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1.
Adv Healthc Mater ; : e2402253, 2024 Sep 25.
Article in English | MEDLINE | ID: mdl-39319494

ABSTRACT

Drug-eluting bead transcatheter arterial chemoembolization (D-TACE) is one of the first-line treatment for intermediate hepatocellular carcinoma (HCC). However, the dual hypoxia microenvironment, due to inherent tumor hypoxia and TACE-induced hypoxia, triggers drug resistance in HCC. To address this challenge, the study develops multicavitary microspheres capable of encapsulating oxygen and harnessing magnetic hyperthermia to enhance oxygen permeability. The novel multicavitary oxygen-encapsulated magnetothermal drug-eluting microspheres (OTD-Ms) effectively reduce hypoxia-related proteins (HIF-1α, VEGF-A) and drug resistance (P-gp) both in vitro and in vivo. Moreover, these microspheres demonstrate improved TACE efficacy and enhance survival rates in a rabbit VX-2 tumor model, suggesting their potential for HCC treatment.

2.
J Mol Model ; 28(11): 360, 2022 Oct 13.
Article in English | MEDLINE | ID: mdl-36227347

ABSTRACT

The vibrational, mechanical, electronic, and optical properties of the ƎĀµ-O8 phase in the pressure range of 11.4-70 GPa were studied by the first-principle calculation method. The phonon dispersion curves have a tiny virtual frequency at 60 GPa, which indicates that ƎĀµ-O8 is dynamically unstable at 60 GPa. However, the 3-BM EOS demonstrates that the unit cell is stable up to 70 GPa. It has been shown that ƎĀµ-O8 remains ductile within the whole applied pressure range. Concurrently, we calculated the variation of the band gap of ƎĀµ-O8 in the pressure range of 11.4-70 GPa. The results show that the band gap of ƎĀµ-O8 decreases with increasing pressure. Notably, the band gap disappears within the range of 50-60 GPa, which reveals that the metallic phase transition occurs within this pressure range.

3.
Chin Med J (Engl) ; 120(18): 1626-31, 2007 Sep 20.
Article in English | MEDLINE | ID: mdl-17908484

ABSTRACT

BACKGROUND: Aberrant DNA methylation plays a key role in human carcinogenesis. 5-aza-2'-deoxycytidine inhibits DNA methylation and induces the expression of genes putatively silenced by promoter methylation in vitro. There are few studies of the biological and clinical significance of 5-aza-2'-deoxycytidine in human hepatocellular carcinoma. This study explored the mechanism of 5-aza-2'-deoxycytidine targeting transcriptional repressor complexes affecting global gene expression in hepatocellular carcinoma cell line. METHODS: High density oligonucleotide gene expression microarrays were used to examine the effects of 5-aza-2'-deoxycytidine treatments on human hepatocellular carcinoma cell line SMMC-7721. The 5' ends of the genes upregulated or downregulated in this manner were compared with BLAST database to determine whether they might have promoter CpG islands. Flow cytometry was used to detect stages of the cell cycle and apoptosis of SMMC-7721 after being treated with 5-aza-2'-deoxycytidine. RESULTS: Data obtained 3 days after 4 days of treatment with 5-aza-2'-deoxycytidine showed that more genes were induced in tumorigenic cells including genes that function in cell proliferation, differentiation, regulation of transcription, and cytokine signalling. Approximately 30% of induced genes did not have CpG islands within their 5' regions, suggesting that some genes activated by 5-aza-2'-deoxycytidine may not result from the direct inhibition of promoter methylation. This phenomenon may contribute to a number of upregulated genes involving regulation of transcription in the treated cell. Results showed that 100 micromol/L 5-aza-2'-deoxycytidine blocked cell cycle at S/G2-M phase increasing rate of apoptosis. Notably, we found differential expression of molecular action in the methylation although DNA methyltransferases did not show significant difference in the treated cell line. CONCLUSION: 5-aza-2'-deoxycytidine could restore some silenced genes expression independently of DNA methylation inhibition and expression of DNA methyltransferases.


Subject(s)
Antimetabolites, Antineoplastic/pharmacology , Apoptosis/drug effects , Azacitidine/analogs & derivatives , Carcinoma, Hepatocellular/drug therapy , Gene Expression Regulation, Neoplastic/drug effects , Liver Neoplasms/drug therapy , Azacitidine/pharmacology , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Cell Cycle/drug effects , Cell Line, Tumor , CpG Islands , DNA Modification Methylases/genetics , Decitabine , Humans , Liver Neoplasms/genetics , Liver Neoplasms/pathology , Transcriptional Activation
4.
J Infect Dev Ctries ; 10(8): 851-6, 2016 Aug 31.
Article in English | MEDLINE | ID: mdl-27580331

ABSTRACT

INTRODUCTION: Maternal 25-hydroxyvitamin D [25(OH)D] deficiency has a negative influence on the health of the mother and the developing fetus. The aim of this study was to assess serum 25(OH)D status and its relationship to virologic and biochemical parameters in pregnant women with chronic hepatitis B virus (HBV) infection. METHODOLOGY: Serum 25(OH)D levels among 142 pregnant women with chronic HBV infection and 251 healthy pregnant women were measured using enzyme-linked immunosorbent assay. RESULTS: The meanĀ±SD values for serum 25(OH)D levels were 13.63Ā±5.5 ng/mL in healthy pregnant women and 12.05Ā±3.3 ng/mL in pregnant women with chronic HBV infection (pĆ¢Ā€ĀŠ< 0.01). Serum 25(OH)D levels were associated with seasonal variation in healthy pregnant women (p = 0.01); however, similar results were not observed in pregnant women with chronic HBV infection (p = 0.10). Furthermore, multivariate analysis indicated that only ALT level was independently associated with severe vitamin D deficiency (p = 0.01). A significant positive correlation was found between serum 25(OH)D level and ALT level in pregnant women with chronic HBV infection (r = 0.32; p < 0.001). CONCLUSIONS: Vitamin D levels were lower in pregnant women with chronic HBV infection compared with healthy pregnant women. Vitamin D supplementation can be routinely recommended for pregnant women in China.


Subject(s)
Hepatitis B, Chronic/complications , Pregnancy Complications, Infectious/pathology , Serum/chemistry , Vitamin D Deficiency/epidemiology , Vitamin D/analogs & derivatives , Adult , Case-Control Studies , China/epidemiology , Enzyme-Linked Immunosorbent Assay , Female , Humans , Pregnancy , Vitamin D/blood , Young Adult
5.
World J Gastroenterol ; 11(23): 3628-31, 2005 Jun 21.
Article in English | MEDLINE | ID: mdl-15962390

ABSTRACT

AIM: To discuss the expression of human leukocyte antigen (HLA) class I antigens in gastric cancer and correlate these with pathologic type and TNM stage. METHODS: The expression of HLA class I antigen was detected by immunohistochemistry in 185 specimens of gastric cancer, 20 gastric cancer specimens with lymphatic metastasis and 22 controls of normal gastric mucosa using four monoclonal antibodies. RESULTS: The expression of HLA class I antigen (B/C locus) was significantly downregulated in gastric cancer and in lymphatic metastasis than that in normal gastric mucosa (chi2=7.712, P<0.05). The expression of other HLA class I antigens was also downregulated, but the change was slight. There was no relationship between the downregulation of HLA class I antigen and that of beta2m and LMP2. The expression of HLA class I (B/C locus) was statistically correlated with pathologic stage in gastric adenocarcinoma (chi2=4.164, P<0.05). CONCLUSION: The expression of HLA class I antigen (B/C locus) was obviously downregulated in gastric cancer and in lymphatic metastasis. This abnormal expression would provide the tumor cells with a way to avoid immunological recognition.


Subject(s)
Histocompatibility Antigens Class I/genetics , Stomach Neoplasms/genetics , Stomach Neoplasms/immunology , Adult , Aged , Aged, 80 and over , Female , Gastric Mucosa/cytology , Gastric Mucosa/immunology , Gene Expression Regulation, Neoplastic/immunology , HLA Antigens , Humans , Immunohistochemistry , Lymphatic Metastasis/immunology , Male , Middle Aged , Reference Values , Stomach Neoplasms/pathology
6.
Yi Chuan Xue Bao ; 32(11): 1115-27, 2005 Nov.
Article in English | MEDLINE | ID: mdl-16318277

ABSTRACT

Whether DNA methyltransferase 3B (DNMT3B) is deregulated in hepatocellular carcinoma cell lines is still unclear. The expression levels of DNMT3B protein in normal liver cell line, pericacinoma cell line and hepatocellular carcinoma cell lines were compared by both Western blotting and immunocytochemistry. Long-term downregulated DNMT3B in a hepatocellular carcinoma cell line SMMC-7721 was achieved using a RNAi recombinant plasmid. The suppression of DNMT3B induced by RNA interference was confirmed using semi-quantitative RT-PCR and Western blotting. High throughput cDNA microarray was used to analyze the expression profiling of downstream genes of DNMT3B displayed in the treated cell lines and control. In the result,DNMT3B in hepatocellular carcinoma cell lines was expressed at a significantly higher level compared to those in pericacinoma cell line and normal liver cell line. A specific DNMT3B siRNA stably expressed from a plasmid vector effectively suppressed the expression of DNMT3B in SMMC-7721 cell line. By microarray analysis,26 downregulated genes and 115 upregulated genes have been identified in the DNMT3B knockdown cell line,including some important developmental genes and tumor-related genes such as SNCG, NOTCH1, MBD3, WNT11, MAOA and FACL4. The discovery showed DNMT3B was over-expressed in most hepatocellular carcinoma cell lines examined and may be linked to the carcinogenesis of hepatocytes. An array of candidate genes that are involved in the action of DNMT3B have been identified,including those related to development.


Subject(s)
DNA (Cytosine-5-)-Methyltransferases/metabolism , Gene Expression Regulation, Neoplastic/drug effects , RNA Interference/physiology , RNA, Small Interfering/pharmacology , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , DNA (Cytosine-5-)-Methyltransferases/genetics , DNA Methylation , Gene Expression Regulation, Neoplastic/physiology , Humans , Microarray Analysis/methods , DNA Methyltransferase 3B
7.
Bing Du Xue Bao ; 30(2): 188-92, 2014 Mar.
Article in Zh | MEDLINE | ID: mdl-24923174

ABSTRACT

Japanese encephalitis virus (JEV) is a pathogenic mosquito-borne flavivirus which is responsible for outbreaks of severe viral encephalitis. The cellular entry of JEV is a prerequisite for Japanese encephalitis, so the understanding of its underlying mechanisms will provide more approaches for treating such disease. In recent years, increasing research has been conducted to investigate the mechanisms of cellular entry of JEV, and the results of research on other flavivirus have expanded the research directions for JEV. More methods will be used to suppress JEV infection because of the development of E protein antibodies and the discovery of several inhibitors of the cellular entry process. This review will summarize the recent advances in the mechanisms of JEV cellular entry and membrane fusion.


Subject(s)
Encephalitis Virus, Japanese/physiology , Encephalitis, Japanese/virology , Virus Internalization , Animals , Biomedical Research/trends , Encephalitis Virus, Japanese/genetics , Humans
8.
Biomed Mater Eng ; 24(1): 599-607, 2014.
Article in English | MEDLINE | ID: mdl-24211944

ABSTRACT

This paper aimed to investigate the preparation of doxorubicin-loaded bovine serum albumin nanoparticles (DOX/BSANP) and their effect on killing liver cancer cells in vitro and in vivo. DOX/BSANP was prepared using a desolvation-chemical crosslinking method. Their morphology and particle size were observed using transmission electron microscopy (TEM). The envelopment, drug-loading rates and slow-release characteristics were determined spectrophotometrically. Their ability to kill liver cancer cells in vitro was determined using the methyl thiazolyl tetrazolium (MTT) assay and flow cytometry (FCM). The tumor-suppressing effect of the nanoparticles in experimental animals in vivo was also evaluated. Under TEM, DOX/BSANP appeared spherical and was distributed uniformly, with a diameter of about 120 nm and hydrated particle size of 170 nm determined by dynamic light diffraction. The envelopment rate was 82% and the drug-loading rate was 11.2%. The in vitro drug-release experiment showed that about 50% of the drug in drug-loaded nanoparticles was released continuously and slowly for 7 days. The MTT assay showed that DOX/BSANP significantly inhibited cell proliferation, while FCM showed that it induced tumor cell apoptosis. The in vivo tumor suppression test showed that the therapeutic effect of drug-loaded nanoparticles was superior to that of DOX alone.


Subject(s)
Antineoplastic Agents/pharmacology , Doxorubicin/administration & dosage , Liver Neoplasms/drug therapy , Nanoparticles/chemistry , Serum Albumin, Bovine/chemistry , Albumins/chemistry , Animals , Antineoplastic Agents/chemistry , Apoptosis , Cattle , Cell Line, Tumor , Cross-Linking Reagents/chemistry , Disease Models, Animal , Drug Carriers/chemistry , Flow Cytometry , Humans , Hydrogen-Ion Concentration , Light , Linear Models , Mice , Mice, Inbred BALB C , Mice, Nude , Microscopy, Electron, Transmission , Neoplasm Transplantation , Particle Size , Spectrophotometry , Temperature , Time Factors
9.
J Gastroenterol Hepatol ; 22(7): 1155-61, 2007 Jul.
Article in English | MEDLINE | ID: mdl-17608862

ABSTRACT

BACKGROUND: Tumor cells may alter the expression of numerous components involved in antigen-processing machinery to decrease human leukocyte antigen (HLA) class I expression, allowing the tumor cells to escape immune surveillance. The purpose of the present study was to investigate the involvement of these components in the downregulation of HLA class I expression in human hepatocellular carcinoma cell line BEL7,404. METHODS: Expression of HLA-I and antigen presentation-related genes were analyzed by flow cytometry and polymerase chain reaction. The HLA class I-deficient BEL7,404 cell was transfected with the low-molecular-weight protein (LMP) 2 and LMP7 gene and were analyzed by flow cytometry for restoration of surface HLA class I expression. RESULTS: The BEL7,404 cells downregulated the expression of HLA class I antigen and lacked expression of LMP2 and LMP7. Interferon (IFN)-gamma treatment increased the expression of LMP2 but not LMP7. The LMP2-transfected BEL7,404 cells or LMP2 and LMP7-cotransfected cells restored surface HLA class I expression while LMP7-transfected cells did not. However, in IFN-gamma-treated BEL7,404 cells, transfection with the LMP7 gene induced more HLA class I expression than mock transfection. CONCLUSIONS: The LMP2 gene was required for the expression of HLA class I molecules in BEL7,404. The LMP7 was not the major reason for loss of HLA class I in BEL7,404 cells, although the supply of exogenous LMP7 could increase surface expression of HLA class I antigen.


Subject(s)
Carcinoma, Hepatocellular/immunology , Cysteine Endopeptidases/physiology , Down-Regulation , Histocompatibility Antigens Class I/physiology , Leukocytes/immunology , Liver Neoplasms/immunology , Multienzyme Complexes/physiology , Cell Line, Tumor , Humans , Proteasome Endopeptidase Complex
10.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 21(1): 60-3, 2005 Jan.
Article in Zh | MEDLINE | ID: mdl-15629086

ABSTRACT

AIM: To prepare monoclonal antibodies against aldose reductase-like(ARL-1)protein. METHODS: Purified ARL-1 protein (ARL-GST) was used to immunize BALB/c mice, and mAbs were prepared by hybridoma technique. The mAbs against ARL-1 were detected by ELISA, Western blot and immunohistochemical staining respectively. RESULTS: One clone of hybridoma secreting specific mAb against ARL-1 was obtained. The Ig subclass of mAb was of IgG2b and the titre of the antibody in ascites was 1:4.096 x 10(5). Highexpression of ARL-1 protein in liver cancer was detected. CONCLUSION: The specific mAb against ARL-1 lays the foundation for investigation of functions of ARL-1 protein and relationship between ARL-1 protein and liver cancer.


Subject(s)
Aldehyde Reductase/immunology , Antibodies, Monoclonal/immunology , Aldehyde Reductase/metabolism , Animals , Antibodies, Monoclonal/analysis , Enzyme-Linked Immunosorbent Assay , Gene Expression Regulation, Neoplastic , Hybridomas/immunology , Liver Neoplasms/genetics , Liver Neoplasms/immunology , Mice , Mice, Inbred BALB C
11.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 21(6): 738-42, 2005 Nov.
Article in Zh | MEDLINE | ID: mdl-16256039

ABSTRACT

AIM: To prepare monoclonal antibodies (mAbs) against aldose reductase (AR) and compare with anti-aldose reductase-like protein (ARL-1) mAb. METHODS: The AR gene was gained by RT-PCR and inserted into pGEX-4T-1 (His)(6)C. Recombinant protein GST-AR was used to immunize BALB/c mouse. MAb was prepared by hybridoma technique and detected by ELISA and Western blot. Simultaneously, according to the analysis of AR by software Clustalx and Antheprot, GST-dAR(80-142 aa), GST-dA1(1-79 aa), GST-dA2(80-99 aa), GST-dA3(111-142 aa) and GST-dA4(143-316 aa) were expressed in E. coli Rosetta. All the proteins were used to analyze the binding sites of the mAb and AR protein by Western blot. RESULTS: Three clones secreting anti-AR mAb were obtained. They were all of IgG1. And the titer of mAb in ascites was 1:400,000 while in cell culture was 1:10,000. All of the three anti-AR mAbs reacted to GST-AR and proteins of placenta tissues and had no cross-reaction to GST-ARL-1 and GST protein. And the three anti-AR mAb could recognize GST-dA1, GST-dA3 and GST-dA4, respectively. CONCLUSION: Three specific mAbs against AR are obtained and recognize the 1-79, 111-142, 143-316 amino acid sites of AR, respectively. The anti-AR mAb, together with the anti-ARL-1 mAb, may be a useful tool for further study of the function of AR and ARL-1 and the relationship between the two proteins and relevant diseases as well as for the epidemiological investigation.


Subject(s)
Aldehyde Reductase/immunology , Antibodies, Monoclonal/biosynthesis , Antibodies, Monoclonal/immunology , Animals , Antibody Specificity , Blotting, Western , Electrophoresis, Polyacrylamide Gel , Enzyme-Linked Immunosorbent Assay , Humans , Mice , Mice, Inbred BALB C , Reverse Transcriptase Polymerase Chain Reaction , Tumor Cells, Cultured
12.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 19(5): 473-5, 485, 2003 Sep.
Article in Zh | MEDLINE | ID: mdl-15169661

ABSTRACT

AIM: To construct HEV-specific phage combinatorial anti-body library and screen anti-HEV antibodies with neutralizing activity from the library. METHODS: The total RNA was extracted from B-lymphocytes of 6 HE patients. Kappa chain and Fd segment of IgG gene were amplified respectively by RT-PCR using a set of Fab-specific primers. The amplified gene were inserted successively into vector pComb3 and electrotransformed E. coli XLI-Blue cells. Furthermore, the recombinant phage was rescued by being concultured with helper phage VCSM13 to construct HEV-specific phage anti-body library. RESULTS: Fab displayed on the surface a as fusion protein with the N terminal of coat protein III, and 1. 8 x 10(7) clone library was established. Specific antibodies to HEV ORF2 recombinant antigen were acquired after five rounds of panning with HEV ORF2 recombinant antigen including neutralizing epitope. CONCLUSION: Four clones exhibited specific binding to HEV ORF2 recombinant antigen including neutralizing epitope is identified by ELISA. The results show that we have got the recombinant phage antibodies.


Subject(s)
Hepatitis Antibodies/genetics , Hepatitis E virus/immunology , Peptide Library , Viral Proteins/immunology , Humans , Immunoglobulin kappa-Chains/genetics , Polymerase Chain Reaction
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