Nanosilver-loaded PMMA bone cement doped with different bioactive glasses - evaluation of cytocompatibility, antibacterial activity, and mechanical properties.

Nanosilver-loaded PMMA bone cement (BC-AgNp) is a novel cement developed as a replacement for conventional cements. Despite its favorable properties and antibacterial activity, BC-AgNp still lacks biodegradability and bioactivity. Hence, we investigated doping with bioactive glasses (BGs) to create a new bioactive BC characterized by time-varying porosity and gradual release of AgNp. The BC Cemex was used as the base material and modified simultaneously with the AgNp and BGs: melted 45S5 and 13-93B3 glasses with various particle sizes and sol-gel derived SiO2/CaO microparticles. The effect of BG addition was examined by microscopic analysis, an assessment of setting parameters, wettability, FTIR and UV-VIS spectroscopy, mechanical testing, and hemo- and cytocompatibility and antibacterial efficiency studies. The results show that it is possible to incorporate various BGs into BC-AgNp, which leads to different properties depending on the type and size of BGs. The smaller particles of melted BGs showed higher porosity and better antibacterial properties with the moderate deterioration of mechanical properties. The sol-gel derived BGs, however, displayed a tendency for agglomeration and random distribution in BC-AgNp. The BGs with greater solubility more efficiently improve the antibacterial properties of BC-AgNp. Besides, the unreacted MMA monomer release could negatively influence the cellular response. Despite that, cements doped with different BGs are suitable for medical applications.

How to diagnose splenic abscesses?

Splenic abscess is a rare but potentially fatal entity, occurring mainly in patients with underlying risk factors. Mortality of the disease depends on the time of diagnosis and treatment. Due to low sensitivity and specificity of clinical symptoms and laboratory markers, imaging plays the vital role in the diagnostic work-up. The aim of this article is to give a concise overview of the methods of splenic abscess diagnosis.

Essentiality and toxicity of vanadium supplements in health and pathology.

The biological properties of vanadium complexes have become an object of interest due to their therapeutic potential in several diseases. However, the mechanisms of action of vanadium salts are still poorly understood. Vanadium complexes are cofactors for several enzymes and also exhibit insulin-mimetic properties. Thus, they are involved in the regulation of glucose metabolism, including in patients with diabetes. In addition, vanadium salts may also normalize blood pressure and play a key role in the metabolism of the thyroid and of iron as well as in the regulation of total cholesterol, cholesterol HDL and triglyceride (TG) levels in blood. Moreover, in cases of hypoxia, vanadium compounds may improve cardiomyocytes function. They may also exhibit both carcinogenic and anti-cancer properties. These include dose- and exposure-time-dependent induction and inhibition of the proliferation and survival of cancer cells. On the other hand, the balance between vanadium's therapeutic properties and its side effects has not yet been determined. Therefore, any studies on the potential use of vanadium compounds as supplements to support the treatment of a number of diseases must be strictly monitored for adverse effects.

Nitric oxide inhibits von Willebrand factor-mediated platelet adhesion and spreading through regulation of integrin alpha(IIb)beta(3) and myosin light chain.

BACKGROUND: von Willebrand factor (VWF)-mediated platelet adhesion and spreading at sites of vascular injury is a critical step in hemostasis. This process requires two individual receptors: glycoprotein Ib (GPIb)-V-IX and integrin alpha(IIb)beta(3). However, little is known about the negative regulation of these events. OBJECTIVES: To examine if the endogenous platelet inhibitor nitric oxide (NO) has differential effects on adhesion, spreading and aggregation induced by immobilized VWF. RESULTS: S-nitrosoglutathione (GSNO) inhibited platelet aggregation on immobilized VWF under static and flow conditions, but had no effect on platelet adhesion. Primary signaling events underpinning the actions of NO required cyclic GMP but not protein kinase A. Dissecting the roles of GPIb and integrin alpha(IIb)beta(3) demonstrated that NO targeted alpha(IIb)beta(3)-mediated aggregation and spreading, but did not significantly influence GPIb-mediated adhesion. To understand the relationship between the effects of NO on adhesion and subsequent aggregation, we evaluated the activation of alpha(IIb)beta(3) on adherent platelets. NO reduced the phosphorylation of extracellular stimuli-responsive kinase (ERK) and p38, required for integrin activation resulting in reduced binding of the activated alpha(IIb)beta(3)-specific antibody PAC-1 on adherent platelets. Detailed analysis of platelet spreading initiated by VWF demonstrated key roles for integrin alpha(IIb)beta(3) and myosin light chain (MLC) phosphorylation. NO targeted both of these pathways by directly modulating integrin affinity and activating MLC phosphatase. CONCLUSION: These data demonstrate that initial activation-independent platelet adhesion to VWF via GPIb is resistant to NO, however, NO inhibits GPIb-mediated activation of alpha(IIb)beta(3) and MLC leading to reduced platelet spreading and aggregation.