Miracle-dz/UniFAR-FTUs huggingface dataset:
RELACIÓN ENTRE EL METABOLISMO DE LOS TRIGLICÉRIDOS Y ATEROSCLEROSIS EN LA HIPERCOLESTEROLEMIA FAMILIAR

Familial hypercholesterolaemia (FH) is a genetic disorder, with the heterozygous form affecting one in 500 deliveries. FH is associated with atherosclerosis due to elevated LDL concentrations but also, triglyceride levels and postprandial hypertriglyceridemia have been reported as possible independent risk factors for atherosclerosis. In the present review article available literature in the data basesinformation from database PubMed as well as historical articles, texts and references cited in public published papers to date were analyzed, searching a possible relationship between triglyceride metabolism in FH and atherosclerosis. The information obtained was organizedPertinent information related with the objectives proposed in the present review was found and analyzed. It was then divided into three sections as follows: triglyceride metabolism, triglyceride metabolism in familiar hypercholesterolaemia, triglycerides in familiar hypercholesterolaemia and atherosclerosis. Among the conclusions iIt was found that can be concluded that high levels of triglycerides are associated to with high risk of early coronary heart disease in FH patients.
Ric1-Rgp1 Complex Is a Guanine Nucleotide Exchange Factor for the Late Golgi Rab6A GTPase and an Effector of the Medial Golgi Rab33B GTPase*

Background: The guanine nucleotide exchange factor that activates Rab6A GTPase is not known. Results: Ric1-Rgp1 binds Rab33B-GTP and catalyzes nucleotide exchange on Rab6A GTPase. Conclusion: Ric1 and Rgp1 are needed to generate and maintain active Rab6A on the Golgi. Significance: This evidence supports the presence of a Rab cascade on the Golgi complex of human cells. Rab GTPases are master regulators of membrane trafficking events and template the directionality of protein transport through the secretory and endocytic pathways. Certain Rabs recruit the guanine nucleotide exchange factor (GEF) that activates a subsequent acting Rab protein in a given pathway; this process has been termed a Rab cascade. We show here that the medial Golgi-localized Rab33B GTPase has the potential to link functionally to the late Golgi, Rab6 GTPase, by its capacity for association with Ric1 and Rgp1 proteins. In yeast, Ric1p and Rgp1p form a complex that catalyzes guanine nucleotide exchange by Ypt6p, the Rab6 homolog. Human Ric1 and Rgp1 both bind Rab6A with preference for the GDP-bound conformation, characteristic of a GEF. Nevertheless, both Ric1 and Rgp1 proteins are needed to catalyze nucleotide exchange on Rab6A protein. Ric1 and Rgp1 form a complex, but unlike their yeast counterparts, most of the subunits are not associated, and most of the proteins are cytosolic. Loss of Ric1 or Rgp1 leads to destabilization of Rab6, concomitant with a block in Rab6-dependent retrograde transport of mannose 6-phosphate receptors to the Golgi. The C terminus of Ric1 protein contains a distinct binding site for Rab33B-GTP, supporting the existence of a Rab cascade between the medial and trans Golgi. This study thus identifies a GEF for Rab6A in human cells.
CD3-T Cell Receptor Co-stimulation through SLAMF3 and SLAMF6 Receptors Enhances RORγt Recruitment to the IL17A Promoter in Human T Lymphocytes*

Background: CD3-T cell receptor co-stimulation through SLAMF3/SLAMF6 promotes IL-17A production. Results: SLAMF3/SLAMF6 and CD28 co-stimulation induces NFAT recruitment to IL17A. SLAMF3/SLAMF6 signaling increases nuclear RORγt abundance and recruitment to the IL17A promoter. Conclusion: SLAMF3/SLAMF6 promote Th17 subsets in a RORγt-dependent fashion. Significance: Deciphering the molecular mechanisms that control receptor-specific cytokine expression will help to understand immune regulation in health and disease. Th17 lymphocytes play a key role during immune responses against bacteria and fungi and are involved in the pathophysiology of multiple autoimmune disorders. The co-stimulatory molecules SLAMF3 and SLAMF6 have been implicated in the formation of Th17 phenotypes and IL-17A expression. Increased surface expression of SLAMF3 and SLAMF6 has been linked with disease activity in systemic lupus erythematosus. Here we demonstrate that in human total T lymphocytes the canonical CD28 and the non-canonical SLAMF3/SLAMF6 co-stimulatory pathways cooperate in the recruitment of the transcription factor NFAT1 to the IL17A promoter. Furthermore, the dominance of the SLAMF3/SLAMF6 pathway in inducing IL-17A production can be attributed to an increased nuclear abundance and recruitment of RORγt to the IL17A promoter. Thus, we have identified an additional mechanism that may be central for the specific control of IL17A gene regulation in systemic lupus erythematosus T lymphocytes.
Association of CDH11 with non‐syndromic ASD

We report a sporadic patient with Autism Spectrum Disorder (ASD), mild intellectual disability and attention deficit hyperactivity disorder (ADHD) with a de novo partial deletion of CADHERIN 11 (CDH11). The deletion is associated with one of the breakpoints of a de novo complex chromosomal rearrangement 46,XY,t(3;16;5)(q29;q22;q15)inv4(p14;q21)ins(4;5)(q21;q14.3q15). Cadherins are cell adhesion molecules involved in synaptic plasticity. Since genetic evidence points towards a role for cadherins in ASD, we studied the possible contribution of CDH11 to ASD. A case‐control association study for 14 SNP variants in 519 ASD cases and 1,192 controls showed significant overrepresentation of rs7187376C/C genotypes in the patient group [P = 0.0049 (Chi‐square = 7.90 1 df) and O.R. 3.88 C.I. = 1.403–10.733]. There was no association for C/T versus T/T [P = 0.6772 (Chi‐square = 0.17 1 df)] nor was there association at the allelic level [P = 0.4373 (Chi‐square = 0.6 1 df)]. In addition to the association of common variants in CDH11 with ASD, we studied the possible contribution of rare variants by sequencing CDH11 in 247 patients, and found three novel variants in the coding region of CDH1, of which two variants were unlikely to be causal. Targeted CNV screening in these 247 patients did not reveal copy number variation in CDH11. In conclusion, the data provide evidence for the involvement of CDH11 in ASD which is consistent with the association of other cadherins with ASD and neuropsychiatric diseases. © 2014 Wiley Periodicals, Inc.
HONEY TREATMENT IN VETERINARY MEDICINE, WHERE TO?

Investigations into the microbial flora of wounds began in the late 19th century. Since then, improvements in techniques have facilitated the recovery, identification and enumeration of a wide variety of microbial species. The increased antibiotic resistance of numerous bacterial species isolated from various wounds and inflammatory lesions constitutes an increasingly important problem. Honey and propolis are bee products that have been used for centuries in traditional medicine (Ghisalberti 1979; Zumla and Lulat 1989) and have received attention from the general population because of their health claims (Dobrowolski et al. 1991). These products could easily represent an alternative to drug therapy, with both increased bioavailability and healing effects.
Kuppfer Cells Trigger Nonalcoholic Steatohepatitis Development in Diet-induced Mouse Model through Tumor Necrosis Factor-α Production*

Background: The mechanisms triggering nonalcoholic steatohepatitis (NASH) remain poorly defined. Results: Kupffer cells are the first responding cells to hepatocyte injuries, leading to TNFα production, chemokine induction, and monocyte recruitment. The silencing of TNFα in myeloid cells reduces NASH progression. Conclusion: Increase of TNFα-producing Kupffer cells is crucial for triggering NASH via monocyte recruitment. Significance: Myeloid cells-targeted silencing of TNFα might be a tenable therapeutic approach. Nonalcoholic steatohepatitis (NASH), characterized by lipid deposits within hepatocytes (steatosis), is associated with hepatic injury and inflammation and leads to the development of fibrosis, cirrhosis, and hepatocarcinoma. However, the pathogenic mechanism of NASH is not well understood. To determine the role of distinct innate myeloid subsets in the development of NASH, we examined the contribution of liver resident macrophages (i.e. Kupffer cells) and blood-derived monocytes in triggering liver inflammation and hepatic damage. Employing a murine model of NASH, we discovered a previously unappreciated role for TNFα and Kupffer cells in the initiation and progression of NASH. Sequential depletion of Kupffer cells reduced the incidence of liver injury, steatosis, and proinflammatory monocyte infiltration. Furthermore, our data show a differential contribution of Kupffer cells and blood monocytes during the development of NASH; Kupffer cells increased their production of TNFα, followed by infiltration of CD11bintLy6Chi monocytes, 2 and 10 days, respectively, after starting the methionine/choline-deficient (MCD) diet. Importantly, targeted knockdown of TNFα expression in myeloid cells decreased the incidence of NASH development by decreasing steatosis, liver damage, monocyte infiltration, and the production of inflammatory chemokines. Our findings suggest that the increase of TNFα-producing Kupffer cells in the liver is crucial for the early phase of NASH development by promoting blood monocyte infiltration through the production of IP-10 and MCP-1.
Bayesian Phylogenetic Estimation of Clade Ages Supports Trans-Atlantic Dispersal of Cichlid Fishes.

Divergence-time estimation based on molecular phylogenies and the fossil record has provided insights into fundamental questions of evolutionary biology. In Bayesian node dating, phylogenies are commonly time calibrated through the specification of calibration densities on nodes representing clades with known fossil occurrences. Unfortunately, the optimal shape of these calibration densities is usually unknown and they are therefore often chosen arbitrarily, which directly impacts the reliability of the resulting age estimates. As possible solutions to this problem, two nonexclusive alternative approaches have recently been developed, the "fossilized birth-death" (FBD) model and "total-evidence dating. " While these approaches have been shown to perform well under certain conditions, they require including all (or a random subset) of the fossils of each clade in the analysis, rather than just relying on the oldest fossils of clades. In addition, both approaches assume that fossil records of different clades in the phylogeny are all the product of the same underlying fossil sampling rate, even though this rate has been shown to differ strongly between higher level taxa. We here develop a flexible new approach to Bayesian age estimation that combines advantages of node dating and the FBD model. In our new approach, calibration densities are defined on the basis of first fossil occurrences and sampling rate estimates that can be specified separately for all clades. We verify our approach with a large number of simulated data sets, and compare its performance to that of the FBD model. We find that our approach produces reliable age estimates that are robust to model violation, on par with the FBD model. By applying our approach to a large data set including sequence data from over 1000 species of teleost fishes as well as 147 carefully selected fossil constraints, we recover a timeline of teleost diversification that is incompatible with previously assumed vicariant divergences of freshwater fishes. Our results instead provide strong evidence for transoceanic dispersal of cichlids and other groups of teleost fishes. [Bayesian inference; calibration density; Cichlidae; fossil record; marine dispersal; phylogeny; relaxed molecular clock].
Genetics of cognitive control: Implications for Nimh's research domain criteria initiative

Cognitive control refers to a set of mental processes that modulate other cognitive and emotional systems in service of goal‐directed adaptive behavior. There is growing support for the notion that cognitive control abnormalities are a central component of many of the neuropsychological deficits observed in individuals with mental illnesses, particularly those with psychotic disorders. NIMH's research domain criteria (RDoC) initiative, which is designed to develop biologically informed constructs to better understand psychopathology, designated cognitive control a construct within the cognitive systems domain. Identification of genes that influence cognitive control or its supportive brain systems will improve our understating of the RDoC construct and provide candidate genes for psychotic disorders. We examine evidence for cognitive control deficits in psychosis, determine if these measures could be useful endophenotypes, and explore work linking genetic variation to cognitive control performance. While there is a wealth of evidence to support the notion the cognitive control is a valid endophenotype for psychosis, its genetic underpinning remains ill characterized. However, existing work provides a promising foundation on which future endeavors might build. Confirming existing individual gene associations will go some way to expanding our understanding of the genetics of cognitive control, and by extension, psychotic disorders. Yet, to truly understand the molecular underpinnings of such complex traits, it may be necessary to evaluate genes in tandem, focusing not on single genes but rather on empirically derived gene sets or on functionally defined networks of genes. © 2015 Wiley Periodicals, Inc.
The Size and Conservation of a Coiled-coil Structure in the Ectodomain of Human BST-2/Tetherin Is Dispensable for Inhibition of HIV-1 Virion Release*

Background: BST-2 inhibits virus release by tethering virions to the cell surface. Results: The length of the BST-2 ectodomain can be increased or reduced without loss of function. Conclusion: The positioning of ectodomain deletions rather than their size determines the impact on BST-2 function. Significance: Understanding the importance of structural elements in BST-2 is critical for developing antiviral strategies. BST-2/CD317/tetherin is a host factor that inhibits HIV-1 release and is counteracted by HIV-1 Vpu. Structural studies indicate that the BST-2 ectodomain assumes a coiled-coil conformation. Here we studied the role of the BST-2 ectodomain for tethering function. First, we addressed the importance of the length and structure of the ectodomain by adding or substituting heterologous coiled-coil or non-coiled-coil sequences. We found that extending or replacing the BST-2 ectodomain using non-coiled-coil sequences resulted in loss of BST-2 function. Doubling the size of the BST-2 ectodomain by insertion of a heterologous coiled-coil motif or substituting the BST-2 coiled-coil domain with a heterologous coiled-coil motif maintained tethering function. Reductions in the size of the BST-2 coiled-coil domain were tolerated as well. In fact, deletion of the C-terminal half of the BST-2 ectodomain, including a series of seven consecutive heptad motifs did not abolish tethering function. However, slight changes in the positioning of deletions affecting the relative placing of charged or hydrophobic residues on the helix severely impacted the functional properties of BST-2. Overall, we conclude that the size of the BST-2 ectodomain is highly flexible and can be reduced or extended as long as the positioning of residues important for the stability of the dimer interface is maintained.
New laboratory methods of diagnosing allergic disease - Part II - Where are we going? : review article

A great number of advances have been made in the diagnostic tools and testing methods used for allergy diagnosis. Improved and new methodologies are under development, not only to identify the presence of an allergy, but also to determine the severity of an allergy and the likelihood of its resolution. The role of laboratory testing for allergy should be thought of in context of the suspected mechanism of pathogenesis (i.e. IgE or non-IgE mediated) and the limitations of available testing. These results should always be interpreted in correlation with the clinical history. This article reviews currently available diagnostic tests, recent improvements to diagnostic tools and touches on new testing methods that are in development.
LEVOSULPIRIDE Y DOMPERIDONA EN EL TRATAMIENTO DE LA DISPEPSIA FUNCIONAL: ESTUDIO COMPARATIVO

Objetivo: Comparar la eficiencia en la reduccion de los sintomas de pacientes diagnosticados mediante los criterios de Roma III con el diagnostico de dispepsia funcional, a las 4 semanas de estar tomando levosulpiride o domperidona. Metodo: Se incluyeron 105 pacientes que consultaron con los sintomas de dispepsia funcional, al Servicio de Gastroenterologia del Hospital Universitario de Caracas, que cumplian con los criterios de ROMA III, en un estudio prospectivo aleatorio. A todos se les realizo gastroscopia y biopsia para diagnosticar Helicobacter pylori. Tiempo de duracion del estudio por cada paciente 30 dias. Tiempo total del estudio 6 meses de noviembre de 2006 a abril de 2007. Resultados: El 94,28 % de los pacientes que recibieron levosulpiride reportaron sintomas leves o ausentes en comparacion con el 71,42 % del grupo que recibio dinoprostona y el 14,28 % del grupo control. Conclusion: Levosulpiride es mas eficaz que domperidona en el control de los sintomas de dispepsia funcional en los pacientes estudiados. Las drogas comparadas no presentaron efectos adversos severos. Levosulpiride, deberia considerarse entre los farmacos de eleccion en el tratamiento de la dispepsia funcional. ABSTRACT: Objective: Compare efficiency in the reduction of symptoms of patients diagnosed according Rome III classification of functional dyspepsia, for 4 weeks of are taking Levosulpiride or Domperidona. Methods: Were included 105 patients that consulted with the symptoms of Functional Dyspepsia, to the Service of Gastroenterology of the University Hospital of Caracas, in a study prospective randomized. To all they are carried out Gastroscopy and biopsy to diagnose Helicobacter Pylori. Time of duration of the study for each patient 30 days. Total time of the study 6 months of November of 2006 to April of 2007. Results: 94.28 % of patients that received Levosulpiride was asyntomatic, comparing with 71.42 % Domperidona group and 14.28 % Control group. Conclusion: Levosulpiride is more effective than Domperidona in the control of the symptoms of functional dyspepsia in the studied patients. The compared drugs didn’t present severe adverse effects. Levosulpiride, it should be considered among the drugs of choice for the treatment of the functional dyspepsia.
MTHFR methylation moderates the impact of smoking on DNA methylation at AHRR for African American young adults

Smoking has been shown to have a large, reliable, and rapid effect on demethylation of AHRR, particularly at cg05575921, suggesting that methylation may be used as an index of cigarette consumption. Because the availability of methyl donors may also influence the degree of demethylation in response to smoking, factors that affect the activity of methylene tetrahydrofolate reductase (MTHFR), a key regulator of methyl group availability, may be of interest. In the current investigation, we examined the extent to which individual differences in methylation of MTHFR moderated the association between smoking and demethylation at cg05575921 as well as at other loci on AHRR associated with a main effect of smoking. Using a discovery sample (AIM, N = 293), and a confirmatory sample (SHAPE, N = 368) of young adult African Americans, degree of methylation of loci in the first exon of MTHFR was associated with amplification of the association between smoking and AHRR demethylation at cg05575921. However, genetic variation at a commonly studied MTHFR variant, C677T, did not influence cg05575921 methylation. The significant interaction between MTHFR methylation and the smoking‐induced response at cg05575921 suggests a role for individual differences in methyl cycle regulation in understanding the effects of cigarette consumption on genome wide DNA methylation.
Therapeutic Management of concurrent Sarcoptic and Psoroptic Acariosis in Rabbits

Eight New Zealand white rabbits were presented with clinical signs of pruritus, alopecia, scab and crust formation and lichenification initially on upper lip which later extended to full face, ear pinnae, eyelids, lower jaw and limbs. Skin scrapping revealed mixed infestations of Sarcoptes cuniculi and Psoroptes cuniculi. Subcutaneous injection of ivermectin at weekly intervals for four weeks resulted in remission of clinical signs and improvement.
Cambios de los arcos dentales deciduos clase I con apiñamiento, utilizando pistas planas directas. Medellín 2012-2013

Abstract Introduction and objective: Crowding has become one of the leading causes of morbidity and consultation in pediatric dentistry, early treatment has been proposed as the best alternative to intercept malocclusions, preventing these from getting worse or perpetuate to the permanent dentition. Planas Direct Tracks (PPD) are devices with bimaxillary action aimed at neurooclusal rehabilitation at an early age, in order to rehabilitate the laterals movements of the jaw and enhace the masticatory function alternation. The objective of this study is to evaluate the dentoalveolar changes occurring in the transverse plane using PPD in patients Class I with anterior crowding between 4-5 years old. Materials and methods: The sample consisted of 6 subjects were models were performed before mounting them in the gnatostato, preparation and cementation of PPD and models six and twelve months later, to observe differences. Results: Statistically significant differences were found in the maxillary intercanine width, in maxillary intermolar distance and right space required maxillary, between the initial model and after 6 and 12 months of installed the therapy. Conclusion: Patients treated early with PPD have higher transverse development and decreased crowding, when compared with longitudinal studies in untreated patients