Percutaneous & Mini Invasive Achilles tendon repair

Rupture of the Achilles tendon is a considerable cause of morbidity with reduced function following injury. Recent studies have shown little difference in outcome between the techniques of open and non-operative treatment using an early active rehabilitation programme. Meta-analyses have shown that non-operative management has increased risk of re-rupture whereas surgical intervention has risks of complications related to the wound and iatrogenic nerve injury. Minimally invasive surgery has been adopted as a way of reducing infections rates and wound breakdown however avoiding iatrogenic nerve injury must be considered. We discuss the techniques and outcomes of percutaneous and minimally invasive repairs of the Achilles tendon

Cytotoxicity of CD56bright NK Cells towards Autologous Activated CD4+ T Cells Is Mediated through NKG2D, LFA-1 and TRAIL and Dampened via CD94/NKG2A

In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation

Main results of the first experimental campaign in the stellarator W7-X

A summary of the first operational phase (OP1.1) at the stellarator W7-X is given. The operational setup of heating and diagnostics as well the results of experiments are briefly described. Plasma parameters and confinement are better than expected: Te > 8 keV and Ti > 2 keV at ne ≈ 3×1019 m-3 yielding β0 ≈ 2.5 %. The results for ECR heating with X2-mode as well the ECCD are in good agreement with the theory predictions. The heating scenario with the O2-mode alone was successfully first time performed. Stellarator specific regime of core “electron root” confinement was obtained

NK cell activity in tuberculosis is associated with impaired CD11a and ICAM-1 expression: a regulatory role of monocytes in NK activation

Although the role of natural killer (NK) cells in mycobacterial infections is unclear, it has been postulated that they contribute to protective immunity through the production of interferon (IFN)-γ. In this study, we evaluate the effect of interleukin (IL)-10, IL-15 and IL-18 on NK lytic activity through the expression of CD16, CD11a and CD69 molecules and the induction of IFN-γ production in patients with tuberculosis (TB) and healthy individuals (N). Our results showed an impairment of NK lytic activity and a gradual down-regulation of costimulatory and adhesion molecules on NK cells which were dependent on the severity of the disease. NK lytic activity was increased by exogenous IL-15 and IL-18 in both TB and N, and by neutralization of endogenous IL-10 only in TB; IL-15 and IL-18 increased CD69 receptor expression, while anti-IL-10 up-regulated CD16 and CD11a expression in TB. Mycobacterium tuberculosis reduced the number of intracellular adhesion molecule (ICAM)-1(+) CD14(+) cells, but in the presence of IL-15, IL-18 and anti-IL-10 its expression was up-regulated. In cells from TB patients, the observed effects of IL-15 and IL-18 on NK function were not dependent on IL-10 modulation of the surface expression of activator/adhesion molecules. In the absence of monocytes, IL-10 activated NK cells, suggesting an indirect effect on their function. Furthermore, in TB patients the depletion of monocytes increased the production of IFN-γ by NK cells. Therefore, monocytes from TB patients regulated the NK function involving IL-10 which, through an indirect mechanism, led to the down-regulation of costimulatory/adhesion molecules and/or IFN-γ production

Author Correction: Magnetic configuration effects on the Wendelstein 7-X stellarator

\u3cp\u3eIn the version of this Article originally published, and in the associated Publisher Correction, the members of the W7-X Team were not included. All versions of the Article, and the Publisher Correction, have now been amended to include these team members.\u3c/p\u3