Development of a Shape Memory Polymer Soft Microgripper

The ability to control microrobots by means of magnetic fields has become of increasing interest to researchers. These robots’ ability to reach places tethered microrobots otherwise could not leads to many possible applications in the body, such as delivering drugs to targeted locations and performing biopsies. This study shows the use of shape memory polymer (SMP) to wirelessly actuate a microgripper to be used by a controllable microrobot to achieve these functions. Many smart materials were analyzed in order to find the material that most effectively would accomplish wirelessly gripping, manipulating, and releasing a microobject. Multiple microgripper designs were designed, analyzed, and constructed at a macroscale from acrylic, simulating a microscale counterpart. Simulated and experimental data were compared to determine the design that would require the least amount of inputted force and displacement from the SMP. This study shows a proposal for scaling this final design to the microscale involving experimentation with different forms of SMP in order to make the gripper actuatable in biologically relevant conditions. This technology could provide an inexpensive and effective solution for manipulating cells and other microobjects in vitro and in vivo

Staphylococcus aureus and Acinetobacter baumannii Inhibit Osseointegration of Orthopedic Implants

Bacterial infections routinely cause inflammation and thereby impair osseointegration of orthopedic implants. Acinetobacter spp., which cause osteomyelitis following trauma, on or off the battlefield, were, however, reported to cause neither osteomyelitis nor osteolysis in rodents. We therefore compared the effects of Acinetobacter strain M2 to those of Staphylococcus aureus in a murine implant infection model. Sterile implants and implants with adherent bacteria were inserted in the femur of mice. Bacterial burden, levels of proinflammatory cytokines, and osseointegration were measured. All infections were localized to the implant site. Infection with either S. aureus or Acinetobacter strain M2 increased the levels of proinflammatory cytokines and the chemokine CCL2 in the surrounding femurs, inhibited bone formation around the implant, and caused loss of the surrounding cortical bone, leading to decreases in both histomorphometric and biomechanical measures of osseointegration. Genetic deletion of TLR2 and TLR4 from the mice partially reduced the effects of Acinetobacter strain M2 on osseointegration but did not alter the effects of S. aureus. This is the first report that Acinetobacter spp. impair osseointegration of orthopedic implants in mice, and the murine model developed for this study will be useful for future efforts to clarify the mechanism of implant failure due to Acinetobacter spp. and to assess novel diagnostic tools or therapeutic agents

Bacterial Pathogen-associated Molecular Patterns Stimulate Biological Activity of Orthopaedic Wear Particles by Activating Cognate Toll-like Receptors*

Aseptic loosening of orthopaedic implants is induced by wear particles generated from the polymeric and metallic components of the implants. Substantial evidence suggests that activation of Toll-like receptors (TLRs) may contribute to the biological activity of the wear particles. Although pathogen-associated molecular patterns (PAMPs) produced by Gram-positive bacteria are likely to be more common in patients with aseptic loosening, prior studies have focused on LPS, a TLR4-specific PAMP produced by Gram-negative bacteria. Here we show that both TLR2 and TLR4 contribute to the biological activity of titanium particles with adherent bacterial debris. In addition, lipoteichoic acid, a PAMP produced by Gram-positive bacteria that activates TLR2, can, like LPS, adhere to the particles and increase their biological activity, and the increased biological activity requires the presence of the cognate TLR. Moreover, three lines of evidence support the conclusion that TLR activation requires bacterially derived PAMPs and that endogenously produced alarmins are not sufficient. First, neither TLR2 nor TLR4 contribute to the activity of “endotoxin-free” particles as would be expected if alarmins are sufficient to activate the TLRs. Second, noncognate TLRs do not contribute to the activity of particles with adherent LPS or lipoteichoic acid as would be expected if alarmins are sufficient to activate the TLRs. Third, polymyxin B, which inactivates LPS, blocks the activity of particles with adherent LPS. These results support the hypothesis that PAMPs produced by low levels of bacterial colonization may contribute to aseptic loosening of orthopaedic implants

Thermal Cracking of Massive Concrete Structures, State of the Art Report of the RILEM Technical Committee 254-CMS: Chapter 3: Thermal properties

info:eu-repo/semantics/inPres