The Central Hospital of Wuhan
The Central Hospital of Wuhan
Wang Y.,The Central Hospital of Wuhan |
Chen M.,The Central Hospital of Wuhan
Medical Science Monitor | Year: 2017
Background: Acute pancreatitis (AP) is a sudden inflammation of the pancreas. It results in multiple, severe complications, and 15–20% of patients develop severe acute pancreatitis (SAP) with mortality as high as 30%. Consequently, it is imperative to develop an effective therapy for SAP. Material/Methods: We used 30 adult male Sprague Dawley (SD) rats. Rats were randomly divided into 3 groups – sham, SAP, and fentanyl+SAP – with 10 rats in each group. An automatic biochemical analyzer was used to analyze the concentration of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH). Terminal-deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay was applied to assess the cell apoptosis rate. Pathological changes in pancreas/heart were detected with hematoxylin and eosin (HE) staining. Western immunoblot assay was used to analyze protein levels of interleukin (IL)-1β, IL-6, and IkB. Results: Fentanyl pre-treatment inhibits SAP-induced elevation of CK-MB/LDH concentrations in serum. Compared with the sham group, SAP generates a higher brown/yellow staining rate, which is abated by fentanyl. In the pancreas, SAP generated more serious interstitial edema/hemorrhage and fat necrosis than in the sham group, which are attenuated by fentanyl. Likewise, compared to the sham group, SAP generates swelled/disordered myocardial fibers and congested blood vessels in myocardium, which are ameliorated by fentanyl. In the sham group, there was little IL-1β/IL-6, and fentanyl significantly inhibited SAP-induced up-regulation of IL-1β/IL-6 levels. Compared with the sham group, SAP significantly reduced IkB level, which was rescued by fentanyl. Conclusions: Fentanyl effectively alleviates SAP-induced pancreas and heart injuries through regulating the nuclear factor-κB (NF-κB) signaling pathway. © Med Sci Monit, 2017.
He A.-Y.,Wuhan University |
Qiu L.-J.,The Central Hospital of Wuhan |
Gao Y.,Wuhan University |
Zhu Y.,Wuhan University |
And 3 more authors.
Neuroscience | Year: 2011
Previous research has indicated that neuromelanin (NM) is involved in the pathogenesis of Parkinson's disease (PD). Increased reactive oxygen species (ROS) generation in PD sufferers is thought to be related to enhanced tyrosine hydroxylase (TH) activity and NM production. However, few reports have confirmed this hypothesis. In this study, PC12 cells of all experiments were exposed to 50 μmol/L levodopa (l-DOPA) to generate a model for NM synthesis. Meanwhile, PC12 cells were treated with glucose oxidase (GO) at different concentrations to generate oxidative stress. Finally, cell viability, TH activity, and NM generation in PC12 cells were measured. The results showed that GO dose-dependently stimulated oxidative stress generation in PC12 cells. Moderate increases in oxidative stress enhanced the viability of PC12 cells. However, an excessive level of oxidative stress can lead to the degeneration of PC12 cells. Notably, in the surviving PC12 cells, ROS significantly increased the TH activity, and the NM production was also upregulated. Thus, oxidative stress may upregulate the synthesis of NM, which may be a result of the increased TH activity observed in response to the elevated ROS in l-DOPA-treated PC12 cells. © 2011 IBRO.
Chen W.,The Central hospital of Wuhan |
Yuan K.,The Central hospital of Wuhan |
Tao Z.-Z.,Wuhan University |
Xiao B.-K.,Wuhan University
Asian Pacific Journal of Cancer Prevention | Year: 2011
The transcription factor, Forkhead Box M1 (FoxM1), has a specific expression pattern during the cell cycle. It also plays an important role in cellular developmental pathways and in the maintenance of homeostasis between cell proliferation and apoptosis. However, the precise role and molecular mechanisms associated with FoxM1 in laryngeal squamous carcinoma remain unclear. Therefore, laryngeal squamous carcinoma cells were transfected with FoxM1-targeted small interfering RNA (siRNA) and compared with cells transfected with a control siRNA. Assays of these two treatment groups detected a decrease in cell viability associated with down-regulation of FoxM1 expression, and resulted in an inhibition of cell proliferation, migration, and invasion. These phenotypes were also associated changes in expression of VEGF and MMP-2, a decrease in expression of cyclin B, and an increase in expression of p27. These findings suggest that deregulation of FoxM1 protein signaling is sufficient to affect tumorigenesis and cancer progression. These results also indicate that inhibition of FoxM1 represents an attractive target for cancer therapy.
Gan L.-L.,Hubei University |
Zhang H.,The Central Hospital of Wuhan |
Guo J.-H.,Hubei University |
Fan M.-W.,Hubei University
Asian Pacific Journal of Cancer Prevention | Year: 2014
High risk forms of the human papilloma virus (HPV) are generally accepted as necessary causative agents for cervical cancer. Recently, a possible relation between HPV and oral squamous cell carcinoma (OSCC) has also been noticed. The present study was conducted to investigate the prevalence of HPV infection in OSCCs in Wuhan city. DNA samples were collected from fresh tissues in 200 patients with OSCC and 68 normal controls. The polymerase chain reaction and direct sequencing were used to identify the HPV types in the samples. The prevalence of HPV of all types in the OSCC group was higher than in the control group (55/200 vs 2/68, OR=11.5, 95% CI=2.6-50.2). HPV16 and HPV18 were the main types detected, with HPV6 was the only low-risk type identified. High-risk HPV types HPV16 and HPV18 are prevalent in OSCC patients and may participate in the development of OSCC with traditional risk factors, tobacco and alcohol, possibly exerting synergistic effects. The results of multinomial logistic regression showed that those who smoked, consumed alcohol and with HPV infection have the highest risk of developing oral cancer (OR=13.3, 95% CI=3.1-56.8). Adjusted for age, smoking and alcohol use, HPV infection was independently associated with oral squamous cell carcinoma.
Zhang Y.,University of Missouri |
Zhang Y.,The Central Hospital of Wuhan |
Yue Y.,University of Missouri |
Li L.,Cedars Sinai Medical Center |
And 4 more authors.
Human Molecular Genetics | Year: 2013
Neuronal nitric oxide synthase (nNOS) membrane delocalization contributes to the pathogenesis of Duchenne muscular dystrophy (DMD) by promoting functional muscle ischemia and exacerbating muscle injury during exercise. We have previously shown that supra-physiological expression of nNOS-binding mini-dystrophin restores normal blood flow regulation and prevents functional ischemia in transgenic mdx mice, a DMD model. A critical next issue is whether systemic dual adeno-associated virus (AAV) gene therapy can restore nNOS-binding mini-dystrophin expression and mitigate muscle activity-related functional ischemia and injury. Here, we performed systemic gene transfer in mdx and mdx4cv mice using a pair of dual AAV vectors that expressed a 6 kb nNOS-binding mini-dystrophin gene. Vectors were packaged in tyrosine mutant AAV-9 and co-injected (5 × 1012 viral genome particles/vector/mouse) via the tail vein to 1-month-old dystrophin-null mice. Four months later, we observed 30-50% mini-dystrophin positive myofibers in limb muscles. Treatment ameliorated histopathology, increased muscle force and protected against eccentric contractioninduced injury. Importantly, dual AAV therapy successfully prevented chronic exercise-induced muscle force drop. Doppler hemodynamic assay further showed that therapy attenuated adrenergic vasoconstriction in contracting muscle. Our results suggest that partial transduction can still ameliorate nNOS delocalization-associated functional deficiency. Further evaluation of nNOS binding mini-dystrophin dual AAV vectors is warranted in dystrophic dogs and eventually in human patients. © The Author 2013. Published by Oxford University Press. All rights reserved.
Jiang J.,The Central Hospital of Wuhan |
Lv X.,The Central Hospital of Wuhan |
Fan L.,The Central Hospital of Wuhan |
Huang G.,The Central Hospital of Wuhan |
And 3 more authors.
Tumor Biology | Year: 2014
Non-small cell lung cancer (NSCLC) is the major cause of cancer death worldwide. Increasing evidence shows that microRNAs (miRNAs), evolutionally conserved noncoding RNAs, are widely involved in the development and progression of NSCLC. Aberrant alteration of miRNAs expression has been implicated in NSCLC initiation and progression. Herein, we studied the role of miR-27b in NSCLC cells. We found that miR-27b was significantly decreased in several NSCLC cell lines. Forced overexpression of miR-27 inhibited both the growth and invasion of NSCLC cells. Furthermore, we identified Sp1 transcription factor (Sp1) as a target of miR-27b in NSCLC cells.Moreover, we found that miR-27 suppressed growth and invasion of NSCLC cells partially by targeting Sp1. Our data indicate that miR-27b may play a critical role in the development of NSCLC. © International Society of Oncology and BioMarkers (ISOBM) 2014.
Li S.,The Central Hospital of Wuhan |
Fu X.-A.,The Central Hospital of Wuhan
International Eye Science | Year: 2014
AIM: To analyze the clinical data of patients with cataract in our hospital practicing clinical pathway and evaluate the value of clinical pathway. METHODS: Two hundred eyes (200 eyes) of two hundred patients who suffered cataract from January 2012 to December 2012 were treated with ultrasound emulsification and intraocular lens planting by managing with clinical path. They are considered as clinical pathway group. The control group was another 200 patients (200 eyes) from December 2010 to December 2011 who suffered the same disease and treated with the same surgery not by managing with clinical path. The average length of stay, preoperative average length of stay, average cost of hospitalization (except the cost of IOL), drug cost, inspection fee, curative effect, degree of satisfaction of patients and medical staff, and readmission rate were analyzed. RESULTS: In the clinical pathway group, the average length of stay was 6.01±0.13 d, the preoperative average length of stay was 1.02±0.15 d, the average cost of hospitalization was 4401.23±129.07 Yuan, drug cost was 720.35±23.21 Yuan, inspection fee was 700.37±46.25 Yuan, and patient satisfaction was 96.4%. In the control group, the average length of stay was 10.21±0.05 d, the preoperative average length of stay was 2.20±0.07 d, average hospitalization cost was 4827.43±132.13 Yuan, drug cost was 1206.21±53.64 Yuan, inspection fee was 850.35±24.26 Yuan, and patient satisfaction was 93.1%. The difference between the two groups was significant (P<0.05). The cure rate was 97.2% in the clinical pathway group and 96.2% in the control group. The difference was not statistically significant (P>0.05). Satisfaction of the medical staff was 98.2% in the clinical pathway group and 96.4% in the control group, with no statistically significant difference (P>0.05). Clinical pathway group and control group had a readmission rate of 1% and 0.9%, with no statistically significant difference (P>0.05). CONCLUSION: Implementation of clinical pathway on cataract patients will not reduce the quality of medical care. On the contrary, it will standardize the medical behavior, improve patient satisfaction, and reduce health care costs, and ease the tension in the doctor-patient relationship, and provide a theoretical basis for the realization of the medical system of prepaid. Copyright 2014 by the Press.
Wang F.,The Central Hospital of Wuhan |
Zhang L.,The Central Hospital of Wuhan
Aging Clinical and Experimental Research | Year: 2015
Background and aims: Cyclin-dependent kinase inhibitor p15INK4b is thought to be an important player in regulating astrocytic cell cycle. However, little is known with regard to the expression of p15INK4b and its function in hippocampal astrocytes. This study evaluated the expression of p15INK4b and its function during different development stages in hippocampal astrocytes. Methods: In this study, we cultured hippocampal astrocytes from neonatal adult and aged rats. The expression of p15INK4b in neonatal, adult and aged astrocytes was examined. Short interfering RNA (siRNA) was then used to study the functional effects of p15INK4b down-regulation during cell cycle regulation. Results: We found the expression of p15INK4b in hippocampal astrocytes was detectable on postnatal day 7, was expressed at moderate levels in adult mice (9 months old) astrocytes and peaked in aged rat (24 months old) astrocytes. Incubation with siRNA significantly suppressed p15INK4b expression at the mRNA and protein levels in astrocytes. Down-regulation of p15INK4b increased [3H]-thymidine incorporation into DNA and allowed cells to pass the G0/G1-S checkpoint in aged but not in neonatal or adult astrocytes. Conclusions: These observations suggest p15INK4b is expressed at a steady level in neonatal and adult rat hippocampal astrocytes with no effect on cell cycle regulation. Importantly, aged astrocyte cell cycle regulation was significantly affected by high expression levels of p15INK4b suggesting a role for p15INK4b in cell cycle regulation when it is expressed at high but not moderate or low levels in hippocampal astrocytes. © 2015 Springer International Publishing Switzerland
Becker L.E.,University of Louisville |
Lu Z.,The Central Hospital of Wuhan |
Chen W.,The Central Hospital of Wuhan |
Xiong W.,Central South University |
And 2 more authors.
PLoS ONE | Year: 2012
MicroRNAs (miRNAs) are encoded in the genome as individual miRNA genes or as gene clusters transcribed as polycistronic units. About 50% of all miRNAs are estimated to be co-expressed with neighboring miRNAs. Recent studies have begun to illuminate the importance of the clustering of miRNAs from an evolutionary, as well as a functional standpoint. Many miRNA clusters coordinately regulate multiple members of cellular signaling pathways or protein interaction networks. This cooperative method of targeting could produce effects on an overall process that are much more dramatic than the smaller effects often associated with regulation by an individual miRNA. In this study, we screened 366 human miRNA minigenes to determine their effects on the major signaling pathways culminating in AP-1, NF-κB, c-Myc, or p53 transcriptional activity. By stratifying these data into miRNA clusters, this systematic screen provides experimental evidence for the combined effects of clustered miRNAs on these signaling pathways. We also verify p53 as a direct target of miR-200a. This study is the first to provide a panoramic view of miRNA clusters' effects on cellular pathways. © 2012 Becker et al.
Liu W.,Huazhong University of Science and Technology |
Liu W.,the central hospital of Wuhan |
He P.,Huazhong University of Science and Technology |
Cheng B.,Huazhong University of Science and Technology |
And 3 more authors.
Microbes and Infection | Year: 2010
Chlamydia pneumoniae (C. pneumoniae) induces macrophage-derived foam cell formation, a hallmark of early atherosclerosis, in the presence of low density lipoprotein (LDL). However, its mechanisms have yet to be elucidated. In this study we examined the effects of live, heat-killed and UV-inactivated C. pneumoniae on cholesterol metabolism in THP-1-derived macrophages and the role of c-Jun NH2 terminal kinase (JNK), which may participate in the C. pneumoniae-induced disruption of intracellular cholesterol homeostasis. We investigated whether SP600125, a special JNK inhibitor, affects the expression of peroxisome proliferator-activated receptor gamma (PPARγ), and also its downstream target genes Acyl-CoA cholesterol acyltransferase-1 (ACAT1), ATP-binding cassette transporter A1 and G1 (ABCA1/G1) in human THP-1 macrophages infected with C. pneumoniae. In this paper we found that both live and inactivated C. pneumoniae infection induce intracellular cholesterol accumulation and foam cell formation. C. pneumoniae infection increased the expression of ACAT1 and decreased the expression of ABCA1/G1, all of which facilitated cholesterol accumulation and promoted macrophage-derived foam cell formation. However, these responses were attenuated by SP600125 in a dose-dependent manner. These results demonstrate for the first time that both live and inactivated C. pneumoniae infections disturb cholesterol homeostasis in human THP-1 macrophages and C. pneumoniae infection disturbs cholesterol homeostasis via JNK-PPARγ dependent signal transduction pathways. © 2010 Institut Pasteur.