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Fang K.,Zhengzhou University | Liu F.,Zhengzhou University | Wen J.,Hunan Province Peoples Hospital | Liu H.,Hunan Province Peoples Hospital | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2017

Since TAP polymorphisms were associated with accelerated progression of post-infection tuberculosis (TB), and TB could account for development of spinal TB (STB), the present study was intended to investigate whether the mutations of TAP polymorphisms could predict risk and prognosis of pediatric patients suffering from STB. Altogether 85 pediatric STB (PSTB) patients and 97 healthy children were recruited, and their peripheral blood samples were gathered to extract genomic DNA for genotyping. According to previously published investigations, 2SNPs located within TAP1 and 7SNPs situated within TAP2 were finally selected for this investigation. Genotyping of the SNPs were implemented utilizing method of polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP), and potential haplotypes were obtained with application of SHESIS software. The odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated to assess correlations between SNPs/ haplotypes and prevalence of PSTB. The G allele of TAP1 rs1135216 and A allele of TAP2 rs4148871 were both closely linked with elevated susceptibility to PSTB when, respectively, compared with A allele and G allele (G vs. A, OR = 2.06, 95% CI: 1.28-3.30, P < 0.01; A vs. G, OR = 2.45, 95% CI: 1.48-4.04, P < 0.01), whereas A allele of TAP2 rs2857103 was significantly associated with lessened PSTB risk in comparison to C allele (OR = 0.35, 95% CI: 0.23-0.55, P < 0.01). Besides, mutations of rs241447 (G>A) and rs4148876 (G>A) could significantly modify PSTB risk (AA vs. GG+GA, OR = 2.44, 95% CI: 1.27-4.72, P < 0.01; AA+GA vs. GG, OR = 2.00, 95% CI: 1.08-3.70, P = 0.03). Haplotypes A-G-A-G-G and A-A-A-G-G were also demonstrated to decrease PSTB risk significantly (OR = 0.25, 95% CI: 0.07-0.95, P = 0.03; OR = 0.35, 95% CI: 0.12-0.96, P = 0.03). SNPs within TAP1 (rs1135216) and TAP2 (rs241447, rs2857103, rs4148871 and rs4148876) appeared as potential targets for both prediction and treatment of PSTB, yet further studies were in demand. © 2017, E-Century Publishing Corporation. All rights reserved.


Zhao Y.,PLA Fourth Military Medical University | Wang W.J.,PLA Fourth Military Medical University | Guan S.,Zhengzhou University | Li H.L.,Henan Tumor Hospital | And 10 more authors.
Annals of Oncology | Year: 2013

Background: Data on the efficacy and safety of sorafenib in combination with transarterial chemoembolization (TACE) in patients with advanced hepatocellular carcinoma (HCC) are lacking. Patients and methods: In this multicenter retrospective study, 222 consecutive HCC patients receiving combination therapy were enrolled between June 2008 and July 2011. Results: Chronic hepatitis B was the predominant cause of HCC (86%). Eighty percent patients were at Barcelona Clinic Liver Cancer (BCLC) stage C, and 86% patients were in Child-Pugh (CP) A class. The overall median survival was 12 months (95% CI 10.1-13.9). The overall incidence of adverse events (AEs) was 87%. In 177 BCLC-C patients, performance status, the number of HCC nodules, Child-Pugh score and macrovascular invasion were significantly associated with overall survival (OS) and were included in the final risk scores (R), where R = 5 × (vascular invasion: 0 if no, 1 yes) + 6 × (CP: 0 if A, 1 if B) + 7 × (no. of lesions: 0 if 1-2, 1 =3) + 8 × (Eastern Cooperative Oncology Group, ECOG: 0 if 0, 1 =1). Conclusions: Sorafenib in combination with TACE should be considered a safe and effective therapy for advanced HCC. Further validation of the new subgroup of BCLC-C stage is warranted in an independent patient cohort. © The Author 2013. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.


Xiong F.,Hunan Normal University | Fan P.-Z.,Hunan Province Peoples Hospital | Zhang C.-J.,Hunan Province Peoples Hospital
Journal of Dalian Medical University | Year: 2015

Thyroid carcinoma is the most common malignant tumor of thyroid, derived from thyroid follicular epithelial cells. It represents approximately 1.3% -1.5% of all malignant tumors and the incidence is increasing in recent years. Mutation, deletion and recombinant p53 gene inactivation play important roles in the process of formation and development of many human tumors. Ubiquitin ligase Pirh2 is a new protein with E3 ligase activity. It promotes p53 ubiquitination and subsequent degradation, and thus inhibit the anti - tumor function of p53, resulting in tumor formation and deterioration. With progression in cancer research, identification of novel genes related to the occurrence, development and prognosis of thyroid cancer has become a hot research spot. This review summarizes research progress of Pirh2 and p53 in thyroid carcinoma.


Huang F.,Central South University | Wang H.,Henan Province Peoples Hospital | Zou Y.,Hunan Province Maternity and Childrens Health Care Center | Liu Q.,Hunan Province Peoples Hospital | And 2 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2013

Objective: To study the effect of GnRH-II on the cell proliferation, apoptosis and secreting vascular endothelial growth factor (VEGF) of ectopic, eutopic and normal endometrial stromal cells (ESC) from patients with or without endometriosis (EMs) in vitro. Methods: The ectopic, eutopic and normal ESC were isolated, cultured and identified, then added 0 M, 10-10 M, 10-8 M, 10-6 M GnRH-II. The growth and proliferation of three ESC were measured by MTT assay; the cell apoptosis were detected with the method of Hoechst staining and Flow Cytometry test; ELISA was used to measure the VEGF concentration change by three ESC secretion. Results: GnRH-II inhibited the proliferation of ectopic, eutopic ESC from patients with endometriosis and normal ESC from control patients, in a dose- and time-dependent manner (P<0.05); GnRH-II increased the apoptotic rate of three ESC in a dose-dependent manner (P<0.05); The concentration of VEGF in three ESC was significantly decreased after the treatment of GnRH-II, in a dose-dependent manner (P<0.01); And these above effects were the strongest on the ectopic than on the eutopic or normal, there were statistical significance (P<0.05); and three was no significantly difference between the eutopic and normal (P>0.05). Conclusions: GnRH-II significantly inhibited the cell proliferation, induced cell apoptosis and decreased the VEGF secreting of ectopic, eutopic and normal ESC in EMs in vitro, and these effects were the strongest on ectopic ESC, which suggested that GnRH-II may become a new effective treatment for endometriosis.


Xiao H.,Hunan University | Li P.,Hunan University | Li P.,Guangzhou Mechanical Engineering Research Institute | Guo D.,Hunan University | And 3 more authors.
Medicinal Chemistry Research | Year: 2014

The reaction of 5,5′-(pyridine-2,6-diyl)bis(4-amino-3-mercapto-1,2,4- triazole) with various carboxylic acid in phosphorus oxychloride yielded the corresponding 2,6-bis(6-substituted-1,2,4-triazolo[3,4-b][1,3,4]thiadiazol-3-yl) pyridine derivatives 6a-l. The structures of the newly synthesized compounds were confirmed by elemental analysis, 1H NMR and 13C NMR spectral, mass spectral, and Infrared spectral studies. All the synthesized target compounds have been investigated for their in vitro antibacterial activity, and the preliminary results revealed that the compounds 6b and 6k exhibited very promising activity against Escherichia coli and Pseudomonas aeruginosa. © Springer Science+Business Media 2013.


Luo Y.,Central South University | Luo Y.,Hunan Province Children Hospital | Wang Y.,Hunan Province Peoples Hospital | Shu Y.,Central South University | And 3 more authors.
International Journal of Biochemistry and Cell Biology | Year: 2015

Systemic sclerosis (SSc) is a heterogeneous and life-threatening autoimmune disease characterized by damage to small blood vessels, interruption of immune homeostasis and ultimately, fibrosis. Currently, the mechanisms involved in SSc pathogenesis remain unknown. An increasing amount of data shows that, via certain signaling pathways, epigenetic mechanisms, including DNA methylation, histone modification, and miRNAs, are closely related to the three primary processes that characterize SSc: vascular abnormalities, activation of immune system, and excessive extracellular matrix deposition. In the clinical setting, identification of molecules and biomarkers for determining disease severity, predicting disease progression and assessing response to treatment remains challenging. In this review, we aim to summarize the key epigenetic mechanisms involved in the pathogenesis of SSc. Certain cytokines or molecules, such as CD40, CD70, and Fli-1, are expressed at varying rates in SSc due to epigenetic modification and play important roles in SSc. It is therefore likely that these molecules may be biomarkers for SSc. In addition, epigenetic changes of certain genes, including Fli-1, BMPRII, CD11a, Foxp3, and eNOS, influence the expression of these genes to ultimately result in an anti-fibrotic effect. The influence that epigenetics has on SSc pathogenesis suggests that epigenetics-targeting drugs may have potential therapeutic effects against SSc. This article is part of a Directed Issue entitled: Epigenetics dynamics in development and disease. © 2015 Elsevier Ltd.


PubMed | Central South University and Hunan Province Peoples Hospital
Type: | Journal: The international journal of biochemistry & cell biology | Year: 2015

Systemic sclerosis (SSc) is a heterogeneous and life-threatening autoimmune disease characterized by damage to small blood vessels, interruption of immune homeostasis and ultimately, fibrosis. Currently, the mechanisms involved in SSc pathogenesis remain unknown. An increasing amount of data shows that, via certain signaling pathways, epigenetic mechanisms, including DNA methylation, histone modification, and miRNAs, are closely related to the three primary processes that characterize SSc: vascular abnormalities, activation of immune system, and excessive extracellular matrix deposition. In the clinical setting, identification of molecules and biomarkers for determining disease severity, predicting disease progression and assessing response to treatment remains challenging. In this review, we aim to summarize the key epigenetic mechanisms involved in the pathogenesis of SSc. Certain cytokines or molecules, such as CD40, CD70, and Fli-1, are expressed at varying rates in SSc due to epigenetic modification and play important roles in SSc. It is therefore likely that these molecules may be biomarkers for SSc. In addition, epigenetic changes of certain genes, including Fli-1, BMPRII, CD11a, Foxp3, and eNOS, influence the expression of these genes to ultimately result in an anti-fibrotic effect. The influence that epigenetics has on SSc pathogenesis suggests that epigenetics-targeting drugs may have potential therapeutic effects against SSc. This article is part of a Directed Issue entitled: Epigenetics dynamics in development and disease.


Yu J.-M.,Chinese National Institute for Viral Disease Control and Prevention | Chen Q.-Q.,Hunan Province Peoples Hospital | Hao Y.-X.,Chinese National Institute for Viral Disease Control and Prevention | Yu T.,Hunan Province Peoples Hospital | And 4 more authors.
Journal of Clinical Virology | Year: 2013

Background: Encephalitis is a major cause of death and disability in adults and children; different members in the family Parvoviridae are known to be associated with encephalitis to some extent. Objectives: To determine the presence of human bocaviruses (HBoVs) and corresponding HBoV-specific immunoglobulins (Igs) in cerebrospinal fluid from children with suspected viral encephalitis. Study design: Employing real-time PCR and nested touchdown PCR, 67 cerebrospinal fluid (CSF) samples from children with suspected viral encephalitis were screened for HBoV and routine encephalitis-causing viruses. Using ELISA, Western blot and IFA, HBoV-specific Ig were determined in the samples. Results: Nine samples (134%) were HBoV1 DNA-positive, while one sample (15%) was HBoV2 DNA-positive. HBoV-specific IgM and IgG antibodies were detected in the CSF samples from three children; two samples were HBoV1 DNA-positive and one sample was negative. One death was recorded; CSF from this child was the only HBoV-IgM-positive CSF samples among the 67 CSF tested. Conclusion: We screened CSF samples obtained from children with encephalitis for the presence of HBoV1 and HBoV2 and specific IgM- or IgG-responses. Detection of viral DNA and/or immunological response to HBoV1/HBoV2 highlights the significance of these viruses as causes of encephalitis in children. Further studies are needed to examine the role of HBoV infection in children encephalitis. © 2013 Elsevier B.V.


Yi H.M.,Hunan Province Peoples Hospital
Zhonghua zhong liu za zhi [Chinese journal of oncology] | Year: 2010

To investigate the expression of LTF mRNA in several nasopharyngeal cancer (NPC) cell lines, and analyze the relationship between the genetic and epigenetic changes and expression of LTF gene. The expression level of LTF was detected in NPC cell lines HNE1, HNE2, HNE3, CNE1, CNE2, 5-8F, 6-10B cells and tissues of 15 cases of chronic nasopharyngitis by RT-PCR. The LTF protein level was analyzed by Western blotting in 6-10B cells. Then LOH, mutation and methylation status of LTF was examined by microsatellites analysis, PCR-SSCP, MSP and bisulfite genomic sequencing, respectively. 15 chronic nasopharyngitis tissues showed stable LTF expression, while there were weak expression in 6-10B cells and absent expression in remaining detected NPC cell lines. There was a significantly lower LTF expression in chronic nasopharyngitis tissues (Z = -3.738, P = 0.000). No LTF protein expression was observed in 6-10B cells. LOH analysis demonstrated that allele loss of LTF wasn't found in NPC cell lines. LTF mutation was noted in 14.3% (1/7) of NPC cell lines. DNA sequencing confirmed the mutation point in the promoter region (-305 bp to -50 bp) was at -218 bp (del T) of LTF gene in the HNE1 cell line. Methylation of LTF gene was not found in chronic nasopharyngitis. However, methylation of LTF promoter was detected in all NPC cell lines. LTF mRNA expression was increased in 5-8F and 6-10B cell lines after treatment with 5-aza-2-deoxycytidine. There is an inactivation of expression of LTF gene in the NPC cell lines. Its molecular mechanism may be related with methylation of promoter region and deletion mutation.


PubMed | Hunan Province Peoples Hospital
Type: Journal Article | Journal: Zhonghua zhong liu za zhi [Chinese journal of oncology] | Year: 2010

To investigate the expression of LTF mRNA in several nasopharyngeal cancer (NPC) cell lines, and analyze the relationship between the genetic and epigenetic changes and expression of LTF gene.The expression level of LTF was detected in NPC cell lines HNE1, HNE2, HNE3, CNE1, CNE2, 5-8F, 6-10B cells and tissues of 15 cases of chronic nasopharyngitis by RT-PCR. The LTF protein level was analyzed by Western blotting in 6-10B cells. Then LOH, mutation and methylation status of LTF was examined by microsatellites analysis, PCR-SSCP, MSP and bisulfite genomic sequencing, respectively.15 chronic nasopharyngitis tissues showed stable LTF expression, while there were weak expression in 6-10B cells and absent expression in remaining detected NPC cell lines. There was a significantly lower LTF expression in chronic nasopharyngitis tissues (Z = -3.738, P = 0.000). No LTF protein expression was observed in 6-10B cells. LOH analysis demonstrated that allele loss of LTF wasnt found in NPC cell lines. LTF mutation was noted in 14.3% (1/7) of NPC cell lines. DNA sequencing confirmed the mutation point in the promoter region (-305 bp to -50 bp) was at -218 bp (del T) of LTF gene in the HNE1 cell line. Methylation of LTF gene was not found in chronic nasopharyngitis. However, methylation of LTF promoter was detected in all NPC cell lines. LTF mRNA expression was increased in 5-8F and 6-10B cell lines after treatment with 5-aza-2-deoxycytidine.There is an inactivation of expression of LTF gene in the NPC cell lines. Its molecular mechanism may be related with methylation of promoter region and deletion mutation.

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