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Biomedical subjects

B Du

Publications and source records attributed to B Du.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Study on pathogenicity of sputum from cavity of sputum negative patients with pulmonary tuberculosis after short course chemotherapy].

OBJECTIVE: To find out whether or not the sputa of pulmonary tuberculosis(PTB) patients with cavitation but sputum negative have pathogenicity after short course chemotherapy. METHODS: Guinea pigs were inoculated with sputa of PTB patients who were with cavitation but sputum negative after having finished short course chemotherapy. Then their body weight, enlargement of local lymph nodes and other ordinary symptom were observed. Six weeks later, pathological changes of TB in the internal organs were examined by dissecting these guinea pigs. Culture and drug resistance test of tubercle bacillus were also conducted. All of which were with negative and positive controls. RESULTS: Of the 63 cases included, 3(5%) patients' sputa resulted in tuberculous nodulation varying in amount in lung, liver and spleen of these guinea pigs, and the culture for tubercle bacillus of these sputa was positive too. CONCLUSIONS: 5% of sputum collected from PTB patients with cavitation but sputum negative still show pathogenicity after short course chemotherapy. For the cases with drug-resistant PTB and slow sputum negative conversion, the treatment should be prolonged and tubercle bacilli in their sputa should be monitored.

Animals↗
PubMed2000

[Clinical observation on ganrening granule in treating common cold].

OBJECTIVE: To explore the therapeutic effect of Ganrening Granule (GRN) in treating common cold. METHODS: Four hundred cases of common cold were randomly divided into three groups, the GRN group (160 Patients), the control group (100 Patients) and the opened group (140 Patients). The changes in symptoms and body temperature of patients were observed before and after treatment by single blind method, and the therapeutic effect was assessed according to the "Guideline of Clinical Research of TCM New Drugs". RESULTS: The markedly effective rate and total effective rate of the GRN group were 81.25% and 96.88% respectively, while those of the control group were 44.44% and 88.00% respectively. The difference between the two groups was significant (P < 0.01). GRN showed significant effect in subsiding fever. CONCLUSION: GRN has good effect in treating common cold (Syndrome of both Weifen and Qifen). No adverse effect was found in the clinical trial.

Adolescent↗
PubMed2000

Right ventricular function of patients with septic shock: clinical significance.

OBJECTIVE: To understand the effect of right ventricular dysfunction on circulatory supportive therapy in patients with septic shock. METHODS: 25 patients with septic shock who were admitted consecutively to the intensive care unit (ICU) of Peking Union Medical College Hospital were observed prospectively. Hemodynamic profile of the left side and right side heart was monitored with right ventricular ejection fraction catheter and transthoracic echocardiography. Intramucosal pH (pHi) and oxygen delivery were also monitored to illustrate any relation with patient outcome. RESULTS: Stroke volume index (SVI) and right ventricular ejection fraction (RVEF) were significantly higher in survivors than in nonsurvivors (P < 0.01 and < 0.05, respectively). The pulmonary vascular resistance index (PVRI) was significantly lower in survivors (P < 0.01). At the onset of shock, the left ventricular end-diastolic volume index (LVEDVI) of both groups was very low, and steadily increased in survivors but not in nonsurvivors. Left ventricular ejection fraction (LVEF) and systemic vascular resistance index (SVRI) decreased during treatment, which were not different in both groups. Right ventricular end-diastolic volume index (RVEDVI) increased in both survivors and nonsurvivors. Oxygen delivery of nonsurvivors was significantly lower than that of survivors. LVEDVI and RVEF were correlated with SVI in both survivors and nonsurvivors. CONCLUSIONS: The impairment of right heart function may be more severe than that of left heart function in the patients with early septic shock. "Right heart priority" must be seriously considered in supportive treatment of patients with septic shock. The present treatment of septic shock has significant limitations, and even aggravates the existing cardiac dysfunction.

Adult↗
PubMed1999

In vitro release of 5-fluorouracil with cyclic core dendritic polymer.

This paper describes the first synthesis of a series of dendritic polymers with a core of 1,4,7,10-tetraazacyclododecane. This core was allowed to react with methyl acrylate through a Michael addition and was then amidated with ethylenediamine. Repeating the two steps led to controlled molecular weight increasing and branching on the molecular level and produced four direction poly(amide-amine) dendrimers. We successfully synthesized dendrimers from generation 0. 5 to generation 5.5. Each generation was analyzed by Fourier- transform infrared (FT-IR) spectroscopy, 1H NMR and elemental analysis. Titrimetry was also used to determine the number of -NH2 of each full generation (2.0, 3.0, 4.0, 5.0). SEC (size exclusion chromatography) was performed to test the purity of G-3.0, G-4.0 and G-5.0. Parts of the outer layer -NH2 groups of the dendrimers generation 4 and generation 5 were acylated by acetic anhydride. The solubility in water of the dendrimer was thus greatly enhanced. The acetylated dendrimers were then reacted with 1-bromoacetyl-5-fluorouracil to form dendrimer-5FU conjugates. Hydrolysis of the conjugates in a phosphate buffer solution (pH 7.4) at 37 degreesC will release free 5FU. Different generation of dendrimer-5FU conjugates exert marking influence on the amount of 5FU released. The dendritic polymer seems to be a promising carrier for the controlled release of antitumor drugs.

Antimetabolites, Antineoplastic↗
PubMed1999

Recombinant adeno-associated virus-based vectors provide short-term rather than long-term transduction of primitive hematopoietic stem cells.

Bone marrow stem cells collected from B6-Gpi-1a mice pretreated with 5-fluorouracil were incubated for 2 h at 37 degrees C in the presence of the recombinant adenovirus-associated virus-based vector (rAAV) SSV9. As measured in vitro immediately following transduction, SSV9 was found to be effective in transducing the primitive cobble-stone-area-forming cell (CAFC)-35 subset (60% transduction efficiency). However, this did not predict long-term expression as the presence of the transgene could not be detected six months after transplantation of 1-2 x 106 transduced bone marrow stem cells into lethally irradiated recipients. CAFC analysis of bone marrow cells and Southern blot analysis of bone marrow and spleen cells were negative, and polymerase chain reaction analysis showed less than 0.1% transduction in bone marrow cells. Therefore, based on our study we conclude that rAAV transiently transduces hematopoietic stem cells but fails to integrate into the genome, leading to the loss of the reporter gene within the first six months after transplantation in vivo.

Animals↗
PubMed1999

The expression of TGF-beta receptors in human atherosclerosis: evidence for acquired resistance to apoptosis due to receptor imbalance.

The degree of cellularity in vascular lesions is determined by the balance between the migration and proliferation of cells relative to their rate of egress and apoptosis. Transforming growth factor-beta(1) can act as a potent antiproliferative and apoptotic factor for proliferating vascular cells. Our laboratory has previously identified cells cultured from human vascular lesions that are resistant to the antiproliferative effect of TGF-beta(1) due to an acquired mutation in the Type II receptor for TGF-beta(1). In the present studies, the expression of the Type I and II receptors in coronary and carotid atherosclerotic lesions was analysed by immunostaining, RT-PCR, and in situ RT-PCR. Levels of the Type I and Type II receptors varied widely within lesions, with the highest levels in the fibrous cap and at discrete foci within the lesion. Regions of smooth muscle-like cells (SMC) were commonly found that were Type I positive but Type II receptor negative. In 43 cell lines cultured from 126 human lesions, 84% of the lesion-derived cell (LDC) cultures exhibited functional resistance to the antiproliferative effect of TGF-beta(1). This resistance was conferred against TGF-beta(1), TGF-beta(2), and TGF- beta(3), but not interferon-gamma or mimosine. While normal SMC exhibited a four-fold increase in the rate of apoptosis after TGF- beta(1) treatment, most LDC were resistant to apoptosis in response to TGF-beta(1). Resistant cells exhibited selective loss of Type II receptor expression, and retroviral transfection of Type II receptor cDNA partially corrected the functional deficit. Thus, resistance to apoptosis may lead to the slow proliferation of resistant cell subsets, thereby contributing to the progression of atherosclerotic and restenotic lesions.

Activin Receptors, Type I↗
PubMed1999

Expression of membrane type 1-matrix metalloproteinase in laryngeal carcinoma.

Membrane type 1-matrix metalloproteinase (MT1-MMP) is a member of the recently identified unique membrane-type subgroup in the matrix metalloproteinase (MMP) family. MT1-MMP has proteolytic activity against components of the extracellular matrix and activates progelatinase A (MMP-2) at the cell surface. In this study, we analyzed the expression of MT1-MMP mRNA in 45 cases of laryngeal carcinoma by RT-PCR and investigated the relationship between MT1-MMP expression and survival in 18 cases. The result showed that the expression of MT1-MMP mRNA was higher in tumor tissue than in corresponding normal tissue. The tumoral expression in clinical stage III was higher than in stage II. The tumoral expression level of MT1-MMP mRNA in patients with lymph node metastasis was signigicantly higher than those with negative lymph nodes. The patients with high expression level showed significantly poorer 5 year survival than those with low expression level. Collectively, our findings suggest that the high level of MT1-MMP expression is closely related to the invasion and metastasis of laryngeal carcinoma, and indicates poorer prognosis.

Actins↗
PubMed1999

Glucocorticoid resistance caused by reduced expression of the glucocorticoid receptor in cells from human vascular lesions.

Mechanisms that control the balance between cell proliferation and death are important in the development of vascular lesions. Rat primary smooth muscle cells were 80% inhibited by low microgram doses of hydrocortisone (HC) and 50% inhibited by nanogram concentrations of transforming growth factor-beta1 (TGF-beta1), although some lines acquired resistance in late passage. However, comparable doses of HC, or TGF-beta1, failed to inhibit most human lesion-derived cell (LDC) lines. In sensitive LDC, HC (10 microg/mL) inhibited proliferation by up to 50%, with obvious apoptosis in some lines, and TGF-beta1 inhibited proliferation by more than 90%. Collagen production, as measured by [3H]proline incorporation or RIA for type III pro-collagen, was either unaffected or increased in the LDCs by HC. These divergent responses between LDC lines were partially explained by the absence of the glucocorticoid receptor (GR) and heat shock protein 90 mRNA in 10 of 12 LDC lines, but the presence of the mineralocorticoid receptor and 11beta-hydroxysteroid dehydrogenase type II. Western blot analysis confirmed the absence of the GR protein in cells lacking GR mRNA. Immunohistochemistry of human carotid lesions showed high levels of GR in the tunica media, but large areas lacking GR in the fibrous lesion. Considering the absence of the GR in most lines, the effects of HC may be elicited through the mineralocorticoid receptor. Functional resistance to the antiproliferative and antifibrotic effects of HC may contribute to excessive wound repair in atherosclerosis and restenosis.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1999

CD4 receptor-dependent entry of human immunodeficiency virus type-1 env-pseudotypes into CCR5-, CCR3-, and CXCR4-expressing human alveolar macrophages is preferentially mediated by the CCR5 coreceptor.

Alveolar macrophages (AM) are important host-defense cells and targets of human immunodeficiency virus type 1 (HIV-1) infection. However, the receptors mediating HIV-1 entry into AM are not completely characterized. We observed that, in addition to CD4 receptors, AM from healthy adults expressed low levels of CCR5, CCR3, and CXCR4 chemokine receptors by flow cytometry, and specific messenger RNA was detected for all three receptors by reverse transcriptase/polymerase chain reaction. The macrophage monocytotropic (M-tropic; YU2) and dual-tropic (89.6) HIV-1 env-pseudotypes entered AM efficiently, as expected given CCR3 and CCR5 expression. However, the T-lymphocytotropic (T-tropic; HXB2) pseudotype did not enter AM despite expression of the appropriate chemokine coreceptor CXCR4. Incubation of AM with regulated on activation, normal T cells expressed and secreted (RANTES) significantly impaired entry of the M-tropic (YU2) HIV-1 pseudotype, whereas SDF-1beta or eotaxin did not impair entry. The entry of simian immunodeficiency virus (SIV) pbj1.9 env-pseudotype into AM was not blocked by RANTES, SDF-1beta, or eotaxin. The competence of these chemokine receptors for virus entry was confirmed in Cf2Th canine thymocytes cotransfected with the human CD4 and chemokine receptors. Entry of the M-tropic (YU2) HIV-1 pseudotype was shown to be mediated by either CCR3 or CCR5, the T-tropic (HXB2) HIV-1 pseudotype by CXCR4, and the dual-tropic (89.6) HIV-1 or the SIVpbj1. 9 pseudotype by CCR5, CCR3, or CXCR4. Our data indicate that the mechanisms for HIV-1 entry are both receptor-specific and cell type-specific, and that chemokine receptor expression on AM does not fully explain cell susceptibility to different virus isolates.

Adult↗
PubMed1998

Recombinant adeno-associated virus vector: use for transgene expression and anterograde tract tracing in the CNS.

We used a recombinant adeno-associated virus vector (AAV) to deliver a foreign gene, green fluorescent protein (GFP), into mature neurons in adult rat CNS in vivo. Microinjections of AAV as small as 50 nl transduced hundreds of neurons at the injection site. There was virtually no retrograde transport as fewer than one neuron per brain was found distant from the injection site that exhibited GFP immunoreactivity. The gene product, GFP, filled the entire neuronal cytoplasmic compartment; GFP immunoreactivity was robust in cell bodies, axons, and nerve terminals. There was no tissue damage at the injection sites or pathogenicity indicated by changes in astrocytic or microglial markers. There was no inflammatory response as judged by leukocytic invasion. Gene expression in transduced cells was robust and apparently permanent: there was no evidence of phenotypic reversion up to 12 weeks following infection. AAV is an excellent vector for introducing foreign genes into mature CNS neurons. Not only might it be an ideal vehicle for gene therapy, but also the GFP-containing AAV presents a new strategy for tracing long axonal pathways in the CNS, which is difficult with current tracers (PHAL, biotinylated dextrans).

Animals↗
PubMed1998

[Analysis of critically ill patients with bacteremia].

OBJECTIVE: To study the epidemiology of bacteremia of critically ill patients and the mortality associated with bacteremia and risk factors for death in an intensive care unit. METHOD: 75 patients with 116 episodes of bacteremia were retrospectively studied. RESULTS: The mortality rate of the patients was 43%. Staphylococci (29%), Enterococci (12%), Class I inducible beta-lactamase-producing Enterobacter (12%), extensive spectrum beta-lactamase-producing Enterobacter (10%) were the most common pathogens, among which gram-positive organisms constitute a major part. The most commonly affected organs were respiratory (77%), hepatic (53%), circulatory (53%), gastrointestinal (50%), renal (47%), central nervous (36%), and hemopoietic systems (27%). Multiple organ failure accounted for 76%. Univariate analysis revealed that the severity of underlying illness, multiple organ failure (MOF), septic shock, hepatic failure, renal failure and infection focus were the risk factors for in-hospital death (P < 0.05). Cox proportional hazard model analysis suggested central nervous system failure, septic shock, hemopoietic failure, hepatic failure and respiratory manipulation significantly affected the survival time of patients with bacteremia (P < 0.05). CONCLUSION: Gram-positive organisms are major pathogens of bacteremia in critically ill patients. Antibiotic therapy can not prevent the occurence of bacteremia, nor can it improve the prognosis.

Adult↗
PubMed1998

[Clinical study of physiologic work of breathing as a weaning parameter in mechanically ventilated patients].

OBJECTIVE: To evaluate the physiologic work of breathing (WOBphy) as a predicting Parameter of weaning and extubation. METHODS: WOBphy was obtained by the patient's work of breathing (WOBt), minuting the imposed work of breathing (WOBimp). In weaning trial, if the patients could not meet predefined extubation criteria, but WOBphy < 0.70 J/L, the patients were also extubated immediately. RESULTS: In a group of 28 patients who met the predefined criteria (group 1), 27 patients were successfully extubated. In another group of 13 patients who could not meet the criteria, but WOBphy < 0.70 J/L (group 2), extubation was successful in 12 patients. WOBt and WOBimp were significantly higher in group 2 (1.37 +/- 0.50 and 0.82 +/- 0.37 J/L) than group 1 (0.96 +/- 0.38 and 0.55 +/- 0.27 J/L, P < 0.05), while WOBphy was higher in group 2, but did not reach statistical significance. CONCLUSIONS: WOBphy < 0.70 J/L may be safe as the weaning and extubation criterion and enables earlier extubation.

Adult↗
PubMed1997

Genomic instability in the type II TGF-beta1 receptor gene in atherosclerotic and restenotic vascular cells.

Cells proliferating from human atherosclerotic lesions are resistant to the antiproliferative effect of TGF-beta1, a key factor in wound repair. DNA from human atherosclerotic and restenotic lesions was used to test the hypothesis that microsatellite instability leads to specific loss of the Type II receptor for TGF-beta1 (TbetaR-II), causing acquired resistance to TGF-beta1. High fidelity PCR and restriction analysis was adapted to analyze deletions in an A10 microsatellite within TbetaR-II. DNA from lesions, and cells grown from lesions, showed acquired 1 and 2 bp deletions in TbetaR-II, while microsatellites in the hMSH3 and hMSH6 genes, and hypermutable regions of p53 were unaffected. Sequencing confirmed that these deletions occurred principally in the replication error-prone A10 microsatellite region, though nonmicrosatellite mutations were observed. The mutations could be identified within specific patches of the lesion, while the surrounding tissue, or unaffected arteries, exhibited the wild-type genotype. This microsatellite deletion causes frameshift loss of receptor function, and thus, resistance to the antiproliferative and apoptotic effects of TGF-beta1. We propose that microsatellite instability in TbetaR-II disables growth inhibitory pathways, allowing monoclonal selection of a disease-prone cell type within some vascular lesions.

Arteriosclerosis↗
PubMed1997

Identification of HIV-1 determinants for replication in vivo.

Pathogenic organisms are frequently attenuated after long-term culture in vitro. The mechanisms of the attenuation process are not clear, but probably involve mutations of functions required for replication and pathogenicity in vivo. To identify these functions, a direct comparison must be made between attenuated genomes and those that remain pathogenic in vivo. In this study, we used the heterochimeric SCID-hu Thy/Liv mouse as an in vivo model to define human immunodeficiency virus type 1 (HIV-1) determinants which are uniquely required for replication in vivo. The Lai/IIIB isolate and its associated infectious molecular clones (e.g., HXB2) were found to infect T cell lines but failed to replicate in the SCID-hu Thy/Liv model. When a lab worker was accidentally infected by Lai/IIIB, however, HIV-1 was isolated only from infection of primary PBMC, and not from infection of T cell lines. We hypothesized that the lab worker was exposed to a heterogeneous viral stock which had been attenuated by passage in immortalized T cell lines. Either a rare family member from this stock was selected for in vivo replication or, alternatively, an attenuated genotype dominant in vitro may have reverted to become more infectious in vivo. To address this hypothesis, we have used the SCID-hu Thy/Liv model to study the replication of HXB2 and of HXB2 recombinant viruses with HIV-1 fragments isolated from the infected lab worker. HXB2 showed no or very low levels of replication in the Thy/Liv organ. Replacement of its subgenomic fragment encoding the envelope gene with a corresponding fragment from the lab worker isolate generated a recombinant virus (HXB2/LW) which replicated actively in SCID-hu mice. The NEF mutation in the HXB2 genome is still present in HXB2/LW. Thus, the LW sequences encode HIV-1 determinants which enhance HIV replication in vivo in a NEF-independent mechanism. The specific determinants have been mapped to the V1-V3 regions of the HIV-1 genome. Six unique mutations in the V3 loop region of HXB2/LW have been identified which contribute to the increased replication in vivo.

Amino Acid Sequence↗
PubMed1997

Potent inhibition of human immunodeficiency virus type 1 in primary T cells and alveolar macrophages by a combination anti-Rev strategy delivered in an adeno-associated virus vector.

The rate of viral replication appears to play a pivotal role in human immunodeficiency virus type 1 (HIV-1) pathogenesis and disease progression as it outstrips the capacity of the immune system to respond. Important cellular sites for HIV-1 production include T lymphocytes and tissue macrophages. Antiviral strategies, including newer treatment modalities such as gene therapy of HIV-1-susceptible cell populations, must be capable of engendering durable inhibitory effects to HIV-1 replication in both of these primary cell types in order to be effective. Among the potential genetic targets for intervention in the HIV-1 life cycle, the Rev regulatory system, consisting of Rev and its binding site, the Rev-responsive element (RRE), stands out as particularly attractive. Rev is essential for maintaining the stability of the viral genomic RNA as well as viral mRNAs encoding key structural and regulatory proteins. Moreover, it exhibits favorable threshold kinetics, in that Rev concentrations must rise above a critical level to exert their effect. To disable Rev function, primary T cells or macrophages were transduced with anti-Rev single-chain immunoglobulin (SFv) or RRE decoy genes either singly or in combination by employing adeno-associated virus vectors and then challenged with HIV-1. By directing both a protein and a nucleic acid against the normal interaction between Rev and the RRE, this genetic antiviral strategy effectively inhibited infection by either clinical or laboratory virus isolates. These results provide a framework for novel interventions to reduce virus production in the infected host.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Effects of dexamethasone, ibuprofen, and ligustrazini on lipopolysaccharides-induced tumor necrosis factor alpha production.

AIM: To study the influence of dexamethasone (Dex), ibuprofen (Ibu), and ligustrazini (Lig) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression (both mRNA and protein). METHODS: TNF alpha in supernatants of human whole blood was measured by ELISA; The TNF alpha mRNA was assessed by slot blot analysis. RESULTS: LPS-induced TNF alpha production was in a dose-dependent manner. TNF alpha levels in the whole blood increased markedly at 3 h and peaked at 6 h. The induction of TNF alpha mRNA was very rapid, peaking at 2 h after LPS challenge. Dex exerted inhibitory effects on TNF alpha production in a dose-dependent manner. Ibu and Lig had 2-phase effects on TNF alpha release. CONCLUSION: Dex, Ibu, and Lig affected TNF alpha gene expression, so they may be new approaches of anti-TNF alpha for treatment of sepsis.

Anti-Inflammatory Agents↗
PubMed1997

[Prospective study of central venous catheter-related sepsis in critically ill patients].

To evaluate the incidence of central venous catheter-related sepsis (CRS) in critically ill patients, we performed a prospective study of the central venous catheters (CVCs) in ICU of the Peking Union Medical College Hospital from Jan. 1995 to March 1996. Of 151 CVCs, 13 (8.6%) had CRS, with an incidence of 16.7 episodes per 1000 catheter-days. Presence of infectious focus at catheterization, catheter insertion site, duration of catheterization, and the decrease of body temperature after catheter removal correlated with definite CRS, while difficulty of insertion, body temperature at catheter removal, as well as the decrease of body temperature after catheter removal correlated well with no CRS. The study showed that CRS is a serious problem in critically ill patients. Careful manipulation of CVCs is a major determinant in reducing the incidence of CRS.

Catheterization, Central Venous↗