43 research outputs found

    The healing pattern of the wounds in different conditions.

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    <p>(A) Scaffold treated and (B) injury wound after 0, 1, 2, 3, 4, 5, 7 and 10 days after injury. The wound healing efficacy of the scaffold was evaluated in a full thickness wound model. Following anaesthetized a full thickness excisions of 2 cm in diameter were created by a surgical knife of male Wistar rats. For treatment group after excision was made, the scaffold was covered on the wound immediately. For injury group wounds were not covered for comparison. From the first day after injury, the healing of wound from injury group was slower than scaffold treated wound until 10 days after injury. Scale bar  = 0.5 cm. (C) Wound contraction ratios of scaffold and injury at different times. By examining the wound area at definite days, the reduction of wound area was calculated. The surface area of the excisional wounds was calculated as described in methods. The wound area decreased rapidly in the presence of scaffold when compared with the control since first day after injury. The wound area in control group was 60% of the original size on day 7. This percentage was reached almost 3 days earlier at scaffold group. The difference between wounds of injury and scaffold group were statistically significant at day 10. Data are presented as the mean ± standard error.</p

    The swelling studies of the scaffolds fabricated with collagen (0.6%, w/v), HA (0.01%, w/v), and gelatin (1.0%, w/v) and crosslinked with EDC (50 mM) (n = 3).

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    <p>Without EDC crosslinking reactions, the scaffolds were dissoluble into water (symbol: ×). Compared with commercial materials include, Du (DuoDERM 9C52552), Hy (Hydro Coll), Te (Tegaderm M1635), and ME (MEDPOR<sup>®</sup>).</p

    Collagen amount secreted from cells seeded on plate or in the scaffold.

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    <p>On the plate or in the scaffold, FBs raised for the first 7 days, after that, KCs and MCs seeded in for another 7 days. (A), the total collagen amounts on the plate or in the scaffold were shown. (B), the specific collagen amount measured with dividing collagen amount by cell amount.</p

    H&E stained sections for the morphological evaluation of skin wounds.

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    <p>Ten days after injury, rats were scarified, wound skin was fixing in 4% of paraformaldehyde. The skin was stained with H&E for histological observation. Ten randomly selected areas of dermis from each sample were examined at a magnification of 400× for counting neutrophil. Scaffold group (A), injury group (B) and control (C) wounds at 10 days after injury. Both scaffold and injury group wounds have granulation tissue. The epidermis of treatment group was denser than injury epidermis. Wounds of treatment group were had less neutrophil infiltrated compare to injury group (D). Scale bar  = 200 μm. EP, epithelial layer, GT, granulation tissue.</p

    The manufacturing process and structural diagram.

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    <p>(A) The biomaterial manufacture, skin culture and mouse skin wound healing model. (B) Proposed schematic presentation of collagen (0.6%, w/v, 93.75 mM), HA (0.01%, w/v, 0.05 mM), gelatin (1%, w/v, 2 mM) cross-linked by EDC. (C), (D) SEM of collagen/HA/gelatin scaffolds. The pore size was 132.5±8.4 μm.</p

    The degradation rates of the enzymes.

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    <p>(A) Lysozyme, (B) hyaluronidase, and (C) collagenase. A significant difference compare to the control group was defined as *<i>p</i><0.05 and **<i>p</i><0.01.</p

    The protocols and fluorescent photos of 3D human skin equivalent.

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    <p>(A) The protocols of 3D human skin equivalent. (B) Paraffin section of the 3D human skin equivalent under microscope in bright view (400×). (C–E) Fluorescent images of KCs, MCs, and FBs cultured in scaffold for 14 days, and were stained with DAPI (blue); anti-cytokeratin to mark KCs (green); anti-s-100 for MCs (red). (F) The merged image was of KCs, MCs, and FBs together. Arrows pointed to KCs, MCs, and FBs with specific colors.</p

    Novel Synthetic <i>Medea</i> Selfish Genetic Elements Drive Population Replacement in <i>Drosophila</i>; a Theoretical Exploration of <i>Medea</i>-Dependent Population Suppression

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    Insects act as vectors for diseases of plants, animals, and humans. Replacement of wild insect populations with genetically modified individuals unable to transmit disease provides a potentially self-perpetuating method of disease prevention. Population replacement requires a gene drive mechanism in order to spread linked genes mediating disease refractoriness through wild populations. We previously reported the creation of synthetic <i>Medea</i> selfish genetic elements able to drive population replacement in <i>Drosophila</i>. These elements use microRNA-mediated silencing of myd88, a maternally expressed gene required for embryonic dorso-ventral pattern formation, coupled with early zygotic expression of a rescuing transgene, to bring about gene drive. <i>Medea</i> elements that work through additional mechanisms are needed in order to be able to carry out cycles of population replacement and/or remove existing transgenes from the population, using second-generation elements that spread while driving first-generation elements out of the population. Here we report the synthesis and population genetic behavior of two new synthetic <i>Medea</i> elements that drive population replacement through manipulation of signaling pathways involved in cellular blastoderm formation or Notch signaling, demonstrating that in <i>Drosophila Medea</i> elements can be generated through manipulation of diverse signaling pathways. We also describe the mRNA and small RNA changes in ovaries and early embryos associated from <i>Medea</i>-bearing females. Finally, we use modeling to illustrate how <i>Medea</i> elements carrying genes that result in diapause-dependent female lethality could be used to bring about population suppression
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