Behavior characteristics of bimolecular reactive transport in heterogeneous porous media.

In order to study the mechanism of bimolecular reactive solute transport in heterogeneous porous media, the chemical reaction (CuSO4 + Na2EDTA2-→CuEDTA2) was carried out by laboratory experiments and numerical simulation in heterogeneous porous media. Three different kinds of heterogeneous porous media (Sd2 = 1.72, 1.67 and 0.80 mm2) and flow rates (1.5, 2.5 and 5.0 mL/s) were considered. The increase of flow rate would promote the mixing between reactants, resulting in a greater peak value and a slighter "tailing" of product concentration, while the increase of medium heterogeneity would result in a more significant "tailing". It was found that the concentration breakthrough curves of reactant CuSO4 had a peak in the early stage of the transport, and the peak value increased with the increase of flow rate and medium heterogeneity. The concentration peak of CuSO4 was caused by the delayed mixing and reaction of reactants. The IM-ADRE (The advection-dispersion-reaction equation considering incomplete mixing) model could well simulate the experimental results. The simulation error of IM-ADRE model for the concentration peak of product was less than 6.15%, and the fitting accuracy for "tailing" increased with the increase of flow. The dispersion coefficient increased logarithmically with the increase of flow, and was negatively correlated to the heterogeneity of the medium. In addition, the dispersion coefficient of CuSO4 simulated by IM-ADRE model was one order of magnitude larger than that simulated by ADE model, indicating that the reaction promoted dispersion.

[Mechanism investigation of platelet apoptosis inhibition by N-Arachidonoylethanolamine].

OBJECTIVE: To investigate the mechanism of N- Arachidonoylethanolamine (ANA) on inhibiting platelets (PLT) apoptosis under standard blood bank storage conditions. METHODS: Samples taken from collected apheresis PLT by the Amicus instrument were split into three parts. An aliquot of 0.5 µmol/L ANA were added to one part of storage PLT as the ANA group; an aliquot of 0.5 µmol/L ANA and 1 µmol/L SR141716 was added to the another part as the ANA + SR141716 group; and the third part without ANA and SR141716 as the control group. These samples were stored on a flat-bed shaker at (22 ± 2) °C for 7 days. The expression of phosphatidyl serine (PS) positive, phospho (p)-Akt, Akt, p-Bad, Bad, caspase-3, caspase-9, cytochrome C (Cyt-C) and BCL-XL interaction with Bak were detected. RESULTS: The rate of PLT PS positive in ANA group decreased significantly than that in control group[ (8.29 ± 1.44) % vs (14.24 ± 2.47) %, P<0.05]. The release of Cyt-C from mitochondria to cytosol in ANA group decreased significantly compared with control group[ (3.29 ± 1.44) % vs (15.24 ± 3.40) %, P<0.05]. Also the expressions of p-Akt and p-Bad in ANA group increased significantly than those in control group[ (71.33 ± 10.26) % vs (35.00 ± 6.00) %, P<0.05; (39.00 ± 9.64) % vs (10.33 ± 1.53) %, P<0.05, respectively]. Higher amounts of Bak protein were co-precipitated with BCL-XL in ANA group than that in control group (about 2.6 fold, P<0.05). The expressions of cleaved caspase- 9 and caspase- 3 in ANA group decreased significantly than those in control group[ (9.63 ± 1.47) % vs (23.24 ± 2.47) %, P<0.05; (6.30 ± 1.40) % vs (13.20 ± 2.50) %, P<0.05, respectively]. There were no significantly changes between ANA+SR141716 and control groups (P>0.05). CONCLUSION: ANA protected PLTs from apoptosis as a result of inhibiting the release of Cyt-C from mitochondria to cytosol by modifying the expressions of apoptosis-relative proteins.

Differentiation of lymphatic endothelial cells from bone marrow mesenchymal stem cells with VEGFs.

Although there have been many experimental studies demonstrating that bone marrow-derived mesenchymal stem cells (MSCs) have the potential to differentiate into mesenchymal tissues such as osteocytes, chondrocytes, and adipocytes in vivo and in vitro, little information is available regarding their potential to differentiate into lymphatic endothelial cells. Therefore, we chose to investigate differentiation of MSCs into lymphatic endothelial cells using stimulation with members of the vascular endothelial growth factor (VEGFs) family. Rat MSCs were isolated from bone marrow aspirate of Sprague-Dawley rats as previously described and characterized with flow cytometry for surface markers CD14, CD34, CD29, and CD90. Purified MSCs were plated and cultured in the presence of VEGF-A, VEGF-C, or the combination of both for 10 days. We examined the cells for Prox-1 and LYVE-1 by immunocytochemistry, RT-PCR, and Western blot analysis. Results demonstrated that compared to controls, cell differentiated with VEGF-A, VEGF-C and VEGF-A+VEGF-C expressed Prox-1 and LYVE-1. Our results indicate that MSCs induced by VEGFs are capable of differentiating into lymphatic endothelial-like cells in vitro, and this response has the potential to make them attractive candidates for the development of autologous tissue grafts for future therapy.

[Identification of a novel allele HLA-DRB1*1219].

OBJECTIVE: To identify a novel HLA DRB1 allele in a Chinese leukemia family. METHODS: A new HLA-DRB1 allele was initially detected by polymerase chain reaction-sequence specific primer and unusual reaction pattern by Luminex RSSO, then DNA sequencing was performed to identify the sequence of the novel allele. RESULTS: The DNA sequencing revealed the presence of the new allele which differs from the closest matching HLA-DRB1*120201 by a single nucleotide substitution at position (341 C > T in exon 2), resulting in an amino acid change from Ala to Val at coden 85. CONCLUSION: A novel allele was confirmed by DNA sequencing and has been designated HLA-DRB1*1219 by the WHO Nomenclature Committee.

Effect of vascular endothelial growth factor C (VEGF-C) gene transfer in rat model of secondary lymphedema.

Secondary lymphedema has been clinically well described, but a cure is still lacking. Although there have been previous investigations using plasmid DNA for gene therapy, few have focused on the use for the treatment of lymphedema. Therefore, we investigated the effects of VEGF-C gene transfer for the treatment of lymphedema using our plasmid pcDNA3.1-VEGF-C. We produced a surgical model of secondary lymphedema in the rat hindlimb and treated with local intradermal VEGF-C transfection to investigate the efficacy of gene transfer. Magnetic resonance imaging (MRI) (P<0.05), B ultrasound (P<0.05), and water displacement volumetry (P<0.05) demonstrated a reduction of lymphedema in therapy group as compared to controls. Histological and immunofluorescent studies demonstrated numerous newly formed lymphatic vessels in therapy group. Our results indicate that VEGF-C gene therapy has produced new lymphatic vessels which may have improved functional lymphatic drainage to reduce lymphedema volume in our model.

Negative pressure in pharyngo-oral cavity can treat lymphedema and related disorders.

With the finding of specific markers and growth factors for lymphatic vessels, more and more attentions were paid to research on lymphatic vascular system. But the treatment of lymphedema and related disorders is still difficult. Waldeyer's ring is the lymphoid tissues that form a ring around the opening of the throat including tonsils laterally, adenoids superiorly, and lingual tonsil at the base. We hypothesized that negative pressure in pharyngo-oral cavity can improve lymphatic system circulation by affect Waldeyer's ring. And this treatment is proved to be useful in the therapy of lymphedema and chyloperitoneum. So we came to the conclusion that negative pressure in pharyngo-oral cavity was helpful in the treatment of lymphedema and related disorders. But the mechanism of this treatment still need further study. The future of this field of research is very promising and may eventually lead to better treatment of lymphedema and related disorders.