Biomedical subjects
Publications and source records attributed to H Ding.
Protein iron-sulfur (FeS) centers have recently been implicated in the regulation of gene expression. In the redox-sensing SoxR protein, the oxidation state of [2Fe-2S] centers controls its activity as a transcription activator independent of DNA-binding ability. Thus, FeS centers allosterically link cellular oxidative stress to the expression of defense genes.
Binding of 125I-labelled alpha 2-macroglobulin (alpha 2M) to Actinomyces pyogenes was investigated. The binding of alpha 2M proved to be time dependent, saturable, and could be inhibited by unlabelled alpha 2M, but not by fibrinogen, haptoglobin, fibronectin, or albumin. The alpha 2M binding site was sensitive to treatment with proteolytic enzymes and heat, indicating its protein nature. The dissociation constant (Kd) was 4.447 x 10(-9) M, and the number of binding sites per bacterial cell was calculated to be 5200. The kinetic analysis indicated an homogeneous population of binding sites. Binding of alpha 2M to the surface of A. pyogenes had no significant influence on the phagocytosis of the bacteria by polymorphonuclear leucocytes.
The relationship between maternal exposure to air pollution during periods of pregnancy (entire and specific periods) and birth weight was investigated in a well-defined cohort. Between 1988 and 1991, all pregnant women living in four residential areas of Beijing were registered and followed from early pregnancy until delivery. Information on individual mothers and infants was collected. Daily air pollution data were obtained independently. The sample for analysis included 74,671 first-parity live births were gestational age 37-44 weeks. Multiple linear regression and logistic regression were used to estimate the effects of air pollution on birth weight and low birth weight (< 2,500 g), adjusting for gestational age, residence, year of birth, maternal age, and infant gender. There was a significant exposure-response relationship between maternal exposures to sulfur dioxide (SO2) and total suspended particles (TSP) during the third trimester of pregnancy and infant birth weight. The adjusted odds ratio for low birth weight was 1.11 (95% CI, 1.06-1.16) for each 100 micrograms/m3 increase in SO2 and 1.10 (95% CI, 1.05-1.14) for each 100 micrograms/m3 increase in TSP. The estimated reduction in birth weight was 7.3 g and 6.9 g for each 100 micrograms/m3 increase in SO2 and in TSP, respectively. The birth weight distribution of the high-exposure group was more skewed toward the left tail (i.e., with higher proportion of births < 2,500 g) than that of the low-exposure group. Although the effects of other unmeasured risk factors cannot be excluded with certainty, our data suggests that TSP and SO2, or a more complex pollution mixture associated with these pollutants, contribute to an excess risk of low birth weight in the Beijing population.
The effects of high dietary zinc on alloxan induced diabetic mice were studied. The results showed that high zinc could sharply decrease the body weight and increase food intake, water intake and urine of diabetic mice, and increase blood sugar levels in diabetic mice. After alloxan injection in diabetic model group, urine sugar levels reached [symbol: see text] at the 2nd day and [symbol: see text] at the 6th day. After alloxan injection in high-zinc-diabetic mice group, urine sugar levels reached [symbol: see text] and [symbol: see text] at the 2nd and the 4th day, respectively. These results suggested that the high level of dietary zinc may be damage to diabetic patients.
The effects of high-dietary-zinc (HZ, 1.5 g/kg) on growth, blood composition and immune function were studied with a high-dietary-zinc model of mice. By 3 weeks, the body weight and food consumption of mice were significantly lower in HZ group than those in control group. The concentrations of hemoglobin and blood calcium decreased significantly and the platelet and cholesterol levels increased significantly in HZ group. The HZ group showed a spleen swelling and depressed immune function.
In order to investigate the expression of Epstein-Barr virus in human laryngeal carcinoma, immunohistochemical study for Epstein-Barr virus latent membrane protein (EBV LMP) was performed on 90 laryngeal specimens taken from laryngeal carcinoma patients. The results showed that LMP was localized on the cell membrane and in cytoplasm. LMP was detected in 41 of 90 (45.5%) laryngeal squamous cell carcinoma, among them the positive rates of poorly differentiated, middle differentiated and well differentiated squamous carcinoma were 44% (12/27), 52% (25/47) and 26.6% (4/15) respectively. This study indicated that EB virus was not only presented in poorly differentiated carcinoma, it was also presented in well differentiated carcinoma. The development of laryngeal squamous carcinoma is related to the infection of EB virus.
A chiral RP-HPLC method was developed to assay the 5-(p-hydroxyphenyl)-5-Phenylhydantoin (p-HPPH) enantiomers, the major metabolite of antiepileptic drug phenytoin, in rat hepatic microsomes. A 50 mm FLC-C8 column was used as the analytical column, beta-cyclodextrin (beta-CD) as chiral mobile phase additive and phenobarbital as the internal standard. The detection wavelength was 250 nm. The linear range of p-HPPH enantiomers was 0.5-110 mg/L. The detection limit was 5 ng (S/N = 3). The recoveries of S- and R-p-HPPH were 93.6% +/- 2.8% and 94.7% +/- 1.8% respectively. The RSD within day and between days were less than 2%. The concentration of beta-CD played an important role in separating chiral enantiomers. When the concentration of beta-CD was between 8.8 and 13.2 mmol/L the resolution of p-HPPH enantiomers had the largest value Rs = -1.1. In this work, 8.8 mmol/L beta-CD solution (4 g beta-CD, 6 g urea, and 1.5 g ammonium acetate in 400 mL water) was selected in considering some factors such as column efficiency, solubility of beta-CD etc. Urea can increase the solubility of beta-CD. When urea: beta-CD = 1:1-1.5:1 (g/g), the solubilization of beta-CD was significant. Methanol concentration in mobile phase affected retention time, resolution of p-HPPH enantiomers and solubility of beta-CD.
The surface pressure/molecular area isotherms ( pi approximately A ) of lanthanium bisphthalocyanine were investigated, showing an edge-on molecular orientation of the macrocycle rings on the water subphase. Langmuir-Blodgett films of this compound were prepared and characterized using IR, UV-vis absorption spectroscopy.
The structure of tris- (2, 4-di-t-amylpheoxy) - (8-quinolinoxy) copper phthalocyanine (CuPc) thin solid films has been characterized by Fourier transform infrared (FTIR) transmission, polarized transmission and reflection absorption (RA) spectroscopy. The following conclusions can be obtained from the above measurements: (1)in LB films, the hydrocarbon chains of CuPc are in hexagonal or pseudohexagonal subcell packing, the CH2 asymmetric vibrational vector is oriented with respect to the substrate surface and the RA spectroscopy can distinguish the two CH2 streching modes of benzene cycle; (2)in sublimed films, the molecules of CuPc are out of order.
The apparatus of Faraday effect LMR used for the detection of 14N 16O and 15N 16O is described in this paper. We gave and analyzed the spectra of FLMR of 14N 16OX2pi3/2 (1. 5) v =0-->1 transition and 15N 16OX2pi3/2Q(1.5) v =0-->1 transition. The dependence of FLMR signal on the sample molecular concentration has been stadied.
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SoxR protein is a redox-responsive transcription factor that governs a regulon of oxidative stress and antibiotic resistance genes in Escherichia coli. Purified SoxR contains oxidized [2Fe-2S] clusters and stimulates in vitro transcription of its target gene soxS up to 100-fold. SoxR transcriptional activity, but not DNA binding, is completely dependent on the [2Fe-2S] clusters; apo-SoxR prepared in vitro binds the soxS promoter with unchanged affinity but does not have transcription activity. Thus, modulation of the SoxR [2Fe-2S] clusters was proposed to control the protein's function in transcription. Here, we provide evidence that SoxR with reduced [2Fe-2S] clusters is inactive. Redox titration of purified SoxR revealed a midpoint potential of -285 +/- 10 mV (pH 7.6). In vitro transcription assays showed that SoxR was inactivated when the [2Fe-2S] cluster was reduced (-380 mV), and full activity was restored upon reoxidation (+100 mV). The results suggest that one-electron oxidation and reduction of the [2Fe-2S] cluster regulate SoxR transcriptional activity.
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SoxR is a transcription factor that governs a global defense against the oxidative stress caused by nitric oxide or excess superoxide in Escherichia coli. SoxR is a homodimer containing a pair of [2Fe-2S] clusters essential for its transcriptional activity, and changes in the stability of these metal centers could contribute to the activation or inactivation of SoxR in vivo. Herein we show that reduced glutathione (GSH) in aerobic solution disrupts the SoxR [2Fe-2S] clusters, releasing Fe from the protein and eliminating SoxR transcriptional activity. This disassembly process evidently involves oxygen-derived free radicals. The loss of [2Fe-2S] clusters does not occur in anaerobic solution and is blocked in aerobic solution by the addition of superoxide dismutase and catalase. Although H2O2 or xanthine oxidase and hypoxanthine (to generate superoxide) were insufficient on their own to cause [2Fe-2S] cluster loss, they did accelerate the rate of disassembly after GSH addition. Oxidized GSH alone was ineffective in disrupting the clusters, but the rate of [2Fe-2S] cluster disassembly was maximal when reduced and oxidized GSH were present at a ratio of approximately 1:3, which suggests the critical involvement of a GSH-based free radical in the disassembly process. Such a reaction might occur in vivo: we found that the induction by paraquat of SoxR-dependent soxS transcription was much higher in a GSH-deficient E. coli strain than in its GSH-containing parent. The results imply that GSH may play a significant role during the deactivation process of SoxR in vivo. Ironically, superoxide production seems both to activate SoxR and, in the GSH-dependent disassembly process, to switch off this transcription factor.
Monocyte adhesion to the vascular endothelium is a pivotal step during their egress to tissues at sites of inflammation and immune reactions, and during atherogenesis. In this study, an in vitro flow model and blocking mAb were used to define the role of adhesion molecules in monocyte interactions with activated HUVEC under flow conditions. By videomicroscopy, freely flowing monocytes abruptly halted (initial attachment) on 6-h TNF-alpha-activated HUVEC under flow via L- and P-selectin, whereas E-selectin was not involved. CD49d/CD29 integrin (VLA-4), which can mediate initial attachment of certain T cells to VCAM-1 under flow, did not support monocyte initial attachment. Once initially attached, a small number of monocytes began rolling at 9 microns/s through a mechanism involving L-selectin, as well as CD49d and CD11/CD18 integrins, while the remaining monocytes became firmly adherent, or released to the flow stream. Monocyte stable arrest and subsequent transendothelial migration occurred rapidly and efficiently through either CD49d or CD18 integrin adhesion pathways. Transendothelial passage was also dependent on PECAM-1 (CD31). These data reveal monocytes initially attach to activated endothelium via an L-selectin-dependent mechanism, with a smaller contribution from P-selectin and no contribution by CD49d. Subsequent monocyte rolling, arrest, and transmigration require overlapping functions between multiple members of the selectin, integrin, and Ig gene families.
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The expression of leukocyte adhesion molecules on endothelial cells is induced by TNF-alpha and other inflammatory cytokines. This induction of endothelial-leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 requires the transcription factor nuclear factor-kappa B (NF-kappa B). Recent work has suggested that some nonsteroidal anti-inflammatory agents, including sodium salicylate and aspirin, can inhibit NF-kappa B-dependent gene activation. We studied the effects of salicylates on expression of adhesion molecules in HUVECs. We found that sodium salicylate inhibited activation of NF-kappa B (p50/p65 and p65/p65) by preventing phosphorylation and subsequent degradation of the inhibitor 1 kappa B-alpha. Salicylate treatment had no effect on TNF-alpha-induced phosphorylation of the transcription factor ATF-2. Salicylate blocked the TNF-alpha-induced increase in mRNA levels of adhesion molecules and gave a dose-dependent inhibition of TNF-alpha-induced surface expression of vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 with higher doses required to inhibit endothelial-leukocyte adhesion molecule-1 expression. Indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression of adhesion molecules, suggesting that the effects were not due to inhibition of cyclooxygenase. Treatment of endothelial cell monolayers with sodium salicylate inhibited transendothelial migration of neutrophils but had no significant effect on neutrophil adhesion under flow conditions. The clinical importance of high-dose salicylates in inflammation may be due, in part, to the ability to prevent expression of inducible adhesion molecules and recruitment of leukocytes.