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Biomedical subjects

B Du

Publications and source records attributed to B Du.

At least 19 recordsLinked to original sources

Perforator stroke after elective stenting of symptomatic intracranial stenosis.

OBJECTIVE: To study the frequency, clinical course, and functional outcome of perforator stroke (PS) resulting from elective stenting of symptomatic intracranial stenosis. METHODS: Between September 2001 and November 2004, 169 consecutive patients with 181 symptomatic intracranial stenoses underwent stenting procedure at our institute. The preoperative perforator infarct adjacent to the stenotic segment (PIAS) on MRI was evaluated blindly. Patients who developed PS after stenting were enrolled. Each patient was assessed by an experienced stroke neurologist by neurologic examination and NIH Stroke Scale score every day until discharge and at day 30, and by modified Rankin Scale (mRS) score at the end of the first, third, and sixth month, and then at intervals of 6 months. RESULTS: PS frequency was 3.0% (5/169 patients). The patients with preoperative PIAS had a higher frequency of PS and PS exacerbation, resulting from intracranial stenting (8.2%, 4/49), vs patients without preoperative PIAS (0.8%, 1/120; p = 0.031). Four PSs occurred during the procedure and one 10 hours after stenting. Four PSs reached the maximum deficit almost at once, and one after 2 hours from onset. All five patients were functionally independent (mRS <or= 1) within 12 months. CONCLUSION: Patients with preoperative perforator infarct adjacent to the stenotic segment have a higher perforator stroke frequency after elective stenting of intracranial stenosis. Most perforator strokes occur during the procedure and reach the maximum deficit almost immediately. Functional outcomes are relatively good.

Adolescent↗

Ascites, but not hyponatremia, is associated with high intraoperative transfusion and vasopressor requirements during liver transplantation.

BACKGROUND: We previously demonstrated that patients with high MELD scores required significantly higher volumes of blood transfusion and vasopressor usage during orthotopic liver transplantation (OLT) compared with patients with low MELD scores. Now we investigated whether hyponatremia or ascites were associated with increased transfusion and vasopressor requirements during OLT. METHODS: Medical records of 192 OLT patients between January 1, 2004, and May 5, 2005, were retrospectively reviewed. Intraoperative transfusion of red blood cells (RBC) or fresh frozen plasma (FFP) and administration of vasopressors were compared. RESULTS: As expected, patients with high (>30) MELD scores were associated with higher requirements for intraoperative transfusion and vasopressors than those with low ( or 30) MELD plus ascites scores (MELD+A, 4.5 points added to MELD if ascites was present) had higher requirements for transfusion and vasopressors compared with patients with low (<or=30) MELD+A scores (16.1+/-9.9 versus 11.4+/-8.6 for RBC; 21.7+/-12.7 versus 15.2+/- 9.6; and 63.4% versus 28.2% for vasopressors, P=.001 to <.001). CONCLUSION: Although hyponatremia and ascites are indicators for liver disease severity, ascites, but not hyponatremia, is associated with increased intraoperative transfusion and vasopressor requirements during OLT.

Ascites↗

Estrogen and raloxifene induce apoptosis by activating p38 mitogen-activated protein kinase cascade in synthetic vascular smooth muscle cells.

Proliferation of vascular smooth muscle cells (VSMC) plays a major role as an initiating event of atherosclerosis. Although estrogen directly inhibits the proliferation of VSMC, the mechanism has not been firmly established. In addition, the effect of raloxifene on VSMC remains unknown. 17Beta-estradiol (E(2)) and raloxifene significantly inhibited the growth of VSMC under growth-stimulated conditions. Since mitogen-activated protein (MAP) kinases have been implicated in VSMC proliferation, the role of MAP kinases in both the E(2)- and raloxifene-induced growth inhibition of VSMC was studied. Both E(2) and raloxifene caused rapid, transient phosphorylation and activation of p38 that was not affected by actinomycin D and was blocked by ICI 182,780. In contrast with p38 phosphorylation, extracellular signal-regulated protein kinase (ERK) phosphorylation was significantly inhibited and c-Jun N-terminal kinase (JNK) phosphorylation was not changed by E(2). Because VSMC expressed both estrogen receptor (ER) alpha and ERbeta, it is not known which of them mediates the E(2)-induced phosphorylation of p38. Although E(2) did not affect the p38 phosphorylation in A10 smooth muscle cells, which express ERbeta but not ERalpha, transfection of ERalpha expression vector into A10 cells rendered them susceptible to induction of p38 phosphorylation by E(2). We then examined whether E(2) and raloxifene induce apoptosis through a p38 cascade. Both E(2) and raloxifene induced apoptosis under growth-stimulated conditions. The p38 inhibitor SB 203580 completely blocked the E(2)-induced apoptosis. Our findings suggest that both E(2)- and raloxifene-induced inhibition of VSMC growth is due to induction of apoptosis through a p38 cascade whose activation is mediated by ERalpha via a nongenomic mechanism.

Animals↗

Branched crystal morphology of linear polyethylene crystallized in a two-dimensional diffusion-controlled growth field.

The branched crystal morphology of linear polyethylene formed at various temperatures from thin films has been studied by atomic-force microscopy (AFM), transmission electron microscopy (TEM), electron diffraction (ED) pattern and polymer decoration technique. Two types of branched patterns, i.e. dendrite and seaweed patterns, have been visualized. The fractal dimension d(f) = 1.65 of both dendrite and some of seaweed patterns was obtained by using the box-counting method, although most of the seaweed patterns are compact. Selected-area ED patterns indicate that the fold stems tilt about 34.5( degrees ) around the b-axis and polymer decoration patterns show that the chain folding direction and regularity in two (200) regions are quite different from each other. Because of chain tilting, branched crystals show three striking features: 1) the lamella-like branches show two (200) regions with different thickness; 2) the crystals usually bend towards the thin region; 3) the thick region grows faster by developing branches, thus branches usually occur outside the thick region. The branched patterns show a characteristic width w, which gives a linear relationship with the crystallization temperature on a semilogarithmic plot.

Journal Article↗

Syntheses and structural characterizations of sheet- and column-like lanthanide-transition metal arrays: the effect of hydrogen bonding on the structure when K(+) is replaced by [NH4]+.

Sheet- and column-like cyanide bridged lanthanide-transition metal arrays were synthesized through metathesis reactions between anhydrous LnCl(3) (Ln = Eu, Yb) and A(2)[M(CN)(4)] (A = K(+), NH(4)(+); M = Ni, Pt) in a 1:2 molar ratio in DMF (DMF = N,N-dimethylformamide) solution. Single-crystal X-ray analysis revealed that complexes of formula [K(DMF)(7)Ln[M(CN)(4)](2)](infinity) (Ln = Eu, M = Ni, 1; Ln = Yb, M = Pt, 2) consist of infinite layers of neutral, puckered sheets that contain hexagonal rings of composition [(DMF)(10)Ln(2)[M(CN)(4)](3)](6) with interstitial (DMF)(4)K(2)[M(CN)(4)] units located between the layers. The sheet structure is generated through the repeating (DMF)(10)Ln(2)[M(CN)(4)](3) unit with trans cyanide ligands in [M(CN)(4)](2)(-) serving as bridges. The column-like complex [(NH(4))(DMF)(4)Yb[Pt(CN)(4)](2)](infinity), 3, is formed when NH(4)(+) replaces K(+). It consists of infinite, negatively charged, square, parallel columns bundled through N-H...NC hydrogen bonds between NH(4)(+) and terminal CN from the columns. Cis cyanide ligands in [Pt(CN)(4)](2)(-) units serve as bridges. Complex 3 is the first known example where Ln(III) centers are coordinated to four [M(CN)(4)](2)(-) units. Bicapped (square face) trigonal prismatic coordination geometries were observed for Ln(III) centers in 1 and 2. Square antiprismatic geometry for Yb(III) centers are observed in 3. Crystal data for 1: triclinic space group P1, a = 8.797(2) A, b = 15.621(3) A, c = 17.973(6) A, alpha = 105.48(2) degrees, beta = 98.60(2) degrees, gamma = 98.15(2) degrees, Z = 2. Crystal data for 2: triclinic space group P1, a = 8.825(1) A, b = 15.673(1) A, c = 17.946(1) A, alpha = 105.46(2) degrees, beta = 99.10(1) degrees, gamma = 98.59(1) degrees, Z = 2. Crystal data for 3: monoclinic space group P2(1)/c, a = 9.032(1) A, b = 29.062(1) A, c = 15.316(1) A, beta = 94.51(1) degrees, Z = 2.

Journal Article↗

[Prediction of prognosis of patients with multiple organ dysfunction syndrome by sepsis-related organ failure assessment].

OBJECTIVE: To describe the clinical properties of multiple organ dysfunction syndromB (MODS) with sepsis-related organ failure assessment (SOFA). METHODS: A total of 366 MODS patients admitted to the 5 participating ICUs from 1990 to 1996 were included in this study. SOFA score and demographic data were retrospectively evaluated. RESULTS: Total maximum SOFA score, delta SOFA and admission total SOFA score exhibited a good correlation with hospital mortality rate, with the area under the ROC curve of 0.819, 0.750 and 0.616, respectively. The SOFA score for patients without organ failure was 3.7 +/- 1.2, with a mortality rate of 21.7%, and the SOFA score for patients with failure of all 6 organs was 20.2 +/- 1.4, with a mortality rate of 77.8%. A maximum score was firstly reached for respiratory system (1.41 days after admission), and last for cardiovascular system (4.89 days). Logistic regression model revealed that the central nervous system was associated with the highest relative contribution (odds ratio 1.75) to hospital outcome, followed by renal (OR 1.42), cardiovascular (OR 1.38), coagulation (OR 1.34) and respiratory (OR 1.17) systems. No independent contribution was found for the hepatic score (OR 0.99). CONCLUSION: Total maximum SOFA score and delta SOFA can be used to quantify the progress of MODS during ICU stay.

Adult↗

Beta-chemokine induction of activation protein-1 and cyclic AMP responsive element activation in human myeloid cells.

Chemokines effect leukocyte chemotaxis and activation through their binding to specific G protein-coupled receptors. Although early steps in chemokine signal transduction pathways have been characterized, there is relatively limited information available at the transcription factor level. To that end, we have examined the binding activity on activation protein-1 (AP-1) and cyclic AMP responsive element (CRE) target sequences in human THP-1 myeloid cells after treatment with the beta-chemokine macrophage inflammatory protein (MIP-1alpha). MIP-1alpha induced both AP-1 and CRE activation. Although inhibition of protein kinase C blocked the AP-1 activity induced by this chemokine, there was no decrease in CRE activation in the presence of a protein kinase A inhibitor. Using kinase assays, it appeared that mitogen-activated protein kinase pathways were involved in CRE activation. In addition, HIV-1 infection of THP-1 cells resulted in constitutive activation of AP-1 and CRE elements but no further response to MIP-1alpha treatment. These results suggest that beta-chemokines act via protein kinase C-dependent pathways and mitogen-activated protein kinase pathways to modulate the host transcriptional response in myeloid cells, and that this response is altered by HIV infection.

Cell Line↗

Present situation in preventing and treating liver fibrosis with TCM drugs.

Considerable evidences have shown that the mechanism of TCM drugs for preventing and treating liver fibrosis is very complicated. TCM treatment can not only inhibit viral replication, ameliorate inflammation and promote blood circulation in the liver, and enhance regeneration of the hepatic cells, but also inhibit HSC proliferation, intra- and extracellular secretion, decrease the secretion of collagen and promote its degradation and re-absorption. However, most of the animal models are only suitable for studies of acute hepatitis. Establishment of cell lines suitable for studies of fibrosis is still at its initial stage. What we expect is that comprehensive clinical studies in TCM treatment of liver fibrosis will be carried out and evaluation of each datum given, both of which are of importance.

Animals↗

[Study on graft-versus-leukemia effects of donor lymphocyte infusion after nonmyeloablative allogeneic bone marrow transplantation].

OBJECTIVE: To explore the graft-versus-leukemia effects of donor lymphocyte infusion(DLI) after nonmyeloablative allogeneic bone marrow transplantation while attenuating treatment-associated morbidity, mortality and graft-versus-host disease. METHODS: 615(H-2k) mice were loaded with L615 cells and 3 days later received total body irradiation (TBI) 5 Gy (60 Co gamma-ray) followed by allogeneic bone marrow transplantation (allo-BMT). The allo-grafts consisted of 3 x 10(7) bone marrow cells and 1 x 10(7) spleen cells from BALB/c (H-2d) donor mice. Two days after allo-BMT, the recipient mice were given 200 mg/kg of CTX. Afterwards these recipient mice were infused either donor spleen cells (2 x 10(7)) on d14 and d21 or hydrocortison (HC) and cyclosporine A (CsA) treated donor spleen cells (5 x 10(7)) on d14 post-BMT. RESULTS: Survival time of mice received DLI on d21 and pretreated DLI on d14 post-BMT was longer than that of control group and d14 DLI group(P < 0.01) and without severe graft-versus-host disease. CONCLUSION: Donor lymphocyte infusion after nonmyeloablative bone marrow transplantation could reduce transplantation-associated morbidity and mortality while strengthening graft-versus-leukemia effects.

Animals↗

[Study of a mutation in connexin 26 gene associated with congenital sensorineural deafness].

OBJECTIVE: So far, at least 39 deafness gene loci have been mapped in human chromosome including the connexin 26 gene coding for a gap-junction protein. This gene is thought to be linked to hereditary non-syndromic sensorineural hearing loss. About 80% of cases of DFNB1 hereditary deafness carry a 30 mer G mutation of connexin 26. METHOD: To investigate this relationship, we obtained DNA samples from 15 cases with autosomal recessive and autosomal dominant forms of non-syndromic deafness. In addition, DNA samples were obtained from 252 unrelated subjects with sporadic hearing loss; parents of these subjects were symptom free. We analyzed the coding region for the connexin 26 gene for mutation using PCR-SSCP and sequence analysis and PCR-mediated site-directed mutagensis. RESULT: We detected 46 mutations with SSCP. The PCR products that of 5 cases mutations had similar abnormalities in their electrophoresis bands were sequenced. Results from 2 cases of families with hereditary hearing loss and 3 cases of sporadic hearing loss had a G-to-A transversion at nucleotide 79. In addition, 2 cases sporadic hearing loss with 251 delT and 233 delC were found, 35 delG was not detected in 46 cases abnormal PCR products using PSDM assay. CONCLUSION: High mutation rates were found in China deafness population of connexin 26 gene, but the mutation loci is different from those previously reported. Finding hot spot of connexin 26 gene mutation in China population is important for deafness etiologic diagnosis and affect genetic counseling.

Adolescent↗

Elevated Egr-1 in human atherosclerotic cells transcriptionally represses the transforming growth factor-beta type II receptor.

Atherosclerotic lesions may progress due to a "failure to die" by vascular repair cells. Egr-1, a zinc finger transcription factor, is elevated more than 5-fold in human carotid lesions relative to the adjacent tunica media. Lesion cells in vitro also express 2-3-fold higher Egr-1 mRNA and protein levels but express much lower levels of the transforming growth factor-beta (TGF-beta) Type II receptor (TbetaR-2) and are functionally resistant to the antiproliferative effects of TGF-beta. Lesion cells fail to express a TbetaR-2 promoter/chloramphenicol acetyltransferase (CAT) construct but overexpress an Egr-1-inducible platelet-derived growth factor-A promoter/CAT construct. Transfection of Egr-1 cDNA represses TbetaR-2/CAT constructs but induces PDGF-A/CAT. Egr-1 transfection reduces the levels of TbetaR-2 and confers resistance to the antiproliferative effect of TGF-beta1. Egr-1 can interact directly with both the -143 Sp1 site and the positive regulatory element 2 (PRE2) (ERT/ets) region of the TbetaR-2 promoter. Thus, although activating a family of stress-responsive genes, Egr-1 also transcriptionally represses one of the major inhibitory pathways that restrains vascular repair.

Arteries↗

Recurrent chromosome changes in 62 primary gastric carcinomas detected by comparative genomic hybridization.

Comparative genomic hybridization (CGH) has been applied to detect recurrent chromosome alterations in 62 primary gastric carcinomas. Several nonrandom chromosomal changes, including gains of 8q (31 cases, 50%), 20q (29 cases, 47%) with a minimum gain region at 20q11. 2-q12, 13q (21 cases, 34%) with a minimum gain region at 13q22, and 3q (19 cases, 31%) were commonly observed. The regions most frequently lost included: 19p (23 cases, 37%), 17p (21 cases, 33%), and 1p (14 cases, 23%). High copy number gain (DNA sequence amplification) was detected in 6 cases. Amplification of 8q23-q24.2 and 20q11.2-q12 were observed in 3 cases. Gain of 20q and loss of 19p were confirmed by fluorescence in situ hybridization using corresponding bacterial artificial chromosomes (BAC) clones from those regions. The gain and loss of chromosomal regions identified in this study provide candidate regions involved in gastric tumorigenesis.

Adult↗

Cyclic core dendrimer as a new kind of vector for gene transfer into mammalian cells.

Cyclic core dendritic polymer is a new type of synthetic polymers. The ability of generation 4 of the dendrimer with a core of 1,4,7,10-tetraazacyclododecane to function as an effective gene delivery vector was investigated. Results from fluorescence in situ hybridization (FISH) show that the pCH 110 plasmid DNA was transferred into human small intestine cancer metastatic ascites (HICMA) cells induced by this kind of dendrimer as a vector. The transferred LacZ, GFP and luciferase genes were highly expressed in the transfected HICMA, COS-7 and 293 cells. These studies demonstrate that the dendrimer can transfect mammalian cells in vitro which offers an alternatively efficient method for mammalian gene transfer.

Animals↗

High-level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis.

To understand the mRNA transcript profile in the human atherosclerotic lesion, RNA was prepared from the fibrous cap versus adjacent media of 13 patients undergoing carotid endarterectomy. cDNA expression arrays bearing 588 known genes indicated that lesions express unexpectedly high levels of the early growth response gene, Egr-1 (NGFI-A), a zinc-finger transcription factor that modulates a cluster of stress-responsive genes including PDGF and TGF-beta. Expression of Egr-1 was an average of 5-fold higher in the lesion than in the adjacent media, a result confirmed by RT-PCR, and many Egr-1-inducible genes were also strongly elevated in the lesion. Time-course analyses revealed that Egr-1 was not induced ex vivo. Immunocytochemistry indicated that Egr-1 was expressed prominently in the smooth muscle-actin positive cells, particularly in areas of macrophage infiltration, and in other cell types, including endothelial cells. Induction of atherosclerosis in LDL receptor-null mice by feeding them a high-fat diet resulted in a progressive increase in Egr-1 expression in the aorta. Thus, induction of Egr-1 by atherogenic factors may be a key step in coordinating the cellular events that result in vascular lesions.

Animals↗