Effect of root perforation repair with mineral aggregate-based cements on the retention of customized fiberglass posts

Odontology - The purpose of this study was to investigate whether the root perforation repair with mineral aggregate-based cements affects the retention of customized fiberglass posts to bovine...     

Partial life-cycle and acute toxicity of perfluoroalkyl acids to freshwater mussels

Freshwater mussels are among the most sensitive aquatic organisms to many contaminants and have complex life-cycles that include several distinct life stages with unique contaminant exposure pathways. Standard acute (24-96 h) and chronic (28 d) toxicity tests with free larva (glochidia) and juvenile mussels are effective at generating data on contaminant effects at two discrete life stages but do not incorporate effects on brooded glochidia. We developed a novel partial life-cycle assay that incorporates exposures to brooding adult female mussels and used this method in combination with acute toxicity tests to assess adverse effects of perfluoroctanesulfonic acid (PFOS) and perfluoroctanoic acid (PFOA) on freshwater mussels. Fatmucket (Lampsilis siliquoidea) were exposed to PFOS at two life stages: brooding glochidia (in marsupia) for 36 d and free glochidia in water for 24 h. In standard acute tests with glochidia (24-48 h exposures) and juveniles (48-96 h exposures) of fatmucket and black sandshell (Ligumia recta), glochidia were 8 to 25 times more sensitive than juveniles. Perfluoroctanesulfonic acid significantly reduced the duration of glochidia viability and reduced probability of metamorphosis at concentrations 3,000 times lower than the most sensitive acute endpoint (24-h EC50). The partial life-cycle test is adaptable to a variety of endpoints and research objectives and is useful for identifying adverse effects at contaminant concentrations below those required for an acute lethal response.     

The RS685012 Polymorphism of ACCN2, the Human Ortholog of Murine Acid-Sensing Ion Channel (ASIC1) Gene,is Highly Represented in Patients with Panic Disorder

Panic disorder (PD) is a disabling anxiety disorder that is characterized by unexpected, recurrent panic attacks, associated with fear of dying and worrying about possible future attacks or other behavioral changes as a consequence of the attacks. The acid-sensing ion channels (ASICs) are a family of proton-sensing channels expressed throughout the nervous system. Their activity is linked to a variety of behaviors including fear, anxiety, pain, depression, learning, and memory. The human analog of ASIC1a is the amiloride-sensitive cation channel 2 (ACCN2). Adenosine A2A receptors are suggested to play an important role in different brain circuits and pathways involved in anxiety reactions. In this work we aimed to evaluate the distribution of ACCN2 rs685012 and ADORA2A rs2298383 polymorphisms in PD patients compared with healthy subjects. We found no association between ADORA2A polymorphism and PD. Instead, the C mutated allele for ACCN2 rs685012 polymorphism was significantly more frequent in patients than in controls. On the contrary, the TT homozygous wild-type genotype and also the ACCN2 TT/ADORA2A CT diplotype were significantly more represented in controls. These results are suggestive for a role of ACCN2 rs685012 polymorphism in PD development in Caucasian people.     

Computed tomography halo sign in pulmonary nodules: frequency and diagnostic value

On computed tomography (CT) scanning, a ground-glass opacity zone surrounding a pulmonary nodule has been named the computed tomography (CT) halo sign. To investigate the frequency and diagnostic value of the CT halo sign, the authors reviewed the CT examinations of 305 patients with proven diseases producing solitary or multiple nodules. The CT halo sign was seen in 22 patients (7%). Eleven patients had a solitary nodule; five patients had multiple nodules; and six patients had nodules associated with areas of pulmonary consolidation, or ground-glass opacity, or both. Solitary nodules were the result of bronchioloalveolar carcinoma (n = 5), tuberculoma (n = 2), squamous cell carcinoma, non-Hodgkin lymphoma, myxovirus infection, and metastasis (n = 1 each). Multiple nodules were the result of metastasis (n = 2), Kaposi sarcoma (n = 2), and Wegener granulomatosis (n = 1). Nodules associated with areas of consolidation or ground-glass opacity were the result of metastasis (n = 2), bronchioloalveolar carcinoma, bronchiolitis obliterans organizing pneumonia, eosinophilic pneumonia, and invasive pulmonary aspergillosis (n = 1 each). The data showed that the CT halo sign is a nonspecific finding. It is known that in immunocompromised patients the CT halo sign should suggest invasive pulmonary aspergillosis, Kaposi sarcoma, and lymphoproliferative pulmonary disorders. However, in immunocompetent patients, the authors found that a solitary nodule with the CT halo sign and pseudocavitations has a high likelihood of being a bronchioloalveolar carcinoma.     

Communication via gap junctions underlies early functional and beneficial interactions between grafted neural stem cells and the host

How grafted neural stem cells (NSCs) and their progeny integrate into recipient brain tissue and functionally interact with host cells is as yet unanswered. We report that, in organotypic slice cultures analyzed by ratiometric time-lapse calcium imaging, current-clamp recordings, and dye-coupling methods, an early and essential way in which grafted murine or human NSCs integrate functionally into host neural circuitry and affect host cells is via gap-junctional coupling, even before electrophysiologically mature neuronal differentiation. The gap junctions, which are established rapidly, permit exogenous NSCs to influence directly host network activity, including synchronized calcium transients with host cells in fluctuating networks. The exogenous NSCs also protect host neurons from death and reduce such signs of secondary injury as reactive astrogliosis. To determine whether gap junctions between NSCs and host cells may also mediate neuroprotection in vivo, we examined NSC transplantation in two murine models characterized by degeneration of the same cell type (Purkinje neurons) from different etiologies, namely, the nervous and SCA1 mutants. In both, gap junctions (containing connexin 43) formed between NSCs and host cells at risk, and were associated with rescue of neurons and behavior (when implantation was performed before overt neuron loss). Both in vitro and in vivo beneficial NSC effects were abrogated when gap junction formation or function was suppressed by pharmacologic and/or RNA-inhibition strategies, supporting the pivotal mediation by gap-junctional coupling of some modulatory, homeostatic, and protective actions on host systems as well as establishing a template for the subsequent development of electrochemical synaptic intercellular communication.Reestablishment of functional networks in the central nervous system (CNS) has been proffered as one of the goals of stem cell–mediated therapeutics. Although this is clearly one strategy, it may not be the easiest, or even the most likely basis for the beneficial outcomes in most reported cases of recovery to date. The number of neural stem cells (NSCs), for example, that differentiate into mature well-integrated neurons, and the lengthy time this process requires, are usually insufficient to account for the improvement. Although it is becoming recognized that grafted NSCs interact with—indeed, sustain, rescue, or protect—endogenous imperiled neurons in vivo (1–3), the underlying mechanisms are poorly characterized. Although, in some cases, we and others have attributed this action to the release of diffusible cytokines from NSCs (1, 2), this mechanism alone is inadequate for explaining all cases (3). A better understanding of the iterative developmental process by which grafted NSCs integrate into host neural tissue may provide insights into the interplay between donor and host. Here we report that an early and essential step in the functional integration of grafted murine and human NSCs into host neural circuitry, even before (and perhaps establishing a template for) mature electrochemical synaptic communication, is cell–cell coupling via gap junctions that modulate network activity. When we observed that such gap junction formation also seemed to inhibit death of host neurons and suppress such inimical processes as gliosis, we further hypothesized that this mode of direct intercellular communication between exogenous NSCs and host cells might constitute an underappreciated mechanism by which stem cells exert a homeostatic and/or protective effect on endangered host cells. Indeed, these therapeutic actions by NSCs could be abrogated by blocking gap junction formation or function. That such gap junctions may mediate translationally relevant neuroprotection was suggested by observing their role in the NSC-mediated rescue of host neurons and their projections in representative models of neurodegeneration—effects noted only when direct cell–cell contact via functional gap junctions were made.     

Rapid decline of Zika virus NS1 antigen-specific antibody responses,northeastern Brazil

Virus Genes - Zika virus (ZIKV) is a positive-stranded RNA virus within the Flaviviridae family. After decades of circulation in Asia, ZIKV was introduced to Brazil in 2014–2015, associated...