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Biomedical subjects

D W Wang

Publications and source records attributed to D W Wang.

At least 19 recordsLinked to original sources
PubMed2006

Prolonged cardiac allograft survival in presensitized rats after a high activity Yunnan-cobra venom factor therapy.

UNLABELLED: Complement-dependent antibody-mediated acute humoral rejection is the major obstacle of clinical transplantation across ABO incompatibility and human leukocyte antigen presensitization. We previously demonstrated that Yunnan-cobra venom factor (Y-CVF) could almost completely abrogate complement activity and successfully prevent hyperacute rejection in some xenotransplant models without any obvious toxicity. In this study we investigated whether depletion of complement by Y-CVF prevented acute humoral allograft rejection in presensitized rats thereby prolonging graft survival. METHODS: Presensitization was achieved in Lewis rats by sequential grafting of three full-thickness skin pieces from Brown Norway rats. Serum cytotoxic alloantibody titers were determined by a modified in vitro complement-dependent microcytotoxicity assay. After presensitization, each Lewis rat received a heterotopic Brown Norway cardiac allograft. Fifteen recipients were divided into two groups: (1) no treatment control (n = 7); (2) Y-CVF therapy group (86 u/kg, IV, day -1) (n = 8). After cessation of the heart beat, allograft rejection was confirmed by pathologic as well as IgG and C3 immunohistochemical examinations. RESULTS: The mean graft survival time was significantly prolonged to 99.50 +/- 38.72 hours among rats that received Y-CVF vs 12.71 +/- 13.94 hours in nontreated controls (P < .001). Upon pathological and immunohistochemical examination, acute humoral rejection was mainly exhibited in the control group, whereas acute cellular rejection was mainly displayed in the Y-CVF therapy group. CONCLUSIONS: Our study demonstrated that complement depletion by Y-CVF significantly inhibited acute humoral allograft rejection in presensitized rats. As a therapeutic immunointervention tool for complement, Y-CVF has shown potential efficacy across ABO incompatible and positive cross-match barriers.

Animals↗
PubMed2006

Electrophoretic ink using urea-formaldehyde microspheres.

A kind of electronic ink, which is supported on indium-tin-oxide (ITO) glass before polymerization, is prepared using urea and formaldehyde resin as wall materials, in which TiO(2) modified with PMMA are dispersed in tetrachloroethylene (TCE) using a mixture of oil blue dyes and charge control additive (span80). Rotary viscometer, Fourier transform infrared spectroscopy (FT-IR) and optical microscopy are used to characterize the particles, respectively. The electrophoretic mobility of the microcapsules to electric field is also investigated with two parallel electrodes.

Capsules↗
PubMed2004

Recombinant adeno-associated virus-mediated kallikrein gene therapy reduces hypertension and attenuates its cardiovascular injuries.

Gene therapy of hypertension requires long-term expression of a therapeutic gene to achieve stable reduction of blood pressure. Human tissue kallikrein (HK) cleaves kininogen to produce a potent vasoactive peptide kinin, which plays an important role in the regulation of the cardiovascular and renal functions. In the present study, we have delivered human kallikrein cDNA with an rAAV vector to explore the potential therapeutic effects of kallikrein on hypertension and related secondary complications. A single tail vein injection of the rAAV-HK vector into the adult spontaneously hypertensive rats resulted in a significant reduction (12.0+/-2.55 mmHg, P<0.05, n=6, ANOVA) of the systolic blood pressure from 2 weeks after vector injection, when compared with the control rAAV-lacZ vector-injected rats. Weekly blood pressure monitoring showed stable hypertension-reduction effect throughout the course of the 20-week experiments. In addition, total urine microalbumin contents decreased as a result of rAAV-HK treatment. Histological analysis of various tissues showed remarkable amelioration of cardiovascular hypertrophy, renal injury and collagen depositions in the rAAV-treated group. Finally, persistent expression of the transgene product HK was confirmed by the enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction. We conclude that rAAV-mediated HK delivery rendered a long-term and stable reduction of hypertension and protected against renal injury, cardiac remodeling in the spontaneously hypertensive rat model. Further studies are warranted for the development of a gene therapy strategy for human hypertension.

Animals↗
PubMed2001

Adenoma of the posterior urethra: 131 case report.

AIM: A case-report on adenoma of the posterior urethra. METHODS: In 131 cases of adenoma of the posterior urethra, aged 17-79 (mean: 36.4) years, a detailed medical history was taken and urinalysis, urethroscopy, and prostatic specific antigen (PSA) immunohistochemical staining were performed. They were then treated with transurethral resection (TUR) or transurethral electric coagulation (TUEC). RESULTS: Hemospermia occurred in 51% of the cases, hematuria in 38%, blood overflow from the urethral orifice in 6%, and dysuria in 5%. The position of the tumor was at or around the verumontanum. The appearance of the tumor was similar to those of a papilla, a villus, a dactyl or polyp, or simply an engorgement. The tumor contained glandular alveoli and adeno-epithelial cells. PSA immunohistochemistry was positive in the cytoplasm and nucleus of the adeno-epithelial cell. One hundred and tweenty-nine cases were cured after TUR or TUEC, while 2 patients recurred and were operated again. CONCLUSION: Adenoma of the posterior urethra is a common cause of hemospermia and hematuria in young men. Urethroscopic examination and biopsy are the principal diagnostic measures. TUR or TUEC are believed to be the treatment of choice with a short-term recurrence rate of around 1. 5%.

Adenoma↗
PubMed2001

[Study on the relationship between postmortem interval and the change of absorbance in vitreous humor of rabbit after death].

OBJECTIVE: To seek a exact method of estimating Postmortem interval (PMI). METHODS: This study was preformed to investigate the relationship between postmortem interval and absorbance in vitreous humor of rabbit after death. The absorbance in vitreous humor of 48 rabbits after death were investigated with Model 754 spectrophotometer in apt wavelength (420 nm). RESULTS: There exists positive linear regression association between postmortem interval (Y) and absorbance in vitreous humor (X) (r = 0.98327, P < 0.05), during rabbits after death 0 to 72 hours. The formula of linear regression is Y = 453.30 X + 0.75 (Y = postmortem interval = PMI, X = absorbance in vitreous humor). CONCLUSION: The absorbance in vitreous humor can be as reference indicator to estimate PMI within hour 72.

Animals↗
PubMed2001

[Study on the relationship between PMI and the concentration of zincum and nickel in the vitreous humor of rabbit after death].

OBJECTIVE: To seek a exact method of estimating postmortem interval (PMI). METHODS: This study detected the concentration of zincum(Zn) and nickel(Ni) in vitreous humor of rabbit at hour 96 after death and explored the relationship between their concentration and PMI using a method ICP-MS. RESULTS: The concentration of Zn and Ni in vitreous humor of rabbit at hour 24 after death were related to PMI significantly; The formulae of the relationship between PMI and Zn concentrations is y = 0.1404x2 - 1.3351x + 3.8298 (within 24 h; R2 = 0.9202). The formula of the relationship between PMI and Ni concentrations is y = 0.0043x2 - 0.0596x + 0.2665(within 24 h; R2 = 0.9103). CONCLUSION: The concentration of Zn and Ni in vitreous humor of rabbit may be a reference indicator to estimate early PMI.

Animals↗
PubMed2000

Enhanced Na(+) channel intermediate inactivation in Brugada syndrome.

Brugada syndrome is an inherited cardiac disease that causes sudden death related to idiopathic ventricular fibrillation in a structurally normal heart. The disease is characterized by ST-segment elevation in the right precordial ECG leads and is frequently accompanied by an apparent right bundle-branch block. The biophysical properties of the SCN5A mutation T1620M associated with Brugada syndrome were examined for defects in intermediate inactivation (I:(M)), a gating process in Na(+) channels with kinetic features intermediate between fast and slow inactivation. Cultured mammalian cells expressing T1620M Na(+) channels in the presence of the human beta(1) subunit exhibit enhanced intermediate inactivation at both 22 degrees C and 32 degrees C compared with wild-type recombinant human heart Na(+) channels (WT-hH1). Our findings support the hypothesis that Brugada syndrome is caused, in part, by functionally reduced Na(+) current in the myocardium due to an increased proportion of Na(+) channels that enter the I:(M) state. This phenomenon may contribute significantly to arrhythmogenesis in patients with Brugada syndrome. The full text of this article is available at http://www.circresaha.org.

Amino Acid Substitution↗
PubMed2000

Many-body renormalization of semiconductor quantum wire excitons: absorption, gain, binding, and unbinding.

We consider theoretically the formation and stability of quasi-one-dimensional many-body excitons in GaAs quantum wire structures under external photoexcitation conditions by solving the dynamically screened Bethe-Salpeter equation for realistic Coulomb interaction. In agreement with several recent experimental findings the calculated excitonic peak shows weak carrier-density dependence up to (and even above) the Mott transition density, nc approximately 3 x 10(5) cm(-1). Above nc we find considerable optical gain demonstrating compellingly the possibility of a one-dimensional quantum wire laser operation.

Journal Article↗
PubMed2000

[A preliminary analysis on a group of low molecular weight RNases in wheat and related species].

By employing RNase activity gel analysis, we detected a novel group of RNases in wheat and related species. The molecular weight of the RNases varied from 8-14 kDa, which was lower than that of most plant RNases characterized previously. The small RNases expressed abundantly in seedlings and differed in their optimal pH and ionic requirement in digesting RNA substrate. Several members of the small RNases were detected in dormant and germinating wheat seeds. During germination, the activity of two RNases did not change significantly whereas that of the other two RNases showed a gradual pattern of decrease and increase, respectively.

Molecular Weight↗
PubMed2000

[Determination of ecdysterone in Achyranthes bidentata Bl. and its activity promoting proliferation of osteoblast-like cells].

AIM: To study the activity of ecdysterone from Achyranthes bidentata Bl. (AB) promoting proliferation of osteoblast-like (OB-like) UMR106 cells and to determine its content in AB by HPLC method. METHODS: Ecdysterone isolated from AB was cultured with OB-like cells UMR106 together in vitro and the proliferation of OB-like cells was determined by MTT assay. The chromatographic conditions for determining ecdysterone included an ODS column (250 mm x 4.6 mm, 5 microns), a mobile phase consisting of a mixture of water-acetontrile-tetrahydrofuran (86:11:3), detection wavelength of 243 nm, and column temperature of 27 degrees C. Phenacetin was used as the internal standard. RESULTS: The ecdysterone from AB had significant activity promoting proliferation of OB-like cells, the proliferation was promoted by 41% (n = 3). The average recovery of ecdysterone was 96.2% (RSD = 2.1%), the calibration was linear in the range of 30-300 micrograms.mL-1 (gamma = 0.9998). CONCLUSION: Ecdysterone was screened quickly by cultivating with OB-like cells together in vitro. The HPLC method is accurate, fast and reproducible for the determination of ecdysterone in AB.

Achyranthes↗
PubMed1999

Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel.

BACKGROUND: Congenital long-QT syndrome (LQTS) is an inherited condition of abnormal cardiac excitability characterized clinically by an increased risk of ventricular tachyarrhythmias. One form, LQT3, is caused by mutations in the cardiac voltage-dependent sodium channel gene, SCN5A. Only 5 SCN5A mutations have been associated with LQTS, and more work is needed to improve correlations between SCN5A genotypes and associated clinical syndromes. METHODS AND RESULTS: We researched a 3-generation white family with autosomal dominant LQTS who exhibited a wide clinical spectrum from mild bradycardia to sudden death. Molecular genetic studies revealed a single nucleotide substitution in SCN5A exon 28 that caused the substitution of Glu1784 by Lys (E1784K). The mutation occurs in a highly conserved domain within the C-terminus of the cardiac sodium channel containing multiple, negatively charged amino acids. Two-electrode voltage-clamp recordings of a recombinant E1784K mutant channel expressed in Xenopus oocytes revealed a defect in fast inactivation characterized by a small, persistent current during long membrane depolarizations. Coexpression of the mutant with the human sodium channel beta1-subunit did not affect the persistent current, even though we did observe shifts in the voltage dependence of steady-state inactivation. Neutralizing multiple, negatively charged residues in the same region of the sodium channel C-terminus did not cause a more severe functional defect. CONCLUSIONS: We characterized the genetics and molecular pathophysiology of a novel SCN5A sodium channel mutation, E1784K. The functional defect exhibited by the mutant channel causes delayed myocardial repolarization, and our data on the effects of multiple charge neutralizations in this region of the C-terminus suggest that the molecular mechanism of channel dysfunction involves an allosteric rather than a direct effect on channel gating.

Adolescent↗
PubMed1999

Functional consequences of a domain 1/S6 segment sodium channel mutation associated with painful congenital myotonia.

An unusual form of painful congenital myotonia is associated with a novel SCN4A mutation causing a valine to methionine substitution in the domain 1/S6 segment of the skeletal muscle sodium channel. We studied the functional characteristics of this mutant allele using a recombinant channel to gain understanding about the nature of the biophysical defect responsible for this unique phenotype. When expressed heterologously in a cultured mammalian cell line (tsA201), the mutant channel exhibits subtle defects in its gating properties similar, but not identical, to other myotonia-producing sodium channel mutations. The main abnormalities are the presence of a small non-inactivating current that occurs during short test depolarizations, a shift in the voltage-dependence of channel activation to more negative potentials, and a slowing of the time course of recovery from inactivation. Flecainide, a potent sodium channel blocker previously reported to benefit patients affected by this form of myotonia, effectively inhibits the abnormal sodium current associated with expression of the mutant channel. Our findings demonstrate the unique pattern of sodium channel dysfunction associated with a D1/S6 myotonia-producing sodium channel mutation, and provide a mechanism for the beneficial effects of flecainide in this setting.

Animals↗
PubMed1999

Transfection of an active cytochrome P450 arachidonic acid epoxygenase indicates that 14,15-epoxyeicosatrienoic acid functions as an intracellular second messenger in response to epidermal growth factor.

A common feature of most isolated cell systems is low or undetectable levels of bioactive cytochrome P450. We therefore developed stable transfectants of the renal epithelial cell line, LLCPKcl4, that expressed an active regio- and enantioselective arachidonic acid (AA) epoxygenase. Site-specific mutagenesis was used to convert bacterial P450 BM-3 into an active regio- and stereoselective 14S,15R-epoxygenase (F87V BM-3). In clones expressing F87V BM-3 (F87V BM-3 cells), exogenous AA induced significant 14S,15R-epoxyeicosatrienoic acid (EET) production (241. 82 ng/10(8) cells, >97% of total EETs), whereas no detectable EETs were seen in cells transfected with vector alone. In F87V BM-3 cells, AA stimulated [3H]thymidine incorporation and increased cell proliferation, which was blocked by the tyrosine kinase inhibitor, genistein, by the phosphatidylinositol 3 (PI-3) kinase inhibitors, wortmannin and LY294002, and by the mitogen-activated protein kinase kinase inhibitor, PD98059. AA also induced tyrosine phosphorylation of extracellular signal-regulated kinase (ERK) and PI-3 kinase that was inhibited by the cytochrome P450 BM-3 inhibitor, 17-ODYA. Epidermal growth factor (EGF) increased EET production in F87V BM-3 cells, which was completely abolished by pretreatment with either 17-ODYA or the phospholipase A2 (PLA2) inhibitor, quinacrine. Compared with vector-transfected cells, F87 BM-3 transfected cells demonstrated marked increases in both the extent and sensitivity of DNA synthesis in response to EGF. These changes occurred in the absence of significant differences in EGF receptor expression. As seen with exogenous AA, EGF increased ERK tyrosine phosphorylation to a significantly greater extent in F87V BM-3 cells than in vector-transfected cells. Furthermore, in these control cells, neither 17-ODYA nor quinacrine inhibited EGF-induced ERK tyrosine phosphorylation. On the other hand, in F87V BM-3 cells, both inhibitors reduced ERK tyrosine phosphorylation to levels indistinguishable from that seen in cells transfected with vector alone. These studies provide the first unequivocal evidence for a role for the AA epoxygenase pathway and endogenous EET synthesis in EGF-mediated signaling and mitogenesis and provide compelling evidence for the PLA2-AA-EET pathway as an important intracellular-signaling pathway in cells expressing high levels of cytochrome P450 epoxygenase.

8,11,14-Eicosatrienoic Acid↗
PubMed1999

Modulation of HERG potassium channels by extracellular magnesium and quinidine.

Torsades de pointes is a polymorphic ventricular arrhythmia resulting from congenital or drug-induced (acquired) QT prolongation. Pharmacologic suppression of repolarizing potassium currents is one mechanism causing the acquired long QT (LQT) syndrome. Recent studies have linked mutations in a gene encoding a potassium channel subunit (HERG) to the LQT syndrome. Clinical experience indicates that intravenous magnesium sulfate is effective in reversing torsades de pointes, but the molecular basis of this effect is not understood. This study was designed to investigate the effects of extracellular magnesium (Mg2+) on HERG potassium currents. HERG potassium channels were expressed in Xenopus oocytes and in a human cell line and were examined by voltage-clamp methods. Extracellular Mg2+ (0.3-10 mM) caused a concentration-dependent shift in the membrane-potential dependence of HERG channel opening, causing a reduction in K+ current. This effect was much greater than that observed in another human delayed rectifier K+ channel, hKv1.5, suggesting a specific interaction with the HERG channel. Quinidine is an antiarrhythmic drug that also causes torsades de pointes under certain conditions. Quinidine (3 microM) inhibited HERG currents expressed in oocytes by 32.1 +/- 3.2% (n = 5), whereas 1 microM quinidine inhibited HERG currents in tsA201 cells by 75.8 +/- 2.4% (n = 12). Increasing extracellular Mg2+ did not relieve the inhibition by quinidine, but caused additional suppression. These results indicate that extracellular Mg2+ exerts a direct action on HERG potassium channels, resulting in suppression of outward repolarizing potassium current. It is concluded that modulation of this important K+ current is not the mechanism by which intravenous magnesium terminates drug-induced LQT and torsades de pointes. Potent suppression of HERG channel current by quinidine, compared with that of I(Ks) and I(Na), is a likely contributor to torsades de pointes arrhythmias.

Animals↗
PubMed1999

[The changes of GFAP, PCNA after brain contusion: an immunohistochemical study in forensic pathology].

After the model of experimental brain contusion was set up, the changes of GFAP, PCNA were studied by immunohistochemistry SP method combined with image quantity analysis. After contusion, the gray degrees and areas of GFAP-positive cells increased significantly at the 3rd hour, reached the highest level in the 4th day and kept until the 7th day. PCNA-positive cells appeared in the 12th hour, simultaneously, their gray degrees tended to increase and positive areas tended to decrease. It showed regular changes of GFAP, PCNA with various survival times, and these changes were useful in the diagnosis of brain contusion especially in the period from the second to 7th day after injury. The numbers of astrocytes increased and reached the highest level in the 3rd day after contusion while the reactive proliferation of astrocytes is only a minor phenomenon.

Animals↗
PubMed1999

Apoptosis of lymphocytes in canine peripheral blood induced by shock vibration and its mechanism.

We investigated the mechanism of apoptosis induced by shock vibration in canine peripheral lymphocytes, the T-lymphocyte changes, and the expression of p53 and bax gene products related to apoptosis using the techniques of immuno- and enzyme cytochemistry. We noted obvious apoptosis after delivery of 80, 100, and 200 acceleration of gravity values (G values). The percentage of apoptotic lymphocytes was directly proportional to the G value. On the 3rd day after injury, the number of apoptotic lymphocytes reached the peak value, which was about 5 to 8 times the amount in the control group. On the contrary, on day 3 after injury, T lymphocytes decreased and were about 50% of the control group. On the other hand, we found that the percentage of p53 and bax-positive lymphocytes distinctly increased and, on the 3rd day after injury, their number was, respectively, about 2.3 and 1.8 times that in the control groups, suggesting that they may play an important role in lymphocyte apoptosis. The above-mentioned results provide an important basis for further study of the mechanism of shock-vibration injury, its prevention, and treatment.

Animals↗