Aspergillosis of the larynx: a report of 8 cases.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
Z Chen
Publications and source records attributed to Z Chen.
Clinical and biological relevance of flow cytometric determination of P-glycoprotein expression in acute non-lymphocytic leukemia.
OBJECTIVE: To evaluate the characteristics of P-glycoprotein (P-gp) expression of acute non-lymphocytic leukemia (ANLL) at different status and the prognostic and biological features in ANLL at diagnosis. METHODS: Monoclonal antibody UIC2 and indirect immunofluorescence assay by flow cytometry were used to determine P-gp expression of 169 patients with ANLL, including 152 previously untreated, 7 refractory and 10 at remission. RESULTS: P-gp was expressed in 28.9% of the previously untreated ANLL cases and P-gp was lower than that in 71.4% of the refractory cases (P < 0.05). No P-gp expression was found in the patients at remission. For previously untreated AN-LL, P-gp was highly expressed in hybrid acute leukemia (66.7%) and acute monoblastic leukemia (47.4%). P-gp expression was highly associated with surface markers [cluster of differentiation (CD) 34, CD7, CD14, CD42b and CD61] and unfavorable cytogenetic abnormalities. About 23% of P-gp-ANLL obtained complete remission, which was significantly lower than that (76%) in P-gp-cases. CONCLUSIONS: P-gp expression is higher in refractory ANLL cases than that in cases at diagnosis or at remission. P-gp is an index of poor prognosis in adults with ANLL. P-gp+ ANLL cases have unique clinical and biological characteristics.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
[Inhibition of hepatitis C virus by antisense oligodeoxynucleotide in vitro].
OBJECTIVE: To study inhibitory effect of antisense oligodeoxynucleotide (asODN) on HCV in vitro. METHODS: The H9 cells transfected by pCD-HCV, a recombinant HCV containing total HCV structural gene, were treated with two 15-mers phosphorothioate (PS) ODNs complementary (PS-ASON) and homologous (PS-ODN) to HCV core genomic region, which were labeled with digoxin (DIG). Spot blot hybridization was carried out. Treated by the two ODNs, rPS-ODN (a 15-mers PS ODN of random sequence) or PS-ASON were modified with two liposomes (DOTAP and Lipofectin) and calcium phosphate precipitation respectively. With a half-ration, the variation of level of HCV mRNA and HCV antigen expression was observed by RT-PCR and dot ELISA. 3H-TdR adding test was done to observe PS-ASON cytotoxicity. RESULTS: PS-ODN and PS-ASON were detected in the H9 cells. The target gene was hybridized to PS-ASON and PS-ODN labeled with DIG. PS-ASON cut down level of HCV mRNA and HCV antigen expression obviously. However, PS-ODN and rPS-ODN did not influence the level of the both. The time-dependent and dose-dependent inhibition of PS-ASON was observed. In contrast to free PS-ASON, both of liposomal PS-ASON showed more highly effective inhibition, but calcium phosphate precipitation-PS-ASON complex did not. The results showed PS-ASON did not influence the H9 cells growth at 10 mumol/L. CONCLUSION: PS-ASON complementary to HCV core gene is asODN and exerts antisense-inhibitory effect on the level of HCV translation obviously, but not on the level of HCV replication and transcription.
CD4-Positive T-Lymphocytes↗
[The relation between expression of PML-RAR alpha gene and effects of ATRA on proliferation and differentiation of NB4 cells].
OBJECTIVE: To study the relation between the PML-RAR alpha gene and the effects of ATRA on proliferation and differentiation in acute promyelocytic leukemia cell line NB4 cells. METHODS: ASODN-mediated inactivation of the PML-RAR alpha mRNA was measured by RT-PCR. The proliferation and differentiation of NB4 cells were determined by proliferation curve, morphology, CD antigen of membrane and NBT test. NB4 Cell cycle was analyzed by FACS. RESULTS: The inactivation of PML-RAR alpha mRNA by ASODN could egnhance the maturation effects and growth suppression of ATRA on NB4 cells. The percentage of S phase cell was decreased from 52% to 29%, and NBT rate increased. All suggest that the sensitivity of NB4 cell to ATRA was improved. CONCLUSION: The PML-RAR alpha gene, as a molecular marker of APL, is responsible for pathogenesis of APL, and it also decreases the sensitivity of ATRA to APL cells.
Antineoplastic Agents↗
[Progresses in the study of orthopedics in China, 1997].
Explore the source record for details and available documents.
Animals↗
[Immediate and late repair of the midface fracture].
A new method of repairing midface fracture is reported. The authors emphasize that midface fracture should be treated by early open reduction in order to recover good function and external contour. The paper presents the causes, the classification of injury, and the symptoms and diagnosis of midface fracture in 65 cases. Four types of operative approaches were used: 1. hemi-coronal or coronal incision; 2. intraoral incision; 3. transconjunctival approach; and 4. Le-Fort I osteotomy. Postoperative roentgenographic examinations after 1-3 months showed bony healing of all the fractures and good external contour as well. Both functional and cosmetic results were achieved. The indications, advantages, disadvantages of the operation and the operative approaches were discussed.
Adult↗
[Morphometric study of collagen fibers during healing following partial and complete section of extensor tendons in rats].
In order to study the influence of severity of tendon injury on the morphology of collagen fibers during healing process of extensor tendons, 40 female Wistal rats were used for investigation. The rats were divided into 2 groups. Transection of the tendon of extensor digitorum longus was performed in one group, while partial section of the same tendon was performed in the other group. Morphometric analysis was undertaken on the 15th, 30th, 60th and 90th day after operation. The result was that there was no significant difference between the two groups both in distribution and diameter of collagen fibers on the 15th and 30th days (P > 0.05). However, there was significent difference between those on the 60th and 90th days (P < 0.05). It was concluded that the severity of the tendon injury could influence the morphology of collagen fibers during the late stage of tendon healing.
Animals↗
[Experimental study of peripheral nerve regeneration influenced inverted and non-inverted distal nerve segments].
The sciatic nerves of adult rats were sectioned bilaterally and the ends of the nerves were placed in silicone tubes. One side of the distal nerve segment was inverted and that of the contralateral side was non-inverted. After 2, 4, 6 weeks, the rats were killed and the specimens were removed for macroscopic, histologic and morphometric analysis. The results showed that either the inverted or non-inverted distal nerve segments had no influence on the number of the myelinated axons in the regenerated nerves, but the number and density of the myelinated axons was markedly diminished in the inverted distal nerve segments.
Animals↗
The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic.
Acute promyelocytic leukemia (APL) is specifically associated to a t(15; 17) translocation which fuses a gene encoding a nuclear receptor for retinoic acid, RARalpha, to a previously unknown gene PML. The PML protein is localized in the nucleus on a specific domain of unknown function (PML nuclear bodies, NB) previously detected with autoimmune sera from patients with primary biliary cirrhosis (PBC). These bodies are nuclear matrix-associated and all of their identified components (PML, Sp100, and NDP52) are sharply upregulated by interferons. We show that autoantibodies against both PML and Sp100 are usually associated in sera with multiple nuclear dot anti-nuclear antibodies and demonstrate that PML is an autoantigen, not only in PBC, but also in other autoimmune diseases. In APL, the PML/RARalpha fusion interferes with both the retinoic acid (RA) response and PML localization on nuclear bodies, but the respective contribution of each defect to leukemogenesis is unclear. RA induces the terminal differentiation of APL blasts, yielding to complete remissions, and corrects the localization of NB antigens. Arsenic trioxide (As2O3) also induces remissions in APL, seemingly through induction of apoptosis. We show that in APL, As2O3 leads to the rapid reformation of PML bodies. Thus, both agents correct the defect in NB antigen localization, stressing the role of nuclear bodies in the pathogenesis of APL.
Animals↗
Interleukin-13, in combination with anti-interleukin-12, increases graft prolongation after portal venous immunization with cultured allogeneic bone marrow-derived dendritic cells.
Portal venous (pv) transfusion before transplant with large numbers (100 x 10(6)) of irradiated multiple minor histoincompatible spleen cells (B10.Br) augments allogeneic skin graft survival in C3H mice. We have shown in earlier studies that this is correlated with preferential activation for production of type 2 cytokines (interleukin [IL]-4 and IL-10) and decreased production of type 1 cytokines (IL-2 and interferon [IFN] gamma). We have also shown that recombinant (r)IL-12, in association with anti-IL-10 monoclonal antibody, can reverse in vivo the graft prolongation afforded by pv immunization and the altered cytokine production that follows. Adoptive transfer of inhibition of graft rejection is possible at early times after pv immunization, using plastic adherent cells obtained from the liver of treated mice. We show below that within 4 days of pv immunization, dendritic cells (NLDC-145+) isolated from the thymus, mesenteric lymph node (MLN), and.
Adoptive Transfer↗
Synthesis and dopamine transporter affinity of 2-(methoxycarbonyl)-9-methyl-3-phenyl-9-azabicyclo[3.3.1]nonane derivatives.
A series of 9-methyl-3 beta-phenyl-2-substituted-9-azabicyclo[3.3.1]nonane derivatives were synthesized and evaluated as cocaine-binding site ligands at the dopamine transporter (DAT). The conformation of the bicyclic structures and the stereochemistry of the substituents were determined by NMR and X-ray crystallography. The in vitro binding affinity (Ki) of the 9-azabicyclo[3.3.1]nonane derivatives was measured in rat caudate-putamen tissue, and they were found to be 100-fold (Ki = 2-14 microM) less potent than cocaine and other tropane analogs. From these results it is evident that the cocaine-binding site at the DAT is very sensitive to structural modifications of the unsubstituted methylene bridge [C(6)-C(7)] of cocaine and cocaine-like compounds.
Animals↗
Activation of actin-cleavable interleukin 1beta-converting enzyme (ICE) family protease CPP-32 during chemotherapeutic agent-induced apoptosis in ovarian carcinoma cells.
We have previously reported that actin cleavage activity (ACA) by interleukin 1beta-converting enzyme (ICE) family protease was elevated during anticancer drug-induced apoptosis in human leukemia U937 cells. In this study, the involvement of ACA in the drug-induced apoptosis in solid tumor cells was investigated. Human ovarian carcinoma OVCAR-3 cells undergo apoptotic cell death when cells are treated with chemotherapeutic agents such as cisplatin and etoposide. The induction of the actin cleavage activity accompanied the development of apoptosis. ICE/ced-3 family protease inhibitors such as Z-VAD-CH2DCB and Z-EVD-CH2DCB at 100 microg/ml prevented both the emergence of ACA and the morphological change, characteristics of apoptosis, in cisplatin-treated OVCAR-3 cells. The ACA in apoptotic OVCAR-3 cell lysate was greatly adsorbed by antibody against CPP-32, an ICE family protease. Furthermore, the immunoprecipitated CPP-32 from OVCAR-3 lysate could cleave actin to generate a 15-kDa fragment, as did the apoptotic OVCAR-3 cell lysate, indicating that CPP-32 is a major protease responsible for the ACA. The activation of CPP-32 in the drug-treated cell lysate was verified with Western blot analysis. Our present results indicate that CPP-32, an actin cleavage ICE/ced-3 family protease, could be a common mediator involved in the process of chemotherapy-induced apoptosis of cancer cells.
Actins↗
Avian reovirus-induced syncytium formation is independent of infectious progeny virus production and enhances the rate, but is not essential, for virus-induced cytopathology and virus egress.
The nonenveloped avian reoviruses represent a distinct antigenic subgroup of orthoreoviruses. Unlike their mammalian counterparts, the avian reoviruses exhibit the unusual property of inducing rapid and extensive syncytium formation in cell cultures, a cytopathic effect more commonly associated with enveloped virus replication. While the syncytium-inducing capability of avian reovirus has been known for quite some time, the relationship between cell fusion and the virus replication cycle has not been determined. The conservation of the syncytial phenotype among all field isolates of avian reovirus suggests that avian reovirus-induced syncytium formation either reflects an essential step in the virus replication cycle involving intracellular membrane interactions or that cell fusion contributes to enhanced virus replication in infected animals. In order to distinguish between these possibilities, we have examined several aspects of virus replication in the presence of inhibitors of syncytium formation. Inhibitors of intracellular vesicle transport and O-linked glycosylation eliminated or markedly reduced syncytium formation with little effect on the rate or extent of virus macromolecular synthesis and infectious progeny virus production. Moreover, syncytium formation was not required for virus-induced cytopathology or virus egress but did significantly enhance the rate of both of these processes. The data indicate that, unlike the syncytium-inducing enveloped viruses, the membrane interactions and protein trafficking required for avian reovirus-induced syncytium formation do not reflect the sequelae of an essential step in the virus replication cycle. These results suggest that the conservation of the avian reovirus syncytial phenotype may reflect a fortuitous aspect of virus replication which confers advantages associated with the rapid spread of the virus within an infected host.
Animals↗
Rapid shortening during relaxation increases activation and improves systolic performance.
BACKGROUND: Previous studies in cardiac muscle and isolated heart preparations generally have attributed positive effects of ejection to greater length-dependent activation. However, there have been some reports of an ejection-related increase in contractile function that is independent of end-diastolic volume (EDV) history. The present study was designed to more fully characterize the mechanoenergetic results of the latter effect in the intact ventricle. METHODS AND RESULTS: A servomotor was used to initiate left ventricular volume reduction (VR) at end systole, with EDV kept constant. Seven isolated, red blood cell-perfused rabbit hearts were studied at constant EDV during isovolumic contraction, slow VR (5.0 +/- 0.9 EDV/s), and rapid VR (26.8 +/- 5.1 EDV/s). Compared with isovolumic beats, VR caused an enhancement in contractility. This effect was greater for rapid VR and required > 50 beats to attain steady state. Rapid VR increased developed pressure by 15% (92.2 +/- 23.7 [mean +/- SD] versus 105.9 +/- 27.6 mm Hg), maximum dP/dt by 17% (1223 +/- 401 versus 1435 +/- 505 mm Hg.s-1), and Emax (slope of the end-systolic pressure-volume relation) by 13% (69.4 +/- 19.9 versus 78.6 +/- 23.0 mm Hg/mL) (all P < .01). Left ventricular oxygen consumption (VO2) was unchanged with slow VR and decreased by 8% with rapid VR (0.0744 +/- 0.0194 versus 0.0683 +/- 0.0141 mL O2.beat-1.100 g-1; P < .05). In separate hearts (n = 8), costs (basal metabolism and excitation-contraction coupling) were estimated by use of 2,3-butanedione monoxime. Compared with control, rapid VR was associated with a 26% increase in nonmechanical VO2 (0.0248 +/- 0.0021 versus 0.0312 +/- 0.0022 mL O2.beat-1.100 g-1; P < .01), consistent with an increase in calcium cycled per beat. CONCLUSIONS: Ejection after end systole has a positive effect on ventricular performance that cannot be ascribed to length-dependent activation and is likely related to an increase in calcium available for activation. Similarly, an increase in nonmechanical VO2 associated with ejection suggests a positive interaction between myofilament shortening and activator calcium cycling.
Animals↗
Role of the low density lipoprotein (LDL) receptor pathway in the metabolism of chylomicron remnants. A quantitative study in knockout mice lacking the LDL receptor, apolipoprotein E, or both.
Two receptor pathways are thought to mediate the hepatic clearance of chylomicron remnants, (i) the low density lipoprotein receptor (LDLR) pathway and (ii) non-LDLR pathway. The current study was undertaken to quantitatively assess the contribution of each receptor pathway to hepatic catabolism of chylomicron remnants, by using mice that are deficient in apolipoprotein E (apoE) (apoE(-/-)), the LDLR (LDLR(-/-)), and both (apoE(-/-);LDLR(-/-)). Vitamin A fat tolerance tests showed that the area under the curves of the plasma excursions of retinyl ester in the LDLR(-/-), apoE(-/-), and apoE(-/-);LDLR(-/-) mice were 4, 12, and 12 times larger than those in wild-type mice. The retinyl ester accumulated in the plasma of the LDLR(-/-) mice was distributed in larger subfractions of triglyceride-rich lipoproteins, chylomicrons through very low density lipoprotein-C. These results indicate that the LDLR constitutes the major pathway for the clearance of retinyl ester. In support of this, agarose gel electrophoresis revealed that an oral fat load resulted in retention of chylomicrons in the LDLR(-/-) mice, which was not seen in wild-type mice. The observation that the apoE(-/-) mice showed larger retinyl ester excursion than LDLR(-/-) mice indicates that an apoE-dependent non-LDLR pathway is involved in the rest of the clearance of the retinyl ester. Together, we conclude that the LDLR pathway plays a significant role in the chylomicron remnant metabolism in mice fed a normal chow.
Animals↗
Regional perfusion with hemofiltration (chemofiltration) for the treatment of patients with regionally advanced cancer.
BACKGROUND: Regionally advanced cancer is a common, often unresolved problem. Effective local control with chemotherapy is limited by the toxicity following systemic administration. Chemofiltration (CF) is a form of regional perfusion that enables the administration of cytotoxic drugs into one body area while limiting systemic toxicity. The drug is infused into the artery supplying the involved area. The venous effluent of the same organ is pumped out into a hemofiltration unit at a high flow rate. The drug is then filtered away and the blood returned to systemic circulation. METHODS: Forty-one patients underwent 45 CF. Twenty-four patients had CF of the pelvis for advanced rectal carcinoma (10), malignant melanoma (6), and cancers of the uterine cervix (3), ovary (2), vulva (1), endometrium (1), and anus (1). Seventeen patients underwent CF of the liver for metastatic colon (10), breast (4), pancreas (1), ovary (1), and unknown primary (1) cancer. 5-fluorouracil (1 g/m2) and mitomycin-C (30 mg/m2); cisplatinum (200 mg/m2) alone or combined with bleomycin (50 mg/m2) and mitomycin-C (20 mg/m2); or melphalan (1 mg/kg) were the combinations used. RESULTS: Generally the procedure was well tolerated. Complications included transient leukopenia (18), paralytic ileus (2), hair loss (2), renal failure (1). Two patients died within 40 days following CF. Of 36 evaluable patients, 16 (44%) had partial response, 14 (38%) had stable disease, and 6 (18%) had disease progression. A decrease of at least 30% in carcinoembryonic antigen levels occurred in 12 of 24 patients (50%). Median time to progression was 7 months. Ten of 13 patients (77%) achieved good symptomatic palliation. CONCLUSIONS: The results of CF in our study are not superior to alternative methods of drug delivery to the liver and pelvis. However, considering that previous systemic chemotherapy had failed two-thirds of the patients, some benefit may be attributed to this regional delivery modality. Furthermore, pelvic CF afforded very significant symptomatic relief which was definitely superior to other methods.
Adult↗
Cloning and characterization of murine endothelial constitutive nitric oxide synthase.
Complementary DNA clones encoding mouse endothelial constitutive nitric oxide synthase (ecNOS) were isolated by plaque hybridization from a murine fetal cardiac lambda ZAP II cDNA expression library using a full-length human ecNOS cDNA as the hybridization probe. DNA sequence analysis indicates a 1202 amino acid protein showing significant sequence identity with human as well as bovine ecNOS.
Amino Acid Sequence↗
In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RAR alpha/PML proteins.
It has been shown recently in China that arsenic trioxide (As2O3) is a very effective treatment for acute promyelocytic leukemia (APL). APL patients resistant to all-trans retinoic acid (ATRA) and conventional chemotherapy can still respond to AS2O3. In this study, we addressed the possible cellular and molecular mechanisms of this treatment by using NB4 cells as a model. The results show that: (1) As2O3 triggers relatively specific NB4 cell apoptosis at micromolar concentration, as proved by morphology, histogramic related nuclear DNA contents, and DNA gel eletrophoresis. (2) As2O3 does not influence bax, bcl-x, c-myc, and p53 gene expression, but downregulates bcl-2 gene expression at both mRNA and protein levels. (3) As2O3 induces a significant modulation of the PML staining pattern in NB4 cells and HL-60 cells. The micropunctates characteristic of PML-RAR alpha in NB4 cells dissappear after treatment with As2O3, whereas a diffuse PML staining occurs in the perinuclear cytoplasmic region. In addition, a low percentage of untreated NB4 cells exhibits an accumulation of PML positive particles in a compartment of cytoplasm. The percentage of these cells can be significantly increased after As2O3 treatment. A similar PML staining pattern is observed in apoptotic cells. (4) ATRA pretreatment does not influence As2O3-induced apoptosis. These results suggest that induction of cell apoptosis can be one of the mechanisms of the therapeutic effect of As2O3. Moreover, this apoptosis induction occurs independently of the retinoid pathway and may be mediated, at least partly, through the modulation of bcl-2, as well as PML-RAR alpha and/ or PML proteins.
Apoptosis↗