ELECTRICAL CONDUCTIVITY OF POTASSIUM CHLORIDE

The electrical conductivity of potassium chloride is discussed within the framework of a four-defect model of the crystal. The four defects are mobile anion and cation vacancies and immobile divalent cation impurities and divalent cation impurity-cation vacancy complexes. The Teltow formulation of the four-defect mode1 fails to describe precisely the measured electrical conductivity of KCl over the entire intrinsic and extrinsic range

Ionic Transport in Potassium Chloride

The electrical conductivity and chlorine ion diffusion in KC1 and KCl:SrC12 single crystals have been analyzed by least-squares methods, using as a model a perfect crystal perturbed by five defects: isolated anion vacancies, isolated cation vacancies, divalent cation impurities, divalent cation-impurity-cation-vacancy complexes, and vacancy pairs. The transport equations were derived from this five-defect model using a simple theory for noninteracting particles, except for the nearest-neighbor binding to form complexes and vacancy pairs, and using the same theory including long-range Coulomb interactions between the isolated defects. This latter theory yielded the better description of the experimental results. However, the analyses showed that significant nonrandom deviations exist between theory and experiment. These deviations exist in both the intrinsic and extrinsic regions of conductivity. The failure of existing concepts for these transport properties is discussed in terms of possible additional mechanisms, i.e., electrons, cationic Frenkel defects, or trivacancies, and in terms of more complete theoretical treatment

Social media for research discourse, dissemination, and collaboration in rheumatology

Social media has become an important venue for rheumatologists, patients, organizations, and other stakeholders to discuss recent research advances in diagnosis and management of rheumatic disorders. In this article, we describe the current state of how social media may enhance dissemination, discourse, and collaboration in rheumatology research. Social media may refer to social platforms like Twitter and Instagram or digital media like podcasts and other websites that are operated for providing as free, open-access medical education (FOAM). Twitter has been one of the most active social media venues and continues to host a vibrant rheumatology community. Examples of research discussions on Twitter include organic user tweets, educational threads ( tweetorials ), live-tweeting academic conferences, and journals posting recently-accepted articles. Some research collaborations have been initiated through social media interactions. Social media may also directly contribute to research by facilitating the recruitment of study participants and the collection of survey-based data. Thus, social media is an evolving and important tool to enhance research discourse, dissemination, and collaboration in rheumatology

Expression of an Arc-Immunoreactive Protein in the Adult Zebrafish Brain Increases in Response to a Novel Environment

Zebrafish are a powerful research tool in the field of neuroscience, offering several logistical and physiological advantages over rodents as a research model. However, the molecular dynamics of this model organism, especially with regards to learning and memory, are scarcely known. The current study explored the zebrafish brain for the presence of a protein bearing a similar function to the activity-regulated, cytoskeleton-associated protein (Arc), a critical player in synaptic plasticity. The adult zebrafish brain was found to express a protein with immunoreactivity against the anti-Arc antibody H-300. Immunoreactivity was detected ubiquitously, especially in areas known as adult progenitor cell zones. The protein, termed Arc-immunoreactive protein (AIP), increased in the telencephalon but not the optic tectum 60 min after exposure to a novel environment. Epileptiform brain activity, however, did not induce AIP expression. Evidence presented herein suggests AIP may be the neuropeptide Y receptor rather than a zebrafish homolog of Arc

SS25. Cryopreserved Venous Allograft: An Alternative Conduit for Reconstruction of Infected Prosthetic Aortic Grafts

Olivé Milián, ArmandPla general picat del mosaic format per tres cercles: el central, amb un sol de color ocre sobre un cel blau. El sol, somrient, està encarat cap al sud. Aquest està envoltat d'un primer anell dentat i un segon on s'hi representen les fases d

Fibroblast activation and inflammation in frozen shoulder

Introduction: Frozen shoulder is a common, fibro-proliferative disease characterised by the insidious onset of pain and progressively restricted range of shoulder movement. Despite the prevalence of this disease, there is limited understanding of the molecular mechanisms underpinning the pathogenesis of this debilitating disease. Previous studies have identified increased myofibroblast differentiation and proliferation, immune cell influx and dysregulated cytokine production. We hypothesised that subpopulations within the fibroblast compartment may take on an activated phenotype, thus initiating the inflammatory processes observed in frozen shoulder. Therefore, we sought to evaluate the presence and possible pathogenic role of known stromal activation proteins in Frozen shoulder, Methods: Shoulder capsule samples were collected from 10 patients with idiopathic frozen shoulder and 10 patients undergoing shoulder stabilisation surgery. Fibroblast activation marker expression (CD248, CD146, VCAM and PDPN, FAP) was quantified using immunohistochemistry. Control and diseased fibroblasts were cultured for in vitro studies from capsule biopsies from instability and frozen shoulder surgeries, respectively. The inflammatory profile and effects of IL-1β upon diseased and control fibroblasts was assessed using ELISA, immunohistochemistry and qPCR. Results: Immunohistochemistry demonstrated increased expression of fibroblast activation markers CD248, CD146, VCAM and PDPN in the frozen shoulder group compared with control (p < 0.05). Fibroblasts cultured from diseased capsule produced elevated levels of inflammatory protein (IL-6, IL-8 & CCL-20) in comparison to control fibroblasts. Exposing control fibroblasts to an inflammatory stimuli, (IL-1ß) significantly increased stromal activation marker transcript and protein expression (CD248, PDPN and VCAM). Conclusions: These results show that fibroblasts have an activated phenotype in frozen shoulder and this is associated with inflammatory cytokine dysregulation. Furthermore, it supports the hypothesis that activated fibroblasts may be involved in regulating the inflammatory and fibrotic processes involved in this disease

S100A8 & S100A9: alarmin mediated inflammation in tendinopathy

Alarmins S100A8 and S100A9 are endogenous molecules released in response to environmental triggers and cellular damage. They are constitutively expressed in immune cells such as monocytes and neutrophils and their expression is upregulated under inflammatory conditions. The molecular mechanisms that regulate inflammatory pathways in tendinopathy are largely unknown therefore identifying early immune effectors is essential to understanding the pathology. Based on our previous investigations highlighting tendinopathy as an alarmin mediated pathology we sought evidence of S100A8 & A9 expression in a human model of tendinopathy and thereafter, to explore mechanisms whereby S100 proteins may regulate release of inflammatory mediators and matrix synthesis in human tenocytes. Immunohistochemistry and quantitative RT-PCR showed S100A8 & A9 expression was significantly upregulated in tendinopathic tissue compared with control. Furthermore, treating primary human tenocytes with exogenous S100A8 & A9 significantly increased protein release of IL-6, IL-8, CCL2, CCL20 and CXCL10; however, no alterations in genes associated with matrix remodelling were observed at a transcript level. We propose S100A8 & A9 participate in early pathology by modulating the stromal microenvironment and influencing the inflammatory profile observed in tendinopathy. S100A8 and S100A9 may participate in a positive feedback mechanism involving enhanced leukocyte recruitment and release of pro-inflammatory cytokines from tenocytes that perpetuates the inflammatory response within the tendon in the early stages of disease

Temperature Dependence of Spin-Split Peaks in Transverse Electron Focusing

We present experimental results of transverse electron-focusing measurements performed using n-type GaAs. In the presence of a small transverse magnetic field (B⊥), electrons are focused from the injector to detector leading to focusing peaks periodic in B⊥. We show that the odd-focusing peaks exhibit a split, where each sub-peak represents a population of a particular spin branch emanating from the injector. The temperature dependence reveals that the peak splitting is well defined at low temperature whereas it smears out at high temperature indicating the exchange-driven spin polarisation in the injector is dominant at low temperatures

Novel mutations expand the clinical spectrum of DYNC1H1-associated spinal muscular atrophy

OBJECTIVE To expand the clinical phenotype of autosomal dominant congenital spinal muscular atrophy with lower extremity predominance (SMA-LED) due to mutations in the dynein, cytoplasmic 1, heavy chain 1 (DYNC1H1) gene. METHODS Patients with a phenotype suggestive of a motor, non-length-dependent neuronopathy predominantly affecting the lower limbs were identified at participating neuromuscular centers and referred for targeted sequencing of DYNC1H1. RESULTS We report a cohort of 30 cases of SMA-LED from 16 families, carrying mutations in the tail and motor domains of DYNC1H1, including 10 novel mutations. These patients are characterized by congenital or childhood-onset lower limb wasting and weakness frequently associated with cognitive impairment. The clinical severity is variable, ranging from generalized arthrogryposis and inability to ambulate to exclusive and mild lower limb weakness. In many individuals with cognitive impairment (9/30 had cognitive impairment) who underwent brain MRI, there was an underlying structural malformation resulting in polymicrogyric appearance. The lower limb muscle MRI shows a distinctive pattern suggestive of denervation characterized by sparing and relative hypertrophy of the adductor longus and semitendinosus muscles at the thigh level, and diffuse involvement with relative sparing of the anterior-medial muscles at the calf level. Proximal muscle histopathology did not always show classic neurogenic features. CONCLUSION Our report expands the clinical spectrum of DYNC1H1-related SMA-LED to include generalized arthrogryposis. In addition, we report that the neurogenic peripheral pathology and the CNS neuronal migration defects are often associated, reinforcing the importance of DYNC1H1 in both central and peripheral neuronal functions