Development of Scheelite Tailings-Based Ceramic Formulations with the Potential to Manufacture Porcelain Tiles,Semi-Stoneware and Stoneware

New ceramic formulations based on scheelite tailing were developed, and their potential in the ceramic industry was evaluated. Green bodies with different contents of scheelite tailing (0–8 wt%) were sintered (1150 °C, 1200 °C, and 1250 °C) and characterized in terms of the main mineralogical phases, microstructure, and physico-mechanical properties. The mullite was the main phase identified in all sintered temperatures. This result was also ratified with the aid of scanning electron microscope (SEM) images, in which small needles of the mullite were detected. The presence of mullite is required because it contributes to increasing the mechanical resistance of the material. The physico-mechanical properties measured (water absorption, linear shrinkage, apparent porosity, and flexural strength) were compared to the ISO 13006, and the samples sintered at 1150 °C presented potential to be used as semi-stoneware, while those sintered at 1200 °C and 1250 °C can be employed stoneware and porcelain tiles, respectively.     

Markers of oxidative stress in adipose tissue during Trypanosoma cruzi infection

The protozoan parasite Trypanosoma cruzi causes Chagas disease. Cardiac and adipose tissues are among the early targets of infection and are sites of persistent infection. In the heart and adipose tissue, T. cruzi infection results in an upregulation of pro-inflammatory mediators. In the heart, infection is associated with an increase in the markers of oxidative stress. To date, markers of oxidative stress have not been evaluated in adipose tissue in this infection. Brown and white adipose tissues were obtained from CD-1 mice infected with the Brazil strain of T. cruzi for 15, 30, and 130 days post infection. Protein carbonylation and lipid peroxidation assays were performed on these samples. There was an upregulation of these markers of oxidative stress at all time-points in both white and brown adipose tissue. Determinants of anti-oxidative stress were downregulated at similar time-points. This increase in oxidative stress during T. cruzi infection most likely has a deleterious effect on host metabolism and on the heart.     

Anandamide produced by Ca2+-insensitive enzymes induces excitation in primary sensory neurons

The endogenous lipid agent N-arachidonoylethanolamine (anandamide), among other effects, has been shown to be involved in nociceptive processing both in the central and peripheral nervous systems. Anandamide is thought to be synthesised by several enzymatic pathways both in a Ca²⁺-sensitive and Ca²⁺-insensitive manner, and rat primary sensory neurons produce anandamide. Here, we show for the first time, that cultured rat primary sensory neurons express at least four of the five known Ca²⁺-insensitive enzymes implicated in the synthesis of anandamide, and that application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl, the common substrate of the anandamide-synthesising pathways, results in anandamide production which is not changed by the removal of extracellular Ca²⁺. We also show that anandamide, which has been synthesised in primary sensory neurons following the application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl induces a transient receptor potential vanilloid type 1 ion channel-mediated excitatory effect that is not inhibited by concomitant activation of the cannabinoid type 1 receptor. Finally, we show that sub-populations of transient receptor potential vanilloid type 1 ion channel-expressing primary sensory neurons also express some of the putative Ca²⁺-insensitive anandamide-synthesising enzymes. Together, these findings indicate that anandamide synthesised by primary sensory neuron via a Ca²⁺-insensitive manner has an excitatory rather than an inhibitory role in primary sensory neurons and that excitation is mediated predominantly through autocrine signalling. Regulation of the activity of the Ca²⁺-insensitive anandamide-synthesising enzymes in these neurons may be capable of regulating the activity of these cells, with potential relevance to controlling nociceptive processing.     

Impaired participation of potassium channels and Na+/K+‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury

Mercury intoxication is a public health risk factor due to its hazardous effect to several organs, including the cardiovascular system. There is evidence of endothelial dysfunction after exposure to mercury, but the effects on endothelium‐dependent vasodilatation are still unknown. In the present study, we aimed to evaluate the chronic effects of high HgCl₂ doses on the mechanisms of vasodilatation. Wistar rats were injected with HgCl₂ (1st dose 10.86 μg/kg, and daily doses 0.014 μg/kg for 30 days i.m.), and saline was used as control. Mercury exposure reduced the acetylcholine‐induced vasodilatation in aortic rings, which was restored by incubation with antioxidant tiron. Inhibition of the NO synthase, Na⁺/K⁺‐ATPase and K⁺ channels indicates reduced participation of these factors. In the mercury group, there were an increased local anion superoxide and a reduced NO. The vasodilatation to exogenous NO was partially inhibited by co‐incubation with TEA plus tiron, suggesting that reduced NO bioavailability is the responsible to that decreased the participation of K⁺ channels. Moreover, there was an increased participation of the Na⁺/K⁺‐ATPase associated with an up‐regulation of its alpha‐1 subunit. In conclusion, reduced NO bioavailability plays a major role in the impaired participation of K⁺ channels and Na⁺/K⁺‐ATPase in the acetylcholine‐mediated relaxation, although sodium pump is up‐regulated probably as a compensatory mechanism.     

Hepatitis B and C virus reactivation in immunosuppressed patients with inflammatory bowel disease

In recent years,a number of case reports and clinical studies have highlighted the risk of hepatitis B and C virus reactivation in patients with inflammatory bowel disease who are treated with immunosuppressive drugs.The cases of viral hepatitis reactivation that have been reported are characterized by a wide range of clinical manifestations,from viremia without clinically relevant manifestations to fulminant life-threatening hepatitis.The development and dissemination of biological immunosuppressive drugs have led to a significant increase in the number of reports of interest to physicians in a variety of clinical settings.On this topic,there have been a number of published guidelines and reviews that have collected the available evidence,providing recommendations on prophylactic and therapeutic strategies and methods for monitoring patients at risk.However,it should be noted that,to date,very few clinical studies have been published,and most of the recommendations have been borrowed from otherclinical settings.The published studies are mostly retrospective and are based on very heterogeneous populations,using different therapeutic and prophylactic regimens and obtaining conflicting results.Thus,it seems clear that it is desirable to concentrate our efforts on prospective studies,not conducting further reviews of the literature in the continued absence of new evidence.     

Systemic venous atrium stimulation in transvenous pacing after mustard procedure

We present the case of a young woman corrected with a Mustard procedure undergoing successful transvenous double chamber pacemaker implantation with the atrial lead placed in the systemic venous channel. The case presented demonstrates that, when the systemic venous atrium is separate from the left atrial appendage, the lead can be easily and safely placed in the systemic venous left atrium gaining satisfactory sensing and pacing thresholds despite consisting partially of pericardial tissue.     

The endocannabinoid 2-AG controls skeletal muscle cell differentiation via CB1 receptor-dependent inhibition of Kv7 channels

Little is known of the involvement of endocannabinoids and cannabinoid receptors in skeletal muscle cell differentiation. We report that, due to changes in the expression of genes involved in its metabolism, the levels of the endocannabinoid 2-arachidonoylglycerol (2-AG) are decreased both during myotube formation in vitro from murine C₂C₁₂ myoblasts and during mouse muscle growth in vivo. The endocannabinoid, as well as the CB1 agonist arachidonoyl-2-chloroethylamide, prevent myotube formation in a manner antagonized by CB1 knockdown and by CB1 antagonists, which, per se, instead stimulate differentiation. Importantly, 2-AG also inhibits differentiation of primary human satellite cells. Muscle fascicles from CB1 knockout embryos contain more muscle fibers, and postnatal mice show muscle fibers of an increased diameter relative to wild-type littermates. Inhibition of K_v7.4 channel activity, which plays a permissive role in myogenesis and depends on phosphatidylinositol 4,5-bisphosphate (PIP2), underlies the effects of 2-AG. We find that CB1 stimulation reduces both total and K_v7.4-bound PIP2 levels in C₂C₁₂ cells and inhibits K_v7.4 currents in transfected CHO cells. We suggest that 2-AG is an endogenous repressor of myoblast differentiation via CB1-mediated inhibition of K_v7.4 channels.The endocannabinoid system (ECS) refers to a large group of endogenous molecules including the two major arachidonate-derived neuromodulatory mediators, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), known as endocannabinoids (EC); several enzymes involved in the metabolism of AEA (NAPE-PLD, ABDH4, GDE1, PTPN22 for biosynthesis and FAAH for degradation) and 2-AG (DAGLα and DAGLβ for biosynthesis and MAGL, ABDH6, ABDH12, and FAAH for degradation); and two G protein-coupled receptors known as cannabinoid receptor of type-1 (CB1) and type-2 (CB2). AEA also activates the cation permeant transient receptor potential vanilloid type-1 (TRPV1) channels (1). In mammals, the ECS regulates a large number of physiological processes; alterations in its activity are in fact responsible for the onset or progression of many types of disorders affecting both the central and the peripheral nervous system as well as other organs (2–5). So far, a few studies have reported that CB1 receptor activity controls key skeletal muscle metabolic processes such as insulin signaling, glucose uptake, and fatty acid oxidation (6, 7). However, little, if anything at all, is known about the expression profile and the functional role played by the ECS during skeletal muscle development.Skeletal myogenesis is a tightly regulated process that requires coordinated changes in a large number of genes allowing proliferating myoblasts to withdraw from the cell cycle and fuse to form large multinucleated myotubes (8). Several classes of ion channels play a pivotal role in the initiation of the differentiation process. For example, the sequential activation of two distinct classes of K⁺ channels, the ether-a-go-go K_v10.1 and the inward-rectifier KIR2.1 (9, 10), is known to be one of the first molecular events that causes myoblast hyperpolarization. This event, in turn, leads to the activation of voltage-dependent T-type Ca²⁺ channels, which increase the [Ca²⁺]_i necessary to initiate myoblast commitment to differentiation into myotubes (11). More recently, members of the K_v7 (KCNQ) subfamily of voltage-activated K⁺ channels have been found to be expressed in both myoblasts and myotubes (12, 13), and, in particular, it has been shown that K_v7.4 channel expression plays a permissive role in skeletal myogenesis (14).The K_v7 subfamily comprises five subunits (K_v7.1–K_v7.5), each showing distinct tissue distribution and physiological properties. K_v7 channel function is regulated by several classes of G_q/11-coupled receptors including muscarinic (15), bradikynin (16), serotonin (17), and somatostatin receptors (18). Stimulation of these receptors leads to phospholipase C (PLC) activation and subsequent hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Thus, considering that PIP2 is strictly required for K_v7 channels activity, G_q/11-coupled receptor stimulation represents one of the most important cellular mechanisms through which this subclass of K⁺ channels is kept under negative control (19). Interestingly, the M current, which is underlied by K_v7 channels, can be also inhibited following CB1 receptor stimulation by AEA at the postsynaptic level in hippocampal neurons (20) or by stimulation of the G_q/11-coupled orphan receptor GPR55 (21).In this study, we have endeavored to understand the role played by the ECS in muscle development and its impact on K_v7 activity during myogenesis by using molecular biology, biochemical, pharmacological, morphological, and electrophysiological techniques. Our results indicate that the endocannabinoid 2-AG tonically inhibits differentiation of mouse and human myoblasts via sequential activation of CB1 receptors, reduction of PIP2 levels, and inhibition of K_v7 channel activity.     

MOLECULAR IDENTIFICATION OF Bartonella henselae IN A SERONEGATIVE CAT SCRATCH DISEASE PATIENT WITH AIDS IN RIO DE JANEIRO, BRAZIL

Bartonella henselae is associated with a wide spectrum of clinical manifestations, including cat scratch disease, endocarditis and meningoencephalitis, in immunocompetent and immunocompromised patients. We report the first molecularly confirmed case of B. henselae infection in an AIDS patient in state of Rio de Janeiro, Brazil. Although DNA sequence of B. henselae has been detected by polymerase chain reaction in a lymph node biopsy, acute and convalescent sera were nonreactive.