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3D Systems Corporation Message Board

servpro9002 19 posts  |  Last Activity: Apr 25, 2016 5:18 PM Member since: Jan 4, 2013
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  • servpro9002@sbcglobal.net servpro9002 Apr 25, 2016 5:18 PM Flag

    nikki,

    Check out Organovo Holdings Inc. v. Dimitrov, case number 10536, in the Delaware Court of Chancery.

    Also, Organovo Holdings Inc. v. Simeon Research LLC, case number 9563, in the same venue.

    That is how we deal with fraudulent entities. Sucks to be you.

  • servpro9002@sbcglobal.net servpro9002 Apr 14, 2016 7:08 PM Flag

    Thanks for the info Stan. June should be interesting with fiscal year end update, partner presentations further validating future uses, and hopefully early kidney testing for select clients commencing (if it hasn't already!)

  • servpro9002@sbcglobal.net servpro9002 Apr 14, 2016 6:55 PM Flag

    venturecapitalizt
    6 posts | Last Activity: 1 minute 43 seconds ago
    Member since: Apr 14, 2016

    Ignored since: Apr 14, 2016

  • Reply to

    Shorts are working hard with their BS ...

    by spangle26 Apr 13, 2016 6:24 AM
    servpro9002@sbcglobal.net servpro9002 Apr 13, 2016 9:31 AM Flag

    It can also be used to dispense condiments at the local burger joint.

  • Reply to

    Big Sky Montana

    by ournightowl Apr 1, 2016 1:43 PM
    servpro9002@sbcglobal.net servpro9002 Apr 4, 2016 12:29 PM Flag

    We were there in Aug also just after the road reopened. One buddy swam in the river, I was content to soak my feet.

  • Reply to

    Big Sky Montana

    by ournightowl Apr 1, 2016 1:43 PM
    servpro9002@sbcglobal.net servpro9002 Apr 4, 2016 11:14 AM Flag

    I agree, it's a great park and area. Backpacked 58 miles there last summer with 4 buddies. Had to visit before all the glaciers melted!

  • Reply to

    OT IGGY was in my stompin'grounds

    by toppadred Mar 31, 2016 9:47 PM
    servpro9002@sbcglobal.net servpro9002 Apr 1, 2016 11:47 AM Flag

    I believe he's recovering from a snowboard accident. Best wishes ig!

  • servpro9002@sbcglobal.net servpro9002 Mar 31, 2016 5:20 PM Flag

    Kidney product promised in 2nd calendar qtr.

  • servpro9002@sbcglobal.net servpro9002 Mar 31, 2016 3:04 PM Flag

    and the 2nd qtr starts tomorrow!

  • Reply to

    Just back from SOT 2016 New Orleans (I)

    by drzzzzzzz Mar 16, 2016 12:31 AM
    servpro9002@sbcglobal.net servpro9002 Mar 16, 2016 5:55 PM Flag

    Thanks drz for investing the time and money to attend and report back to the rest of us. One of my favorite cities for food and fun, I'm sure you had a great time.

  • servpro9002@sbcglobal.net by servpro9002 Mar 11, 2016 12:21 PM Flag

    Anybody have any info on what progress has been made on the use of 3D bioprinted human breast cancer for in vitro screening of therapeutics targeted against cancer progression using patients own cells?

    Or what Janssen ( Johnson & Johnson) is doing with their tissues (or what tissues they are using?)

    Somebody needs to go to happy hour where the lab techs hangout and buy them a few drinks!

  • Reply to

    Why ONVO's product is BAD for drug companies

    by alex_nemese Mar 5, 2016 10:24 PM
    servpro9002@sbcglobal.net servpro9002 Mar 7, 2016 8:37 AM Flag

    " almost exactly " is closer to almost than exactly.

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 5, 2016 10:36 AM Flag

    My take aways from these SOT poster abstracts are the continued validation of the liver product from both internal and external sources and the disclosure of potential partner / customer Astellas Pharma Inc from Japan. Keith alluded to the faster pace of approval / adoption in that market for tissue products.

  • servpro9002@sbcglobal.net servpro9002 Mar 5, 2016 10:29 AM Flag

    Don't confuse the failed theory of Supply Side (Reaganomics) with the core ideas in microeconomics. Supply, demand and equilibrium.

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 4, 2016 6:27 PM Flag

    2001 Functional Evaluation of Bioprinted Human Liver
    Tissue as a Liver Injury Model
    K. Tetsuka1, M. Ohbuchi1, H. Moriguchi1, E. Kobayashi2, M. Kanki2, A.
    Miyashita1 and K. Tabata1. 1Analysis & Pharmacokinetics Research
    Labs., Astellas Pharma Inc., Tsukuba-shi, Japan and 2Drug Safety
    Research Labs., Astellas Pharma Inc., Osaka-shi, Japan. Sponsor:
    A. Okada.
    Purpose: As drug-induced liver injury is a major cause of drug withdrawal
    from market, culture models that can accurately predict and evaluate
    the toxic potential of chemicals are required. Three-dimensional (3D)
    bioprinting technology enables the alignment of different cell types in a
    spatially-controlled manner. Here, we characterized the long- and shortterm
    effects of acetaminophen (APAP) in a 3D-bioprinted model of the
    human liver. Materials and Methods: The exVive3D Liver (Organovo
    Holdings Inc., San Diego, CA, USA) was used as a three-dimensional
    human liver tissue model (3DHLT). Briefly, 3DHLTs were constructed
    from human hepatocytes, stellate cells, and endothelial cells of the
    umbilical vein using a Novogen Bioprinter (Organovo Holdings Inc.). To
    measure the long-term effects of APAP, 3DHLTs underwent treatment
    with APAP at 0, 0.3, 1, 3, 10, or 30 mM for 1, 7, 14, or 28 days. To measure
    the short-term effects of APAP, 3DHLTs underwent treatment with APAP
    at 30 mM for 6 h, followed by either termination of culture or further culture
    without APAP for 1, 3, or 18 h as a washout stage. Intracellular ATP
    and glutathione (GSH) levels in these specimens were then measured
    as described in the manufacturer’s instructions. Results and Discussion:
    Treatment of 3DHLTs with APAP at 30 mM for 1 day significantly reduced
    mean ATP level to 27.9% of that of controls. Prolonged APAP
    treatment also reduced mean ATP levels, even with treatment at lower
    concentrations. IC50 values decreased over the APAP treatment period.
    Short-term APAP treatment of 3DHLTs at 30 mM for 6 h significantly reduced
    mean GSH level to 56% of that

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 4, 2016 4:01 PM Flag

    2003 Utilization of exVive 3D Human Liver Tissues for
    the Evaluation of Valproic Acid-Induced Liver
    Injury
    C. Grundy, R. Smith, J. Nickel, R. N. Hardwick and D. G. Nguyen.
    Tissue Applications, Organovo, Inc., San Diego, CA; Tissue Testing,
    Organovo, Inc., San Diego, CA. Sponsor: D. Nguyen.
    Conventional (2D) cell culture models do not accurately reflect the
    complex microenvironment of liver tissue, and pre-clinical animal trials
    are often inadequate due to species-specific variation in hepatocellular
    functions. 3D bioprinted human liver tissues better approximate
    human tissue composition and physiology, and therefore enable the
    assessment of drug-induced liver injury (DILI) and related mechanisms
    at the tissue level, including biochemical and histologic outcomes. In
    this study, we assessed the DILI response to Valproic Acid (VPA), a compound
    known to induce steatosis in humans, in 3D-bioprinted human
    liver tissue mimetics comprised of primary hepatocytes, hepatic stellate
    cells, and endothelial cells. 3D-bioprinted human liver tissues (exVive3D;
    Organovo, San Diego CA), were treated daily for 14 days with VPA, which
    resulted in dose-dependent decreases in tissue health as assessed by
    ATP, GSH and histology. Tissue ATP levels were decreased 70% and
    45% relative to vehicle following 14 day treatment with 1mM and 5mM
    VPA, respectively. Following the observations seen with ATP levels, the
    higher doses of 200µm, 1mM and 5mM were selected to further evaluate
    the mechanism of observed tissue damage. GSH levels were measured
    at 24hr and 72hr to determine the acute oxidative stress response.
    A significant decrease in the ratio of reduced to oxidized GSH was observed
    at 24hr treatment, indicating increased oxidative stress. Recovery
    of GSH ratios was noted with 200µm and 1mM treatment groups at
    72hr, while the 5mM treatment group exhibited prolonged oxidative
    stress. Histological evaluation of tissues revealed dose-dependent damage
    with abundant vacuolization in 5mM VPA treate

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 4, 2016 3:31 PM Flag

    1996 Modeling Drug-Induced Hepatic Fibrosis In Vitro
    Using Three-Dimensional Liver Tissue Constructs
    L. M. Norona2,3, D. G. Nguyen1, D. A. Gerber3, S. C. Presnell1 and
    E. L. LeCluyse2,3. 1Organovo, Inc., San Diego, CA; 2The Hamner
    Institutes, Research Triangle Park, NC and 3The University of North
    Carolina at Chapel Hill, Chapel Hill, NC.
    Compound-induced hepatotoxicity leading to fibrosis remains a challenge
    for human toxicity risk assessment. Latency to detection and lack
    of early biomarkers make it difficult to characterize the dynamic and
    complex intercellular interactions that occur during progressive liver
    injury. Animal models only partially address this challenge however; the
    development of a truly mechanistic understanding requires the use of
    human tissue-like model systems that can be interrogated over time
    to identify key cellular and molecular events underlying fibrogenesis.
    Here we demonstrate the utility of bioprinted tissue (exVive3D Human
    Liver, Organovo) comprising hepatocytes, stellate cells and endothelial
    cells to conduct repeated low concentration modeling of compound-induced
    liver injury leading to fibrosis. Significant time dependent elevations
    of LDH were observed for both TAA (by Day 3) and MTX (by Day
    11) and were accompanied by the acquisition of a fibrogenic phenotype
    as supported by preliminary cytokine, gene expression data, and histologic
    evidence of collagen deposition. In comparison, treatment with
    TGF-β1, a known pro-fibrogenic cytokine, yielded moderate to severe
    fibrotic change in the tissue with little evidence of hepatocellular damage.
    These preliminary data provide strong proof-of-concept that 3D
    bioprinted liver tissues can recapitulate drug-, chemical- and TGF-β1-
    induced fibrogenesis on a cellular, molecular, and histological basis. The
    use of this novel system and strategy will enable the integration of initial
    and adaptive cellular mechanisms during the onset and progression of
    injury to better characterize key attributes

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 4, 2016 12:19 PM Flag

    I tried posting them all but they seem to be stuck in the cloud.....maybe they'll show up eventually.

  • Reply to

    Research Partners Presentation

    by marc9871 Mar 4, 2016 10:32 AM
    servpro9002@sbcglobal.net servpro9002 Mar 4, 2016 12:04 PM Flag

    1959 Inflammatory Response of Kupffer Cells in 3D
    Bioprinted Human Liver Tissues
    R. N. Hardwick, J. Hampton, D. Perusse and D. G. Nguyen. Tissue
    Applications, Organovo, Inc., San Diego, CA.
    Hepatic inflammation, mediated by Kupffer cells (KC), can exacerbate
    hepatocellular damage during drug-induced liver injury. KC are often
    employed in co-culture with hepatocytes to investigate the potential
    for inflammation in response to stimuli, such as the prototypical inducer
    lipopolysaccharide (LPS); however, such systems seldom include other
    nonparenchymal cells and fail to recapitulate the complex 3D interactions
    present in native liver. In the current study, LPS-mediated activation
    of KC at 24 and 72hrs was investigated in 3D bioprinted human liver
    tissues (exVive3D; Organovo, San Diego, CA). Induction of pro- and anti-inflammatory
    cytokines was measured via electrochemiluminescence
    in tissues comprising primary hepatocytes, stellate cells, and endothelial
    cells (Hep:KC-), and compared to tissues containing KC. Independent
    experiments were conducted comparing two KC donors (Hep:KC+D1
    ♂ and Hep:KC+D2 ♀) with all other cell donors held constant. LPS
    stimulated TNF-α, IL-1β, IL-12p70, IL-10, IL-2, IL-13, and IL-4 levels in
    Hep:KC+D1 tissues at 24hrs compared to untreated, with sustained induction
    to 72hrs. TNF-α, IL-10, and IL-8 exhibited greater induction in
    Hep:KC+D1 tissues compared to Hep:KC-. All cytokines were increased
    at 24hrs in Hep:KC+D2 tissues treated with LPS compared to untreated,
    with sustained induction of IL-8, IL-1β, IFN-γ, IL-2, and IL-12p70. IL-8,
    IL-6, and IL-10 induction was greater in Hep:KC+D2 tissues compared
    to Hep:KC-. To compare donor-specific responses to LPS, cytokine levels
    were normalized to untreated Hep:KC-, and the fold change in LPStreated
    Hep:KC+ tissues was calculated. Patterns of LPS-induced cytokine
    release were distinct between KC donors, with greater induction
    in the female donor. However, IL-1β, IL-10, IL-2, and IL-13 exhibited no
    v

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