oleic acid with sonophoresis to enhance the permeation of propranolol (PRO) though the skin. The system was evaluated by applying 24 statistical fractional factorial design. In aforesaid study ultrasound treatment time (A), probe to skin distance (B), duty cycle (C), and oleic acid (D) were independent variables while in vitro drug release though skin (Y1) was considered as dependent variable. The isolated human abdomen cadaver skin was used for ultrasonic treatment and in vitro permeation of drug. All selected independent variables were found to be statistically significant (p < 0.05). PRO gel was prepared using chitosan as polymer and oleic acid as permeation enhancer. PRO gel without permeation enhancer and without ultrasonic treatment (controlled condition) showed permeation about 245 μg/cm2 and deposition 81.66 μg/cm2, while the same formulation showed the permeation of the 330 μg/cm2 and deposition 152.90 μg/cm2 when the skin was ultrasonically treated. While the maximum in vitro drug permeation in 12 h was found to be in the range of 835.9 μg/cm2 (Run 13) and deposition 278.63 and 152.90 μg/cm2 after passive delivery. So from the present investigation it can be concluded that the sonophoresis mediated PRO delivery along with permeation enhancer is a potential delivery system that could enhance the bioavailability of PRO. © 2016, Colegio de Farmaceuticos de la Provincia de Buenos Aires. All rights reserved.


Tian Y.,The Zhumadian City Center Hospital | Liu X.,The Zhumadian City Center Hospital | Liu H.,The Zhumadian City Center Hospital | Xing J.,The Zhumadian City Center Hospital
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: This study aims to observe the pathological changes of inner ear in deaf mice at different time after mouse cytomegalovirus infection. Methods: A total of 60 BALB/C mice were divided into 2 groups randomly: model group (A) and control group (B). In model group, 10 μl of MCMV was injected into the brain of each mouse while 10 μl of physiological saline was injected in control group. 10 cochlear samples were taken from 5 mice selected from each group randomly after infection for 1, 3, 5, 7, 14 and 21 days respectively. They were detected with PCR and HE staining methods. Auditory brain stem response was determined. The apoptosis of spiral ganglion (SGN) cells was detected by apoptosis assay kit. The levels of Bcl-2 and Bax were detected by RT-PCR and western blotting methods. Results: In group A, PCR results were negative after infection for 1 day, they were positive after infection for 3 days to 21 days. In group B, PCR results were negative in the experimental period. Compared with group B, ABR I wave latency and threshold increased while ABR I wave decreased in group A. There were no obvious hyperemia and inflammatory cells infiltration in group B, In group A, hemorrhage of scala tympani and scala vestibule appeared and reached highest peak after infection for 3 days accompanied by inflammatory cell infiltration; the vestibular membrane thickened after infection for 5 days; cell gap of SGN cells widened, arranged more sparsely with cell edema after infection for 7 days accompanied by infiltration of plasma cells; fibroblast proliferation and fibrosis appeared after infection for 14 days. Conclusions: MCMV infection occurred in cochlear after MCMV infection for 3 days and could sustain, the continues pathological changes of inner will bring difficulties to the treatment of CMV deafness, further studies on the specific mechanism of SGN changes caused by CMV infection will provide an important target for the treatment of CMV deafness. © 2015, E-Century Publishing Corporation. All rights reserved.

Loading The Zhumadian City Center Hospital collaborators
Loading The Zhumadian City Center Hospital collaborators