High levels of circulating CXC chemokine ligand 10 are associated with chronic autoimmune thyroiditis and hypothyroidism

CXC chemokine ligand 10 (CXCL10), an interferon-gamma-inducible chemokine associated with Th1-mediated immune responses, has been proposed as a marker of inflammation in autoimmune diseases. We measured serum CXCL10 concentrations in 223 consecutive patients with newly diagnosed autoimmune thyroiditis (AT), 97 euthyroid controls, and 29 patients with nontoxic multinodular goiter and related this parameter to the clinical phenotype. The three groups were similar in gender distribution and age; among the AT patients, 24% had subclinical hypothyroidism. Serum CXCL10 level was significantly higher in AT patients (157 +/- 139 pg/ml) than in controls (79 +/- 38) or patients with multinodular goiter (90 +/- 32; P < 0.0001). Among patients with AT, CXCL10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern and hypothyroidism. In a multiple linear regression model including age, thyroid volume, hypoechogenicity, hypervascularity, TSH, free T(4), and antithyroid peroxidase, only age (standardized coefficient = 0.39; P = 0.0001) and TSH (standardized coefficient = 0.41; P < 0.0002) were significantly related to serum CXCL10 levels. We conclude that circulating CXCL10 is increased in patients with AT and is associated with hypothyroidism. CXCL10 may be regarded as a marker of a more aggressive thyroiditis leading to thyroid destruction.     

Perioperative venous thromboembolic disease and the emerging role of the novel oral anticoagulants: An analysis of the implications for perioperative management

Venous thromboembolism includes 2 inter-related conditions: Deep venous thrombosis and pulmonary embolism. Heparin and low-molecular-weight heparin followed by oral anticoagulation with vitamin K agonists is the first line and current accepted standard therapy with good efficacy. However, this therapeutic strategy has many limitations including the significant risk of bleeding and drug, food and disease interactions that require frequent monitoring. Dabigatran, rivaroxaban, apixaban, and edoxaban are the novel oral anticoagulants that are available for use in stroke prevention in atrial fibrillation and for the treatment and prevention of venous thromboembolism (HYPERLINK\l ”1). Recent prospective randomized trials comparing the NOACs with warfarin have shown similar efficacy between the treatment strategies but fewer bleeding episodes with the NOACs. This paper presents an evidence-based review describing the efficacy and safety of the new anticoagulants compared to warfarin.     

Polysialic acid on SynCAM 1 in NG2 cells and on neuropilin‐2 in microglia is confined to intracellular pools that are rapidly depleted upon stimulation

NG2 cells comprise a heterogeneous precursor population but molecular markers distinguishing between the assumed NG2 cell subpopulations are lacking. Previously, we described that a subfraction of the synaptic cell adhesion molecule SynCAM 1 is modified with the glycan polysialic acid (polySia) in NG2 cells. As for its major carrier, the neural cell adhesion molecule NCAM, polySia attenuates SynCAM 1 adhesion. Functions, as well as cellular and subcellular distribution of polySia‐SynCAM 1 are elusive. Using murine glial cultures we now demonstrate that polySia‐SynCAM 1 is confined to the Golgi compartment of a subset of NG2 cells and transiently recruited to the cell surface in response to depolarization. NG2 cells with Golgi‐confined polySia were NCAM‐negative, but positive for markers of oligodendrocyte precursor cells (OPCs). Consistent with previous data on polySia‐SynCAM 1, polySia in Ncam^?/? NG2 cells was exclusively attached to N‐glycans and synthesized by ST8SIA2, one out of two mammalian polysialyltransferases. Unexpectedly, Golgi‐confined polySia was also detected in Ncam^?/? microglia, but this fraction resided on O‐glycans and was produced by the second polysialyltransferase, ST8SIA4, indicating the presence of yet another polySia carrier in microglia. Searching for this carrier, we identified polysialylated neuropilin‐2, so far only known from dendritic cells and exudate macrophages. Microglia activation by LPS, but not interleukin‐4, caused a transient translocation of Golgi‐localized polySia to the cell surface, resulting in complete depletion. Finally, NO‐production of LPS‐stimulated microglia was attenuated by addition of polySia suggesting that the observed loss of polySia‐neuropilin‐2 is involved in negative feedback regulation of pro‐inflammatory microglia polarization. GLIA 2015;63:1240–1255     

Long‐Term Stability of Root Coverage by Coronally Advanced Flap Procedures

Background: This study compared 6‐month and 3‐year outcomes for root coverage (RC) by coronally advanced flap (CAF) procedures in localized gingival recessions. Methods: Two centers, that had participated in a 6‐month multinational multicenter randomized clinical trial (RCT), followed up 18 patients with 36 Miller Class I and II defects that had been treated in a split‐mouth design with CAF procedures or CAF + xenogeneic collagen matrix (CMX). Percentage of RC, complete root coverage (CRC), width, and thickness of keratinized tissue were assessed by the same masked examiners as after the 6‐month RCT. Results: There was a high correlation between 6‐month and 3‐year RC outcomes for both CAF procedures. Mean RC after CAF + CMX amounted to 89.9% after 6 months and 91.7% after 3 years (Pearson’s correlation: 0.91). Corresponding values for CAF were 83.7% versus 82.8% (Pearson’s correlation: 0.94). Likewise, CRC was stable with 61%/61% for CAF + CMX and 39%/39% for CAF after 6 months/3 years, respectively. Conclusions: In this 3‐year follow‐up of a subgroup of patients from a previous 6‐month RCT, there was a high correlation between the results for RC after 6 months and 3 years, indicating their stability. These data suggest that 6‐month outcomes may be useful to predict long‐term outcomes in CAF procedures with or without additional use of CMX.