13 research outputs found
Enhanced Photothermocatalytic Synergetic Activity Toward Gaseous Benzene for Mo+C-Codoped Titanate Nanobelts
In the present paper, a simple and facile method is proposed
to
synthesize Mo+C-codoped titanate (H<sub>2</sub>Ti<sub>5</sub>O<sub>11</sub>·3H<sub>2</sub>O) nanobelts by using hydrothermal method
together with sol–gel technique, and various Mo-doped and Mo+C-codoped
titanate nanobelts are realized by controlling the precursor’s
contents. It is found that the photocatalytic activity of titanate
nanobelts toward gaseous benzene will be greatly enhanced by Mo+C-codoping
if comparing with that of the pure titanate nanobelts, Mo-doped titanate
nanobelts, and C-doped titanate nanobelts, and the optimal Mo doping
content is confirmed to be 0.33 wt % for Mo/Ti ratio. The reason lies
in the fact that by Mo+C-codoping (Mo/Ti ratio of 0.33 wt %, C/Ti
ratio of 0.33 wt %), the band gap of titanate nanobelts will be narrowed
and the allowed paths for photoexcitation will be increased with the
generation of impurity energy level, which results in an obvious red-shift
in their UV–vis absorption spectra and the increased utilization
of the solar energy, and thus enhances their photocatalytic activity.
On the basis of the above experimental results, the current photocatalytic
mechanism is proposed
Formylpeptide Receptors Mediate Rapid Neutrophil Mobilization to Accelerate Wound Healing
<div><p>Wound healing is a multi-phased pathophysiological process requiring chemoattractant receptor-dependent accumulation of myeloid cells in the lesion. Two G protein-coupled formylpeptide receptors Fpr1 and Fpr2 mediate rapid neutrophil infiltration in the liver of <i>Listeria</i>-infected mice by sensing pathogen-derived chemotactic ligands. These receptors also recognize host-derived chemotactic peptides in inflammation and injury. Here we report the capacity of Fprs to promote the healing of sterile skin wound in mice by initiating neutrophil infiltration. We found that in normal miceneutrophils rapidly infiltrated the dermis in the wound before the production of neutrophil-specific chemokines by the injured tissue. In contrast, rapid neutrophil infiltration was markedly reduced with delayed wound closure in mice deficient in both Fprs. In addition, we detected Fpr ligand activity that chemoattracted neutrophils into the wound tissue. Our study thus demonstrates that Fprs are critical for normal healing of the sterile skin wound by mediating the first wave of neutrophil infiltration.</p></div
Fpr agonist activity in the skin wound.
<p><i>A - C,</i> inhibition of homogenate-induced migration of neutrophils from WT mice by Fpr antagonists (n = 5). Neutrophils from WT mice were pretreated with Boc-1 (4 µM and 8 µM, <i>A</i>), WRW4 (4 µM and 8 µM, <i>B</i>) or Boc-2 (5 µM and 10 µM, <i>C</i>) for 30 min and then were measured for chemotaxis in response to homogenates of wounded skin collected at 4 h. *, significantly decreased number of migrating cells treated with Fpr antagonists as compared to neutrophils without pretreatment (<i>p</i>< 0.05). #, significantly decreased number of migrating cells treated with Fpr antagonists as compared to neutrophils without pretreatment (<i>p</i>< 0.05). <i>D</i>, inhibition of the chemotactic activity of skin wound homogenates by a neutralizing CRAMP antibody. HEK293/Fpr2 cells were measured for chemotaxis in response to CRAMP or skin wound homogenates with or without pretreatment by a neutralizing CRAMP antibody (10 µg/ml for 45 min) (n = 5). *, significantly increased number of migrating cells in response to CRAMP or homogenates as compared to medium control (0) (<i>p</i>< 0.05). #, significantly decreased number of migrating cells as compared to neutrophils without pretreatment by CRAMP antibody (<i>p</i>< 0.05).</p
Reduced neutrophil infiltration in the wounds of Fpr-deficient mice and the production of chemokines.
<p><i>A</i>, representative immunofluorescence of skin wound showing Ly6G<sup>+</sup> cells 4 h after injury. Cryosections of wounded skin from WT and Fpr-deficient mice were labeled with Ly6G and DAPI (Red: Ly6G; Blue: DAPI) (n = 5, scale bar: 20 µm). Insert: control IgG staining. <i>B</i>, Kinetics of infiltrating Ly6G<sup>+</sup> neutrophils in 3 consecutive high power fields (HPF). *, significantly reduced Ly6G<sup>+</sup> cells in the wounds of Fpr-deficient micecompared with WT mice (<i>p</i>< 0.05). #, significantly reduced Ly6G<sup>+</sup> cells in the wounds of Boc-2 pretreated WT mice, compared with WT mice without pretreatment (<i>p</i>< 0.05). <i>C&D</i>, chemokinesCXCL1 and CXCL2 in the homogenates of skin wound from WT and Fpr-deficient mice. Skin (1 cm×1 cm) with wounds in the center was excised and homogenized in 5 ml DPBS. The homogenates were centrifuged and the supernatants were collected for measurement of CXCL1 and CXCL2 by ELISA (n = 15).</p
Chemokine production and chemotactic activity of homogenates of skin wound.
<p><i>A-C</i>, chemokine production of skin wound at 72 h (n = 15). WT and Fpr-deficient mice were subjected to full-thickness skin wound and the wounds were harvested at 72 h after injury and then homogenized for chemokine measurement with ELISA. <i>D</i>, homogenate-induced migration of parental and Fpr-transfected HEK293 cells. Migrating cells in response to different concentration of the homogenate in 3 HPF were counted. *, significantly increased migrating cells in response to homogenates as compared to medium control (0) (<i>p</i><0.05). <i>E</i>, chemotactic activity of skin homogenates for neutrophils from WT and Fpr-deficient mice. *, significantly increased migrating neutrophils in response to homogenates as compared to medium control (0) (<i>p</i><0.05).</p
Delayed skin wound healing in Fpr double deficient Fpr1/2<sup>-/-</sup>mice.
<p><i>A</i>, representative pictures of skin wound of WT and Fpr1/2<sup>-/-</sup> mice. A 6-mm full-thickness (including the Panniluluscarnosus) skin was excised from the right and left upper paravertebral regions of each animal and the injured areas were measured daily using NIH Image J software (version 1.37) (n = 5). <i>B</i>, the areas of wounds. Mice were punched to generate two 6-mm full thickness skin wounds with or without IP injection CRAMP (10 µg/100 µl) or Boc-2 (5 µM, 100 µl) (n = 15). The areas of wound were calculated. *, significantly increased wound area in Fpr1/2<sup>-/-</sup>and Boc-2 treated mice, compared with the wound area of WT mice at the same time points (<i>p</i>< 0.05).</p
The absence of MCP-1 in tumor stroma reduces the lung metastasis of 4T1 cells and prolongs survival.
<p>A. 1×10<sup>5</sup> 4T1 cells were injected into a mammary pad of WT or MCP-1<sup>−/−</sup> mice. The size of each primary tumor was measured and the area was calculated. <i>n = 9</i> for WT, <i>n = 8</i> for MCP-1<sup>−/−</sup> mice. B. Primary tumors were excised from WT and MCP-1<sup>−/−</sup> mice 31 days after tumor cell injection and weighed. <i>n = 9</i> for WT, <i>n = 8</i> for MCP-1<sup>−/−</sup> mice. C. Mice were euthanized on day 31, and lungs were harvested and fixed in Bouin's solution. The number of metastatic tumor nodules on the surface of lungs of each mouse was counted by eye. <i>n = 9</i> for WT, <i>n = 8</i> for MCP-1<sup>−/−</sup> mice. D. Ten thousand 4T1 cells were injected in a mammary pad of each mouse and the survival of each mouse was examined. <i>n = 8</i> for WT, <i>n = 8</i> for MCP-1<sup>−/−</sup> mice.</p
MCP-1-deficiency in tumor stroma results in early necrosis, reduced macrophage infiltration and reduced angiogenesis.
<p>A. 1×10<sup>5</sup> 4T1 cells were injected into a mammary pad of WT or MCP-1<sup>−/−</sup> mice. Primary tumors were excised two weeks after 4T1 cell injection and fixed in formalin. Tissue sections were prepared from the center of each tumor, stained by H&E, and the area of necrosis was measured. % of necrotic area was calculated by using a formula, area of necrosis/area of tumor×100. <i>n = 5</i> for each group. B. H&E section of tumor tissue away from necrosis. C. Immunohistochemical examination of tumor sections. Green, cytokeratin; Red, F4/80 or CD31.</p
The expression of MCP-1 and CCR2 by 4T1 cells.
<p>A. The expression of MCP-1 mRNA by 4T1 cells was examined and compared to that of LLC by Northern blotting. B. The concentration of MCP-1 in the culture supernatants of 4T1 or LLC cells incubated for 24 h with 1 or 10 ng/ml of murine TNFα or 100 ng/ml of LPS or without any stimulus was measured by ELISA. C. The surface expression of CCR2 on 4T1 cells was examined by FACS. D. The expression of CCR2 mRNA in 4T1 cells was examined by RT-PCR. Thioglycollate-induced mouse peritoneal exudates cells were used as control.</p
Increased MCP-1 expression in 4T1 cells has no effect on spontaneous lung metastasis in MCP-1<sup>−/−</sup> mice, but increases lung metastasis after intravenous injection.
<p>A. 1×10<sup>5</sup> 4T1-L10 cells were injected into a mammary pad of WT or MCP-1<sup>−/−</sup> mice. The size of each primary tumor was measured and the area was calculated. <i>n = 4</i> for WT, <i>n = 3</i> for MCP-1<sup>−/−</sup> mice. B. 1×10<sup>5</sup> 4T1-L10 cells were injected into a mammary pad of WT or MCP-1<sup>−/−</sup> mice. All mice were euthanized 4 weeks after the injection and the number of metastatic tumor nodules on the surface of each lung was counted by eye. C. Total RNA was extracted from each tumor and the expression of MCP-1 mRNA was examined by Northern analysis. Ten µg of total RNA was used. D. Sera were collected 2 weeks after the injection of 4T1-L10 cells and MCP-1 concentrations were measured by ELISA. E. 4T1-L5 or 4T1-L10 cells (5×10<sup>4</sup> cells in 0.2 ml PBS) were intravenously injected into WT (left panel) or MCP-1<sup>−/−</sup> mice (right panel). Two weeks later, mice were euthanized and the number of metastatic tumor nodules on the lung was counted. The results are the summary of two independent experiments. <i>n = 8</i> for WT, and <i>n = 8</i> (4T1-L5) or <i>n = 9</i> (4Y1-L10) for MCP-1<sup>−/−</sup> mice.</p