Miracle-dz/UniFAR-FTUs huggingface dataset:
Cirugía de los trastornos del comportamiento: el estado del arte

Introducción: La cirugía de los trastornos del comportamiento (CTC) se está convirtiendo en un tratamiento más común desde el desarrollo de la neuromodulación. Métodos: Este artículo es una revisión no sistemática de la historia, indicaciones actuales, técnicas y blancos quirúrgicos de la CTC. Dividimos su historia en 3 eras: la primera comienza en los inicios de la psicocirugía y termina con el desarrollo de las tícnicas estereotácticas, cuando comienza la segunda era. Ésta se caracteriza por la realización de lesiones estereotácticas. Nos encontramos transitando la tercera era, que comienza cuando la estimulación cerebral profunda (ECP) comienza a ser usada en CTC. Resultados: A pesar de los errores graves cometidos en el pasado, hoy en día, la CTC está renaciendo. Los trastornos psiquiátricos que se más frecuentemente se tratan con cirugía son: depresión refractaria, trastorno obsesivo-compulsivo y síndrome de Tourette. Además, algunos pacientes con agresividad fueron tratados quirúrgicamente. Hay varios blancos estereotácticos descriptos para estos trastornos. La estimulación vagal puede ser usada también para depresión. Conclusión: Los resultados de la ECP en estos trastornos parecen alentadores. Sin embargo, se necesitan más estudios randomizados para establecer la efectividad de la CTC. Debe tenerse en cuenta que una apropiada selección de pacientes nos ayudará a realizar un procedimiento más seguro así como también a lograr mejores resultados quirúrgicos, conduciendo a la CTC a ser más aceptada por psiquiatras, pacientes y sus familias. Se necesita mayor investigación en varios temas como: fisiopatología de los trastornos del comportamiento, indicaciones de CTC y nuevos blancos quirúrgicos.
HsAtg4B/HsApg4B/Autophagin-1 Cleaves the Carboxyl Termini of Three Human Atg8 Homologues and Delipidates Microtubule-associated Protein Light Chain 3- and GABAA Receptor-associated Protein-Phospholipid Conjugates*

In yeast, Atg4/Apg4 is a unique cysteine protease responsible for the cleavage of the carboxyl terminus of Atg8/Apg8/Aut7, a reaction essential for its lipidation during the formation of autophagosomes. However, it is still unclear whether four human Atg4 homologues cleave the carboxyl termini of the three human Atg8 homologues, microtubule-associated protein light chain 3 (LC3), GABARAP, and GATE-16. Using a cell-free system, we found that HsAtg4B, one of the human Atg4 homologues, cleaves the carboxyl termini of these three Atg8 homologues. In contrast, the mutant HsAtg4BC74A, in which a predicted active site Cys74 was changed to Ala, lacked proteolytic activity, indicating that Cys74 is essential for the cleavage activity of cysteine protease. Using phospholipase D, we showed that the modified forms of endogenous LC3 and GABARAP are lipidated and therefore were designated LC3-PL and GABARAP-PL. When purified glutathione S-transferase-tagged HsAtg4B was incubated in vitro with a membrane fraction enriched with endogenous LC3-PL and GABARAP-PL, the mobility of LC3-PL and GABARAP-PL was changed to those of the unmodified proteins. These mobility shifts were not seen when Cys74 of HsAtg4B was changed to Ala. Overexpression of wild-type HsAtg4B decreased the amount of LC3-PL and GABARAP-PL and increased the amount of unmodified endogenous LC3 and GABARAP in HeLa cells. Expression of CFP-tagged HsAtg4B (CFP-HsAtg4B) and YFP-tagged LC3 in HeLa cells under starvation conditions resulted in a significant decrease in the punctate pattern of distribution of YFP-tagged LC3 and an increase in its cytoplasmic distribution. RNA interference of HsAtg4B increased the amount of LC3-PL in HEK293 cells. Taken together, these results suggest that HsAtg4B negatively regulates the localization of LC3 to a membrane compartment by delipidation.
Intrinsic disorder as a mechanism to optimize allosteric coupling in proteins

Transcription factors and other allosteric cell signaling proteins contain a disproportionate number of domains or segments that are intrinsically disordered (ID) under native conditions. In many cases folding of these segments is coupled to binding with one or more of their interaction partners, suggesting that intrinsic disorder plays an important functional role. Despite numerous hypotheses for the role of ID domains in regulation, a mechanistic model has yet to be established that can quantitatively assess the importance of intrinsic disorder for intramolecular site-to-site communication, the hallmark property of allosteric proteins. Here, we present such a model and show that site-to-site allosteric coupling is maximized when intrinsic disorder is present in the domains or segments containing one or both of the coupled binding sites. This result not only explains the prevalence of ID domains in regulatory proteins, it also calls into question the classical mechanical view of energy propagation in proteins, which predicts that site-to-site coupling would be maximized when a well defined pathway of folded structure connects the two sites. Furthermore, in showing that the coupling mechanism conferred by intrinsic disorder is robust and independent of the network of interactions that physically link the coupled sites, unique insights are gained into the energetic ground rules that govern site-to-site communication in all proteins.
Finding Fusin/CXCR4, the First “2nd Receptor” for HIV Entry

Shortly after the pioneering Montagnier/Gallo discoveries of HIV as the etiologic agent of AIDS, the CD4 antigen was identified as the primary receptor for HIV entry. The focus of the present story begins with 1986 report from Richard Axel’s group that recombinant human CD4 conferred permissiveness to HIV-1 infection when expressed on diverse human cell types, but not on mouse cells. The block was at an early replication step after virion binding, perhaps virus internalization (1).
Acyl carrier protein/SpoT interaction, the switch linking SpoT‐dependent stress response to fatty acid metabolism

Bacteria respond to nutritional stresses by producing an intracellular alarmone, guanosine 5′‐(tri)diphosphate, 3′‐diphosphate [(p)ppGpp], which triggers the stringent response resulting in growth arrest and expression of resistance genes. In Escherichia coli, upon fatty acid or carbon starvation, SpoT enzyme activity switches from (p)ppGpp degradation to (p)ppGpp synthesis, but the signal and mechanism for this response remain totally unknown. Here, we characterize for the first time a physical interaction between SpoT and acyl carrier protein (ACP) using affinity co‐purifications and two‐hybrid in E. coli. ACP, as a central cofactor in fatty acid synthesis, may be an ideal candidate as a mediator signalling starvation to SpoT. Accordingly, we show that the ACP/SpoT interaction is specific of SpoT and ACP functions because ACP does not interact with the homologous RelA protein and because SpoT does not interact with a non‐functional ACP. Using truncated SpoT fusion proteins, we demonstrate further that ACP binds the central TGS domain of SpoT, consistent with a role in regulation. The behaviours of SpoT point mutants that do not interact with ACP reveal modifications of the balance between the two opposite SpoT catalytic activities thereby changing (p)ppGpp levels. More importantly, these mutants fail to trigger (p)ppGpp accumulation in response to fatty acid synthesis inhibition, supporting the hypothesis that the ACP/SpoT interaction may be involved in SpoT‐dependent stress response. This leads us to propose a model in which ACP carries information describing the status of cellular fatty acid metabolism, which in turn can trigger the conformational switch in SpoT leading to (p)ppGpp accumulation.
Donald Davidson on Truth, Meaning, and the Mental

Introduction: Davidson's Philosophical Project PART I: TRUTH-THEORY, MEANING, AND LOGICAL FORM 1. Davidson's Contribution to the Philosophy of Language 2. Truth Theories, Competence, and Semantic Computation 3. Davidson's Explication of Meaning 4. Against Logical Form 5. A Truth Predicate in the Object Language 6. Swampman, Response-Dependence, and Meaning PART II: RADICAL INTERPRETATION, PERCEPTION, AND THE MENTAL 7. Knowledge and Error: A New Approach to Radical Interpretation 8. Perception and Intermediaries 9. On Davidson's View of First Person Authority 10. Davidson, First Person Authority, and the Evidence for Semantics 11. Davidsonian Holism in Recent Philosophy of Psychiatry 12. Taking Back the Excitement: Construing 'Theoretical Concepts' so as to Avoid the Threat of Underdetermination Index
Literature and bibliography of the social sciences

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Immunopathological Basis of Virus-induced Myocarditis

Heart diseases are an important cause of morbidity and mortality in industrialized countries. Dilated cardiomyopathy (DCM), one of the most common heart diseases, may be the consequence of infectionassociated myocardits. Coxsackievirus B3 (CVB3) can be frequently detected in the inflamed heart muscle. CVB3-induced acute myocarditis is most likely the consequence of direct virus-induced myocyte damage, whereas chronic CVB3 infection-associated heart disease is dominated by its immunopathological sequelae. Bona fide autoimmunity, for example, directed against cardiac myosin, may favor chronic destructive immune damage in the heart muscle and thereby promote the development of DCM. The immunopathogenesis of myocarditis and subsequent DCM induced either by pathogens or autoantigens can be investigated in well-established animal models. In this article, we review recent studies on the role of viruses, with particular emphasis on CVB3, and different immunological effector mechanisms in initiation and progression of myocarditis.
Acid Precipitation: Natural Versus Anthropogenic Components

The concentrations of H+, SO42-, and NO3- in the precipitation of eastern North America are greater now than they were historically as a result of fossil-fuel combustion. Because of a lack of data prior to 1950, the absolute increases in the concentrations of these three ions are unknown. This problem can be addressed by comparing the composition of precipitation from areas sensitive to acidic deposition with that of precipitation from remote areas. An analysis of precipitation data indicates that many areas of eastern North America receive precipitation with substantially greater H+, SO42-, and NO3- concentrations than remote areas. For example, SO42-, the most ecologically significant indicator of change, is enriched 2 to 16 times in eastern North American precipitation relative to its concentration in remote areas.
Analysis on Effect of SFCL Applied to an Isolated Microgrid With a Dynamic Load Model

This paper analyzes the effect of a resistive superconducting fault current limiter (R-SFCL) applied to an isolated microgrid with a dynamic load model. The isolated microgrid with high penetration of distributed generators (DGs) is vulnerable to faults in aspect of frequency stability. For the more accurate analysis of the isolated microgrid, the dynamic composite load model, which consists of a static part with the constant impedance—current–power model and a dynamic part with the high-order induction motor model, is applied in this study. The R-SFCL in isolated microgrid can effectively mitigate the fault current by rapidly providing protection during the fault as well as improve the transient stability by using the fast response characteristics of the R-SFCL as a transition signal for the DG. To evaluate the performance of the proposed model, a case study is carried out by a time-domain simulation based on the DIgSILENT PowerFactory software
War at the Wall Street Journal: Inside the Struggle to Control an American Business Empire

* War at the Wall Street Journal: Inside the Struggle to Control an American Business Empire. Sarah Ellison. New York, NY: Houghton Mifflin Harcourt, Inc., 2010. 274 pp. $27 hbk. $14.95 pbk. The sale of the Wall Street Journal in 2007 was a major news event, and rightly so. After all, the newspaper had (and still has) the largest circulation of any daily newspaper in the United States. Founded in 1889, it soon came to be recognized as the nation's preeminent business publication. When it was sold by the Bancroft family, which held a controlling interest, the buyer was perhaps the best-known and most controversial figure in modern journalism: Rupert Murdoch, the owner of global media giant News Corporation. Many of the circumstances surrounding the sale only added to the story's appeal. At the time, Sarah Ellison was the Journal's media reporter and assigned to cover the story. She has taken advantage of her unique knowledge and insight, along with her first-rate writing skills, to provide a detailed, balanced, and thoroughly engaging account of the sale. Beginning with Murdoch's dealings with Jimmy Lee from J. P. Morgan to put in place the funding for his offer, and continuing through the transition in the Journal's newsroom after the sale, Ellison leads the reader through the developments as they unfolded. Her account has a novel-like quality to it: The story's character development is outstanding, and she interjects enough suspense around the many conflicts that arose to make this a book that is hard to put down. Most of the news coverage of this sale portrayed Murdoch as arch-villain, who would almost certainly destroy the tremendous journalistic equity that the Bancroft family and existing management had worked so hard to develop - many envisioned the Journal becoming nothing more than a right-wing tabloid. Coverage tended to ignore how poorly the Journal was doing financially (attributing this to the downturn in the economy and /or to what the Internet was doing to all newspapers), or how little involvement (or interest in journalism) most of the Bancrofts had. There was significant discord among Bancroft family members, many of whom were interested only in their dividend checks; none actually worked for the Journal at the time of the sale. Coverage also tended to ignore Murdoch's love of and commitment to print journalism. Ellison's account provides an excellent counterbalance to the hyperbole that typically permeated most coverage of the WS/'s transition, as she painstakingly takes the reader through each important step leading to the final outcome. Along the way, she offers considerable evidence, both direct and indirect, to support her conclusions regarding the priorities, motivations, and dominant personal characteristics of all the key players. As such, this account represents a good example of what solid, in-depth journalism looks like. That said, if this is all that the book represented, it would have little to recommend itself to mass communication scholars, other than as a good read. …
Sucrose Control of Translation Mediated by an Upstream Open Reading Frame-Encoded Peptide1[W][OA]

Regulation of gene expression through translational control is common in many organisms. The Arabidopsis (Arabidopsis thaliana) transcription factor bZIP11 is translational repressed in response to sucrose (Suc), resulting in Suc-regulated changes in amino acid metabolism. The 5′ leader of the bZIP11 mRNA harbors several upstream open reading frames (uORFs), of which the second uORF is well conserved among bZIP11 homologous genes. The uORF2 element encodes a Suc control peptide (SC-peptide) of 28 residues that is sufficient for imposing Suc-induced repression of translation (SIRT) on a heterologous mRNA. Detailed analysis of the SC-peptide suggests that it functions as an attenuator peptide. Results suggest that the SC-peptide inhibits bZIP11 translation in response to high Suc levels by stalling the ribosome on the mRNA. The conserved noncanonical AUG contexts of bZIP11 uORFs allow inefficient translational initiation of the uORF, resulting in translation initiation of the scanning ribosome at the AUG codon of the bZIP11 main ORF. The results presented show that Suc-dependent signaling mediates differential translation of mRNAs containing SC-peptides encoding uORFs.
Bagging and Boosting a Treebank Parser

Bagging and boosting, two effective machine learning techniques, are applied to natural language parsing. Experiments using these techniques with a trainable statistical parser are described. The best resulting system provides roughly as large of a gain in F-measure as doubling the corpus size. Error analysis of the result of the boosting technique reveals some inconsistent annotations in the Penn Treebank, suggesting a semi-automatic method for finding inconsistent treebank annotations.
AN AGENT-BASED SYSTEM FOR PRODUCTS PENETRATION STRATEGY SELECTION

This paper describes an agent-based system implementing an original consumer-based methodology for product penetration strategy selection in real-world situations. Agents are simultaneously considered according to two different levels: a functional and a structural level. In the functional level, we have three types of agents: task agents, information agents, and interface agents assuming task fulfillment through cooperation, information gathering tasks, and mediation between users and artificial agents, respectively. In the structural level, we have elementary agents based on a generic reusable architecture and complex agents considered as an agent organization created dynamically in an hierarchical way.
Residues in the Heptad Repeat A Region of the Fusion Protein Modulate the Virulence of Sendai Virus in Mice

ABSTRACT While the molecular basis of fusion (F) protein refolding during membrane fusion has been studied extensively in vitro, little is known about the biological significance of membrane fusion activity in parainfluenza virus replication and pathogenesis in vivo. Two recombinant Sendai viruses, F-L179V and F-K180Q, were generated that contain F protein mutations in the heptad repeat A region of the ectodomain, a region of the protein known to regulate F protein activation. In vitro, the F-L179V virus caused increased syncytium formation (cell-cell membrane fusion) yet had a rate of replication and levels of F protein expression and cleavage similar to wild-type virus. The F-K180Q virus had a reduced replication rate along with reduced levels of F protein expression, cleavage, and fusogenicity. In DBA/2 mice, the hyperfusogenic F-L179V virus induced greater morbidity and mortality than wild-type virus, while the attenuated F-K180Q virus was much less pathogenic. During the first week of infection, virus replication and inflammation in the lungs were similar for wild-type and F-L179V viruses. After approximately 1 week of infection, the clearance of F-L179V virus was delayed, and more extensive interstitial inflammation and necrosis were observed in the lungs, affecting entire lobes of the lungs and having significantly greater numbers of syncytial cell masses in alveolar spaces on day 10. On the other hand, the slower-growing F-K180Q virus caused much less extensive inflammation than wild-type virus, presumably due to its reduced replication rate, and did not cause observable syncytium formation in the lungs. Overall, the results show that residues in the heptad repeat A region of the F protein modulate the virulence of Sendai virus in mice by influencing both the spread and clearance of the virus and the extent and severity of inflammation. An understanding of how the F protein contributes to infection and inflammation in vivo may assist in the development of antiviral therapies against respiratory paramyxoviruses.
The Health Care Fraud Detection Using the Pharmacopoeia Spectrum Tree and Neural Network Analytic Contribution Hierarchy Process

Recent years, data mining has used frequently for medical fraud detection and neural network has its special merit. This paper proposed an improved neural network algorithm to detect the medical insurance fraud. Our method combined MPL neural network with neural network analytic contribution hierarchy process and make corresponding improvement according to the characteristics of the medical insurance fraud: (1) build a pharmacopoeia spectrum tree, using neural network analytic contribution hierarchy process to cluster the medical items to obtain reasonable fraud detection factor, (2) for each case, use the method of hierarchy contribution rate and multidimensional space distance to calculate the contribution rate of fraud the fraud detection factor have in the medical items, so as to find out the most possible fraud medical items. Our experiment results show that the accuracy of the improved neural network in health care fraud detection reached 86%, which is better than other unsupervised data mining methods. What is more, our method can calculate each fraud detection factor's contribution rate of fraud, which is the ability that other data mining methods do not have.
Dampening DNA damage checkpoint signalling via coordinated BRCT domain interactions

In response to DNA damage, checkpoint signalling protects genome integrity at the cost of repressing cell cycle progression and DNA replication. Mechanisms for checkpoint down‐regulation are therefore necessary for proper cellular proliferation. We recently uncovered a phosphatase‐independent mechanism for dampening checkpoint signalling, where the checkpoint adaptor Rad9 is counteracted by the repair scaffolds Slx4‐Rtt107. Here, we establish the molecular requirements for this new mode of checkpoint regulation. We engineered a minimal multi‐BRCT‐domain (MBD) module that recapitulates the action of Slx4‐Rtt107 in checkpoint down‐regulation. MBD mimics the damage‐induced Dpb11‐Slx4‐Rtt107 complex by synergistically interacting with lesion‐specific phospho‐sites in Ddc1 and H2A. We propose that efficient recruitment of Dpb11‐Slx4‐Rtt107 or MBD via a cooperative ‘two‐site‐docking’ mechanism displaces Rad9. MBD also interacts with the Mus81 nuclease following checkpoint dampening, suggesting a spatio‐temporal coordination of checkpoint signalling and DNA repair via a combinatorial mode of BRCT‐domains interactions.
Functions of BCL-XL at the Interface between Cell Death and Metabolism

The BCL-2 homolog BCL-XL, one of the two protein products of BCL2L1, has originally been characterized for its prominent prosurvival functions. Similar to BCL-2, BCL-XL binds to its multidomain proapoptotic counterparts BAX and BAK, hence preventing the formation of lethal pores in the mitochondrial outer membrane, as well as to multiple BH3-only proteins, thus interrupting apical proapoptotic signals. In addition, BCL-XL has been suggested to exert cytoprotective functions by sequestering a cytosolic pool of the pro-apoptotic transcription factor p53 and by binding to the voltage-dependent anion channel 1 (VDAC1), thereby inhibiting the so-called mitochondrial permeability transition (MPT). Thus, BCL-XL appears to play a prominent role in the regulation of multiple distinct types of cell death, including apoptosis and regulated necrosis. More recently, great attention has been given to the cell death-unrelated functions of BCL-2-like proteins. In particular, BCL-XL has been shown to modulate a number of pathophysiological processes, including—but not limited to—mitochondrial ATP synthesis, protein acetylation, autophagy and mitosis. In this short review article, we will discuss the functions of BCL-XL at the interface between cell death and metabolism.