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Biomedical subjects

H Qian

Publications and source records attributed to H Qian.

At least 37 records · Page 2Linked to original sources
PubMed2001

TNFalpha induces and insulin inhibits caspase 3-dependent adipocyte apoptosis.

Regulation of fat cell number by apoptosis is proposed to be part of a normal physiological cycle in adipose growth and development. To investigate this process, cultured rat adipocytes were treated with various concentrations of tumor necrosis factor alpha (TNFalpha) and/or insulin to determine the roles of these factors in adipocyte apoptosis. The cells were analyzed by flow cytometry using a TUNEL assay. TNFalpha increased adipocyte apoptosis in a dose-dependent fashion. TNFalpha-mediated apoptosis was detectable within 6 h of treatment and continued to increase with time. Decreasing media insulin concentration from 8.5 to 0.85 nM resulted in increased adipocyte apoptosis, whereas high doses of insulin protected adipocytes from TNFalpha-induced apoptosis. TNFalpha-activated apoptosis was accompanied by an increase in caspase 3 activity and could be inhibited by a caspase 3-specific inhibitor. These data suggest that adipose tissue cell number is regulated, in part, by an apoptotic signaling pathway that involves TNFalpha, insulin, and caspase 3.

Adipocytes↗
PubMed2001

Relative entropy: free energy associated with equilibrium fluctuations and nonequilibrium deviations.

Using a one-dimensional macromolecule in aqueous solution as an illustration, we demonstrate that the relative entropy from information theory, Sigma(k)p(k) ln(p(k)/p(*)(k)), has a natural role in the energetics of equilibrium and nonequilibrium conformational fluctuations of the single molecule. It is identified as the free energy difference associated with a fluctuating density in equilibrium, and is associated with the distribution deviate from the equilibrium in nonequilibrium relaxation. This result can be generalized to any other isothermal macromolecular system using the mathematical theories of large deviations and Markov processes, and at the same time provides the well-known mathematical results with interesting physical interpretations.

Journal Article↗
PubMed2001

Protein and DNA oxidation in spinal injury: neurofilaments--an oxidation target.

This study measured the time courses of protein and DNA oxidation following spinal cord injury (SCI) in rats and characterized oxidative degradation of proteins. Protein carbonyl content-a marker of protein oxidation-significantly increased at 3-9 h postinjury and the ratio 8-hydroxy-2-deoxyguanosine/deoxyguanosine-an indicator of DNA oxidation-was significantly higher at 3-6 h postinjury in the injured cords than in the sham controls. This suggests that oxidative modification of proteins and DNA contributes to secondary damage in SCI. Densities of selected bands on coomassie-stained gels indicated that most proteins were degraded. Neurofilament protein (NFP) was particularly evaluated immunohistochemically; its light chain (NFP-68) was gradually degraded in nerve fibers, neuron bodies, and large dendrites following SCI. A mixture of Mn (III) tetrakis (4-benzoic acid) porphyrin (10 mg/kg)-a novel SOD mimetic-and nitro-L-arginine (1 mg/kg)-an inhibitor of nitric oxide synthase-injected intraperitoneally, increased NFP-68 immunoreactivity and the numbers of NFP-positive nerve fibers post-SCI, correlating NFP degradation in SCI to free radical-triggered oxidative damage for the first time. Therefore, blockage of protein and DNA oxidation in the secondary injury stage may improve long-term recovery-important information for development of the SCI therapies.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

Casein kinase II sites in the intracellular C-terminal domain of the thyrotropin-releasing hormone receptor and chimeric gonadotropin-releasing hormone receptors contribute to beta-arrestin-dependent internalization.

We have previously shown that the mammalian gonadotropin-releasing hormone receptor (GnRHR), a unique G-protein-coupled receptor (GPCR) lacking an intracellular carboxyl tail (C-tail), does not follow a beta-arrestin-dependent internalization pathway. However, internalization of a chimeric GnRHR with the thyrotropin-releasing hormone receptor (TRHR) C-tail does utilize beta-arrestin. Here, we have investigated the sites within the intracellular C-tail domain that are important for conferring beta-arrestin-dependent internalization. In contrast to the chimeric GnRHR with a TRHR C-tail, a chimeric GnRHR with the catfish GnRHR C-tail is not beta-arrestin-dependent. Sequence comparisons between these chimeric receptors show three consensus phosphorylation sites for casein kinase II (CKII) in the TRHR C-tail but none in the catfish GnRHR C-tail. We thus investigated a role for CKII sites in determining GPCR internalization via beta-arrestin. Sequential introduction of three CKII sites into the chimera with the catfish C-tail (H354D,A366E,G371D) resulted in a change in the pattern of receptor phosphorylation and beta-arrestin-dependence, which only occurred when all three sites were introduced. Conversely, mutation of the putative CKII sites (T365A,T371A,S383A) in the C-tail of a beta-arrestin-sensitive GPCR, the TRHR, resulted in decreased receptor phosphorylation and a loss of beta-arrestin-dependence. Mutation of all three CKII sites was necessary before a loss of beta-arrestin-dependence was observed. Visualization of beta-arrestin/GFP redistribution confirmed a loss or gain of beta-arrestin sensitivity for receptor mutants. Internalization of receptors without C-tail CKII sites was promoted by a phosphorylation-independent beta-arrestin mutant (R169E), suggesting that these receptors do not contain the necessary phosphorylation sites required for beta-arrestin-dependent internalization. Apigenin, a specific CKII inhibitor, blocked the increase in receptor internalization by beta-arrestin, thus providing further support for the involvement of CKII. This study presents evidence of a novel role for C-tail CKII consensus sites in targeting these GPCRs to the beta-arrestin-dependent pathway.

Amino Acid Sequence↗
PubMed2001

Responses of small- and large-field bipolar cells to GABA and glycine.

Morphologically distinct subtypes of retinal bipolar cells transmit information along parallel pathways to convey different aspects of the visual scene, but the synaptic mechanisms that regulate signal transmission are largely unknown. The all-rod retina of skate provides a comparatively simple system in which to correlate bipolar cell morphology with responses to the inhibitory neurotransmitters GABA and glycine. Two subtypes of bipolar cells can be identified when isolated in culture: large-field bipolar cells with extensive dendritic arbors, and small-field bipolar cells with one or two dendritic branches. Under voltage-clamp, glycine elicited significant current responses from small-field cells, but not from large-field bipolar cells. Although all bipolar cells displayed GABA-activated chloride currents mediated by both GABA(A) and GABA(C) receptors, the small-field bipolar cells showed a significantly greater contribution from GABA(A) receptors. The results of the present study reveal for the first time that the relative expression of the two classes of GABA receptor on each bipolar cell type correlates with cell morphology and the presence of the glycine receptor.

Animals↗
PubMed2001

p27-p16 Chimera: a superior antiproliferative for the prevention of neointimal hyperplasia.

Cyclin-dependent kinase inhibitors (CDKi's) may be useful to treat hyperproliferative vascular disorders, such as restenosis induced following angioplasty or vein engraftment. We have shown that a novel fusion protein of the CDKi's p27 and p16, named W9, significantly reduces proliferation of human coronary smooth muscle cells in vitro, by blocking cell proliferation without inducing apoptosis. We have now evaluated the efficacy of adenovirus-mediated gene transfer of W9 (AV-W9) in a balloon-injury model, in the carotid arteries of cholesterol-fed rabbits. We observed that intravascular delivery of 2 x 10(11) viral particles of AV-W9 3 days following balloon injury inhibited intimal hyperplasia by 60% compared to a control virus (P > 0.001). PCNA expression in the AV-W9-treated vessels, a marker of injury-induced cell proliferation, was also reduced compared to the control virus-treated vessels. Direct comparison of the efficacy of AV-W9 and AV-p16 and AV-p27 in this model indicated that delivery of either of the parental genes was significantly less effective in inhibiting intimal thickening compared to the AV-W9 treatment. We conclude that combining the activities of multiple cell cycle regulatory proteins greatly increases the potency of cytostatic gene therapy in the treatment of balloon injury-induced intimal hyperplasia and represents a promising potential approach to preventing postangioplasty restenosis.

Adenoviridae↗
PubMed2001

The influence of PDL principal fibers in a 3-dimensional analysis of orthodontic tooth movement.

The effects of mechanical loads on the tooth-alveolus complex are of particular concern in orthodontics. The concepts of center of resistance (CRes) and center of rotation (CRot) are used to characterize tooth responses to orthodontic loads. The mechanical environment (stresses and strains) associated with orthodontic tooth movement is a unique model in bone adaptation physiology. Numerous finite element models of varying complexity have been developed to calculate tooth movements and stress distributions within the alveolar bone and the periodontal ligament (PDL). In general, the PDL has been idealized as a homogeneous isotropic material. For this project, a 3-dimensional tooth/PDL/mandible/finite element model was developed in which, for the first time in such an analysis, the PDL's principal-fiber structure was also incorporated. Parametric analyses showed that the fiber orientation and the mechanical properties do not exert much influence on the locations of the CRes and the CRot and on the stress patterns within the bone and the PDL matrix. However, the absence of principal fibers produces not only different stress magnitudes, but also differences in stress patterns. Furthermore, the no-fiber-associated CRes and CRot are considerably separated from the cluster of fiber-influenced centers. It was concluded that it may be more realistic to incorporate "generic" principal fibers into finite element models than not to include them at all, despite the lack of reliable information about fibers.

Alveolar Process↗
PubMed2001

A mechanism of noncontinuous supraosseous tooth eruption.

Numerous theories have been propounded to explain the various aspects of tooth eruption, but no general consensus exists about some of the underlying mechanisms that govern these aspects. An important unresolved issue is the source of the motive forces that displace teeth. We proposed that supraosseous eruptive forces are generated by tooth socket distortions caused by functional jaw deformations. Previous studies used basic equations of static equilibrium to demonstrate that the concomitant stretching of the oblique periodontal ligament (PDL) fibers give rise to forces that may cause supraosseous tooth eruption. For a more rigorous and expanded analysis, we applied the finite element method (FEM). Three functional loads were considered, but the FEM calculations strongly suggested that all jaw deformations contribute to tooth extrusion. It was also demonstrated that the PDL fiber disruptions that are likely to occur with increased stretching can provide a mechanism to stabilize the erupted position.

Computer Simulation↗
PubMed2001

Association of beta-Arrestin 1 with the type 1A angiotensin II receptor involves phosphorylation of the receptor carboxyl terminus and correlates with receptor internalization.

Arrestins bind to phosphorylated G protein-coupled receptors and participate in receptor desensitization and endocytosis. Although arrestins traffic with activated type 1 (AT(1A)) angiotensin II (AngII) receptors, the contribution of arrestins to AT(1A) receptor internalization is controversial, and the physical association of arrestins with the AT(1A) receptor has not been established. In this study, by coimmunoprecipitating AT(1A) receptors and beta-arrestin 1, we provide direct evidence for an association between arrestins and the AT(1A) receptor that was agonist- and time-dependent and contingent upon the level of beta-arrestin 1 expression. Serial truncation of the receptor carboxyl terminus resulted in a graded loss of beta-arrestin 1 association, which correlated with decreases in receptor phosphorylation. Truncation of the AT(1A) receptor to lysine(325) prevented AngII-induced phosphorylation and beta-arrestin 1 association as well as markedly inhibiting receptor internalization, indicating a close correlation between these receptor parameters. AngII-induced association was also dramatically reduced in a phosphorylation- and internalization-impaired receptor mutant in which four serine and threonine residues in the central portion of the AT(1A) receptor carboxyl terminus (Thr(332), Ser(335), Thr(336), Ser(338)) were substituted with alanine. In contrast, substitutions in another serine/threonine-rich region (Ser(346), Ser(347), Ser(348)) and at three PKC phosphorylation sites (Ser(331), Ser(338), Ser(348)) had no effect on AngII-induced beta-arrestin 1 association or receptor internalization. While AT(1A) receptor internalization could be inhibited by a dominant-negative beta-arrestin 1 mutant (beta arr1(319-418)), treatment with hyperosmotic sucrose to inhibit internalization did not abrogate the differences in arrestin association observed between the wild-type and mutant receptors, indicating that arrestin binding precedes, and is not dependent upon, receptor internalization. Interestingly, a substituted analog of AngII, [Sar(1)Ile(4)Ile(8)]-AngII, which promotes robust phosphorylation of the receptor but does not activate receptor signaling, stimulated strong beta-arrestin 1 association with the full-length AT(1A) receptor. These results identify the central portion of the AT(1A) receptor carboxyl terminus as the important determinant for beta-arrestin 1 binding and internalization and indicate that AT(1A) receptor phosphorylation is crucial for beta-arrestin docking.

Amino Acid Sequence↗
PubMed2001

Dietary boron supplementation enhanced the action of estrogen, but not that of parathyroid hormone, to improve trabecular bone quality in ovariectomized rats.

This study investigated whether boron would enhance the ability of 17beta-estradiol (E2) or parathyroid hormone (PTH) to improve bone quality in ovariectomized OVX rats. Adult OVX rats were treated for 5 wk with vehicle, boron (5 ppm as boric acid), E2 (30 microg/kg/d, sc), PTH (60 microg/kg/d, sc), or a combination of boron and E2 or PTH, respectively. The E2 treatment corrected many adverse effects of OVX on bone quality, increased bone Ca, P, and Mg contents, and decreased trabecular plate separation. Dietary boron supplementation had no effects on these bone parameters in OVX rats. When OVX rats were treated with boron and E2 together, trabecular bone volume (Tb.BS/TV) and plate density were increased significantly more than that caused by E2 alone. The boron and E2 combination also increased trabecular bone surface (Tb.BV/TV) and decreased trabecular plate separation in OVX rats. In contrast, whereas daily PTH injection also increased bone Ca, Mg, and P contents, Tb.BV/TV, Tb.BS/TV, trabecular plate density and thickness, and decreased trabecular plate separation in OVX rats, the combination of boron and PTH had no additional improvement in bone quality over that achieved by PTH alone. In summary, this study shows for the first time that boron enhanced the action of E2, but not that of PTH, to improve trabecular bone quality in OVX rats.

Animals↗
PubMed2001

Central norepinephrine pathways are involved in cardiovascular response to intracerebroventricular substance P.

AIM: To study the role of norepinephrine system in the cardiovascular response to intracerebroventricular substance P (SP) in rabbit. METHODS: SP was given intracerebroventricularly in anesthetized rabbits pretreated with the catecholaminergic neurotoxin, 6-hydroxydopamine (6-OHDA). The density and affinity of SP receptors on synaptosomal membranes of the hypothalamus and the ventral medulla of rabbits were determined by [125I]SP receptor assay. Arterial blood pressure and heart rate were recorded. RESULTS: Intracerebroventricular (icv) pretreatment of rabbits with 6-OHDA, reduced norepinephrine in the hypothalamus (by 86.7 %) and in the ventral medulla (by 77.0 %) respectively. The pressor response and tachycardia of these rabbits to icv SP (3.55 nmol . kg-1) were attenuated. The density and the affinity of SP receptors in the hypothalamus and the ventral medulla of 6-OHDA-lesioned rabbits were decreased. The Bmax (pmol . g-1 protein) of SP receptors in hypothalamus and the ventral medulla are 108 +/- 5, 35.9 +/- 2.2 in control group, and 42 +/- 18, 20 +/- 5 in 6-OHDA-lesioned rabbits, respectively. Kd (nmol . L-1) of SP receptors in the two regions are 0.015 +/- 0.004, 0.014 +/- 0.006 in control group and 0.029 +/- 0.001, 0.015 +/- 0.003 in 6-OHDA group. There is a significant difference of Bmax (P < 0.01) and Kd (P < 0.01, P < 0.05) in both regions between 6-OHDA groups and control groups. CONCLUSION: The results suggested that central norepinephrine pathways are involved in the cardiovascular response to icv SP.

Animals↗
PubMed2001

[Studies on the manufacture and immunogenicity of purified rabies vaccines on humans Vero cell].

OBJECTIVE: Using Vero cell as basic cultural material to improve the quality of rabies vaccines and to produce rabies vaccines for humans. METHODS: CTN-1V10 strain were used for production. Vero cell of 150th generation were used for cultivation. Rotating cultivatal method with rotating bottle was used. Fluids with virus were collected at different time. Puritied rabies vaccine was produced on Vero cell after clarification, condensation, purification and extermination. A batch of vaccines made by this techniques were used for immunological observation. Sixty-three people were injected with this rabies vaccine according to the procedure of time of exposure. Thirty of them were injected with vaccines made in France (Verorab) while the others were injected with vaccines to be tested. Side effect and neutralizing antibody were recorded. RESULTS: The quality of this newly developed rabies vaccines has met the quality set by WHO. After all dosages of injection, the rates of positive antibody were both 100% in two groups. The neutralizing antibody among testing group was 11.94 IU/ml comparing with control as 11.69 IU/ml. CONCLUSION: Purified rabies vaccines on Vero cell for humans had reasonable manufacture technique and less little effect with good technological imnunogenicity.

Animals↗
PubMed2001

[Relationship between Streptococcus mutans, Lactobacillus spp. and lactate-producing level and nursing bottle caries].

OBJECTIVE: The study aimed to investigate the levels of Streptococcus mutans and Lactobacillus spp. as well as the relationship between lactate-productive and aciduric organisms and nursing bottle caries. METHODS: Totally, 30 children of 2- to 2.5-year-old were divided into two groups, including the group of nursing bottle caries and the group of caries-free. Streptococcus mutans and Lactobacillus spp. were isolated from dental plaque of all the children. The amount of lactate produced was measured with a microlitre plate reader. RESULTS: The isolation frequency of Streptococcus mutans and Lactobacillus spp. were both 100 percent in the children with nursing bottle caries, and that the composition of these bacteria from nursing bottle caries lesions was higher than that of caries-free dental surface. Lactate-producing level was higher in the caries group than that of the caries-free group. CONCLUSION: This study suggests Streptococcus mutans and Lactobacillus spp. may be the major pathogenic bacteria leading to nursing bottle caries.

Bottle Feeding↗
PubMed2000

Large-scale processes and the Asian bias in species diversity of temperate plants.

An important issue in the study of biodiversity is the extent to which global patterns of species richness reflect large-scale processes and historical contingencies. Ecological interactions in local assemblages may constrain the number of species that can coexist, but differences in diversity in similar habitats within different regions (diversity anomalies) suggest that this limit is not firm. Variation in rate of species production could influence regional and perhaps local diversity independently of the ecological capacity of an area to support coexisting species, thereby creating diversity anomalies. Temperate Zone genera of plants that are disjunct between similar environments in eastern Asia and eastern North America (EAS-ENA) have twice as many species in Asia as in North America. Because lineages of these genera in Asia and North America are mostly sister pairs, they share a common history of adaptation and ecological relationship before disjunction. Thus, the diversity anomaly in EAS-ENA genera is not an artefact of taxon or habitat sampling but reflects differences in the net diversification (speciation-extinction) of the lineages in each of the continents. Here we propose that the most probable cause of the EAS-ENA anomaly in diversity is the extreme physiographical heterogeneity of temperate eastern Asia, especially compared with eastern North America, which in conjunction with climate and sea-level change has provided abundant opportunities for evolutionary radiation through allopatric speciation.

Asia↗
PubMed2000

A class of flow bifurcation models with lognormal distribution and fractal dispersion.

We report a quantitative analysis of a simple dichotomous branching tree model for blood flow in vascular networks. Using the method of moment-generating function and geometric Brownian motion from stochastic mathematics, our analysis shows that a vascular network with asymmetric branching and random variation at each bifurcating point gives rise to an asymptotic lognormal flow distribution with a positive skewness. The model exhibits a fractal scaling in the dispersion of the regional flow in the branches. Experimentally measurable fractal dimension of the relative dispersion in regional flow is analytically calculated in terms of the asymmetry and the variance at local bifurcation; hence the model suggests a powerful method to obtain the physiological information on local flow bifurcation in terms of flow dispersion analysis. Both the fractal behavior and the lognormal distribution are intimately related to the fact that it is the logarithm of flow, rather than flow itself, which is the natural variable in the tree models. The kinetics of tracer washout is also discussed in terms of the lognormal distribution.

Animals↗