Biomedical subjects

Xuebin Li

Publications and source records attributed to Xuebin Li.

6 recordsLinked to original sources

PubMed2006

Determination of the refractive index and size distribution of aerosol from dual-scattering-angle optical particle counter measurements.

A method is presented for inferring both the refractive index and the size distribution of aerosol from observations of a dual-scattering-angle optical particle counter (OPC). An existing prototype of an OPC with 60 degree and 90 degree dual-scattering angles was used for the experiments. Based on the high sensitivity of the OPC response to the refractive index of particulates, two families of size distribution curves may be calculated. The solution of the refractive index corresponds to the superposition of the two size distributions. This method was applied to the simulation and to the field measurements conducted in Beijing and Hefei, and the results of both are presented.

Journal Article↗

PubMed2006

Electronic confinement and coherence in patterned epitaxial graphene.

Ultrathin epitaxial graphite was grown on single-crystal silicon carbide by vacuum graphitization. The material can be patterned using standard nanolithography methods. The transport properties, which are closely related to those of carbon nanotubes, are dominated by the single epitaxial graphene layer at the silicon carbide interface and reveal the Dirac nature of the charge carriers. Patterned structures show quantum confinement of electrons and phase coherence lengths beyond 1 micrometer at 4 kelvin, with mobilities exceeding 2.5 square meters per volt-second. All-graphene electronically coherent devices and device architectures are envisaged.

Journal Article↗

PubMed2005

Paraformaldehyde induces elevation of intracellular calcium and phosphatidylserine externalization in platelets.

Paraformaldehyde fixation of platelets stabilizes surface antigens while altering some that are associated with cellular activation. Present experiments show that the asymmetric distribution of phosphatidylserine in platelets was especially sensitive to paraformaldehyde treatment. It was found that this reagent induced a dose- and time-dependent translocation of phosphatidylserine to the membrane surface as measured by annexin V binding and flow cytometry. The percent phosphatidylserine-positive cells increased from about 5% to >90%. Chelation of extracellular Ca(2+) with EGTA partially blocked this translocation. Spectrofluorimetric analysis of fluo-3 loaded platelets indicates that paraformaldehyde caused a concomitant elevation of intracellular Ca(2+) concentrations, [Ca(2+)](i). ATP levels also declined in paraformaldehyde-treated cells, suggesting that the rise in [Ca(2+)](i) ensued in part from decreased activity of calcium pumps. Previous studies indicate that phosphatidylserine externalization arises from Ca(2+)-activated randomization of membrane phospholipids and decreased transport of phosphatidylserine from the outer to the inner leaflet of the plasma membrane. In light of present results, paraformaldehyde fixation is best avoided particularly in studies involving platelet apoptosis or activation.

Adenosine Triphosphate↗

PubMed2005

Regulation of FoxO1 transcription factor by nitric oxide and cyclic GMP in cultured rat granulosa cells.

FoxO1 is a transcription factor implicated in a multitude of physiological processes including cell cycle progression, apoptosis and insulin signaling. Recent findings indicate that FoxO1 is a key regulator during the proliferation and maturation of granulosa cells. Over the past several years, it has become evident that nitric oxide (NO) and cGMP modulate ovarian function. There has been no information, however, about whether NO-cGMP affects FoxO1 expression or about the relationship between NO-cGMP and FoxO1. In the present study, we used immunoblot analysis to determine whether NO and cGMP affect FoxO1 expression in cultured granulosa cells. Our results clearly showed that FSH suppressed FoxO1 expression in a time-dependent manner, and that NO-cGMP stimulated FoxO1 expression in cultured granulosa cells. In addition, this stimulatory effects of NO and cGMP can be blocked by FSH in cultured granulosa cells. These findings demonstrate that NO and cGMP influence FoxO1 expression possibly through antagonizing the action of FSH in cultured granulosa cells. Results of both immunoblot analysis and immunohistochemistry also show that estradiol implantation do not affect the expression of FoxO1 in rat granulosa cells as gonadotrophins do, indicating that mechanism of estradiol on granulosa cells is different from gonadotrophins. Together, our experiments suggest that expression of FoxO1 in rat granulosa cells can be regulated by gonadotrophins and the NO/cGMP signaling pathway.

Animals↗

PubMed2004

Nitric oxide infusion alleviates cellular activation during preparation, leukofiltration and storage of platelets.

Nitric oxide (NO) is a reversible inhibitor of platelet activation that generates S-nitrosylated compounds in plasma. Since platelets are activated during processing to platelet concentrates and storage, NO is anticipated to dampen the rate of lesion development. Platelet-rich plasma (PRP) was separated into aliquots that were unfiltered, filtered to remove leukocytes, or treated with NO or nitrite before filtration. Platelets were resuspended and stored up to four days at 22 degrees C. Samples removed were measured for S-nitrosylation of plasma, P-Selectin release, complement activation, and cGMP levels. Direct infusion of a NO solution (authentic NO) to PRP before filtration decreased adherence of platelets and improved yields. An infusion rate resulting in 1/1000 dilution of a saturated NO solution was optimal. C3a formation and soluble P-Selectin released from NO-treated-filtered platelets were about half that in unfiltered and filtered controls after four days (p<0.05 by Student-Newman-Keuls method after ANOVA for repeated measures). Plasma isolated from NO-treated PRP combined with untreated platelets protected the latter to a similar extent. Increases in S-nitrosylated compounds in PRPs were correlated with NO effects on platelet recovery and storage. Sodium nitrite failed to inhibit platelet activation and cyclic GMP levels were significantly increased in NO-treated cells. Results indicate that NO inhibited platelet activation associated with processing and storage and suggest that slow release of NO from S-nitrosylated plasma components afforded long-term protection. The infusion of authentic NO into PRPs is potentially an efficacious method for generating anti-platelet compounds to inhibit storage lesions.

Blood Platelets↗

PubMed2004

The surface electrocardiographic changes after radiofrequency catheter ablation in patients with idiopathic left ventricular tachycardia.

Surface electrocardiographic changes after radiofrequency (RF) catheter ablation (RFCA) were observed in patients with idiopathic left ventricular tachycardia (ILVT), and the possible mechanisms were analysed. In 41 cases with ILVT who underwent the RFCA, the surface electrocardiograms (ECGs) before and after RFCA were recorded and the serum cardiac troponin I (cTnI) were measured before, immediately after, 4 h after and 24 h after RFCA. Seven patients developed different models and degrees of fascicular block after successful RFCA. The configurations of fascicular block had no dynamic alteration during the follow-up periods. No significant difference in the duration of the RF energy delivered, the numbers of RF lesion and the serum levels of cTnI between the patients with or without the electrocardiographic alteration was observed. Thus, the RFCA can cause the fascicular block in some of the patients with ILVT. The different distribution models of the left bundle branch, but not the damage degree to the endocardium induced by RF current, is the primary factor to the changes of ECG.

Adolescent↗