Cpp

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Approximately 4000 human beings experience a traumatic brain injury each day in the United States ranging in severity from mild to fatal. Improvements in initial management, surgical treatment, and neurointensive care have resulted in a better prognosis for traumatic brain injury patients but, to date, there is no available pharmaceutical treatment with proven efficacy, and prevention is the major protective strategy. Many patients are left with disabling changes in cognition, motor function, and personality. Over the past two decades, a number of experimental laboratories have attempted to develop novel and innovative ways to replicate, in animal models, the different aspects of this heterogenous clinical paradigm to better understand and treat patients after traumatic brain injury. Although several clinically-relevant but different experimental models have been developed to reproduce specific characteristics of human traumatic brain injury, its heterogeneity does not allow one single model to reproduce the entire spectrum of events that may occur. The use of these models has resulted in an increased understanding of the pathophysiology of traumatic brain injury, including changes in molecular and cellular pathways and neurobehavioral outcomes. This review provides an up-to-date and critical analysis of the existing models of traumatic brain injury with a view toward guiding and improving future research endeavors.

The purpose of this study is to establish normative values for the smoothed cepstral peak prominence (CPPS) and its sensitivity and specificity as a measure of dysphonia. Prospective cohort study. Voice samples of running speech were obtained from 835 patients and 50 volunteers. Eight laryngologists and four speech-language pathologists performed perceptual ratings of the voice samples on the degree of dysphonia/normality using an analog scale. The mean of their perceptual ratings was used as the gold standard for the detection of the presence or absence of dysphonia. CPPS was measured using the CPPS algorithm of Hillenbrand, and the cut-off value for positivity that has the highest sensitivity and specificity for discriminating between normal and severely dysphonia voices was determined based on ROC-curve analysis. The cut-off value for normal for CPPS was set at 4.0 or higher, which gave a sensitivity of 92.4%, a specificity of 79%, a positive predictive value of 82.5%, and a nega...

Delayed ischemic neurologic deficit (DIND) is a serious and poorly understood complication of aneurysmal subarachnoid hemorrhage. Although advances in treatment have improved prognosis for these patients, long-term clinical outcomes remain disappointing. Historically, angiographic vasospasm was thought to result in a DIND, although an increasing body of evidence suggests that this is an oversimplification, because interventions that have effectively targeted angiographic vasospasm have not improved outcome. Consequently, the relationship between angiographic vasospasm and neurologic outcome may be associative rather than causative. Although our understanding of the underlying molecular processes and pathophysiology is improving, responsible mediators or pathways have yet to be identified. The aim of this review is to summarize the key historical events that have helped shape our understanding of the pathophysiology of this phenomenon (microcirculation, autoregulation, microthrombosi...

This article aims to analyze the technical performance of football teams in the FA Premier League during the 2015/2016 season. Data of twenty clubs over 38 matches for each club are considered using 23 variables. These variables have been explored in the football literature and address different features of technical performance. The different configuration of the data for teams in detached segments motivated the multi-criteria approach, which enables identification of strong and weak sectors in each segment. The uncertainty as to the outcome of football matches and the imprecision of the measures indicated the use of Composition of Probabilistic Preferences (CPP) to model the problem. " R " software was used in the mod-eling and computation. The CPP global scores obtained were more consistent with the final classification than those of other methods. CPP scores revealed different performances of particular groups of variables indicating aspects to be improved and explored.

Sharp waves (SPWs) are endogenous hippocampal network activity that occurs during certain behaviors and it is thought to be involved in the process of memory consolidation. Frequently, SPWs are generated in bursts or clusters of several consecutive events forming discrete episodes of activity, a hitherto unexplored feature of this prominent hippocampal network activity. In the present study, using rat ventral hippocampal slices, we show that clusters of SPWs consist of two to four consecutive events occurring at a frequency of approximately 10 Hz (range, 7-14 Hz). Similarly to the first (primary) event in a cluster the following (secondary) SPWs correspond to inhibitory postsynaptic potentials in CA1 pyramidal cells. Furthermore, the initiation of secondary SPWs in the 23% of cells coincides with postinhibitory rebound excitation. Antagonists of NMDA receptors reversibly abolish secondary but not primary SPWs suggesting that their generation depend on the activation of NMDA receptor...

Peptide–membrane interactions have been gaining increased relevance, mainly in biomedical investigation, as the potential of the natural, nature-based and synthetic peptides as new drugs or drug candidates also expands. These peptides must face the cell membrane when they interfere with or participate in intracellular processes. Additionally, several peptide drugs and drug leads actions occur at the membrane level (e.g., antimicrobial peptides, cell-penetrating peptides and enveloped viruses membrane fusion inhibitors). Here we explore fluorescence spectroscopy methods that can be used to monitor such interactions. Two main approaches are considered, centered either on the peptide or on the membrane. On the first, we consider mainly the methodologies based on the intrinsic fluorescence of the aminoacid residues tryptophan and tyrosine. Regarding membrane-centric approaches, we review methods based on lipophilic probes sensitive to membrane potentials. The use of fluorescence constitutes a simple and sensitive method to measure these events. Unraveling the molecular mechanisms that govern these interactions can unlock the key to understand specific biological processes involving natural peptides or to optimize the action of a peptide drug.

It has been more than a century since the first evidence linking the process of amyloid formation to the pathogenesis of Alzheimer's disease. During the last three decades in particular, increasing evidence from various sources (pathology, genetics, cell culture studies, biochemistry, and biophysics) continues to point to a central role for the pathogenesis of several incurable neurodegenerative and systemic diseases. This is in part driven by our improved understanding of the molecular mechanisms of protein misfolding and aggregation and the structural properties of the different aggregates in the amyloid pathway and the emergence of new tools and experimental approaches that permit better characterization of amyloid formation in vivo. Despite these advances, detailed mechanistic understanding of protein aggregation and amyloid formation in vitro and in vivo presents several challenges that remain to be addressed and several fundamental questions about the molecular and structural determinants of amyloid formation and toxicity and the mechanisms of amyloid-induced toxicity remain unanswered. To address this knowledge gap and technical challenges, there is a critical need for developing novel tools and experimental approaches that will not only permit the detection and monitoring of molecular events that underlie this process but also allow for the manipulation of these events in a spatial and temporal fashion both in and out of the cell. This review is primarily dedicated in highlighting recent results that illustrate how advances in chemistry and chemical biology have been and can be used to address some of the questions and technical challenges mentioned above. We believe that combining recent advances in the development of new fluorescent probes, imaging tools that enabled the visualization and tracking of molecular events with advances in organic synthesis, and novel approaches for protein synthesis and engineering provide unique opportunities to gain a molecular-level understanding of the process of amyloid formation. We hope that this review will stimulate further research in this area and catalyze increased collaboration at the interface of chemistry and biology to decipher the mechanisms and roles of protein folding, misfolding, and aggregation in health and disease.► This review is focused on how recent developments in chemical biology can help understanding the key steps in amyloid formation and toxicity. ► Peptide backbone modifications that block β-sheet formation improve synthesis and handling of amyloid-forming peptides. ► Molecular switches coupled with secondary-structure-inducing units allow controlling the initiation of amyloid assembly in a spatiotemporal manner. ► Photoinduced cross-linking captures early events of amyloid formation. ► The role of posttranslational modifications can be site specifically addressed, either one by one or in combination, thanks to native chemical ligation and protein semisynthesis.