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Biomedical subjects

Chen Liu

Publications and source records attributed to Chen Liu.

At least 55 records · Page 3Linked to original sources
PubMed2005

[Study on the presence of hepatitis B virus in first-trimester villi in pregnant women with hepatitis B surface antigen positive].

OBJECTIVE: To observe the presence of hepatitis B virus (HBV) in first-trimester villi cells from pregnant women carrying HBsAg. METHODS: Immunohistochemical streptavidin-biotin peroxidase complex (SABC) staining with monoclonal HBsAg, hepatitis B core antigen (HBcAg) and PCR, in situ hybridization were used for detection of HBV infection markers in villi. Positive villi ultramicrostructures were observed with transmission electron microscope. RESULTS: HBV was detected in 8 of 25 villi of HBsAg positive pregnant women, the positive rate was 32%. HBsAg was located in the decidual cell, trophoblastic cell and villous mesenchymal cell. HBV analog was detected in rough endoplasmic reticulum of trophoblastic cell. CONCLUSIONS: HBV may infect villous cells in first-trimester pregnancy. It would be impossible for HBV to transmit the desmosomes.

Chorionic Villi↗
PubMed2005

[The tangential excision of razor graft for the giant congenital naevi in children].

OBJECTIVE: To study the therapeutical effect of the tangential excision of razor graft for the spacious giant congenital naevi in children. METHODS: The surface layer of the giant naevi, mainly razor graft, was excised tangentially using electrical dermatome. Then the left naevi was removed by dermabrasion. RESULTS: The satisfactory effects were obtained in 9 of 16 cases. The colour of operative area approached the normal skin, occasionally with scattered pigmentation and hypertrophic scars. In 6 cases, the colour appeared lighter than before. One case relapsed after half a year. CONCLUSIONS: The congenital giant naevi in children could be treated using the tangential excision of razor graft. The short-term results might be expected.

Adolescent↗
PubMed2005

[A study of incision pattern and pedicles in reduction mammaplasty].

OBJECTIVE: To investigate the efficacy, indication, advantage and disadvantage of methods for reduction mammaplasty. METHODS: Thirty one cases with breast hypertrophy received reduction mammaplasty using various incisions and pedicles. Based on the follow-up of the cases, the appearance, nipple-areola complex sensory function and scars were evaluated. RESULTS: Among the skin incision pattern, inverted T, short-horizontal invert T and vertical incision got excellent breast contour (100%), otherwise, periareolar incision got the less scar (100%). The postoperative result of lateral pedicle, lateral inferior pedicle and mammary gland pedicle were satisfactory in terms of the nipple-areola sensation and the amount of mammary tissue removed. CONCLUSIONS: Breast contour and scar formation postoperative are related to incision design, Invert T incision or short-horizontal invert T incision is a good alternative to moderate and large hypertrophies, Periareolar incision is suitable to small hypertrophies. There is a relationship existing between pedicle location and retention of sensation or amount of mammary tissue removed. The inferior pedicle and lateral-inferior pedicle allows better shaping as well as maintaining good sensation.

Adult↗
PubMed2005

[Clinical experience of acupuncture and moxibustion for treatment of chronic cholecystitis].

OBJECTIVE: To sum up clinical experience of acupuncture and moxibustion for treatment of chronic cholecystitis and study on the factors of influencing the therapeutic effect of acupuncture and moxibustion treating chronic cholecystitis. METHODS: The factors of influencing the therapeutic effect were summarized from the indications of acupuncture and moxibustion, meridians, acupoint selection, selection of needling and moxibustion methods, time law of attack, treating the principal aspects and the secondary aspects of a disease, arrival of qi, combined treatment of acupuncture and medicine, lasting time and frequency of treatment, assessment of therapeutic effects, and so on. CONCLUSION: Acupuncture and moxibustion treatment of chronic cholecystitis fully reflects the characteristics and complex nature of the acup-moxibustion therapy. Only when concretely analyze practical condition of the patient and adopt acupuncture and moxibustion treatment, can good therapeutic effect be achieved.

Acupuncture↗
PubMed2005

[Clinical study on method of "tonifying the lung to check the liver" for treatment of chronic cholecystitis].

OBJECTIVE: To evaluate the significance of method of "tonifying the lung to check the liver" for treatment of chronic cholecystitis. METHODS: Forty cases were randomly divided into a treatment group and a control group. The treatment group were treated with acupuncture and moxibustion by the method of "tonifying the lung to check the liver", and the control group with routine moxibustion. RESULTS: After treatment of one day, pain improved significantly in the two groups (P < 0.001), with no significant difference between the two groups; and 15 days after treatment, the treatment group was superior to the control group in the improvement of pain. CONCLUSION: TCM syndrome differentiation has an important significance in clinical acupuncture and moxibustion, and the therapeutic principle "tonifying the lung to check the liver" in classical TCM theories is of scientific basis.

Acupuncture Therapy↗
PubMed2004

Donor T-cell production of RANTES significantly contributes to the development of idiopathic pneumonia syndrome after allogeneic stem cell transplantation.

Idiopathic pneumonia syndrome (IPS) is a major cause of mortality following allogeneic stem cell transplantation (allo-SCT). Clinical and experimental data support a role for conditioning-induced inflammation and alloreactive T-cell responses in IPS pathophysiology, but the mechanisms by which donor leukocytes are ultimately recruited to the lung are not fully understood. RANTES is a chemokine ligand that is up-regulated during inflammation and promotes the recruitment of T cells and macrophages to sites of tissue damage. Using a lethally irradiated murine SCT model (B6 --> B6D2F1), we evaluated the role of donor leukocyte-derived RANTES in the development of IPS. Pulmonary mRNA and protein levels of RANTES were significantly elevated in allo-SCT recipients compared to syngeneic controls and were associated with enhanced mRNA expression of CCR5 and CCR1 and with inflammatory cell infiltration into the lung. Allo-SCT with RANTES-/- donor cells significantly decreased IPS and improved survival. Combinations of allogeneic wild-type or RANTES-/- bone marrow with wild-type or RANTES-/- T cells demonstrated that the expression of RANTES by donor T cells was critical to the development of lung injury after SCT. These data reveal that donor T cells can help regulate leukocyte recruitment to the lung after allo-SCT and provide a possible mechanism through which inflammation engendered by SCT conditioning regimens is linked to allo-specific T-cell responses during the development of IPS.

Animals↗
PubMed2004

STAT3 induces anti-hepatitis C viral activity in liver cells.

Hepatitis C virus (HCV) infection is a leading cause a of chronic liver disease worldwide. The main therapeutic regimen is the combination of interferon alpha (IFN) and the nucleoside analog, Ribavirin. IFN initiates an intracellular antiviral state by the JAK-STAT signaling pathway, including a presumed role for STAT1 and STAT2. We have previously shown that the STAT3 activation occurs during IFN treatment of human hepatoma cells, suggesting that the STAT3-mediated pathway is relevant to IFN-induced antiviral activity. In this study, we investigate the role of activated STAT3 in the induction of anti-HCV activity in human hepatoma cells. We demonstrate that the STAT3 activation is involved in efficient IFN-induced anti-HCV activity. Using an inducible, cytokine-independent, STAT3 activation system, in which the entire coding region of STAT3 is fused with the ligand-binding domain of the estrogen receptor, we demonstrate that: activated STAT3 is tightly regulated in a stably transfected cell line by an estrogen analog, 4-HT; activated STAT3 initiates efficient anti-HCV activity in a HCV subgenomic replicon cell line; and activation of STAT3 is associated with the induction of a potential antiviral gene, 1-8U. In addition, we show that the cytokine IL-6, a potent STAT3 activator, inhibits HCV subgenomic RNA replication through STAT3 activation and ERK pathway. These results strongly suggest that STAT3 activation is capable of initiating intracellular antiviral pathways.

Antiviral Agents↗
PubMed2004

Both perforin and Fas ligand are required for the regulation of alloreactive CD8+ T cells during acute graft-versus-host disease.

Fas ligand (FasL) and perforin pathways not only are the major mechanisms of T cell-mediated cytotoxicity but also are involved in homeostatic regulation of these T cells. In the present study, we tested whether CD8+ donor T cells that are deficient in both perforin and FasL (cytotoxic double deficient [cdd]) could induce graft-versus-host disease (GVHD) in a major histocompatibility complex class I-mismatched lethally irradiated murine model. Interestingly, recipients of cdd CD8+ T cells demonstrated significantly greater serum levels of interferon gamma and tumor necrosis factor alpha and histopathologic damage from GVHD than wild-type (wt) T cells on day 30 after allogeneic bone marrow transplantation (P<.05). Wt and either perforin-deficient or FasL-deficient CD8+ T cells expanded early after transplantation followed by a contraction phase in which the majority of expanded CD8+ T cells were eliminated. In contrast, cdd CD8+ T cells exhibited prolonged expansion and reduced apoptosis to alloantigen stimulation in vivo and in vitro. Together these results suggest that donor cdd CD8+ T cells expand continuously and cause lethal GVHD, and that both perforin and FasL are required for the contraction of allo-reactive CD8+ T cells.

Acute Disease↗
PubMed2004

FAP with concurrent duodenal adenomatous polyposis and carcinoid tumor.

We report a patient with familial adenomatous polyposis (FAP) who developed duodenal adenomatosis with high-grade dysplasia and a periampullary carcinoid tumor several years after total colectomy. Only two prior case reports exist revealing carcinoid tumors in association with FAP. No genetic basis exists explaining the link between FAP and carcinoid tumors. However, the presence of two rare entities in the same patient might suggest an association and further research may be indicated.

Acute Disease↗
PubMed2004

A role for tumor necrosis factor-alpha-mediated endothelial apoptosis in the development of experimental idiopathic pneumonia syndrome.

BACKGROUND: Idiopathic pneumonia syndrome (IPS) is a frequent and often fatal complication of allogeneic bone marrow transplantation (BMT). We have previously shown that experimental IPS is associated with alloreactive donor T cells and the inflammatory mediators TNF-alpha and lipopolysaccharide. Both TNF-alpha and lipopolysaccharide are known contributors to endothelial injury. Although damage to vascular endothelia has been associated with other complications after BMT, its relationship to lung injury has not been explored. METHODS: We used a well-established murine BMT system, in which lung injury and graft-versus-host disease are induced by minor histocompatibility antigenic differences between donor and host, and the DNA terminal transferase nick-end labeling (TUNEL) procedure to evaluate whether significant pulmonary vascular endothelial cell (EC) apoptosis is present during the development of IPS. RESULTS: Our data demonstrate that pulmonary histopathology after allogeneic BMT is accompanied by significant EC apoptosis and the appearance of activated caspase 3. Further evaluation reveals that EC injury coincides with the onset of pulmonary pathology, is associated with elevations in bronchoalveolar lavage fluid tumor necrosis factor (TNF)-alpha levels, and is accompanied by evidence for EC activation. Administration of a soluble TNF-alpha binding protein (recombinant human TNF-alpha receptor:Fc) from week 4 to week 6 after allogeneic BMT significantly reduces EC apoptosis and lung histopathology observed in this setting. CONCLUSIONS: EC damage mediated by TNF-alpha is directly linked to the development of experimental IPS. Methods that protect or maintain the integrity of the pulmonary vascular endothelium may therefore prove effective in reducing the severity of lung injury after BMT.

Animals↗
PubMed2004

Effective gene-viral therapy for telomerase-positive cancers by selective replicative-competent adenovirus combining with endostatin gene.

Gene-viral therapy, which uses replication-selective transgene-expressing viruses to manage tumors, can exploit the virtues of gene therapy and virotherapy and overcome the limitations of conventional gene therapy. Using a human telomerase reverse transcriptase-targeted replicative adenovirus as an antiangiogenic gene transfer vector to target new angiogenesis and making use of its unrestrained proliferation are completely new concepts in tumor management. CNHK300-mE is a selective replication transgene-expressing adenovirus constructed to carry mouse endostatin gene therapeutically. Infection with CNHK300-mE was associated with selective replication of the adenovirus and production of mouse endostatin in telomerase-positive cancer cells. Endostatin secreted from a human gastric cell line, SGC-7901, infected with CNHK300-mE was significantly higher than that infected with nonreplicative adenovirus Ad-mE in vitro (800 +/- 94.7 ng/ml versus 132.9 +/- 9.9 ng/ml) and in vivo (610 +/- 42 ng/ml versus 126 +/- 13 ng/ml). Embryonic chorioallantoic membrane assay showed that the mouse endostatin secreted by CNHK300-mE inhibited angiogenesis efficiently and also induced distortion of pre-existing vasculature. CNHK300-mE exhibited a superior suppression of xenografts in nude mice compared with CNHK300 and Ad-mE. In summary, we provided a more efficient gene-viral therapy strategy by combining oncolysis with antiangiogenesis.

Adenoviridae↗
PubMed2004

Blockade of CXCR3 receptor:ligand interactions reduces leukocyte recruitment to the lung and the severity of experimental idiopathic pneumonia syndrome.

Idiopathic pneumonia syndrome (IPS) is a frequently fatal complication after allogeneic stem cell transplantation (allo-SCT) that responds poorly to standard immunosuppressive therapy. The pathophysiology of IPS involves the secretion of inflammatory cytokines including IFN-gamma and TNF-alpha along with the recruitment of donor T cells to the lung. CXCR3 is a chemokine receptor that is expressed on activated Th1/Tc1 T cell subsets and the expression of its ligands CXCL9 (monokine induced by IFN-gamma (Mig)) and CXCL10 (IFN-gamma-inducible protein 10 (IP-10)) can be induced in a variety of cell types by IFN-gamma alone or in combination with TNF-alpha. We used a lethally irradiated murine SCT model (B6 --> bm1) to evaluate the role of CXCR3 receptor:ligand interactions in the development of IPS. We found that Mig and IP-10 protein levels were significantly elevated in the bronchoalveolar lavage fluid of allo-SCT recipients compared with syngeneic controls and correlated with the infiltration of IFN-gamma-secreting CXCR3(+) donor T cells into the lung. The in vivo neutralization of either Mig or IP-10 significantly reduced the severity of IPS compared with control-treated animals, and an additive effect was observed when both ligands were blocked simultaneously. Complementary experiments using CXCR3(-/-) mice as SCT donors also resulted in a significant decrease in IPS. These data demonstrate that interactions involving CXCR3 and its primary ligands Mig and IP-10 significantly contribute to donor T cell recruitment to the lung after allo-SCT. Therefore, approaches focusing on the abrogation of these interactions may prove successful in preventing or treating lung injury that occurs in this setting.

Animals↗
PubMed2004

Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation.

Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4(+) T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4(+) and CD8(+) T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8(+)-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4(+) or CD8(+) T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4(+)-mediated GVHD but reduced survival in CD8(+)-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8(+) cells. Endogenous IL-18 was critical to GVHD mediated by CD8(+) donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4(+)-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8(+)-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4(+) and CD8(+) cell-mediated GVHD.

Acute Disease↗
PubMed2004

Host dendritic cells alone are sufficient to initiate acute graft-versus-host disease.

Alloantigen expression on host APCs is essential to initiate graft-vs-host disease (GVHD); however, critical APC subset remains to be elucidated. We compared the ability of dendritic cells (DCs) and B cells to initiate acute GVHD by an add-back study of MHC class II-expressing APCs (II(+/+)) into MHC class II-deficient (II(-/-)) mice that were resistant to CD4-dependent GVHD. Injection of host-derived, but not donor-derived, II(+/+) DCs or host-derived II(+/+) B cells, was sufficient to break GVHD resistance of II(-/-) mice and induced lethal acute GVHD. By contrast, host-derived II(+/+) B cells, both naive and LPS stimulated, failed to induce activation or tolerance of donor CD4(+) T cells. Similarly, in a model of CD8-dependent GVHD across MHC class I mismatch injection of allogeneic DCs, but not B cells, induced robust proliferation of donor CD8(+) T cells and broke GVHD resistance of chimeric recipients in which APCs were syngeneic to donors. These results demonstrate that host-derived DCs are critical in priming donor CD4(+) and CD8(+) T cells to cause GVHD, and selective targeting of host DCs may be a promising strategy to prevent GVHD.

Acute Disease↗
PubMed2004

Donor-derived TNF-alpha regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation.

Idiopathic pneumonia syndrome (IPS) is a significant cause of mortality after allogeneic bone marrow transplantation (allo-BMT), and tumor necrosis factor-alpha (TNF-alpha) is a significant effector molecule in this process. However, the relative contribution of donor-versus host-derived TNF-alpha to the development of IPS has not been elucidated. Using a lethally irradiated parent --> F1 mouse IPS model, we showed that 5 weeks after transplantation allo-BMT recipients developed significant lung injury compared with syngeneic controls, which was associated with increased bronchoalveolar lavage (BAL) fluid levels of TNF-alpha, elevated numbers of donor-derived TNF-alpha-secreting T cells, and increased pulmonary macrophage production of TNF-alpha to lipopolysaccharide (LPS) stimulation. Allo-BMT with TNF-alpha(-/-) donor cells resulted in significantly reduced IPS severity, whereas utilization of TNF-alpha-deficient mice as BMT recipients had no effect on IPS. We next determined that TNF-alpha secretion from both donor accessory cells (monocytes/macrophages) and T cells significantly contributed to the development of IPS. Importantly, the absence of donor T-cell-derived TNF-alpha resulted in a significant decrease in inflammatory chemokine production in the lung and near complete abrogation of IPS. Collectively, these data demonstrate that donor TNF-alpha is critical to the development of IPS and reveal a heretofore unknown mechanism for T-cell-derived TNF-alpha in the evolution of this process.

Animals↗
PubMed2004

Histone deacetylase inhibitor suberoylanilide hydroxamic acid reduces acute graft-versus-host disease and preserves graft-versus-leukemia effect.

Acute graft-versus-host disease (GVHD) and leukemic relapse are the two major obstacles to successful outcomes after allogeneic bone marrow transplantation (BMT), an effective therapy for hematological malignancies. Several studies have demonstrated that the dysregulation of proinflammatory cytokines and the loss of gastrointestinal tract integrity contribute to GVHD, whereas the donor cytotoxic responses are critical for graft-versus-leukemia (GVL) preservation. Suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials as an antitumor agent; it inhibits the activity of histone deacetylases and at low doses exhibits antiinflammatory effects by reducing the production of proinflammatory cytokines. Using two well characterized mouse models of BMT, we have studied the effects of SAHA on GVHD severity and GVL activity. Administration of SAHA from day +3 to day +7 after BMT reduced serum levels of the proinflammatory cytokines and decreased intestinal histopathology, clinical severity, and mortality from acute GVHD compared with vehicle-treated animals. However, SAHA had no effect on donor T cell proliferative and cytotoxic responses to host antigens in vivo or in vitro. When mice received lethal doses of tumor cells at the time of BMT, administration of SAHA did not impair GVL activity and resulted in significantly improved leukemia-free survival by using two different tumor and donor/recipient combinations. These findings reveal a critical role for histone deacetylase inhibition in the proinflammatory events contributing to GVHD and suggest that this class of pharmacologic agents may provide a strategy to reduce GVHD while preserving cytotoxic T cell responses to host antigens and maintaining beneficial GVL effects.

Animals↗
PubMed2004

An immunomodulatory role for CD4(+)CD25(+) regulatory T lymphocytes in hepatitis C virus infection.

The CD4(+)CD25(+) regulatory T lymphocytes have been implicated in suppressing T cell immune responses. Our aim was to characterize the frequency, phenotype, function, and specificity of CD4(+)CD25(+) T cells in hepatitis C virus (HCV) infection. Peripheral CD4(+)CD25(+) cells from recovered (n = 15), chronic infected (n = 30), and normal control (n = 15) subjects were analyzed ex vivo for quantitation, phenotype, and effect on HCV-specific interferon gamma production and proliferation. CD4(+)CD25(+) specificity was determined by intracellular cytokine staining for interleukin 10 (IL-10). A higher proportion of CD4(+)CD25(+) were found in chronic infection (mean, 3.02%) when compared with recovered (1.64%, P = .001) and normal controls (2.27%, P = .02). CD4(+)CD25(+) cells display CD45RO(high), CD45RA(low), CD28(high), CD62L(high), and CD95(high) phenotype. HCV-specific interferon gamma activity was enhanced in peripheral blood mononuclear cells depleted of CD4(+)CD25(+) and suppressed in peripheral blood mononuclear cells enriched with CD4(+)CD25(+). Depletion of CD4(+)CD25(+) cells also enhanced HCV-specific CD4(+) and CD8(+) T cell proliferation. Cytokine analysis suggested CD4(+)CD25(+) cells secrete transforming growth factor beta (TGF-beta(1)) and IL-10. The inhibitory role for TGF-beta(1) was confirmed by anti-TGF-beta(1). Transwell studies showed CD4(+)CD25(+) mediated suppression to be dose dependent and requiring cell contact. CD4(+)CD25(+) cells showed HCV-specificity through IL-10 production, with a frequency ranging from 1.9% to 5.3%. A positive correlation was detected between CD4(+)CD25(+) T cell frequency and HCV RNA titer, whereas an inverse relation was found with liver inflammatory activity. In conclusion, CD4(+)CD25(+) T lymphocytes constitute a highly differentiated population and appear to play a role in viral persistence by suppressing HCV-specific T cell responses in a cell-cell contact manner.

Antibodies↗