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Ping Qu

Publications and source records attributed to Ping Qu.

At least 19 recordsLinked to original sources

Tumor cells with B7.1 and transmembrane anchored staphylococcal enterotoxin A generate effective antitumor immunity.

Staphylococcus enterotoxin A (SEA) stimulates T cells bearing certain TCR beta-chain variable regions, when bound to MHC-II molecules, and is a potent inducer of CTL activity and cytokines production. To decrease toxicity of SEA to the normal MHC-II(+) cells and to localize the immune response induced by SEA to the tumor site, my colleague previously genetically fused SEA with B7.1 transmembrane region (named as SEAtm) to make SEA express on the surface of tumor cells and tumor cells modified with SEAtm could induce efficient antitumor immunity in vitro. The tumor cell vaccines modified with multiple immune activators frequently elicited stronger antitumor immune responses than single-modified vaccines. In this study, we modified the tumor cell vaccine with B7.1 and SEAtm to improve efficiency in the application of SEA. First, SEAtm gene was subcloned from recombinant plasmid pLXSNSEP by PCR and murine B7.1 gene was cloned from splenocytes derived from C57BL/6 mice by RT-PCR. Then, the eukaryotic co-expression vector of SEA and murine B7.1 gene was constructed and named as pcDNA-BIS. B16 cell lines stably expressing SEA and/or B7.1 were established by screening with G418 after transfection and inactivated for the preparation of tumor cell vaccines to treat mice bearing established B16 tumors. The results indicated that the dual-modified tumor cell vaccine B16/B7.1+SEAtm (B16-BIS) elicited significantly stronger antitumor immune responses in vivo when compared with the single-modified tumor cell vaccines B16/B7.1 (B16-B7.1) and B16/SEAtm (B16-SEAtm), and supported the feasibility and effectiveness of the dual-modified tumor cell vaccine with superantigen and co-stimulatory molecule.

Animals↗

[Effects of early intervention on learning and memory in young rats of marginal vitamin A deficiency and it's mechanism].

OBJECTIVE: In recent years, some experiments on vitamin A-deprived animals reveal a progressive and ultimately profound impairment of hippocampal CA1 area's long-term potentiation and these losses are fully reversible by dietary vitamin A replenishment in vivo. Our previous study revealed that marginal vitamin A deficiency (MVAD) beginning from embryonic period impairs learning, memory and long-term potentiation (LTP) in young rats. But the losses might not be reversible if the vitamin A supplementation is late, especially when the critical period of hippocampus development is missed. The present study aimed to observe the recovery of learning and memory in vitamin A marginally deficient young rats after early intervention with vitamin A supplementation and begin to study the mechanism. METHODS: Rats were divided into control, MVAD, vitamin A intervention 1 (VAI1) and VAI2 groups in this study. In control group (10 young rats) the dams and pups were fed with normal diet (VA 6500 U/kg). In MVAD group (19 young rats) the dams and pups were fed with MVAD diet (VA 400 U/kg). In VAI1 group (10 young rats) the dams were fed with MVAD diet till day 14 of pregnancy, then were fed with normal diet and the pups were fed with normal diet. In VAI2 group (13 young rats) the dams were fed with MVAD diet till delivery, then were fed with normal diet and the pups were fed with normal diet too. All the young rats were killed at the age of 7 weeks. During the last week of the experiment, the shuttle box active avoidance reaction tests were carried out. At week 7, the hippocampal CA1 LTP was detected by electrophysiological technique. The expression of RAR-alpha, RAR-beta, RXR-beta, RXR-gamma, RC3 and tTG mRNA was detected by using semi-quantified RT-PCR in hippocampus. RESULTS: (1) The times to reach the learning standard in MVAD group (45.6 +/- 12.1) were more than those in control group (17.1 +/- 4.4) (P < 0.01), in both VAI1 group (20.8 +/- 3.1) and VAI2 group (22.1 +/- 4.0) were more than those in group MVAD (P < 0.01), and there were no significant differences among groups VAI1, VAI2 and control (P > 0.05) in active avoidance reaction tests. (2) The changes of field excitatory postsynaptic potentials (fEPSP) slope for MVAD group [(22.9 +/- 9.4)%] and VAI2 group [(39.1 +/- 4.33)%] were less than that of control group [(57.5 +/- 27.3)%], respectively (P < 0.05). No significant difference was found between VAI1 and control group (P > 0.05). (3) The expression of RAR-beta and RXR-beta mRNA decreased by 48.72% and 37.84% respectively (P < 0.05) compared with control, but the expression of RAR-beta mRNA in group VAI1 was higher than that in group MVAD (P = 0.065). The expression of RC3 mRNA in MVAD group was lower than that in control (P = 0.061) and RAR-alpha mRNA in MVAD group was higher than that in control (P = 0.061). The expression of RXR-gamma and tTG mRNA had no significant difference among different groups as determined with semi-quantified RT-PCR in hippocampus. CONCLUSION: Early vitamin A intervention may make the impaired learning and memory behavior due to marginal vitamin A deficiency recover to the normal level in young rats, but lip losses in group VAI2 might not be reversible. Vitamin A may modulate the expression of RC3 mRNA by affecting RAR-alpha, RAR-beta and RXR-beta to influence the LTP, learning and memory.

Animal Nutritional Physiological Phenomena↗

[Synthesis and spectral studies of functionalized L-Cys-CdS nanoparticles as fluorescence probes].

In this work, nano-CdS was successfully prepared. The nano-CdS was also modified with L-cysteine. Absorption and fluorescence spectra of CdS nanoparticles for different pH values, reaction times and different Cys/Cd2+/S ratios were investigated. Meanwhile a fluorescence enhancing effect was observed between trace zinc ions and the functionalized L-Cys-CdS nanoparticles. The response is linearly proportional to the concentration of zinc ions from 1.0 to 15 micromol x L(-1). The functionalized nanoparticles are hopeful of use as fluorescence probes in detecting trace elements in biological samples.

Cadmium Compounds↗

Heat shock protein 70/MAGE-3 fusion protein vaccine can enhance cellular and humoral immune responses to MAGE-3 in vivo.

MAGE-3, a member of melanoma antigen (MAGE) gene family, is recognized as an ideal candidate for tumor vaccine because it is expressed in a significant proportion of tumors of various histological types and can induce antigen-specific immune response in vivo. There is now substantial evidence that heat shock proteins HSPs isolated from cancer cells and virus-infected cells can be used as vaccines to produce cancer-specific or virus-specific immunity. In this research, we investigated whether M. tuberculosis HSP70 can be used as vehicle to elicit immune response to its accompanying MAGE-3 protein. A recombinant protein expression vector was constructed that permitted the production of fusion protein linking amino acids 195-314 of MAGE-3 to the C terminus of HSP70. We found that HSP70-MAGE-3 fusion protein can elicit stronger cellular and humoral immune responses against MAGE-3 expressing murine tumor than those elicited by MAGE-3 protein in vivo, which resulted in potent antitumor immunity against MAGE-3-expressing tumors. Covalent linkage of HSP70 to MAGE-3 was necessary to elicit immune response to MAGE-3. These results indicate that linkage of HSP70 to MAGE-3 enhanced immune responses to MAGE-3 in vivo and HSP70 can be exploited to enhance the cellular and humoral immune responses against any attached tumor-specific antigens.

Animals↗

[Expression of retinoic acid receptor-beta mRNA and p16, p53, Ki67 proteins in esophageal carcinoma and its precursor lesions].

OBJECTIVE: To study the expression of retinoic acid receptor-beta (RAR-beta) mRNA and p16, p53, Ki67 proteins in squamous-cell carcinoma of the esophagus and its precursor lesions in a high risk population. METHODS: A total of 397 tissue specimens were collected from individuals with normal mucosa (NM, n = 25), mild dysplasia (MiD, n = 69), moderate dysplasia (MoD, n = 106), severe dysplasia (SD, n = 51), carcinoma in situ (CIS, n = 78), and squamous-cell carcinoma (SC, n = 68). Expression of RAR-beta mRNA was detected by in situ hybridization, and that of p16, p53 and Ki67 proteins by immunohistochemistry. RESULTS: The frequencies of RAR-beta mRNA expression in NM, MiD, MoD, SD, CIS and SC were 96.0%, 89.9%, 67.9%, 68.6%, 62.8%, and 63.2%, respectively. The frequencies of p16 expression were 88.0%, 71.0%, 64.2%, 51.0%, 53.8% and 52.9%; those of p53 expression were 4.0%, 39.1%, 57.5%, 52.9%, 67.9% and 69.1%; those of Ki67 expression were 0, 40.6%, 61.3%, 58.8%, 59.0% and 75.0%, respectively. CONCLUSION: There are no significant differences in four biomarkers expression between carcinoma of the esophagus and its precursor lesions.

Biomarkers, Tumor↗

[Study on the differentiation of marrow stromal stem cells into neural cells in vitro].

OBJECTIVE: To investigate the neural markers' expression in the differentiation of marrow stromal stem cells (MSCs) into neural cells. METHODS: Rats MSCs were expanded as undifferentiated cells in vitro for 5 to 7 generations and cultured in a modified neuronal medium (MNM) after 24 hours of all-trans retinoid acid (ATRA) pretreatment. Immunocytochemistry was used to detect the expression of nestin, neuron-specific nuclear protein (NeuN), microtubule-associated protein 2 (MAP-2) and glial fibrillary acidic protein (GFAP) at different time points. RESULTS: After ATRA and MNM treatment, MSCs progressively assumed neuronal morphological characteristics. Nestin occurred first after 24 hours of ATRA treatment; then NeuN expressed after 2 hours of MNM treatment; the last one was MAP-2 and it was detected after 9 hours of MNM treatment. Other markers continuously expressed except that the expression of nestin peaked after 18 hours of MNM induction and remarkably decreased after 36 hours. CONCLUSION: ATRA and MNM could promote the differentiation of MSCs into neural cells and the expression of neural-specific markers was consistent with current knowledge regarding the time points of markers expression in the neuronal development which provides a good model in vitro for neuronal development research.

Animals↗

[Effects of marginal vitamin A deficiency and intervention on learning and memory in young rats].

OBJECTIVE: Previous studies have demonstrated that vitamin A and its active derivatives function as essential competence factors for long-term synaptic plasticity within the adult brain. But little is known if marginal vitamin A deficiency (MVAD) beginning from embryonic period affects the brain development and the ability of learning and memory in young rats. The aim of this study was to identify the effects of MVAD and vitamin A intervention (VAI) on learning, memory and the hippocampal CA1 long-term potentiation (LTP) in young rats. METHODS: Rats were divided into control, MVAD and VAI groups in this study. In control group (10 young rats) the dams and pups were fed with normal diet (VA 6500 IU/kg). In MVAD group (19 young rats) the dams and pups were fed with MVAD diet (VA 400 IU/kg). In VAI group (9 young rats) the dams were fed with MVAD diet and the pups were fed with normal diet from postnatal week 4. All the young rats were killed at the age of 7 weeks. During the last week of the experiment, the shuttle box active avoidance reaction tests were carried out. At week 7, the hippocampal CA1 LTP was detected by electrophysiological technique and relative intensity of fluorescence in cells in hippocampal slices was measured by confocal laser scanning microscopy labeled by fluo-3. RESULTS: (1) The times to reach the learning standard in both VAI group (28.8 +/- 4.1) and MVAD group (45.6 +/- 12.1) were more than control group (17.1 +/- 4.4) (P < 0.01), and that of MVAD group was more than VAI group (P < 0.05) in active avoidance reaction tests. (2) The changes of field excitatory postsynaptic potentials (fEPSP) slope for MVAD group (22.9% +/- 9.4%) and VAI group (29.5% +/- 13.7%) were less than that of control group (57.5% +/- 27.3%), respectively (P < 0.01). No significant difference was found between VAI and MVAD groups (P > 0.05). (3) No significant differences of relative intensity of fluorescence in cells were found among the three groups before the tetanus stimulation. However, the significantly low relative intensity of fluorescence in cells was seen in MVAD (65.1 +/- 17.0) and VAI (85.8 +/- 17.1) groups compared with control group (113.6 +/- 20.5) after the tetanus stimulation (P < 0.01), and that of VAI group was higher than that of MVAD group (P < 0.05). CONCLUSION: MVAD beginning from embryonic period impairs learning, memory and LTP in young rats. But the losses might not be reversible if the vitamin A supplementation is late especially missing the critical period of hippocampus development. According to the experimental data, it is speculated that vitamin A may modulate the influx of calcium ion to influence the LTP and lead to the change of learning and memory.

Animals↗

[Effect of RNAi-mediated gene silencing of C-erbB-2 on proliferation of lung adenocarcinoma cell line calu-3].

BACKGROUND & OBJECTIVE: C-erbB-2 gene is amplified or overexpressed in breast cancer, ovarian cancer, and lung cancer, and is related with enhanced malignancy and metastatic ability, intrinsic chemoresistance, and poor prognosis of tumors. RNA interfering (RNAi), a new genetic technique, can efficiently and specifically suppress gene expression. This study was to investigate the effect of small interfering RNA (siRNA)-mediated gene silencing of C-erbB-2 on proliferation of human lung adenocarcinoma cell line calu-3. METHODS: C-erbB-2 siRNA was transfected into calu-3 cells; cell morphology was observed under light microscope. The mRNA and protein levels of C-erbB-2 were detected by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry (FCM). The proliferation of calu-3 cells was assessed by MTT assay. Cell cycle and apoptosis were analyzed by FCM. RESULTS: C-erbB-2 siRNA down-regulated the mRNA and protein levels of C-erbB-2 in calu-3 cells; 48 h after transfection of C-erbB-2 siRNA, the protein level of C-erbB-2 was markedly decreased. The positive rate of C-erbB-2 was significantly lower in C-erbB-2 siRNA group than in untransfected group, empty vector group, and nonspecific siRNA group [(25.04+/-1.56)% vs. (98.24+/-2.23)%, (95.67+/-1.98)%, and (94.79+/-0.87)%, P < 0.01]. C-erbB-2 siRNA inhibited proliferation of calu-3 cells: G(0)/G(1) phase proportion of C-erbB-2 siRNA group was significantly higher than that of untransfected group [(56.6+/-3.6)% vs. (45.5+/-3.2)%, P < 0.01]. C-erbB-2 siRNA also enhanced cell apoptosis. CONCLUSION: Specific siRNA targeting C-erbB-2 can effectively inhibit C-erbB-2 expression and proliferation of calu-3 cells.

Adenocarcinoma↗

Identification of HLA-A2-restricted CTL epitope encoded by the MAGE-n gene of human hepatocellular carcinoma.

BACKGROUND: Identification of the cytotoxic T lymphocytes (CTL) restricted epitopes of tumor antigens opens up possibilities of developing a new cancer vaccine. For the MAGE-n has been demonstrated closely associated with hepatocellular carcinoma (HCC) and HLA-A2.1 is found in over 50% of HCC patients in China, we aim at identifying MAGE-n-encoded peptide presented by HLA-A2.1. MATERIALS: A HLA-A2.1-restricted CTL epitope was identified by using an improved "reverse immunology" strategy: (a) computer-based epitope prediction from the amino acid sequence of MAGE-n antigen; (b) peptide-binding assay to determine the affinity of the predicted peptide with HLA-A2.1 molecule; (c) stimulation of primary T-cell response against the predicted peptides in vitro; and (d) testing of the induced CTLs toward HCC cells expressing MAGE-n antigen and HLA-A2.1. RESULTS: Of the five tested peptides, effectors induced by a peptide of MAGE-n at residue position 159-167(QLVFGIEVV) lysed HCC cells expressing both MAGE-n and HLA-A2.1. Our results indicated that peptide QLVFGIEVV was a new HLA-A2.1-restricted CTL epitope capable of inducing MAGE-n specific CTLs in vitro. CONCLUSIONS: Identification of the MAGE-n /HLA-A2.1 peptide QLVFGIEVV may facilitate peptide-based specific immunotherapy for HCC. The combination of epitope prediction, epitope reconstruction method and immunological methods can improve the efficiency and accuracy of CTL epitope studies.

Amino Acid Sequence↗

Efficient induction of cytotoxic T lymphocytes specific to hepatocellular carcinoma using HLA-A2-restricted MAGE-n peptide in vitro.

MAGE-n is a new member of MAGE gene family and has been demonstrated closely associated with hepatocellular carcinoma (HCC). In this study, MAGE-n-derived peptide-specific cytotoxic T lymphocytes (CTL) were induced from the peripheral blood mononuclear cells of healthy donors by multiple stimulations with HLA-A2-restricted MAGE-n peptide-pulsed T2 cells. The induced CTLs exhibited specific lysis against T2 cells pulsed with the peptide and HLA-A2+ HCC cells expressing MAGE-n, while HLA-A2+ HCC cell lines that did not express MAGE-n could not be recognized by the CTLs. The peptide-specific activity was inhibited by anti-MHC class I monoclonal antibody. These results suggested the MAGE-n peptide could be a potential target of specific immunotherapy for HLA-A2 patients with HCC.

Antibodies, Monoclonal↗

In vivo tumor co-transfection with superantigen and CD80 induces systemic immunity without tolerance and prolongs survival in mice with hepatocellular carcinoma.

BACKGROUND: Since transfection of established tumors with immunostimulatory genes can elicit antitumor immunity, we treat mouse HCC with in vivo transfection of superantigen SEA and/or costimulatory molecule CD80 and evaluated the safety and efficacy. METHODS: Mice with HCC were treated with lipid-complexed plasmid DNA encoding staphylococcal enterotoxin A and/or CD80. Then the mice were evaluated for tumor regression, systemic immunologic responses, survival times and treatment-associated toxicity. RESULTS: Of all treated mice, the overall response rates (complete or partial remission) for SEA, CD80 and SEA/CD80 treated mice in this study were 65%, 60% and 75% separately, and were significantly higher than that of untreated mice. Most of the treat mice completed the therapy without any significant reaction. CTL activity increased with time of treatment and correlated temporally with an objective tumor response. Also our results indicated that local intratumoral expression of SEA did not lead to detectable deletion or anergy of SEA-reactive spleen T cells. Survival times for hepatoma mice in this study treated by intratumoral injection of SEA, CD80 and SEA/CD80 were prolonged significantly (P < 0.01) compared with the control mice.

Animals↗

Heat shock protein 70 / MAGE-1 tumor vaccine can enhance the potency of MAGE-1-specific cellular immune responses in vivo.

The cancer-testis antigen encoded by the MAGE-1 gene is an attractive antigen in tumor immunotherapy because it can be processed as a foreign antigen by the immune system and generate tumor-specific cellular immune response in vivo. However, increase of the potency of MAGE-1 DNA vaccines is still needed. The high degree of sequence homology and intrinsic immunogenicity of heat shock protein 70 (HSP70) have prompted the suggestion that HSP70 might have immunotherapeutic potential, as HSP70 purified from malignant and virally infected cells can transfer and deliver antigenic peptides to antigen-presenting cells to elicit peptide-specific immunity. In this research, we evaluated the enhancement of linkage of Mycobacterium tuberculosis HSP70 to MAGE-1 gene of the potency of antigen-specific immunity elicited by naked DNA vaccines. We found that vaccines containing MAGE-1-HSP70 fusion genes enhanced the frequency of MAGE-1-specific cytotoxic T cells in contract to vaccines containing the MAGE-1 gene alone. More importantly, the fusion converted a less effective DNA vaccine into one with significant potency against established MAGE-1-expressing tumors. These results indicate that linkage of HSP70 to MAGE-1 gene may greatly enhance the potency of DNA vaccines, and generate specific antitumor immunity against MAGE-1-expressing tumors.

Animals↗

Superantigen-SEA gene modified tumor vaccine for hepatocellular carcinoma: an in vitro study.

AIM: To construct an eukaryotic superantigen gene expression vector containing the recombinant gene of SEA and CD80 molecule transmembrane region (CD80TM), and to express staphylococcus enterotoxin A (SEA) on the membrane of hepatocellular carcinoma (HCC) cell to form a superantigen gene modified tumor vaccine for HCC. METHODS: SEA and linker-CD80TM gene were amplified through PCR from plasmid containing cDNA of SEA and CD80. Gene fragments were then subcloned into the multiple cloning sites of retroviral vector pLXSN. Recombinant plasmid was transferred into HepG2 cells mediated with lipofectamine, positive clones were selected in culture medium containing G418. RT-PCR and indirect immunofluorescence studies confirmed that SEA was expressed specifically on HCC cell membrane. INFgamma-ELISPOT study demonstrated that SEA protein was expressed on the membrane of HCC cells. Cytotoxicity of HepG2-SEA primed CTLs (SEA-T) was analyzed by (51)Cr release assay. T cells cultured with rhIL-2 (IL-2-T) were used as control. RESULTS: Restriction digestion and sequence analyses confirmed the correctness of length, position and orientation of inserted fusion genes. SEA was expressed on the surface of HepG2 cells, HepG2-SEA had strong stimulating effect on production of HepG2 specific CTL (P<0.001). SEA-T had enhanced cytotoxicity to HepG2 cells (P<0.05). CONCLUSION: Tumor cell membrane expressed superantigen can be used to reinforce the immune effect of tumor cell vaccine for HCC, which provides a new method of the enhanced active immunotherapy for HCC.

B7-1 Antigen↗

Telomerase activity in cervical intraepithelial neoplasia.

BACKGROUND: It was reported that telomerase expression is closely associated with cellular immortality and cancer. This study was designed to investigate the relationship between telomerase expression and the carcinogenesis of cervical cancer, the possible use of telomerase as a marker of cervical intraepithelial neoplasia (CIN) progression or regression, and the natural history of CIN. METHODS: Telomeric repeat amplification protocol (TRAP) assay was used to measure telomerase activity in cervical scrapings and biopsy samples obtained from 105 cases affected with various cervical conditions, including chronic cervicitis (n = 20), CIN (n = 64, 16 cases of CIN I, 20 cases of CIN II, and 28 cases of CIN III), and invasive squamous cell carcinoma (n = 21). RESULTS: In exfoliated cell samples, telomerase activity was detected in 5 of 20 (25.0%) cases of cervicitis, 10 of 16 (62.5%) cases of CIN I, 11 of 20 (55.0%) cases of CIN II, 23 of 28 (82.1%) cases of CIN III, and 13 of 21 (61.9%) cases of carcinoma. In cervical biopsy samples, telomerase activity was detected in 6 of 20 (30.0%) cases of cervicitis, 8 of 16 (50.0%) cases of CIN I, 9 of 20 (45.0%) cases of CIN II, 27 of 28 (96.4%) cases of CIN III, and 20 of 21 (95.2%) cases of carcinoma. Telomerase activation was significantly higher in CIN samples than in cervicitis samples. Telomerase activity was detected at similar frequency in samples from cervical scrapings and cervical biopsies. CONCLUSION: These results seem to suggest that telomerase expression may be associated with carcinogenesis of the cervix. TRAP assay of cervical scraping samples could be used to monitor and predict the development of CIN in clinical practice.

Adult↗

[Tumor suppression of a constitutively active caspase-3 in the SKBr-3 breast carcinoma xenograft mice model].

AIM: To explore the apoptosis-inducing effect of a constitutively active caspase-3 molecule on human breast carcinoma SKBr-3 cells. METHODS: A revcaspase-3 gene was generated by arranging the coding sequence of the small subunit preceding that of the large one, i.e. in a reverse order of the wild-type caspase-3 gene. A pcDNA3-revcaspase-3 plasmid was constructed and transfected into SKBr-3 cells, and the proapoptotic effect of revcaspase-3 was examined by morphological observation of the cells, cell counting and flow cytometry analysis. The in-vivo tumor suppression was further evaluated following i.t. administration of pcDNA-revcaspase-3, while the apoptosis in tumor tissues was assayed using TUNEL. RESULTS: The apoptosis of SKBr-3 cells was induced after introduction of the revcaspase-3 gene, and tumor growth was strongly suppressed following injection of the pcDNA3 vector harboring revcaspase-3 gene. Revcaspase-3 was expressed in the cells of tumor tissues and apoptosis of the tumor cells was confirmed by TUNEL assays. CONCLUSION: Apoptosis of SKBr-3 cells in a mouse tumor model could be induced by in-vivo expression of a revcaspase-3 gene.

Animals↗

[Decreased peripheral nerve conduction velocity may be associated with lower-serum level of vitamin E in patients with infantile hepatitis syndrome].

OBJECTIVE: To explore the influence of vitamin E (VitE) concentration in serum on peripheral nerve conduction in patients with infantile hepatitis syndrome (IHS). METHODS: A retrospective study was carried out in 58 infants suffered from IHS without congenital biliary atresia and 31 of them were followed up. Thirty-two healthy infants were as control. The level of VitE in serum was detected with high performance liquid chromatography and nerve conduction was tested with surface electrodes along the nerves of limbs. The relationship between the level of VitE or total bilirubin (TB) or direct bilirubin (DB) and the nerve conduction velocity was analyzed comparatively. RESULTS: (1) The serum level of VitE was below the lower limit of 90% the normal value (13.78 micromol/L) in 71% (41/58) of patients, and was below the lower limit of 99% the normal level (9.17 micromol/L) in 48% (28/58) of patients. (2) The level of DB was more than 25.7 micromol/L in 86% (50/58) of the patients and was more than 102.6 micromol/L in 47% (27/58) of patients. Severe conjugated hyperbilirubinemia with cholestasis was demonstrated in most patients. (3) At least one abnormal parameter in nerve conduction test was found in 86% (50/58) patients. In 144 nerves tested, 60.4% (87/144) had at least one abnormal parameter. (4) Analysis for the association between bilirubin levels and VitE concentration in serum: in groups of DB > or = 25.7 micromol/L and DB < 25.7 micromol/L, the percentage of decreased VitE concentrations was 78% (39/50) and 25% (2/8), respectively, and the difference was significant (P < 0.01). Similar association between low VitE concentration and increased level of TB in serum could not be demonstrated. (5) Analysis for the association between abnormal nerve conduction and VitE concentration in serum: in the two groups with low and normal level of VitE, the percentage of abnormal nerve conduction was 93% (38/41) and 71% (12/17), respectively (chi(c)(2) = 4.93, P < 0.05). (6) Analysis for the association between abnormal nerve conduction and bilirubin in serum: There was no significant association between abnormal nerve conduction and serum level of either DB or TB. (7) Eight patients died and 9 patients had motor development delay in 31 patients during follow up. In these 17 patients with poor outcome, 88% (15/17) had very low VitE levels (< 9.17 micromol/L), which was markedly higher than the proportion of cases (43%, 6/14) with better prognosis (chi(c)(2) = 7.235, P < 0.01). CONCLUSIONS: (1) Low VitE serum levels were found in excess of the two thirds of patients with IHS and severely decreased levels in nearly a half of them. (2) A conjugated hyperbilirubinemia with cholestasis could be found in most patients (86%) suffered from IHS without congenital biliary atresia and about a half of them had serious cholestasis. (3) Conjugated hyperbilirubinemia with cholestasis could be the predominant cause of decreased serum VitE level in this study. (4) Abnormality of nerve conduction in patients with IHS might be related to VitE deficiency.

Bilirubin↗

[Expression of a plant associated human cancer antigen in breast cancer].

OBJECTIVE: To study the expression of a glycoprotein of plant origin in normal, benign and malignant breast tissues. METHODS: Expression of a plant glycoprotein was examined in 5 samples of normal breast tissues, 20 fibro-adenoma and 136 breast cancer by SABC immunohistochemical staining and the results were analyzed by SPSS statistics software. RESULTS: No positive staining was detected in normal breast tissues (0/5). Weak staining was observed in 4 of 20 (20.0%) breast fibro-adenoma. Positive staining was demonstrated in 116 out of 136 (85.3%) breast cancer specimens. The differences were statistically significant. The expression of plant-associated human cancer antigen was related to pathological grade (P < 0.05), tissue invasiveness (P < 0.01) and recurrence (P < 0.05), but not to patients' age, tumor size and c-erbB-2 expression. CONCLUSION: The plant glycoprotein studied may be a human cancer-associated antigen which might be a potential marker of breast cancer.

Adenocarcinoma, Mucinous↗

[Prediction synthesis and identification of HLA-A2-restricted cytotoxic T lymphocyte epitopes of the tumor antigen MAGE-n].

OBJECTIVE: To predict, synthesize, and identify HLA-A2-restricted cytotoxic T lymphocyte (CTL) epitopes of the tumor the novel antigen MAGE-n. METHODS: Long-distance prediction system SYFPEITHI combined with polynomial method was used to predict the HLA-A2-restricted CTL epitopes of the tumor antigen MAGE-n. The candidate epitopes were synthesized with solid phase strategies, purified with reverse phase high-performance liquid chromatography and identified by mass spectrometry, The binding affinity and biding stability of the synthesized peptides were examined by cellular competition-based HLA-A2 peptide binding assay, T2 peptide stabilization assay, and peptide-major histocompatibility complex dissociation assay. RESULTS: Five HLA-A2-restricted CTL epitopes of MAGE-n were selected: The epitopes QLVFGIEVV (159-167), IMPKTGGLI (195-203), and FLIIVLMI (201-209) with high HLA-A2 binding affinity (LC(50) < 15 micro mol/L) and binding stability (DT(50) > 6 h) were selected as candidate epitopes for further study in immunotherapy for tumor. CONCLUSION: Epitope prediction combined with epitope reconstruction improves the study of HLA-A2-restricted CTL epitopes of the tumor antigen MAGE-n. The selected epitopes of MAGE-n may be used in the design of therapeutic peptide vaccine for hepatocellular carcinoma.

Amino Acid Sequence↗