Self-healing microcapsules encapsulated with carbon nanotubes for improved thermal and electrical properties

Microcapsules are widely used by researchers in self-healing composites. In this study, multi-walled carbon nanotubes (CNT) were incorporated into the core of the microcapsules, along with the self-healing agent. Dicyclopentadiene (DCPD) and urea-formaldehyde (UF) were chosen as the core and shell materials respectively, and DCPD–CNT–UF based dual core microcapsules were synthesized. Two types of microcapsules, namely, DCPD–UF and DCPD–CNT–UF were successfully synthesized by the in situ polymerization technique. The novelty of this work is the development of dual core microcapsules with DCPD–CNT–UF combination. Surface morphology characterization and elemental analysis of the microcapsules were carried out using a scanning electron microscope (SEM-EDX). TGA and DSC analysis show that DCPD–CNT–UF microcapsules have better thermal stability than DCPD–UF microcapsules. These novel DCPD–CNT–UF microcapsules were found to be compatible with epoxy base resin for making resin castings. The presence of CNT is found to improve the mechanical, thermal and electrical properties of the resin cast specimens without compromising on self-healing efficiency.

Carbon nanotubes incorporated microcapsules based self-heating composites.     

Expression of CD105 and CD34 receptors controls BMP‐induced in vitro mineralization of mouse adipose‐derived stem cells but does not predict their in vivo bone‐forming potential

Adipose‐derived stem cells (ADSCs) can be excellent alternative to bone marrow derived stem cells for enhancing fracture repair since ADSCs can be isolated comparatively in large numbers from discarded lipoaspirates. However, osteogenic potential of ADSCs in vivo is very controversial. We hypothesized that adipose‐derived stem cells (ADSCs) that respond maximally to bone morphogenetic proteins (BMPs) in vitro would possess maximum bone‐forming potential. Four purified populations of mouse ADSCs: CD105⁺CD34⁺, CD105^?CD34^?, CD105⁺CD34^? and CD105^?CD34⁺ were obtained using fluorescence‐activated cell sorting (FACS) and their BMP‐responsiveness was determined in vitro. CD105⁺CD34^? population showed the strongest response to BMPs in terms of robust increase in mineralization. Expression of CD105 correlated with high BMP‐responsive phenotype and larger cell size while expression of CD34 correlated with low BMP‐responsive phenotype and smaller cell size. CD105⁺CD34^? population displayed higher gene expression of Alk1 or Alk6 receptors in comparison with other populations. However, CD105⁺CD34^? ADSCs failed to induce ectopic bone formation in vivo after they were transplanted into syngeneic mice, indicating that in vitro BMP‐responsiveness is not a good indicator to predict in vivo bone forming potential of ADSCs. Therefore greater precautions should be executed during selection of competent ADSCs for bone repair. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:625–632, 2015.

     

An Anatomical Study to Demonstrate the Proximity of Kirschner Wires to Structures at Risk in Percutaneous Pinning of Distal Radius Fractures

Distal radius fractures are often treated using percutaneous Kirschner wires (K-wires). The sensory nerves in this area, extensor tendons, radial artery and cephalic vein are at risk of injury in this procedure. We undertook a cadaveric investigation to identify probability of damage to these ‘at risk’ structures by measuring their distances in relation to standard K-wire sites. Nine upper limbs from six formalin-preserved cadavers were studied. Four K-wires were placed percutaneously simulating fixation of a distal radius fracture. Careful dissection was done preserving the original position of neurovascular and tendinous structures. Distances to relevant soft-tissue structures from each K-wire were measured using an electronic digital caliper. Distance of superficial nerves from radial styloid and Lister’s tubercle was measured to determine their ‘safe distance’ from these fixed landmarks. None of the superficial nerves were injured by a K-wire. Cephalic vein had been pierced on 4 occasions (4/18) and extensor tendons on 3 occasions (3/18). Wilcoxon signed-rank test was used to compare distance of the superficial nerves from radial styloid and Lister tubercle, and the latter was found to be the safer option. This study highlights the inherent danger in percutaneous K-wire fixation of wrist fractures. Limited size of the area, where K-wires can be positioned, and anatomic variations of neurovascular structures pose obstacles in developing guidelines for reducing risk of injury. We advocate use of mini-open approach and guiding devices to avert complications of inadvertent impalement and damage to these structures.     

Identification of a mammalian gene structurally and functionally related to the CDC25 gene of Saccharomyces cerevisiae.

The yeast Saccharomyces cerevisiae CDC25 gene encodes a nucleotide-exchange-factor (NEF) that can convert the inactive GDP-bound state of RAS proteins to an active RAS-GTP complex. CDC25 can activate the yeast RAS proteins as well as the human H-ras protein. CDC25 is a member of a family of yeast genes that likely encode NEFs capable of regulating the RAS-related proteins found in yeast. By aligning the amino acid sequence of CDC25-related gene products we found a number of conserved motifs. Using degenerate oligonucleotides that encode these conserved sequences, we have used polymerase chain reactions to amplify fragments of mouse and human cDNAs related to the yeast CDC25 gene. We show that a chimeric molecule, part mouse and part yeast CDC25, can suppress the loss of CDC25 function in the yeast S. cerevisiae.     

Selective depletion and activation of CD8+ lymphocytes from peripheral blood of patients with polymyalgia rheumatica and giant cell arteritis.

A prospective study of 33 patients with polymyalgia rheumatica/giant cell arteritis (PMR/GCA) was undertaken, firstly, to monitor sequentially peripheral blood CD8+ lymphocyte levels and, secondly, to assess the expression of activation markers on T lymphocyte subsets. The results indicated that there was a significant decrease in absolute numbers and relative percentages of CD8+ T lymphocytes, which returned to normal ranges after approximately 24 months' treatment, and that there was an increased percentage of CD8+ lymphocytes in PMR/GCA which express HLA class II antigens.     

Death-associated protein kinase 1 promotes growth of p53-mutant cancers

Estrogen receptor–negative (ER-negative) breast cancers are extremely aggressive and associated with poor prognosis. In particular, effective treatment strategies are limited for patients diagnosed with triple receptor–negative breast cancer (TNBC), which also carries the worst prognosis of all forms of breast cancer; therefore, extensive studies have focused on the identification of molecularly targeted therapies for this tumor subtype. Here, we sought to identify molecular targets that are capable of suppressing tumorigenesis in TNBCs. Specifically, we found that death-associated protein kinase 1 (DAPK1) is essential for growth of p53-mutant cancers, which account for over 80% of TNBCs. Depletion or inhibition of DAPK1 suppressed growth of p53-mutant but not p53-WT breast cancer cells. Moreover, DAPK1 inhibition limited growth of other p53-mutant cancers, including pancreatic and ovarian cancers. DAPK1 mediated the disruption of the TSC1/TSC2 complex, resulting in activation of the mTOR pathway. Our studies demonstrated that high DAPK1 expression causes increased cancer cell growth and enhanced signaling through the mTOR/S6K pathway; evaluation of multiple breast cancer patient data sets revealed that high DAPK1 expression associates with worse outcomes in individuals with p53-mutant cancers. Together, our data support targeting DAPK1 as a potential therapeutic strategy for p53-mutant cancers.