Small world yields the most effective information spreading

Spreading dynamics of information and diseases are usually analyzed by using a unified framework and analogous models. In this paper, we propose a model to emphasize the essential difference between information spreading and epidemic spreading, where the memory effects, the social reinforcement and the non-redundancy of contacts are taken into account. Under certain conditions, the information spreads faster and broader in regular networks than in random networks, which to some extent supports the recent experimental observation of spreading in online society [D. Centola, Science {\bf 329}, 1194 (2010)]. At the same time, simulation result indicates that the random networks tend to be favorable for effective spreading when the network size increases. This challenges the validity of the above-mentioned experiment for large-scale systems. More significantly, we show that the spreading effectiveness can be sharply enhanced by introducing a little randomness into the regular structure, namely the small-world networks yield the most effective information spreading. Our work provides insights to the understanding of the role of local clustering in information spreading.Comment: 6 pages, 7 figures, accepted by New J. Phy

Excessive extracellular ATP desensitizes P2Y2 and P2X4 ATP receptors provoking surfactant impairment ending in ventilation-induced lung injury

Stretching the alveolar epithelial type I (AT I) cells controls the intercellular signaling for the exocytosis of surfactant by the AT II cells through the extracellular release of adenosine triphosphate (ATP) (purinergic signaling). Extracellular ATP is cleared by extracellular ATPases, maintaining its homeostasis and enabling the lung to adapt the exocytosis of surfactant to the demand. Vigorous deformation of the AT I cells by high mechanical power ventilation causes a massive release of extracellular ATP beyond the clearance capacity of the extracellular ATPases. When extracellular ATP reaches levels >100 μM, the ATP receptors of the AT II cells become desensitized and surfactant impairment is initiated. The resulting alteration in viscoelastic properties and in alveolar opening and collapse time-constants leads to alveolar collapse and the redistribution of inspired air from the alveoli to the alveolar ducts, which become pathologically dilated. The collapsed alveoli connected to these dilated alveolar ducts are subject to a massive strain, exacerbating the ATP release. After reaching concentrations >300 μM extracellular ATP acts as a danger-associated molecular pattern, causing capillary leakage, alveolar space edema, and further deactivation of surfactant by serum proteins. Decreasing the tidal volume to 6 mL/kg or less at this stage cannot prevent further lung injury

Role of the supine lateral radiograph of the spine in vertebroplasty for osteoporotic vertebral compression fracture: a prospective study

<p>Abstract</p> <p>Background</p> <p>Severely collapsed vertebral compression fracture (VCF) is usually considered as a contraindication for vertebroplasty because of critically decreased vertebral height (less than one-third the original height). However, osteoporotic VCF can possess dynamic mobility with intravertebral cleft (IVC), which can be demonstrated on supine lateral radiographs (SuLR) and standing lateral radiographs (StLR). The purposes of this study were to: (1) evaluate the efficacy of SuLR to detect IVCs and assess the intravertebral mobility in VCFs, and (2) evaluate the short-term results of vertebroplasty in severely collapsed VCFs with IVCs.</p> <p>Methods</p> <p>We enrolled 37 patients with 40 symptomatic osteoporotic VCFs for vertebroplasty; 11 had severely collapsed VCFs with concurrent IVCs detected on the SuLR, the others had not-severely collapsed VCFs. A preoperative StLR, SuLR, magnetic resonance imaging (MRI), and postoperative StLR were taken from all patients. Radiographs were digitized to calculate vertebral body morphometrics including vertebral height ratio and Cobb's kyphotic angle. The intensity of the patient's pain was assessed by the visual analogue scale (VAS) on the day before operation and 1 day, 1 month, and 4 months after operation. The patient's VAS scores and image measurement results were assessed with the paired <it>t</it>-test and Pearson correlation tests; Mann-Whitney U test was used for VAS subgroup comparison. Significance was defined as <it>p </it>< 0.05.</p> <p>Results</p> <p>IVCs in patients with not-severely collapsed VCFs were detected in 21 vertebrae (72.4%) by MRI, in 15 vertebrae (51.7%) by preoperative SuLR, and in 7 vertebrae (24.1%) by preoperative StLR. Using the MRI as a gold standard to detect IVCs, SuLR exhibit a sensitivity of 0.71 as compared to StLR that yield a sensitivity of 0.33. In patients with VCFs with IVCs detected on SuLR, the average of the postoperative restoration in vertebral height ratio was significantly higher than that in those without IVCs (17.1% vs. 6.4%). There was no statistical difference in the VAS score between severely collapsed VCFs with IVCs detected on SuLR and not-severely collapsed VCFs at any follow-up time point.</p> <p>Conclusions</p> <p>The SuLR efficiently detects an IVC in VCF, which indicates a better vertebral height correction after vertebroplasty compared to VCF without IVC. Before performing a costly MRI, SuLR can identify more IVCs than StLR in patients with severely collapsed VCFs, whom may become the candidates for vertebroplasty.</p

First histological observations on the incorporation of a novel nanocrystalline hydroxyapatite paste OSTIM(® )in human cancellous bone

BACKGROUND: A commercially available nanocrystalline hydroxyapatite paste Ostim(® )has been reported in few recent studies to surpass other synthetic bone substitutes with respect to the observed clinical results. However, the integration of this implantable material has been histologically evaluated only in animal experimental models up to now. This study aimed to evaluate the tissue incorporation of Ostim(® )in human cancellous bone after reconstructive bone surgery for trauma. METHODS: Biopsy specimens from 6 adult patients with a total of 7 tibial, calcaneal or distal radial fractures were obtained at the time of osteosynthesis removal. The median interval from initial operation to tissue sampling was 13 (range 3–15) months. Samples were stained with Masson-Goldner, von Kossa, and toluidine blue. Osteoid volume, trabecular width and bone volume, and cortical porosity were analyzed. Samples were immunolabeled with antibodies against CD68, CD56 and human prolyl 4-hydroxylase to detect macrophages, osteoblasts, and fibroblasts, respectively. TRAP stainings were used to identify osteoclasts. RESULTS: Histomorphometric data indicated good regeneration with normal bone turnover: mean osteoid volume was 1.93% of the trabecular bone mass, trabecular bone volume – 28.4%, trabecular width – 225.12 μm, and porosity index – 2.6%. Cortical and spongious bone tissue were well structured. Neither inflammatory reaction, nor osteofibrosis or osteonecrosis were observed. The implanted material was widely absorbed. CONCLUSION: The studied nanocrystalline hydroxyapatite paste showed good tissue incorporation. It is highly biocompatible and appears to be a suitable bone substitute for juxtaarticular comminuted fractures in combination with a stable screw-plate osteosynthesis

Angiographic correlations of patients with small vessel disease diagnosed by adenosine-stress cardiac magnetic resonance imaging

Cardiac magnetic resonance imaging (CMR) with adenosine-stress myocardial perfusion is gaining importance for the detection and quantification of coronary artery disease (CAD). However, there is little knowledge about patients with CMR-detected ischemia, but having no relevant stenosis as seen on coronary angiography (CA). The aims of our study were to characterize these patients by CMR and CA and evaluate correlations and potential reasons for the ischemic findings. 73 patients with an indication for CA were first scanned on a 1.5T whole-body CMR-scanner including adenosine-stress first-pass perfusion. The images were analyzed by two independent investigators for myocardial perfusion which was classified as subendocardial ischemia (n = 22), no perfusion deficit (n = 27, control 1), or more than subendocardial ischemia (n = 24, control 2). All patients underwent CA, and a highly significant correlation between the classification of CMR perfusion deficit and the degree of coronary luminal narrowing was found. For quantification of coronary blood flow, corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) was evaluated for the left anterior descending (LAD), circumflex (LCX) and right coronary artery (RCA). The main result was that corrected TFC in all coronaries was significantly increased in study patients compared to both control 1 and to control 2 patients. Study patients had hypertension or diabetes more often than control 1 patients. In conclusion, patients with CMR detected subendocardial ischemia have prolonged coronary blood flow. In connection with normal resting flow values in CAD, this supports the hypothesis of underlying coronary microvascular impairment. CMR stress perfusion differentiates non-invasively between this entity and relevant CAD

Design and rationale of DUTCH-AF:a prospective nationwide registry programme and observational study on long-term oral antithrombotic treatment in patients with atrial fibrillation

Introduction Anticoagulation therapy is pivotal in the management of stroke prevention in atrial fibrillation (AF). Prospective registries, containing longitudinal data are lacking with detailed information on anticoagulant therapy, treatment adherence and AF-related adverse events in practice-based patient cohorts, in particular for non-vitamin K oral anticoagulants (NOAC). With the creation of DUTCH-AF, a nationwide longitudinal AF registry, we aim to provide clinical data and answer questions on the (anticoagulant) management over time and of the clinical course of patients with newly diagnosed AF in routine clinical care. Within DUTCH-AF, our current aim is to assess the effect of non-adherence and non-persistence of anticoagulation therapy on clinical adverse events (eg, bleeding and stroke), to determine predictors for such inadequate anticoagulant treatment, and to validate and refine bleeding prediction models. With DUTCH-AF, we provide the basis for a continuing nationwide AF registry, which will facilitate subsequent research, including future registry-based clinical trials. Methods and analysis The DUTCH-AF registry is a nationwide, prospective registry of patients with newly diagnosed 'non-valvular' AF. Patients will be enrolled from primary, secondary and tertiary care practices across the Netherlands. A target of 6000 patients for this initial cohort will be followed for at least 2 years. Data on thromboembolic and bleeding events, changes in antithrombotic therapy and hospital admissions will be registered. Pharmacy-dispensing data will be obtained to calculate parameters of adherence and persistence to anticoagulant treatment, which will be linked to AF-related outcomes such as ischaemic stroke and major bleeding. In a subset of patients, anticoagulation adherence and beliefs about drugs will be assessed by questionnaire. Ethics and dissemination This study protocol was approved as exempt for formal review according to Dutch law by the Medical Ethics Committee of the Leiden University Medical Centre, Leiden, the Netherlands. Results will be disseminated by publications in peer-reviewed journals and presentations at scientific congresses

HSP60 as a Target of Anti-Ergotypic Regulatory T Cells

The 60 kDa heat shock protein (HSP60) has been reported to influence T-cell responses in two ways: as a ligand of toll-like receptor 2 signalling and as an antigen. Here we describe a new mechanism of T-cell immuno-regulation focused on HSP60: HSP60 is up-regulated and presented by activated T cells (HSP60 is an ergotope) to regulatory (anti-ergotypic) T cells. Presentation of HSP60 by activated T cells was found to be MHC-restricted and dependent on accessory molecules - CD28, CD80 and CD86. Anti-ergotypic T cells responded to T-cell HSP60 by proliferation and secreted IFNγ and TGFβ1. In vitro, the anti-ergotypic T cells inhibited IFNγ production by their activated T-cell targets. In vivo, adoptive transfer of an anti-ergotypic HSP60-specific T-cell line led to decreased secretion of IFNγ by arthritogenic T cells and ameliorated adjuvant arthritis (AA). Thus, the presentation of HSP60 by activated T cells turns them into targets for anti-ergotypic regulatory T cells specific for HSP60. However, the direct interaction between the anti-ergotypic T regulators (anti-HSP60) and the activated T cells also down-regulated the regulators. Thus, by functioning as an ergotope, HSP60 can control both the effector T cells and the regulatory HSP60-specific T cells that control them