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Biomedical subjects

T Liu

Publications and source records attributed to T Liu.

At least 379 records · Page 21Linked to original sources
PubMed1995

Characterization of TAP-independent and brefeldin A-resistant presentation of Sendai virus antigen to CD8+ cytotoxic T lymphocytes.

H-2Kb-transfected T2 cells, which lack both TAP1/2 and LMP2/7 genes, are able to efficiently process and present Sendai virus Antigen to Kb-restricted Sendai virus-specific CTL. This presentation is not inhibited by Brefeldin A (BFA). Here we extend our analysis of this novel antigen presentation pathway. We show that presentation of Sendai virus antigen was not due to sensitization of T2Kb cells by peptides in the virus preparation or peptides released from virus infected cells. Also, the ability to present Sendai virus in a BFA resistant fashion was specific for cells of the T2 lineage. Re-expression of TAP1/2 genes in T2Kb cells did not alter the capability to present antigen in a BFA resistant fashion, i.e. the presence of a functional TAP transporter complex did not relocate (all) peptides to the classical pathway for antigen processing and presentation. We found that co-infection of T2Kb cells with either Sendai virus plus influenza virus or Sendai virus plus VSV did not relocate presentation of influenza or VSV antigen to the TAP independent BFA resistant antigen presentation pathway. Peptide elution experiments and studies with peptide-specific CTL firmly demonstrated that the antigen presented by T2Kb cells after infection with Sendai virus was the natural Sendai virus epitope NP324-332. The same epitope, when expressed as a minigene in vaccinia virus, could be presented also by T2Kb cells but this presentation could be blocked by BFA. Thus, the TAP independent BFA resistant presentation of antigen seem cell (T2 lineage) and virus (Sendai virus) specific, but not epitope specific. The ability of T2Kb cells to present Sendai virus antigen in a TAP independent BFA resistant fashion was only partially blocked by lysosomal inhibitors such as methylamine, ammonium chloride and chloroquine. These findings demonstrate that TAP1/2-independent and BFA-resistant class I processing is only expressed in certain cell types, in parallel with classical MHC class I processing, and that Sendai virus selectively can enter this pathway. Hypothetical models for the TAP-independent class I processing are discussed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Targeted tumor killing via an intracellular antibody against erbB-2.

Specific killing of erbB-2-overexpressing tumor cells can be achieved using expression of an intracellular antibody directed against the erbB-2 oncoprotein. We have developed a strategy using a recombinant adenovirus encoding an anti-erbB-2 single chain antibody to achieve targeted tumor cell killing in vivo and can show significantly prolonged survival of animals carrying a human ovarian carcinoma tumor burden within their peritoneal cavities. This strategy of gene therapy for ovarian carcinoma offers the potential to achieve highly specific, targeted killing of human tumor cells and thus establishes the rationale to undertake human clinical trials on this basis.

Adenoviridae↗
PubMed1995

The effect of fumonisin B1 on isolated chondrocytes and on bone formation.

Toxic effects of fumonisin B1 (FB1) were observed with cultured chondrocytes isolated from epiphyseal growth plates and with growing broiler chicks. Viability of chondrocytes was reduced after 48 h exposure to FB1, and half lethal concentration of FB1 was estimated to be greater than 250 microM. Increase in cell size was inhibited by as low as 25 microM FB1. Dietary inclusion of fumonisins (55 and 110 ppm) caused a reduction in body weight, increase in liver weight, and decrease in feed efficiency (P < .05). However, diarrhea and bone malformation were not observed. It is concluded that fumonisin by itself is not sufficient to cause skeletal problems in poultry.

Animals↗
PubMed1995

A longitudinal analysis of human papillomavirus 16 infection, nutritional status, and cervical dysplasia progression.

To evaluate the effect of potential risk factors, especially human papillomavirus type 16 (HPV-16) infection and nutritional status on the course of cervical dysplasia, we analyzed data from an intervention trial conducted from 1985 to 1990, in Birmingham, Alabama. With the use of data of four repeated evaluations of dysplasia at an interval of 2 months, specific relationships between HPV-16 infection, plasma retinol and zinc levels, and dysplasia progression were evaluated through longitudinal data analysis of generalized estimating equations. Repeated assessments of nutritional status from blood samples, HPV-16 infection, and dysplasia diagnosis were available from 206 women. Dysplasia diagnosis was confirmed by both Papanicolaou smear and colposcopy examinations and was classified as normal, low, or high grade squamous intraepithelial lesions according to the Bethesda system and assigned a score of 0, 1, or 2, respectively. Generalized estimating equation analyses were performed with assumptions of variance of Poisson and link of logarithm. Separate analyses were also conducted for HPV-16-positive and HPV-16-negative women. By multivariate modeling with adjustment for age, race, smoking, oral contraceptive use, and plasma levels of nutrients, HPV-16 infection was found to be related to the progression of cervical dysplasia, with a relative risk of 1.19 and a 95% confidence interval of 1.03-1.38. High plasma levels of retinol were related to the regression of cervical dysplasia, especially in HPV-16-positive women. A protective effect was also observed for high levels of zinc.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

In vivo stability and disposition of a self-stabilized oligodeoxynucleotide phosphorothioate in rats.

The use of antisense oligonucleotides represents a novel, genetically based therapy. The biostability and pharmacokinetics of a 33-mer self-stabilized oligodeoxynucleotide with significant anti-HIV activity was determined in rats after intravenous administration of [35S]oligodeoxynucleotide. Plasma disappearance of the labeled oligodeoxynucleotide could be described by a two-compartment model, with half-lives of 0.54 and 41.44 h. The oligodeoxynucleotide in plasma remained mainly intact. Urinary excretion represented the major elimination pathway, with approximately 27% of the administered dose excreted within 24 h and 57% over 240 h. The majority of radioactivity in urine was attached to degradative products. Fecal excretion was a minor elimination pathway. A wide tissue distribution of the oligonucleotide was observed, with the majority of radioactivity in most tissues being intact. Compared with other linear oligonucleotide phosphorothioates, the self-stabilized oligonucleotide was more stable in vivo, which may be important in development of antisense oligonucleotides as therapeutic agents.

Animals↗
PubMed1995

[Gene expression of growth factors, growth factor receptor and oncogenes in human lung cancer cell lines].

Gene expression of growth factors including epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), epidermal growth factor receptor (EGFR), oncogenes such as c-myc, N-ras, c-erbB2 and tumor suppressor gene P53 were studied in 4 human lung cancer cell lines using Northern blot technique. Among these cell lines were 2 adenocarcinoma cell lines, one large cell carcinoma cell line and one small cell carcinoma cell line. Expression of EGF and TGF alpha mRNAs were found in all 4 cell lines and EFGR mRNA was seen in 3 out of 4 cell lines. Among these cell lines, 2 cell lines with weaker expression of EGF and TGF alpha, expressed c-myc mRNA. Another 2 cell lines had no c-myc but expressed large amounts of EGF and TGF alpha mRNA. No expression of N-ras, c-erbB2 and p53 were found in these cell lines. The results indicate the presence of autocrine loop of growth factors in these cancer cells. The autostimulation of growth factors may be the main cause for the uncontrolled growth of cancer cells. After treating the cancer cells with EGF, anti-EGF and anti-EGFR antibodies, EGF was found to exert a mild stimulating effect on the growth of one cell line, but no effect on the other cell lines. Anti-EGF and anti-EGFR antibodies inhibited the cell growth on all cell lines. These results provided further evidence for the presence of autocrine loop of growth factors in these lung cancer cell lines.

Adenocarcinoma↗
PubMed1995

Effects of antisense epidermal growth factor and its receptor retroviral expression vectors on cell growth of human pancreatic carcinoma cell line.

A 150 bp epidermal growth factor (EGF) cDNA fragment and a 1024 bp epidermal growth factor receptor (EGFR) cDNA fragment were inserted into 5.05 kb pBabe-puro retroviral vectors between BamH I and EcoR I sites in 3'-5' and/or 5'-3' orientation. The vectors were ligated with EGF and EGFR fragments by T-4 Ligase. The recombinant retroviral vectors were then packaged with packaging cell line PA317 through calcium phosphate mediated transfection. The viral supernatant of transfected PA317 cell lines were used to infect the human pancreatic carcinoma cell line PC-7. The resultant transformant cell lines: PC-7/AS-EGF, PC-7/S-EGFR, PC-7/AS-EGFR and PC-7/pBabe were tested for their endogenous EGF and EGFR mRNA expressions, cell growth rate, 3H-TdR incorporation rate, soft agar colony formation and tumorigenicity in nude mice. The results showed that there were noticeable inhibitions of cell growth, 3H-TdR incorporation rate, soft agar colony formation and tumorigenicity in nude mice in PC-7/AS-EGF and PC-7/AS-EGFR transformant cell lines. The endogenous EGF mRNA expression was blocked in PC-7/AS-EGF cell line and the endogenous EGFR mRNA was significantly down-regulated in PC-7/AS-EGFR cell line.

Adenocarcinoma↗
PubMed1995

Phase I trial of an anti-CD19 deglycosylated ricin A chain immunotoxin in non-Hodgkin's lymphoma: effect of an intensive schedule of administration.

In a phase I trial, eight patients with non-Hodgkin's B-cell lymphoma received mouse IgG1k monoclonal antibody HD37 specific for CD19 conjugated to deglycosylated ricin A chain (dgA) administered in four doses at 4-h intervals with total doses ranging from 4-12 mg/m2. This schedule generated serum levels of immunotoxin which were sustained over 36 h. The plasma half-life of HD37-dgA was 17 +/- 4 (SD) h. The HD37-dgA conjugate was stable in vivo as demonstrated by serum levels of HD37-dgA conjugate comparable to those of total HD37 antibody. Peak serum levels attained after the fourth dose ranged from 0.36 to 5.63 micrograms/ml. Two of seven evaluable patients developed modest human anti-immunotoxin antibody responses. Toxicity in patients 1-7 consisted of dose-dependent capillary leak syndrome with hypoalbuminemia, orthostatic hypotension, and weight gain. Patient 8 died on day 8 with severe capillary leak, bronchopneumonia, and rhabdomyolysis. All patients had progressive disease at 4 weeks except patient 8, who exhibited a near-complete remission before his death. This intensive schedule appears to produce inordinate toxicity with a maximal tolerated total dose of 8 mg/m2.

Adult↗
PubMed1995

[Non-functioning adrenal tumor: clinical analysis of 29 cases].

29 patients with adrenal tumors were admitted to our hospital from June 1985 to July 1994. The diagnosis was made preoperatively in 7 patients (5 adrenal cyst, 2 adrenal myelolipoma) by B-US, CT or MRI. Of the 22 patients whose diagnosis was not made before operation, 8 (tumor diameter: < 3cm) had adrenal cortical adenomas, 6 (tumor diameter: 3-6cm) adrenal medullary tumor, 8 (tumor diameter: > 6cm) adrenocortical cancer (2), adrenal neuroblastoma (1), metastatic cancer (2), adrenal pheochromocytoma (1) and adrenal lymphatic hyperplasia (1) respectively. All non-functioning adrenal tumors should be treated operatively except for adrenal cyst smaller than 3 cm or adrenal myelolipoma.

Adrenal Cortex Neoplasms↗
PubMed1995

[Gene therapy of human pancreatic carcinoma by recombinant retroviral vector expressing herpes simplex virus thymidine kinase gene].

A recombinant retroviral vector pNTK expressing the "suicide" gene herpes simplex virus thymidine kinase (HSV-TK) gene was constructed. The recombinant vector was packaged by PA317 cells and viral supernatant was used to infect the human pancreatic carcinoma cell line PC-2. After selection in G418, resistant colonies were identified and isolated. Cytotoxic effects of the non-toxic prodrug Acyclovir (ACV) or Ganciclovir (GCV) to the NTK transformant PC-2 cells was more than 90%, while that of the control PC-2 cells was less that 10%. Furthermore, the "bystander effect" of HSV-TK on PC-2 cells was also observed.

Acyclovir↗
PubMed1995

[Reversal of malignant cell phenotype of human pancreatic adenocarcinoma cell line by recombinant retroviral vector expressing antisense Ki-ras].

A recombinant retroviral vector expressing antisense Ki-ras was constructed. The recombinant virus DNA was packaged with packaging cell line PA317 cells by the calcium phosphate coprecipitation method. The virus supernatant was used to infect human pancreatic carcinoma cell line PC-2. After selection with Puromycin, resistant colonies were obtained. Stable expressions of retrovirus in both PA317 and PC-2 cells were exhibited by Northern blot hybridization. A down regulation of endogenous Ki-ras was found in PC-2 cells infected with antisense Ki-ras construct. It was demonstrated that the antisense Ki-ras did inhibit the cell growth rate and 3H-TdR incorporation rate of PC-2 cells. The ability of colony formation in soft agar and tumorogenicity in nude mice of PC-2 cells were significantly suppressed by the antisense Ki-ras. The results implicate that recombinant retroviral vector containing antisense Ki-ras could inhibit target gene expression and partly reverse malignant phenotype of pancreatic adenocarcinoma cells.

Adenocarcinoma↗
PubMed1994

CD23/IgE-mediated regulation of the specific antibody response in vivo.

We have recently reported that IgE Abs specific for TNP are able to enhance the specific IgG response in mice via the low affinity receptor for IgE, Fc epsilon RII, or CD23. In this study we show that IgE can up-regulate IgM, IgG1, IgG2a, and the IgE response, thereby indicating the possibility of a viscious circle in the maintenance of an allergic response. One of the suggested modes of action of IgE/CD23 is to increase the ability of B cells to present Ag to T cells. The involvement of T cells in IgE-mediated enhancement of the Ab response was studied in several ways: nude mice were resistant to the effect of IgE and a dramatic effect on the induction of immunologic memory was seen, both by in situ secondary immunizations and in adoptive transfer systems. Basic conditions for the ability of IgE to induce enhancement were established, demonstrating critical importance of factors such as type of Ag and temporal relationship between administration of IgE and Ag. Finally, no evidence for the requirement for CD23 for a normal (non-IgE induced) Ab response was found, although modulation of the receptor completely abrogated the IgE-induced Ab response.

Animals↗
PubMed1994

C-reactive proteins, limunectin, lipopolysaccharide-binding protein, and coagulin. Molecules with lectin and agglutinin activities from Limulus polyphemus.

In 1964, Levin and Bang discovered that gram-negative bacterial endotoxin could rapidly induce gelation of Limulus amebocyte lysate. This observation has led to the development of the most sensitive and specific method for the detection of bacterial endotoxin in pharmaceuticals and drugs intended for human use. Over 10 years ago, Bang injected endotoxin into young horseshoe crabs and observed a time and dose-dependent coagulation of the whole hemolymph. Limunectin, LEBP-PI, and Limulus CRP are found together with coagulin as part of the hemolymph clot at the time of endotoxin-induced exocytosis of amebocytes. In this manner, these molecules with agglutinin/lectin activities could work in concert to assist in the recognition and eventual removal of invading microorganisms from the circulating system. Although the mechanism of endotoxin-induced clot formation is to a large extent understood, the mechanism of clot dissolution and removal in the Limulus hemolymph remains to be clarified.

Acute-Phase Proteins↗