Mimicking In Vivo Tissue Microenvironment for In Vitro Testing – Hydrogels for Cell Encapsulation

2022 ◽  
pp. 358-364
Author(s):  
A. Luca ◽  
T. R. Craescu ◽  
L. Verestiuc ◽  
Maria Butnaru
Keyword(s):  
Cell Encapsulation ◽  
In Vitro Testing ◽  
Tissue Microenvironment

In vivo and in vitro testing of gloves for protection against UV-curable acrylate resin systems

1984 ◽  
Vol 11 (5) ◽  
pp. 279-282 ◽  
Author(s):  
Robert L. Rietschel ◽  
Ronald Muggins ◽  
Nicole Levy ◽  
Pat M. Pruitt
Keyword(s):  
In Vitro Testing ◽  
Uv Curable ◽  
Acrylate Resin

Laboratory and in-vitro testing of skin antiseptics: a prediction for in-vivo activity?

1991 ◽  
Vol 18 ◽  
pp. 5-11 ◽  
Author(s):  
F. Baquero ◽  
C. Patrón ◽  
R. Cantón ◽  
M.Martínez Ferrer
Keyword(s):  
In Vitro Testing

Effect of Kallikrein on Sperm Motility: In Vitro Testing of Ejaculate Vs in Vivo Treatment

1982 ◽  
pp. 67-68
Author(s):  
B. Schütte ◽  
C. Schirren
Keyword(s):  
Sperm Motility ◽  
In Vitro Testing ◽  
In Vivo Treatment

Mining a Nanoparticle Dataset, Compiled Within the MODENA-COST Action

2021 ◽  
pp. 1706-1724
Author(s):  
Sabine Van Miert ◽  
Jan Creylman ◽  
Geert R. Verheyen
Keyword(s):  
Chemical Properties ◽  
In Vitro Testing ◽  
Cost Action ◽  
Robust Model ◽  
Physico Chemical ◽  
Classification And Regression ◽  
Toxic Potential ◽  
Sheer Number

Engineered nanomaterials (ENM) have new or enhanced physico-chemical properties compared to their micron-sized counterparts, but may also have an increased toxic potential. Animal and in vitro testing are typically employed to investigate the toxic effects of (nano)materials. The sheer number of ENMs and their physico-chemical parameters make it impossible to only use in vivo and in vitro testing, and modelling technologies are also deployed to find relationships between ENM parameters and toxicity. A heterogenous dataset containing information on 192 nanoparticle endpoints was compiled within the MODENA COST-Action consortium. Here, the available data was mined to identify relationships between nanoparticle properties and cell-death as measured with four cytotoxicity assays. ANOVA, collinearity analyses and classification and regression trees gave indications on potential relations between the NP-properties and toxicity, but could not deliver a robust model. More information and datapoints are necessary to build well-validated models.

Clindamycin anaphylaxis confirmed by in vivo and in vitro testing

2019 ◽  
Vol 7 (1) ◽  
pp. 331-333 ◽  
Author(s):  
Didier G. Ebo ◽  
Christel Mertens ◽  
Marissa Braes ◽  
Isabel Mennes ◽  
Chris H. Bridts ◽  
...  
Keyword(s):  
In Vitro Testing

The Bruton Tyrosine Kinase Inhibitor, PCI-32765, Inhibits Activation and Proliferation of Human Chronic Lymphocytic Leukemia Cells in the NSG Xenograph Mouse Model of the Tissue Microenvironment

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 596-596 ◽  
Author(s):  
Sarah E. M. Herman ◽  
Xiameng Sun ◽  
Joseph J. Buggy ◽  
Georg Aue ◽  
Patricia Perez-Galan ◽  
...  
Keyword(s):  
T Cell ◽  
Peripheral Blood ◽  
Cell Receptor ◽  
Gene Signature ◽  
B Cell Receptor ◽  
Lymphocytic Leukemia ◽  
T Cell Proliferation ◽  
Tissue Microenvironment

Abstract Abstract 596FN2 PCI-32765, a specific inhibitor of Bruton's tyrosine kinase (Btk), can disrupt several signaling pathways involved in tumor microenvironment interactions. In vitro, PCI-32765 has been demonstrated to induce apoptosis, to varying degrees, in tumor cells and prevent CpG-ODN induced proliferation of cultured chronic lymphocytic leukemia (CLL) cells (Herman et al, Blood 2011). PCI-32765 has been shown to be well tolerated in CLL with preliminary clinical trial data showing that >85% (34/39) of patients remained on therapy at a median follow-up of four months. In addition, a significant shrinkage of lymph nodes has been observed in the majority of patients displaying lymphadenopathy. As with other B-cell receptor (BCR) directed therapies, PCI-32765 results in an initial increase in the absolute lymphocyte count. These observations are not explainable by the available in vitro data, demonstrating the need for in vivo investigation. In order to study the effect of PCI-32765 in vivo we chose to use the recently established NOD scid gamma null (NSG) - human CLL xenograft model with some modifications (Bagnara et al., Blood 2011). NSG mice were conditioned with 25 mg/kg busulfan 24 hours before injection of 1 × 108 CLL peripheral blood mononuclear cells previously labeled with 1μM CFSE. We first demonstrated that xenografted CLL cells isolated from the mouse spleen acquire an activated phenotype and proliferate, mimicking the phenotype of CLL cells isolated from human lymph nodes (Sun et al., abstract submitted). Next we sought to use this model to investigate the effect ot PCI-32765 on CLL cell activation and proliferation. Mice received PCI-32765 or vehicle in their drinking water at 0.16 mg/ml dissolved in 1% HP-beta-CD starting at the time of busulfan treatment. Mice were bled weekly and sacrificed between 3 and 4 weeks post xenografting. We found that PCI-32765 treatment resulted in a significant reduction in proliferation (defined as CFSE low cells) compared to mice that received vehicle water; this was observed in all three biological compartments: peripheral blood (84.5% decrease, p=0.007), spleen (72.4% decrease, p=0.012) and bone marrow (92.5% decrease, p=0.049). In comparison, PCI-32765 treatment did not result in a significant reduction in T-cell proliferation in any of the compartments (p>0.4). Although peripheral blood CLL counts were comparable between treated and untreated mice, we found that there were substantially more CLL cells in the spleens of the vehicle treated mice than in those of the PCI-32765 treated mice. In contrast, no differences in T-cell number or localization were observed between treated and untreated mice. Lastly, we sought to determine whether activation of CLL cells in the microenvironment could be blocked by PCI-32765. As we have previously shown, CLL cells in the human lymph node display a gene signature indicating B-cell receptor (BCR) and NF-kB activation compared to CLL cells in the peripheral blood (Herishanu et al., Blood 2011). We used quantitative RT-PCR (pre-designed Taqman Gene Expression assays) to measure expression of representative BCR and NF-kB target genes. PCI-32765 significantly reduced expression of EGR1 (p=0.049), EGR3 (p=0.023) and GFI1 (p=0.023) (BCR signature) and CCL3 (p=0.013) and CCND2 (p=0.046) (NF-kB signature) compared to vehicle treated mice. In addition, we also observed decreases in the proliferation gene signature (CDT1, PCNA and RRM2) (signature score, p=0.035) in the CLL cells from mice treated with PCI-32765; consistent with the assessed CFSE proliferation measurements. Taken together, our results show that PCI-32765 inhibits CLL activation and proliferation in the tissue microenvironment in vivo without affecting T-cell proliferation. These results demonstrate that targeting Btk is sufficient to block key interactions between tumor cells and the microenvironment and thus warrants the use of PCI-32765 as a targeted agent in CLL. Disclosures: Buggy: Pharmacyclics, Inc.: Employment.

A Protocol to Evaluate Semi-Rigid Pedicle Screw Systems

1997 ◽  
Vol 119 (3) ◽  
pp. 364-366 ◽  
Author(s):  
J. D. Clausen ◽  
V. K. Goel ◽  
K. Sairyo ◽  
M. Pfeiffer
Keyword(s):  
Pedicle Screw ◽  
In Vitro Testing ◽  
Cable System ◽  
Spinal Implants ◽  
Testing Protocol

The objective of the current study was to develop an in vitro testing protocol to evaluate semi-rigid pedicle screw devices. A corpectomy model protocol exists to evaluate rigid spinal implants; however, semi-rigid devices are contraindicated for this condition. This paper describes a technique that simulates more closely the conditions a semi-rigid device would see in vivo. Finally, the new testing protocol is used to evaluate the DDS® pedicle screw-cable system. Benefits and shortcomings of the new protocol are discussed.

Evaluation of Phase Stability in Zirconia Femoral Heads From Different Manufacturers After In Vitro Testing or In Vivo Retrieval

2009 ◽  
Vol 24 (8) ◽  
pp. 1225-1230 ◽  
Author(s):  
Kyoju Fukatsu ◽  
Giuseppe Pezzotti ◽  
Yasuhisa Hayaishi ◽  
Nobuhiko Sugano
Keyword(s):  
Phase Stability ◽  
In Vitro Testing ◽  
Femoral Heads

In vivo and in vitro testing of microelectronically fabricated planar sensors designed for applications in cardiology

1993 ◽  
Vol 346 (6-9) ◽  
pp. 584-588 ◽  
Author(s):  
Ern� Lindner ◽  
Vasile V. Cosofret ◽  
Stefan Ufer ◽  
Timothy A. Johnson ◽  
R. Bruce Ash ◽  
...  
Keyword(s):  
In Vitro Testing

Controlled-release components of PZP contraceptive vaccine extend duration of infertility

2008 ◽  
Vol 35 (6) ◽  
pp. 555 ◽  
Author(s):  
John W. Turner ◽  
Allen T. Rutberg ◽  
Ricky E. Naugle ◽  
Manpreet A. Kaur ◽  
Douglas R. Flanagan ◽  
...  
Keyword(s):  
Controlled Release ◽  
Cost Effective ◽  
Field Studies ◽  
In Vitro Testing ◽  
Fertility Reduction ◽  
Contraceptive Vaccine ◽  
Fertility Data ◽  
Controlled Release Formulations

Successful immunocontraception of wildlife relying on repeated access to individuals for boosters has highlighted the need to incorporate primer and booster immunisations into one injection. We have investigated use of controlled-release polymers (lactide–glycolide) in small pellets to provide delayed in vivo delivery of booster porcine zona pellucida (PZP) antigen and adjuvant. This report reviews pellet-making methodology, in vitro testing of controlled-release pellets and in vivo effects of controlled-release PZP vaccine. We assessed 3 different manufacturing approaches for producing reliable, cost-effective pellets: (1) polymer melting and extrusion; (2) solvent evaporation from polymer solution; and (3) punch and die polymer moulding. In vitro testing of release patterns of controlled-release formulations, towards development of a 3-year duration vaccine, provided estimates for in vivo use of pellet preparations. These in vitro studies demonstrated protein release delay up to 22 months using 100% l-lactide or polycaprolactone polymers. For in vivo tests, pellets (1-, 3-, and 12-month release delay) serving as boosters were administered intramuscularly with PZP/adjuvant liquid primer to wild horses (Equus caballus), white-tailed deer (Odocoileus virginanus) and African elephants (Loxodonta africana). Horse field studies assessed fertility via offspring counts and/or faecal-hormone pregnancy testing. Treatment decreased fertility 5.3–9.3-fold in Year 1 and 3.6-fold in Year 2. In preliminary testing in deer, offspring counts revealed treatment-associated fertility reduction of 7.1-fold Year 1 and 3.3-fold Year 2. In elephants, treatment elevated anti-PZP titres 4.5–6.9-fold from pretreatment (no fertility data).

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