Control of polymorphism in coronene by the application of magnetic fields

Coronene, a polyaromatic hydrocarbon, has been crystallized for the first time in a different polymorph using a crystal growth method that utilizes magnetic fields to access a unit cell configuration that was hitherto unknown. Crystals grown in magnetic field of 1 T are larger, have a different appearance to those grown in zero field and retain their structure in ambient conditions. We identify the new form, beta-coronene, as the most stable at low temperatures. As a result of the new supramolecular configuration we report significantly altered electronic, optical and mechanical properties.Comment: 32 pages, 17 figure

Expansion of Foxp3+ T-cell populations by Candida albicans enhances both Th17-cell responses and fungal dissemination after intravenous challenge

Research Funding Wellcome Trust, UK. Grant Numbers: 086827, 080088 NIH. Grant Number: DE022550Peer reviewedPublisher PD

MitoNeoD:a mitochondria-targeted superoxide probe

Mitochondrial superoxide (O2⋅−) underlies much oxidative damage and redox signaling. Fluorescent probes can detect O2⋅−, but are of limited applicability in vivo, while in cells their usefulness is constrained by side reactions and DNA intercalation. To overcome these limitations, we developed a dual-purpose mitochondrial O2⋅− probe, MitoNeoD, which can assess O2⋅− changes in vivo by mass spectrometry and in vitro by fluorescence. MitoNeoD comprises a O2⋅−-sensitive reduced phenanthridinium moiety modified to prevent DNA intercalation, as well as a carbon-deuterium bond to enhance its selectivity for O2⋅− over non-specific oxidation, and a triphenylphosphonium lipophilic cation moiety leading to the rapid accumulation within mitochondria. We demonstrated that MitoNeoD was a versatile and robust probe to assess changes in mitochondrial O2⋅− from isolated mitochondria to animal models, thus offering a way to examine the many roles of mitochondrial O2⋅−production in health and disease

The Caenorhabditis elegans nephrocystins act as global modifiers of cilium structure

Nephronophthisis (NPHP) is the most common genetic cause of end-stage renal disease in children and young adults. In Chlamydomonas reinhardtii, Caenorhabditis elegans, and mammals, the NPHP1 and NPHP4 gene products nephrocystin-1 and nephrocystin-4 localize to basal bodies or ciliary transition zones (TZs), but their function in this location remains unknown. We show here that loss of C. elegans NPHP-1 and NPHP-4 from TZs is tolerated in developing cilia but causes changes in localization of specific ciliary components and a broad range of subtle axonemal ultrastructural defects. In amphid channel cilia, nphp-4 mutations cause B tubule defects that further disrupt intraflagellar transport (IFT). We propose that NPHP-1 and NPHP-4 act globally at the TZ to regulate ciliary access of the IFT machinery, axonemal structural components, and signaling molecules, and that perturbing this balance results in cell type–specific phenotypes

Highly lubricious SPMK-g-PEEK implant surfaces to facilitate rehydration of articular cartilage

To enable long lasting osteochondral defect repairs which preserve the native function of synovial joint counter-face, it is essential to develop surfaces which are optimised to support healthy cartilage function by providing a hydrated, low friction and compliant sliding interface. PEEK surfaces were modified using a biocompatible 3-sulfopropyl methacrylate potassium salt (SPMK) through UV photo-polymerisation, resulting in a ∼350 nm thick hydrophilic coating rich in hydrophilic anionic sulfonic acid groups. Characterisation was done through Fourier Transformed Infrared Spectroscopy, Focused Ion Beam Scanning Electron Microscopy, and Water Contact Angle measurements. Using a Bruker UMT TriboLab, bovine cartilage sliding tests were conducted with real-time strain and shear force measurements, comparing untreated PEEK, SPMK functionalised PEEK (SPMK-g-PEEK), and Cobalt Chrome Molybdenum alloy. Tribological tests over 2.5 h at physiological loads (0.75 MPa) revealed that SPMK-g-PEEK maintains low friction (μ &lt; 0.024) and minimises equilibrium strain, significantly reducing forces on the cartilage interface. Post-test analysis showed no notable damage to the cartilage interfacing against the SPMK functionalised surfaces. The application of a constitutive biphasic cartilage model to the experimental strain data reveals that SPMK surfaces increase the interfacial permeability of cartilage in sliding, facilitating fluid and strain recovery. Unlike previous demonstrations of sliding-induced tribological rehydration requiring specific hydrodynamic conditions, the SPMK-g-PEEK introduces a novel mode of tribological rehydration operating at low speeds and in a stationary contact area. SPMK-g-PEEK surfaces provide an enhanced cartilage counter-surface, which provides a highly hydrated and lubricious boundary layer along with supporting biphasic lubrication. Soft polymer surface functionalisation of orthopaedic implant surfaces are a promising approach for minimally invasive synovial joint repair with an enhanced bioinspired polyelectrolyte interface for sliding against cartilage. These hydrophilic surface coatings offer an enabling technology for the next generation of focal cartilage repair and hemiarthroplasty implant surfaces.</p

Doodles on surfaces

Doodles were introduced in but were restricted to embedded circles in the 2-sphere. Khovanov, extended the idea to immersed circles in the 2-sphere. In this paper we further extend the range of doodles to any closed oriented surfaces. Uniqueness of minimal representatives is proved, and various example of doodles are given with their minimal representatives. We also introduce the notion of virtual doodles, and show that there is a natural one-to-one correspondence between doodles on surfaces and virtual doodles on the plane

Control of mitochondrial superoxide production by reverse electron transport at complex I.

The generation of mitochondrial superoxide (O2̇̄) by reverse electron transport (RET) at complex I causes oxidative damage in pathologies such as ischemia reperfusion injury, but also provides the precursor to H2O2 production in physiological mitochondrial redox signaling. Here, we quantified the factors that determine mitochondrial O2̇̄ production by RET in isolated heart mitochondria. Measuring mitochondrial H2O2 production at a range of proton-motive force (Δp) values and for several coenzyme Q (CoQ) and NADH pool redox states obtained with the uncoupler p-trifluoromethoxyphenylhydrazone, we show that O2̇̄ production by RET responds to changes in O2 concentration, the magnitude of Δp, and the redox states of the CoQ and NADH pools. Moreover, we determined how expressing the alternative oxidase from the tunicate Ciona intestinalis to oxidize the CoQ pool affected RET-mediated O2̇̄ production at complex I, underscoring the importance of the CoQ pool for mitochondrial O2̇̄ production by RET. An analysis of O2̇̄ production at complex I as a function of the thermodynamic forces driving RET at complex I revealed that many molecules that affect mitochondrial reactive oxygen species production do so by altering the overall thermodynamic driving forces of RET, rather than by directly acting on complex I. These findings clarify the factors controlling RET-mediated mitochondrial O2̇̄ production in both pathological and physiological conditions. We conclude that O2̇̄ production by RET is highly responsive to small changes in Δp and the CoQ redox state, indicating that complex I RET represents a major mode of mitochondrial redox signaling