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Biomedical subjects

D Feng

Publications and source records attributed to D Feng.

At least 19 recordsLinked to original sources
PubMed2006

Mechanism of neuroprotective effect induced by QingKaiLing as an adjuvant drug in rabbits with E. coli bacterial meningitis.

OBJECTIVE: To explore the neuroprotective effects and underlying mechanism of QingKaiLing (QKL) as an adjuvant treatment for bacterial meningitis. METHOD: E. coli bacterial meningitis rabbits were treated with antibiotics (ampicillin) alone or in combination with QKL. The number of leukocytes and the concentration of protein in the cerebrospinal fluid (CSF) of rabbits were determined at 0, 16, and 26 hours after treatment. Brain water, sodium, potassium, and calcium contents were determined at the 26-hour time point. The level of matrix metalloproteinase-9 in the brain was also determined by Western blot. RESULT: The average number of leukocytes and the concentration of protein in CSF of the QKL adjuvant treatment group were reduced compared with the ampicillin alone group. Brain water, sodium, and calcium contents were reduced in the QKL adjuvant treatment group. The level of MMP-9 in brain tissue was also reduced in the QKL adjuvant treatment group. CONCLUSION: QKL adjuvant treatment alleviates the aggravated inflammatory reaction and partially protects brain tissue from antibiotic-induced injury. The mechanism of this neuroprotective effect of QKL may be due to decreased levels of Ca2+ and MMP-9 in the brain.

Acute Disease↗
PubMed2006

(-)-Epigallocatechin-3-gallate protects mice from concanavalin A-induced hepatitis through suppressing immune-mediated liver injury.

(-)-Epigallocatechin-3-gallate (EGCG) is the major active component of green tea. Increasing evidence has suggested that EGCG exhibits anti-inflammatory, anti-oxidant and immunosuppressive effects. In this study, we investigated the effect of EGCG on concanavalin A (ConA)-induced hepatitis (CIH) in mice, a model of immune-mediated liver injury in humans. We pretreated mice with EGCG before ConA injection, and then measured alanine aminotransferase (ALT) levels in plasma, inflammatory infiltration and hepatocyte apoptosis in liver. Potential therapeutic mechanisms were elucidated further by measuring several inflammatory mediators. Mice pretreated with EGCG exhibited much less increased ALT levels in plasma, reduced inflammatory infiltration and hepatocyte apoptosis in liver compared with control mice pretreated with vehicle solutions. We further investigated the mechanisms of the protective effects of EGCG. In EGCG-pretreated mice, we found abrogated tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma at both protein levels in plasma and mRNA levels in liver. At the same time, the concentration of nitrite in plasma and inducible nitric oxide synthase production in liver were both down-regulated in these mice. Moreover, IFN-inducible protein-10 and macrophage inflammatory protein-1alpha expressions in liver were decreased significantly. Therefore, EGCG is capable of regulating immune-mediated liver injury in vivo. The protective effect depended on its suppressive effect on the production of important inflammatory mediators.

Alanine Transaminase↗
PubMed2006

Centrosomal protein centrin is not detectable during early pre-implantation development but reappears during late blastocyst stage in porcine embryos.

Centrin is an evolutionarily conserved 20 kDa, Ca+2-binding, calmodulin-related protein associated with centrioles and basal bodies of phylogenetically diverse eukaryotic cells. Earlier studies have shown that residual centrosomes of non-rodent mammalian spermatozoa retain centrin and, in theory, could contribute this protein for the reconstruction of the zygotic centrosome after fertilization. The present work shows that CEN2 and CEN3 mRNA were detected in germinal vesicle-stage (GV) oocytes, MII oocytes, and pre-implantation embryos from the two-cell through the blastocyst stage, but not in spermatozoa. Boar ejaculated spermatozoa possess centrin as revealed by immunofluorescence microscopy and western blotting. Immature, GV oocytes possess speckles of centrin particles in the perinuclear area, visualized by immunofluorescence microscopy and exhibit a 19 kDa band revealed by western blotting. Mature MII stage oocytes lacked centrin that could be detected by immunofluorescence or western blotting. The sperm centrin was lost in zygotes after in vitro fertilization. It was not detectable in embryos by immunofluorescence microscopy until the late blastocyst stage. Embryonic centrin first appeared as fine speckles in the perinuclear area of some interphase blastocyst cells and as putative centrosomes of the spindle poles of dividing cells. The cells of the hatched blastocysts developed centrin spots comparable with those of the cultured cells. Some blastomeres displayed undefined curved plate-like centrin-labeled structures. Anti-centrin antibody labeled interphase centrosomes of cultured pig embryonic fibroblast cells as distinct spots in the juxtanuclear area. Enucleated pig oocytes reconstructed by electrofusion with pig fibroblasts displayed centrin of the donor cell during the early stages of nuclear decondensation but became undetectable in the late pronuclear or cleavage stages. These observations suggest that porcine zygotes and pre-blastocyst embryonic cells lack centrin and do not retain exogenously incorporated centrin. The early embryonic centrosomes function without centrin. Centrin in the blastocyst stage embryos is likely a result of de novo synthesis at the onset of differentiation of the pluripotent blastomeres.

Animals↗
PubMed2005

15-Lipoxygenase is a component of the mammalian sperm cytoplasmic droplet.

Lipoxygenases (LOXs) are a family of enzymes capable of peroxidizing phospholipids. A member of the LOX family of enzymes, 15-LOX, participates in the degradation of mitochondria and other organelles within differentiating red blood cells, the reticulocytes. The present study provides biochemical and immunocytochemical evidence for the presence of 15-LOX in the sperm cytoplasmic droplet (CD). Testicular, epididymal and ejaculated spermatozoa were evaluated for the presence of 15-LOX using an affinity-purified immune serum raised against a synthetic peptide corresponding to the C-terminal sequence of rabbit reticulocyte 15-LOX. Western blotting revealed an appropriate single band of approximately 81 kDa in boar spermatozoa but not in boar seminal plasma. When ejaculated boar spermatozoa were subjected to separation on a 45/90% Percoll gradient, 15-LOX co-migrated with the immotile sperm and cellular debris/CD fractions, but not with the motile sperm fraction containing morphologically normal spermatozoa without CDs. Varied levels of 15-LOX were expressed in ejaculated sperm samples from boars with varied semen quality. By immunofluorescence, prominent 15-LOX immunoreactivity was found within the residual body in the testis and within the CDs from caput, corpus and cauda epididymal and ejaculated spermatozoa. Components of the ubiquitin-dependent proteolytic pathway, which is thought to facilitate both spermiogenesis and reticulocyte organelle degradation, were also detected in the sperm CD. These included ubiquitin, the ubiquitin-conjugating enzyme E2, the ubiquitin C-terminal hydrolase PGP 9.5, and various 20S proteasomal core subunits of the alpha- and beta-type. The 15-LOX and various components of the ubiquitin-proteasome pathway were also detected in sperm CDs of other mammalian species, including the human, mouse, stallion and wild babirusa boar. We conclude that 15-LOX is prominently present in the mammalian sperm CD and thus may contribute to spermiogenesis, CD function or CD removal.

Animals↗
PubMed2001

Giant room-temperature magnetoresistance in polycrystalline Zn(0.41)Fe(2.59)O4 with alpha-Fe2O3 grain boundaries.

A tunneling-type magnetoresistance (MR) as large as 158% is observed at T = 300 K in a polycrystalline Zn0.41Fe2.59O4 sample, in which the Zn0.41Fe2.59O4 grains are separated by insulating alpha-Fe2O3 boundaries. The huge room-temperature MR is attributed to the high spin polarization of Zn(0.41)Fe(2.59)O4 grains and antiferromagnetic correlations between magnetic domains on both sides of the insulating alpha-Fe2O3 boundary. The MR exhibits strong temperature dependence below 100 K and its magnitude is enhanced to reach 1280% at 4.2 K, which may arise from the Coulomb blockade effect.

Journal Article↗
PubMed2001

Platelet glycoprotein IIIa Pl(a) polymorphism, fibrinogen, and platelet aggregability: The Framingham Heart Study.

BACKGROUND: Recent data suggest that the Pl(A2) allele of the platelet glycoprotein IIIa receptor may be a genetic risk factor for cardiovascular disease. We previously reported that the Pl(A2) allele was associated with increased platelet aggregability, as indicated by lower epinephrine threshold concentrations. Paradoxically, however, it has been reported that Pl(A2)-positive platelets have reduced fibrinogen binding. Because fibrinogen mediates platelet aggregability, we hypothesized that plasma fibrinogen levels may interact with Pl(A) genotype in modulating platelet aggregability. Methods and Results-- Glycoprotein IIIa Pl(A) genotype, fibrinogen level, and platelet aggregability were ascertained in 1340 subjects enrolled into the Framingham Offspring Study. Platelet aggregability was evaluated by the Born method. Higher fibrinogen levels were associated with increased epinephrine-induced aggregation (P=0.002) and a trend for ADP-induced aggregation (P=0.07). The fibrinogen effect was genotype specific, however, in that the increase in platelet aggregability with higher fibrinogen was present for the Pl(A1/A1) genotype (P=0.0005 and P=0.03 for epinephrine- and ADP-induced aggregation, respectively) but not for the Pl(A2)-positive genotype (P>0.90). CONCLUSION: Higher fibrinogen levels were associated with increased platelet aggregability. However, the association between fibrinogen and platelet aggregability was genotype specific. This interaction may be responsible for the conflicting findings regarding Pl(A) genotype and platelet aggregability. Further study of this gene-environment interaction may provide insight into cardiovascular disease risk.

Adenosine Diphosphate↗
PubMed2001

Genetic and environmental contributions to platelet aggregation: the Framingham heart study.

BACKGROUND: Platelet aggregation plays an important role in arterial thrombosis in coronary heart disease, stroke, and peripheral arterial disease. However, the contribution of genetic versus environmental influences on interindividual variation in platelet aggregability is poorly characterized. METHODS AND RESULTS: We studied the heritability of platelet aggregation responses in 2413 participants in the Framingham Heart Study. The threshold concentrations of epinephrine and ADP required to produce biphasic platelet aggregation and collagen lag time were determined. Mixed-model linear regression was used to calculate correlation coefficients within sibships and within spouse pairs. Variance and covariance component methods were used to estimate the proportion of platelet aggregation attributable to measured covariates versus additive genetic effects. After accounting for environmental covariates, the adjusted sibling correlations for epinephrine, ADP, and collagen lag time were 0.24, 0.22, and 0.31, respectively (P=0.0001 for each). In contrast, adjusted correlations for spouse-pairs were -0.01, 0.05, and -0.02, respectively (all P>0.30). The estimated heritabilities were 0.48, 0.44, and 0.62, respectively. Measured covariates accounted for only 4% to 7% of the overall variance in platelet aggregation, and heritable factors accounted for 20% to 30%. The platelet glycoprotein IIIa Pl(A2) polymorphism and the fibrinogen Hind III beta-148 polymorphism contributed <1% to the overall variance. CONCLUSIONS: In our large, population-based sample, heritable factors play a major role in determining platelet aggregation, and measured covariates play a lesser role. Future studies are warranted to identify the key genetic variants that regulate platelet function and to lay the groundwork for rational pharmacogenetic approaches.

Adenosine Diphosphate↗
PubMed2001

[Protective effect of c-fos antisense oligonucleotides on brain damage induced by glutamate].

OBJECTIVE: To investigate the relation between glutamate neurotoxicity and c-fos gene expression. METHODS: c-fos antisense oligonucleotides (AS ODN) was injected into the right lateral ventricles of 9 SD rats to block the c-fos gene expression in brain tissue. c-fos sense oligonucleotides (S ODN) was used a control. The numbers and morphology of neurons in both cerebral cortex and hippocampal CA1 were detected by MIAS-300 image analysing instrument. c-fos gene expression in brain was observed by immunohistochemical method. The content of water and electrolytes in the brain tissue and Ca(2+) in the synapse were measured. RESULTS: The c-fos AS ODN blocked the c-fos gene expression and reduced the content of both water and sodium in brain tissue and Ca(2+) in symptosome, thus alleviating the morphological damage in neuron. S ODN did not have such effect. CONCLUSION: c-fos gene expression plays an important role in mediating the effect of glutamate neurotoxicity. Blocking the c-fos gene expression could antagonize glutamate neurotoxicity.

Animals↗
PubMed2001

Hemostatic state and atrial fibrillation (the Framingham Offspring Study).

Atrial fibrillation (AF) is strongly associated with thromboembolic complications, although the mechanism for the increased risk has not been fully explained. To determine whether AF might be associated with a hypercoagulable state, we studied hemostatic factors in subjects with or without AF in the Framingham Heart Study. In 3,577 subjects, we measured fibrinogen, von Willebrand factor antigen, tissue plasminogen activator (tPA) antigen, and plasminogen activator inhibitor-1 antigen. Forty-seven subjects had AF at the index clinic examination and 15 had AF on a prior examination, but not on the current examination. Before matching, the 47 subjects with prevalent AF had higher levels of fibrinogen, von Willebrand factor, and tPA antigen than those without AF, all p < or =0.03. Compared with 167 referent subjects matched for age, sex, and other risk factors, those with AF had higher tPA antigen levels than those without AF, 1 1.8 +/- 4.0 ng/ml versus 10.5 +/- 3.9 ng/ml (p = 0.04). However, when further stratified according to their cardiovascular disease status, the differences in hemostatic factors were no longer significant. We conclude that the prothrombotic profile associated with AF was explained by the risk factors of the subjects and the presence of cardiovascular disease. Nonetheless, the hemostatic changes may contribute toward the propensity for thromboembolic complications in AF. Further prospective studies are needed to evaluate whether measurement of these and other hemostatic factors will identify patients with AF who are at increased risk for thromboembolic complications, and who may therefore benefit from more intensive therapy.

Aged↗
PubMed2001

Glomeruloid microvascular proliferation follows adenoviral vascular permeability factor/vascular endothelial growth factor-164 gene delivery.

Glomeruloid bodies are a defining histological feature of glioblastoma multiforme and some other tumors and vascular malformations. Little is known about their pathogenesis. We injected a nonreplicating adenoviral vector engineered to express vascular permeability factor/vascular endothelial growth factor-164 (VPF/VEGF(164)) into the ears of athymic mice. This vector infected local cells that strongly expressed VPF/VEGF(164) mRNA for 10 to 14 days, after which expression gradually declined. Locally expressed VPF/VEGF(164) induced an early increase in microvascular permeability, leading within 24 hours to edema and deposition of extravascular fibrin; in addition, many pre-existing microvessels enlarged to form thin-walled, pericyte-poor, "mother" vessels. Glomeruloid body precursors were first detected at 3 days as focal accumulations of rapidly proliferating cells in the endothelial lining of mother vessels, immediately adjacent to cells expressing VPF/VEGF(164). Initially, glomeruloid bodies were comprised of endothelial cells but subsequently pericytes and macrophages also participated. As they enlarged by endothelial cell and pericyte proliferation, glomeruloid bodies severely compromised mother vessel lumens and blood flow. Subsequently, as VPF/VEGF(164) expression declined, glomeruloid bodies devolved throughout a period of weeks by apoptosis and reorganization into normal-appearing microvessels. These results provide the first animal model for inducing glomeruloid bodies and indicate that VPF/VEGF(164) is sufficient for their induction and necessary for their maintenance.

Adenoviridae↗
PubMed2001

A general algorithm for optimal sampling schedule design in nuclear medicine imaging.

Optimal sampling schedule (OSS) is of great interest in biomedical experiment design, as it can improve the physiological parameter estimation precision and significantly reduce the samples required. A number of well designed algorithms and software packages have been developed, which deal with the instantaneous measurements at discrete times. However, in nuclear medicine tracer kinetic studies, the imaging systems, such as positron emission tomography (PET) and single photon emission computed tomography (SPECT), take measurements (images) based on continuous accumulation over time intervals. In this case, the existing algorithms cannot be used to design OSS so as to reduce the image frame numbers. In this paper, a general OSS design algorithm for the accumulative measurement is proposed. The potential usefulness of the algorithm is demonstrated by its designing OSS in [18F] fluoro-2-deoxy-D-glucose (FDG) studies with PET to estimate the local cerebral metabolic rate of glucose. The robustness of parameter estimation using the OSS with respect to intra-subject and inter-subject parameter variations is also presented.

Algorithms↗
PubMed2001

Study on examinee's dose delivered in computed tomography.

Dose profiles are presented resulting from computed tomography (CT). The profiles are positioned at the central axis, 1 cm away from the outer surface of the phantom, for single and multiple scans. A Hitachi W-1000 scanner is used with a thermoluminescent dosimeter (TLD), and standard dosimetry head and trunk phantoms. Regression equations are found linking the dose resulting from scattered radiation associated with a single scan to the distance from the scanning centre. The impact on the CT dose index value (CTDI) for varying integrating lengths is analysed. Some problems associated with CT dose measurement are noted, which may assist in the practical application of IBSS (International Basic Standard of Radiation Protection and Safety of Radiation Sources) guide levels.

Abdomen↗
PubMed2001

Simultaneous estimation of physiological parameters and the input function--in vivo PET data.

Dynamic imaging with positron emission tomography (PET) is widely used for the in vivo measurement of regional cerebral metabolic rate for glucose (rCMRGlc) with [18F]fluorodeoxy-D-glucose (FDG) and is used for the clinical evaluation of neurological disease. However, in addition to the acquisition of dynamic images, continuous arterial blood sampling is the conventional method to obtain the tracer time-activity curve in blood (or plasma) for the numeric estimation of rCMRGlc in mg glucose/100-g tissue/min. The insertion of arterial lines and the subsequent collection and processing of multiple blood samples are impractical for clinical PET studies because it is invasive, has the remote, but real potential for producing limb ischemia, and it exposes personnel to additional radiation and risks associated with handling blood. In this paper, based on our previously proposed method for extracting kinetic parameters from dynamic PET images, we developed a modified version (post-estimation method) to improve the numerical identifiability of the parameter estimates when we deal with data obtained from clinical studies. We applied both methods to dynamic neurologic FDG PET studies in three adults. We found that the input function and parameter estimates obtained with our noninvasive methods agreed well with those estimated from the gold standard method of arterial blood sampling and that rCMRGlc estimates were highly correlated (r = 0.973). More importantly, no significant difference was found between rCMRGlc estimated by our methods and the gold standard method (P > 0.16). We suggest that our proposed noninvasive methods may offer an advance over existing methods.

Adult↗
PubMed2001

Microwave-induced thermoacoustic tomography: reconstruction by synthetic aperture.

We have applied the synthetic-aperture method to linear-scanning microwave-induced thermoacoustic tomography in biological tissues. A nonfocused ultrasonic transducer was used to receive thermoacoustic signals, to which the delay-and-sum algorithm was applied for image reconstruction. We greatly improved the lateral resolution of images and acquired a clear view of the circular boundaries of buried cylindrical objects, which could not be obtained in conventional linear-scanning microwave-induced thermoacoustic tomography based on focused transducers. Two microwave sources, which had frequencies of 9 and 3 GHz, respectively, were used in the experiments for comparison. The 3 GHz system had a much larger imaging depth but a lower signal-noise ratio than the 9 GHz system in near-surface imaging.

Acoustics↗
PubMed2001

Ultrastructural localization of vesicle-associated membrane protein(s) to specialized membrane structures in human pericytes, vascular smooth muscle cells, endothelial cells, neutrophils, and eosinophils.

Vesicle-associated membrane proteins (VAMPs) are important to the trafficking of vesicles between membrane-bound intracytoplasmic organelles, in the facilitation of neurosecretion, and in constitutive and regulated secretion in non-neuronal cells. We used a pre-embedding ultrastructural immunonanogold method to localize VAMPs to subcellular sites in human cells of five lineages known to have cytoplasmic vesicles that may function in vesicular transport. We found VAMPs localized to caveolae in pericytes, vascular smooth muscle cells, and endothelial cells of venules, to the vesiculo-vacuolar organelle, recently defined in venular endothelial cells, to the vesicle-rich intergranular cytoplasm and secretory granule membranes of neutrophils, and to perigranular cytoplasmic secretory vesicles and secretory granule membranes in eosinophils. These specific localizations in five human vascular and granulocyte lineages support the notion that VAMPs have vesicle-associated functions in these cells.

Adult↗
PubMed2001

The vesiculo-vacuolar organelle (VVO). A new endothelial cell permeability organelle.

A newly defined endothelial cell permeability structure, termed the vesiculo-vacuolar organelle (VVO), has been identified in the microvasculature that accompanies tumors, in venules associated with allergic inflammation, and in the endothelia of normal venules. This organelle provides the major route of extravasation of macromolecules at sites of increased vascular permeability induced by vascular permeability factor/vascular endothelial growth factor (VPF/VEGF), serotonin, and histamine in animal models. Continuity of these large sessile structures between the vascular lumen and the extracellular space has been demonstrated in kinetic studies with ultrastructural electron-dense tracers, by direct observation of tilted electron micrographs, and by ultrathin serial sections with three-dimensional computer reconstructions. Ultrastructural enzyme-affinity cytochemical and immunocytochemical studies have identified histamine and VPF/VEGF bound to VVOs in vivo in animal models in which these mediators of permeability are released from mast cells and tumor cells, respectively. The high-affinity receptor for VPF/VEGF, VEGFR-2, was localized to VVOs and their substructural components by pre-embedding ultrastructural immunonanogold and immunoperoxidase techniques. Similar methods were used to localize caveolin and vesicle-associated membrane protein (VAMP) to VVOs and caveolae, indicating a possible commonality of formation and function of VVOs to caveolae.

Animals↗
PubMed2001

[Effect of hepatitis C virus nonstructural protein NS3 on telomerase activity].

OBJECTIVE: To study the effect of hepatitis C virus nonstructural protein NS3 (HCV NS3) on telomerase activity and its carcinogenesis, and to observe the practical use of in situ telomerase activity labeling. METHODS: NIH3T3 cells were transfected with plasmid pRcHCNS3-5prime prime or minute (expressing HCV NS3 C-terminal deleted protein), pRcHCNS3-3prime prime or minute (expressing HCV NS3 N-terminal deleted protein) and blank plasmid pRcCMV. Positive clones, 11 with plasmid pRcHCNS3-5prime prime or minute, 11 with pRcHCNS3-3prime prime or minute and 8 with plasmid pRcCMV were harvested respectively. Streptavidin-peroxidase conjugated method (SP) was used to detect the expression of HCV NS3 protein in NIH3T3 cells transfected with plasmid pRcHCNS3-5prime prime or minute and pRcHCNS3-3prime prime or minute. Telomerase activity was detected by in situ telomerase activity labeling method and telomerase PCR ELISA technique in the transfected and non-transfected NIH3T3 cells. RESULTS: HCV NS3 protein was expressed in the cells transfected with plasmid pRcHCNS3-5prime prime or minute or plasmid pRcHCNS3-3prime prime or minute. The positive signals of HCV NS3 protein were localized in the cytoplasm of transfected NIH3T3 cells, and the signal intensity of the former was stronger (chi(2) = 6.667 P < 0.05). There was significant difference on telomerase activity between each group (F = 134.083 P < 0.01). Telomerase activity in all 11 clones with plasmid pRcHCNS3-5prime prime or minute was stronger than cells with plasmid pRcHCNS3-3prime prime or minute (P < 0.01), whereas telomerase activity in NIH3T3 cells transfected with the plasmid pRcCMV or non-transfected NIH3T3 cells were weaker than the cells with the plasmid pRcHCNS3-3prime prime or minute. The expression level of HCV NS3 protein were correlated significantly with the strength of telomerase activity (rs = 0.8084 P < 0.01). The results obtained with in situ telomerase activity labeling corresponded to those with telomerase PCR ELISA technique (rs = 0.50196 P < 0.01). CONCLUSIONS: (1) HCV NS3 protein may activate telomerase through endogenous mechanism to induce host cells transformation. (2) The effect of HCV NS3 C-terminal deleted protein on telomerase activity in host cells may be more intense than that of HCV NS3 N-terminal deleted protein. (3) In situ telomerase activity labeling is a reliable technique for studying pathological morphology and telomerase activity in tissues and cells.

3T3 Cells↗