No 302 Hospital Of Pla

Beijing, China

No 302 Hospital Of Pla

Beijing, China
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Li W.-G.,No 302 Hospital Of Pla | Nie W.-M.,No 302 Hospital Of Pla | Chen W.-W.,No 302 Hospital Of Pla | Jiang T.-J.,No 302 Hospital Of Pla | And 2 more authors.
Gene | Year: 2013

CXCR4-tropic (X4) variants are associated with faster disease progression than CCR5-tropic variants in HIV infection. We previously reported inhibition of CCR5 expression on U937 cells could protect the cells from HIV-1 infection. Here, we established recombinant adenoviruses containing anti-sense CXCR4 cDNA, to investigate its role in the protection of HIV entering into target cells. A fragment of 636. bp cDNA from CXCR4 mRNA was recombined into adenoviral vector and the recombinant adenovirus was obtained from AD-293 cells. The rates of CXCR4 expression on the MT4 cells infected with recombinant adenovirus were measured by FACS. The MT4 cells infected by recombinant adenovirus were challenged by T-tropic HIV-1 strains and then P24 antigen was assayed. The rate of expression of CXCR4 on MT4 cell infected with recombinant adenovirus was decreased from 42% to 1.12% at 24. h, and to 1.03%, 1.39%, and 1.23% at 48. h, 72. h and 10. days respectively. Compared with Ad-control cells, recombinant adenovirus infected MT4 cells produced much less P24 antigen after being challenged with HIV-1. Furthermore, the recombinant adenovirus had no effects on chemotactic activity and proliferation of the MT4 cells. In conclusion, recombinant adenoviruses containing anti-sense can inhibit CXCR4 expression and resist HIV-1 infection on MT4 cell lines. © 2013 Elsevier B.V.


PubMed | No 302 Hospital Of Pla, Mayo Medical School, Peking University, China Japan Friendship Hospital and No 306 Hospital Of Pla
Type: Journal Article | Journal: Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2015

To construct the prokaryotic expression vector of insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), express and purify IGF2BP3 protein in E.coli, and prepare the polyclonal antibody against IGF2BP3.The full open reading frame (ORF) of human IGF2BP3 was amplified by PCR, subcloned into pET-28a vector, and transformed into E.coli BL21(DE3), in which expression of the His-tagged IGF2BP3 protein was induced by IPTG. This protein was subsequently purified by Ni-NTA purification system, refolded by removal of urea from the solution. BALB/c mice were immunized with the purified IGF2BP3 protein to produce polyclonal antibody against IGF2BP3. The resulting anti-sera were further characterized by ELISA, Western blotting and immunohistochemistry.IGF2BP3 gene we amplified was consistent with the sequence reported by GenBank. Prokaryotic expression vector pET-28a-IGF2BP3 was constructed. His-tagged IGF2BP3 protein was successfully expressed in BL21 (DE3) with relative molecular mass (Mr) about 70 000 after IPTG induction. After purified by Ni-NTA resin, the purity of the protein reached above 90%. After immunization, the titer of the IGF2BP3 mouse anti-serum was over 1:50 000 as determined by ELISA. Further, Western blotting and immunohistochemistry showed that the IGF2BP3 antibody could specifically recognize the target protein.The polyclonal antibody specifically recognizing IGF2BP3 has been successfully generated.


Cao Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Chen Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Huang Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Liu Z.,No 302 Hospital Of Pla | Li G.,Weifang Medical University
Irish Journal of Medical Science | Year: 2016

Background: Aberrant promoter methylation of tumor suppressor gene can inhibit corresponding protein expression and promote carcinogenesis. Many studies have demonstrated that human mutL homolog 1(hMLH1) promoter methylation is correlated with occurrence and progression of multiple types of tumors. However, its correlation with esophageal carcinoma drug resistance is still unknown. Aims: To confirm methylation status of hMLH1 promoter in drug-resistance cell line of esophageal carcinoma, further confirm whether hMLH1 promoter methylation is responsible for drug resistance. Methods: Two stable esophageal carcinoma drug-resistance cell lines were successfully established by Cisplatin (DDP) concentration increment method; methylation status of hMLH1 promoter, mRNA and protein expression of hMLH1 were detected by methylation-specific PCR (MSP), RT-PCR and western blot, respectively; Drug-resistance ability assay was used to detect drug-resistance ability. Results: Stronger methylation status of hMLH1 promoter, lower hMLH1 mRNA and protein expression were found in both drug-resistance cell lines; after removing methylated bands using 5-aza-2′-deoxycytidine(5-Aza-CdR) in drug-resistance cell lines, hMLH1 mRNA and protein expression were restored and drug-resistance abilities declined nearly by half. Conclusion: hMLH1 promoter hypermethylation plays important roles in esophageal carcinoma drug-resistance and show us the prospect that combination of demethylation treatment with conventional chemotherapy drugs may bring better therapy effect. © 2016 Royal Academy of Medicine in Ireland


Yin X.,Affiliated Bayi Childrens Hospital | Meng F.,No 302 Hospital Of Pla | Qu W.,Affiliated Bayi Childrens Hospital | Fan H.,Affiliated Bayi Childrens Hospital | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2013

Surfactant protein B (SP-B) deficiency has become increasingly recognized as a cause of severe prolonged respiratory distress. However, little has been reported with regard to the genetic variability of SP-B in Chinese infants with neonatal respiratory distress syndrome (RDS). One case of a Chinese male infant with neonatal RDS was analyzed for clinical manifestation and genetic variability of SP-B. The clinical manifestations, including grunting, intercostal retractions, nasal flaring, cyanosis and tachypnea were discovered in the physical examination. The initial chest X-ray indicated hyperinflation, diffuse opacification and air bronchogram of the lungs. Pathological tests of lung tissue revealed RDS and SP-B deficiency. Atelectasis and pneumonedema were observed in the lobes of the lung. Molecular analysis of genomic DNA revealed a mutation of 121del2 in intron 4 of the SP-B gene. In conclusion, the variant in intron 4 of the SP-B gene was associated with neonatal RDS in a Chinese male infant.


Cui H.,Beijing Institute of Radiation Medicine | Wu F.,Beijing Institute of Radiation Medicine | Sun Y.,No 302 Hospital Of Pla | Fan G.,Beijing Institute of Radiation Medicine | Wang Q.,Beijing Institute of Radiation Medicine
BMC Cancer | Year: 2010

Background: Hepatocellular carcinoma (HCC) is one of the world's leading causes of death among cancer patients. It is important to find a new biomarker that diagnoses HCC and monitors its treatment. In our previous work, we screened a single-chain antibody (scFv) N14, which could specifically recognize human HepG2 HCC cells but not human non-cancerous liver LO2 cells. However, the antigen it recognized in the cells remained unknown.Methods: Recombinant scFv N14 antibody was expressed as an active antibody. Using this antibody with a combination of immunological and proteomic approaches, we identified the antigen of scFv N14 antibody as the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1). The expression of hnRNP A2/B1 in HCC cells was then investigated by semi-quantitative RT-PCR and immunohistochemistry.Results: We found that the up-regulation of hnRNP A2/B1 was measured at both transcriptional and translational levels in rat HCC cells but not in rat hepatic cells. We also found that in various human hepatic tissues, hnRNP A2/B1 was highly expressed in both human hepatitis virus positive liver tissues and human HCC tissues but not in normal liver tissues. Interestingly, we observed that the localization of hnRNP A2/B1 in HCC cells was altered during the development of HCC. In human hepatitis virus infected tissues hnRNP A2/B1 resides exclusively in the nuclei of hepatocytes. However, when the HCC progressed from a well differentiated to a poorly differentiated stage, hnRNP A2/B1 was increasingly localized in the cytoplasm. In contrast, the HCC tissues with hnRNP A2/B1 highly expressed in the nucleus decreased.Conclusions: This work is the first to show that hnRNP A2/B1 is the antigen specifically recognized by the scFv N14 antibody in HCC cells. The over-expression of hnRNP A2/B1 was confirmed in cultured human and rat HCC cell lines, human virus related hepatitis liver tissues and human HCC tissues. The increased localization of hnRNP A2/B1 in the cytoplasm of HCC cells was revealed during the dedifferentiation of hepatocellular carcinoma. Therefore, we suggest that the increased expression and cytoplasmic localization of hnRNP A2/B1 can be used as a diagnostic biomarker to assess the risk of human liver cancer. © 2010 Cui et al; licensee BioMed Central Ltd.


Wang S.Y.,No 302 Hospital Of Pla
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2011

This study attempted to investigate the features of Treg cells in peripheral blood and liver of patients with primary hepatocellular carcinoma (HCC). Peripheral blood samples were obtained from 30 HCC patients and 30 healthy control subjects, then were quantitatively analyzed for Treg cells by using flow cytometry. Liver infiltrating lymphocytes (LIL) isolated from resected tumor samples of 7 HCC patients were simultaneously analyzed. There was a significant increase in the frequency of peripheral Treg cells in HCC patients compared with healthy controls (P < 0.01). Furthermore, we also found that there was a higher frequency of infiltrated Treg within tumor samples than the counterpart in non-tumor region (P < 0.05). In addition, CD4(+) CD25(low) and CD4(+) CD25(-) T cells isolated from resected tumor samples were found to express higher level of FOXP3 molecules. Our findings showed that a dramatic increasing increase of Treg in peripheral blood and liver tissue of HCC patients may be associated with the significant increased development of Treg, which favors the disease progression through the suppressive effect of Treg on host immune response in these patients.


To evaluate the short-term prognostic values for the model of end-stage liver disease-sodium (MELD-Na), end-stage liver disease sodium (MELDNa) and their dynamic changes in patients with acute-on-chronic hepatitis B liver failure (ACLF-HBV). A total of 172 patients diagnosed with ACLF-HBV, admitted between January 2007 to February 2009 and hospitalized for over 2 weeks, were retrospectively recruited. The predictive accuracy of MELD-Na, MELDNa and their dynamic change (Δ) was compared by the method of the area under the receiver operating characteristic curve. The 3-month mortality rate was 43.6%. The largest concordance (c) statistic predicting 3-month mortality was MELDNa score after a 2-week treatment (0.790), followed by MELD-Na (0.728) score, ΔMELDNa (0.713) and ΔMELD-Na (0.646). The average MELD-Na, MELDNa scores after a 2-week treatment and ΔMELD-Na, ΔMELDNa of survival group were 27.7 ± 8.9, 25.9 ± 5.0, -2.1 ± 10.0 and -1.9 ± 4.2 while those of dead group 34.6 ± 8.7, 31.5 ± 5.0, 2.4 ± 10.3 and 2.4 ± 10.3. There was significant difference in MELD-Na, MELDNa, ΔMELD-Na and ΔMELDNa between two groups. The 3-month mortality of the MELD-Na scores group < 25, 25 - 30, 30 - 35 and > 35 were 18.9%, 37.8%, 57.6% and 65.3% while the MELDNa scores group 14.6%, 33.3%, 72.5% and 84.2% respectively. There was significant difference in the 3-month mortality between four groups. The 3-month mortality of the ΔMELD-Na > 0 group was 58.5% while that of the ΔMELD-Na ≤ 0 group 30%; the 3-month mortality of the ΔMELDNa > 0 group was 61.3% while that of the ΔMELDNa ≤ 0 group 29.9%. There was significant difference between two groups. MELDNa score after a 2-week treatment is a promising and useful predictor for 3-month mortality in ACLF-HBV patients. The predictive value may further improve if in conjunctions with dynamic changes.


To explore the etiology, diagnostic methods and procedures for patients with fever of unknown origin (FUO) at department of infectious diseases. A total of 368 FUO patients admitted to department of infectious diseases from 2002 to 2009 were retrospectively reviewed. The correlations of etiologies and diagnostic methods with gender, age and progress of fever were analyzed. Among them, 112 (30.4%) cases were recognized in 2 weeks (diagnosis, n = 107; recovery with unknown causes, n = 5). A final diagnosis was established in 241 (94.1%) from the remaining 256 FUO patients (124 males, 132 females). Among them, the causes were infectious diseases (n = 193), rheumatologic/autoimmune diseases (n = 32) and hematological diseases/tumors (n = 16). The etiologies were infectious diseases (n = 95), rheumatologic/autoimmune diseases (n = 10), hematological diseases/tumors (n = 10) and unknown etiology (n = 9) in males respectively; infectious diseases (n = 98), rheumatologic diseases (n = 22), hematological diseases or tumors (n = 6) and unknown etiology (n = 6) in females respectively. Age of patients: < 14 yr (n = 10), 15 - 20 yr (n = 37), 21 - 50 yr (n = 110), 51 - 60 yr (n = 48) and > 61 yr (n = 51). Thermal process was < 4 weeks (n = 83) including 74 infectious diseases cases and > 8 weeks (n = 63), including infectious diseases (n = 21) and rheumatologic disease (n = 20). Some FUO outpatients may be promptly confirmed by history taking, physical examination and routine examinations. The major cause is infection. Other causes of FUO are infectious diseases, rheumatological/autoimmune diseases and hematological diseases/tumors. For the diagnosis of FUO patients, gender, age and thermal process should be considered.


PubMed | No 302 Hospital Of Pla
Type: Journal Article | Journal: Gene | Year: 2013

CXCR4-tropic (X4) variants are associated with faster disease progression than CCR5-tropic variants in HIV infection. We previously reported inhibition of CCR5 expression on U937 cells could protect the cells from HIV-1 infection. Here, we established recombinant adenoviruses containing anti-sense CXCR4 cDNA, to investigate its role in the protection of HIV entering into target cells. A fragment of 636 bp cDNA from CXCR4 mRNA was recombined into adenoviral vector and the recombinant adenovirus was obtained from AD-293 cells. The rates of CXCR4 expression on the MT4 cells infected with recombinant adenovirus were measured by FACS. The MT4 cells infected by recombinant adenovirus were challenged by T-tropic HIV-1 strains and then P24 antigen was assayed. The rate of expression of CXCR4 on MT4 cell infected with recombinant adenovirus was decreased from 42% to 1.12% at 24 h, and to 1.03%, 1.39%, and 1.23% at 48 h, 72 h and 10 days respectively. Compared with Ad-control cells, recombinant adenovirus infected MT4 cells produced much less P24 antigen after being challenged with HIV-1. Furthermore, the recombinant adenovirus had no effects on chemotactic activity and proliferation of the MT4 cells. In conclusion, recombinant adenoviruses containing anti-sense can inhibit CXCR4 expression and resist HIV-1 infection on MT4 cell lines.


PubMed | No 302 Hospital Of Pla
Type: Comparative Study | Journal: Zhonghua yi xue za zhi | Year: 2011

To evaluate the short-term prognostic values for the model of end-stage liver disease-sodium (MELD-Na), end-stage liver disease sodium (MELDNa) and their dynamic changes in patients with acute-on-chronic hepatitis B liver failure (ACLF-HBV).A total of 172 patients diagnosed with ACLF-HBV, admitted between January 2007 to February 2009 and hospitalized for over 2 weeks, were retrospectively recruited. The predictive accuracy of MELD-Na, MELDNa and their dynamic change () was compared by the method of the area under the receiver operating characteristic curve.The 3-month mortality rate was 43.6%. The largest concordance (c) statistic predicting 3-month mortality was MELDNa score after a 2-week treatment (0.790), followed by MELD-Na (0.728) score, MELDNa (0.713) and MELD-Na (0.646). The average MELD-Na, MELDNa scores after a 2-week treatment and MELD-Na, MELDNa of survival group were 27.7 8.9, 25.9 5.0, -2.1 10.0 and -1.9 4.2 while those of dead group 34.6 8.7, 31.5 5.0, 2.4 10.3 and 2.4 10.3. There was significant difference in MELD-Na, MELDNa, MELD-Na and MELDNa between two groups. The 3-month mortality of the MELD-Na scores group < 25, 25 - 30, 30 - 35 and > 35 were 18.9%, 37.8%, 57.6% and 65.3% while the MELDNa scores group 14.6%, 33.3%, 72.5% and 84.2% respectively. There was significant difference in the 3-month mortality between four groups. The 3-month mortality of the MELD-Na > 0 group was 58.5% while that of the MELD-Na 0 group 30%; the 3-month mortality of the MELDNa > 0 group was 61.3% while that of the MELDNa 0 group 29.9%. There was significant difference between two groups.MELDNa score after a 2-week treatment is a promising and useful predictor for 3-month mortality in ACLF-HBV patients. The predictive value may further improve if in conjunctions with dynamic changes.

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