Distribution of BCR::ABL1 Transcripts in the Different Clinical Phases of Chronic Myeloid Leukemia: Effect on Hematological Parameters and Patient Survival.

Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder characterized by the presence of the Philadelphia chromosome, a product of the reciprocal translocation t(9;22)(q34;q11), in the BCR and ABL genes. These rearrangements in both genes lead to the formation of various fusion mRNA products, with preferential expression of b2a2, b3a2, and other BCR::ABL1 mRNA variants, combined with additional chromosomal abnormalities. Notably, the distribution and frequency of different mRNA variants vary in different populations. However, studies concerning this in Mexico are limited, and the results have been inconclusive. This study therefore aimed to determine the distribution of BCR::ABL1 mRNA variants in different clinical phases of CML and their effect on hematological parameters and patient survival. This study included 33 patients, whose demographic, clinical, and molecular data on BCR::ABL1 mRNA variants and hematological parameters were collected to identify potential associations. A total of 84.8% (n = 28) of patients had BCR::ABL1 translocation and increased platelet and basophil counts. The most frequent mRNA variant was b3a2 (64.3%), followed by b2a2 (28.6%) and e1a2 (3.6%). Concerning the clinical phases of CML, 75.8% (n = 25), 21.2% (n = 7), and 3% (n = 1) of patients were in the chronic, blast, and accelerated phases, respectively. Moreover, the b3a2 mRNA variant was more commonly identified in patients in the chronic phase. No correlation was observed between mRNA variant expression and patient survival. However, b2a2 was indicative of patients with longer survival as well as those treated with imatinib or nilotinib. Additionally, platelet count could be a marker of BCR::ABL1 translocation.

Análisis de la presencia de trisomía 8 en las diferentes fases de leucemia mieloide crónica.

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Ultrafiltration Membranes System: A Proposal to Remove Emerging Pollutants in Urban Wastewater.

Considering the important role that wastewater reuse plays in the water cycle and in the current water scenario immersed in a severe drought, the search for technologies that allow obtaining quality water for reuse is increasingly relevant. In this sense, the membrane biological reactor (MBR) is an alternative to traditional activated sludge systems, in which the separation of biomass and treatment water is carried out by membrane filtration instead of decantation. This study made it possible to confirm the presence of emerging pollutants in the wastewater entering the WWTPs under study, to study the behavior and performance of MBR systems with hollow fiber membranes and flat membranes in obtaining reclaimed wastewater for subsequent reuse, and to compare it with the degree of elimination obtained in conventional biological treatment. It has been demonstrated that this technology is almost 100% effective in the elimination of nutrients, organic matter, pathogens, organic micropollutants, metals, etc., and has achieved different percentages of success in eliminating emerging pollutants depending on their nature: 35% in insecticides and herbicides, 45% in anxiolytics, psychiatric drugs, and industrial disinfectants, 75% in antibiotics, and around 100% in analgesics, anti-inflammatory drugs, and hormones. It has also contributed to the establishment of monitoring protocols for emerging pollutants in the WWTPs under study and to the evaluation of their risks, as well as the development and implementation of advanced regeneration systems that are economically favorable for increasing the quality of WWTP effluents for their reuse.

SIRPα - CD47 axis regulates dendritic cell-T cell interactions and TCR activation during T cell priming in spleen.

The SIRPα-CD47 axis plays an important role in T cell recruitment to sites of immune reaction and inflammation but its role in T cell antigen priming is incompletely understood. Employing OTII TCR transgenic mice bred to Cd47-/- (Cd47KO) or SKI mice, a knock-in transgenic animal expressing non-signaling cytoplasmic-truncated SIRPα, we investigated how the SIRPα-CD47 axis contributes to antigen priming. Here we show that adoptive transfer of Cd47KO or SKI Ova-specific CD4+ T cells (OTII) into Cd47KO and SKI recipients, followed by Ova immunization, elicited reduced T cell division and proliferation indices, increased apoptosis, and reduced expansion compared to transfer into WT mice. We confirmed prior reports that splenic T cell zone, CD4+ conventional dendritic cells (cDCs) and CD4+ T cell numbers were reduced in Cd47KO and SKI mice. We report that in vitro derived DCs from Cd47KO and SKI mice exhibited impaired migration in vivo and exhibited reduced CD11c+ DC proximity to OTII T cells in T cell zones after Ag immunization, which correlates with reduced TCR activation in transferred OTII T cells. These findings suggest that reduced numbers of CD4+ cDCs and their impaired migration contributes to reduced T cell-DC proximity in splenic T cell zone and reduced T cell TCR activation, cell division and proliferation, and indirectly increased T cell apoptosis.

Does hotel management matter to overcoming the COVID-19 crisis? The Spanish case.

This paper analyses the influence that the initial actions and strategies pursued by hotel managers have on the recovery of occupancy after a crisis such as the COVID-19 pandemic. To do this, a specific survey is carried out on managers of Spanish hotels. The main findings show that labour actions, especially plans for temporary employment regulations, innovation and differentiation strategies, reorientation to closer markets and obtaining information from official sources as a guarantee of their certainty, are the measures that have a greater impact on the possibilities of recovering hotel activity. In addition, government measures that contribute to the improvement of the financial situation of firms can also play a relevant role in hotel recovery.

The possibility of spatial mapping of SOC content in olive groves under integrated production using easy-to-obtain ancillary data in a Mediterranean area.

Background: Unlike most of Europe, Andalucía in southern Spain as a Mediterranean area still lacks digital maps of SOC content provided by machine learning algorithms. The wide diversity of climate, geology, hydrology, landscape, topography, vegetation, and micro-relief data as easy-to-obtain covariates facilitated the development of digital soil mapping (DSM). The purpose of this research is to model and map the spatial distribution of SOC at three depths, in an area of approximately 10000 km 2 located in Seville and Cordoba Provinces, and to use R programming to compare two machine learning techniques (cubist and random forest) for developing SOC maps at multiple depths. Methods: Environmental covariates used in this research include nine derivatives from digital elevation models (DEM), three climatic variables and finally eighteen remotely-sensed spectral data (band ratios calculated by the acquired Landsat-8 OLI and Sentinel-2A MSI in July 2019). In total, 300 soil samples from 100 points were taken (0-25 cm). The purpose of this research is to model and map the spatial distribution of SOC, in an area with approximately 10000 km2 located in Seville and Cordoba Provinces, and to compare two machine learning techniques (cubist and random forest) by R programming. Results: The findings showed that the novel approach for integrating the indices using Landsat-8 OLI and Sentinel-2A MSI satellite data had a better result. Conclusions: Finally, we obtained evidence that the resolution of satellite images is more important in modelling and digital mapping.

Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis.

Sialomucin CD43 is a transmembrane protein differentially expressed in leukocytes that include innate and adaptive immune cells. Among a variety of cellular processes, CD43 participates in T cell adhesion to vascular endothelial cells and contributes to the progression of experimental autoimmunity. Sequential infiltration of myeloid cells and T cells in the heart is a hallmark of cardiac inflammation and heart failure (HF). Here, we report that CD43-/- mice have improved survival to HF induced by transverse aortic constriction (TAC). This enhanced survival is associated with improved systolic function, decreased cardiac fibrosis, and significantly reduced T cell cardiac infiltration in response to TAC compared to control wild-type (WT) mice. Lack of CD43 did not alter the number of myeloid cells in the heart, but resulted in decreased cardiac CXCL10 expression, a chemoattractant for T cells, and in a monocyte shift to anti-inflammatory macrophages in vitro. Collectively, these findings unveil a novel role for CD43 in adverse cardiac remodeling in pressure overload induced HF through modulation of cardiac T cell inflammation.

Isolevuglandin-Modified Cardiac Proteins Drive CD4+ T-Cell Activation in the Heart and Promote Cardiac Dysfunction.

BACKGROUND: Despite the well-established association between T-cell-mediated inflammation and nonischemic heart failure, the specific mechanisms triggering T-cell activation during the progression of heart failure and the antigens involved are poorly understood. We hypothesized that myocardial oxidative stress induces the formation of isolevuglandin (IsoLG)-modified proteins that function as cardiac neoantigens to elicit CD4+ T-cell receptor (TCR) activation and promote heart failure. METHODS: We used transverse aortic constriction in mice to trigger myocardial oxidative stress and T-cell infiltration. We profiled the TCR repertoire by mRNA sequencing of intramyocardial activated CD4+ T cells in Nur77GFP reporter mice, which transiently express GFP on TCR engagement. We assessed the role of antigen presentation and TCR specificity in the development of cardiac dysfunction using antigen presentation-deficient MhcII-/- mice and TCR transgenic OTII mice that lack specificity for endogenous antigens. We detected IsoLG protein adducts in failing human hearts. We also evaluated the role of reactive oxygen species and IsoLGs in eliciting T-cell immune responses in vivo by treating mice with the antioxidant TEMPOL and the IsoLG scavenger 2-hydroxybenzylamine during transverse aortic constriction, and ex vivo in mechanistic studies of CD4+ T-cell proliferation in response to IsoLG-modified cardiac proteins. RESULTS: We discovered that TCR antigen recognition increases in the left ventricle as cardiac dysfunction progresses and identified a limited repertoire of activated CD4+ T-cell clonotypes in the left ventricle. Antigen presentation of endogenous antigens was required to develop cardiac dysfunction because MhcII-/- mice reconstituted with CD4+ T cells and OTII mice immunized with their cognate antigen were protected from transverse aortic constriction-induced cardiac dysfunction despite the presence of left ventricle-infiltrated CD4+ T cells. Scavenging IsoLGs with 2-hydroxybenzylamine reduced TCR activation and prevented cardiac dysfunction. Mechanistically, cardiac pressure overload resulted in reactive oxygen species-dependent dendritic cell accumulation of IsoLG protein adducts, which induced robust CD4+ T-cell proliferation. CONCLUSIONS: Our study demonstrates an important role of reactive oxygen species-induced formation of IsoLG-modified cardiac neoantigens that lead to TCR-dependent CD4+ T-cell activation within the heart.

A Highly Conserved Iron-Sulfur Cluster Assembly Machinery between Humans and Amoeba Dictyostelium discoideum: The Characterization of Frataxin.

Several biological activities depend on iron-sulfur clusters ([Fe-S]). Even though they are well-known in several organisms their function and metabolic pathway were poorly understood in the majority of the organisms. We propose to use the amoeba Dictyostelium discoideum, as a biological model to study the biosynthesis of [Fe-S] at the molecular, cellular and organism levels. First, we have explored the D. discoideum genome looking for genes corresponding to the subunits that constitute the molecular machinery for Fe-S cluster assembly and, based on the structure of the mammalian supercomplex and amino acid conservation profiles, we inferred the full functionality of the amoeba machinery. After that, we expressed the recombinant mature form of D. discoideum frataxin protein (DdFXN), the kinetic activator of this pathway. We characterized the protein and its conformational stability. DdFXN is monomeric and compact. The analysis of the secondary structure content, calculated using the far-UV CD spectra, was compatible with the data expected for the FXN fold, and near-UV CD spectra were compatible with the data corresponding to a folded protein. In addition, Tryptophan fluorescence indicated that the emission occurs from an apolar environment. However, the conformation of DdFXN is significantly less stable than that of the human FXN, (4.0 vs. 9.0 kcal mol-1, respectively). Based on a sequence analysis and structural models of DdFXN, we investigated key residues involved in the interaction of DdFXN with the supercomplex and the effect of point mutations on the energetics of the DdFXN tertiary structure. More than 10 residues involved in Friedreich's Ataxia are conserved between the human and DdFXN forms, and a good correlation between mutational effect on the energetics of both proteins were found, suggesting the existence of similar sequence/function/stability relationships. Finally, we integrated this information in an evolutionary context which highlights particular variation patterns between amoeba and humans that may reflect a functional importance of specific protein positions. Moreover, the complete pathway obtained forms a piece of evidence in favor of the hypothesis of a shared and highly conserved [Fe-S] assembly machinery between Human and D. discoideum.

Methodology for Energy Optimization in Wastewater Treatment Plants. Phase III: Implementation of an Integral Control System for the Aeration Stage in the Biological Process of Activated Sludge and the Membrane Biological Reactor.

The proposed methodology for optimizing energy efficiency, based on good management of the aeration process through the implementation of an appropriate control strategy, achieved reductions of more than 40% in energy consumption at the San Pedro del Pinatar Wastewater Treatment Plant (WWTP) (Murcia, Spain). Phases I and II of this methodology managed to reduce the oxygen needs of the microorganisms in the biological system, optimize the efficiency of oxygen transfer to the biological reactor and redesign the installation to correct abnormal energy loss situations. In addition, we established the basis for Phase III, which implemented a control strategy to achieve stable values close to the setpoints of the fundamental operating parameters of the aeration process. The control system is based on the measurements recorded by strategically installed sensors and mathematical algorithms based on models, achieving an expert adaptive-predictive system that regulates aeration both in the biological stage by activated sludge and the aeration of the installed ultrafiltration membrane system. The objectives were: (i) to achieve automatic execution of the best management strategy; (ii) to reduce the energy demand; (iii) to improve the operation and stability of the process; (iv) to reduce operating costs; and (v) to contribute to the fulfillment of the sustainable development objectives.

DOCK8 is essential for LFA-1-dependent positioning of T follicular helper cells in germinal centers.

T follicular helper (Tfh) cell migration into germinal centers (GCs) is essential for the generation of GC B cells and antibody responses to T cell-dependent (TD) antigens. This process requires interactions between lymphocyte function-associated antigen 1 (LFA-1) on Tfh cells and ICAMs on B cells. The mechanisms underlying defective antibody responses to TD antigens in DOCK8 deficiency are incompletely understood. We show that mice selectively lacking DOCK8 in T cells had impaired IgG antibody responses to TD antigens, decreased GC size, and reduced numbers of GC B cells. However, they developed normal numbers of Tfh cells with intact capacity for driving B cell differentiation into a GC phenotype in vitro. Notably, migration of DOCK8-deficient T cells into GCs was defective. Following T cell receptor (TCR)/CD3 ligation, DOCK8-deficient T cells had impaired LFA-1 activation and reduced binding to ICAM-1. Our results therefore indicate that DOCK8 is important for LFA-1-dependent positioning of Tfh cells in GCs, and thereby the generation of GC B cells and IgG antibody responses to TD antigen.

Helping stakeholders select and apply appraisal tools to mitigate soil threats: Researchers' experiences from across Europe.

Soil improvement measures need to be ecologically credible, socially acceptable and economically affordable if they are to enter widespread use. However, in real world decision contexts not all measures can sufficiently meet these criteria. As such, developing, selecting and using appropriate tools to support more systematic appraisal of soil improvement measures in different decision-making contexts represents an important challenge. Tools differ in their aims, ranging from those focused on appraising issues of cost-effectiveness, wider ecosystem services impacts and adoption barriers/opportunities, to those seeking to foster participatory engagement and social learning. Despite the growing complexity of the decision-support tool landscape, comprehensive guidance for selecting tools that are best suited to appraise soil improvement measures, as well as those well-adapted to enable participatory deployment, has generally been lacking. We address this gap using the experience and survey data from an EU-funded project (RECARE: Preventing and REmediating degradation of soils in Europe through land CARE). RECARE applied different socio-cultural, biophysical and monetary appraisal tools to assess the costs, benefits and adoption of soil improvement measures across Europe. We focused on these appraisal tools and evaluated their performance against three broad attributes that gauge their differences and suitability for widespread deployment to aid stakeholder decision making in soil management. Data were collected using an online questionnaire administered to RECARE researchers. Although some tools worked better than others across case studies, the information collated was used to provide guiding strategies for choosing appropriate tools, considering resources and data availability, characterisation of uncertainty, and the purpose for which a specific soil improvement measure is being developed or promoted. This paper provides insights to others working in practical soil improvement contexts as to why getting the tools right matters. It demonstrates how use of the right tools can add value to decision-making in ameliorating soil threats, supporting the sustainable management of the services that our soil ecosystems provide.

Increased lymphocyte activation and atherosclerosis in CD47-deficient mice.

CD47, also known as integrin-associated protein (IAP), is a transmembrane protein with multiple biological functions including regulation of efferocytosis and leukocyte trafficking. In this study we investigated the effect of CD47-deficiency on atherosclerosis using a model of adeno-associated virus (AAV)-induced hypercholesterolemia. We observed increased plaque formation in CD47 null mice compared to wild-type controls. Loss of CD47 caused activation of dendritic cells, T cells and natural killer (NK) cells, indicating an important role for CD47 in regulating immunity. In particular, Cd47 deficiency increased the proportion of IFN-γ producing CD90+ NK cells. Treatment with depleting anti-NK1.1 monoclonal antibody (mAb), but not depleting anti-CD4/CD8 mAbs, equalized atherosclerotic burden, suggesting NK cells were involved in the enhanced disease in Cd47 deficient mice. Additional studies revealed that levels of CD90+ and IFN-γ+ NK cells were expanded in atherosclerotic aorta and that CD90+ NK cells produce more IFN-γ than CD90- NK cells. Finally, we demonstrate that anti-CD47 (MIAP410) causes splenomegaly and activation of DCs and T cells, without affecting NK cell activation. In summary, we demonstrate that loss of CD47 causes increased lymphocyte activation that results in increased atherosclerosis.

Influence of bone quality on the mechanical interaction between implant and bone: A finite element analysis.

OBJECTIVES: To evaluate the influence of bone type in terms of bone density and cortical bone thickness, on the stresses induced by two implants under compressive and oblique loads. METHODS: A numerical simulation technique based on the finite element method was applied. Two implant types (M-12 and Astra Tech) were introduced in a model matrix whose geometry was extracted from a real CBCT radiograph of the posterior mandibular region. The Young's module and Poisson's coefficient of the bone qualities described by Misch were calculated. Loads with amplitude of 400 N were exerted in two directions: compressive and 15° oblique to 5 mm above the uppermost part of the implant. RESULTS: The von Misses variant was analysed. Both implant types presented greater tension in the ​​cortical bone area than in the ​​trabecular bone region under compressive loading. For the oblique load condition, the stresses obtained in the cortical zone were significantly higher than those registered as a consequence of compressive loads in both implant types. CONCLUSIONS: Regardless of bone type, the M-12 implants presented lower tensions in the cortical bone than did the Astra implants. The tensions recorded for D3 and D4 bone types in the trabecular zone surrounding the M-12 implants were greater than those recorded for the Astra implants. CLINICAL SIGNIFICANCE: For both compressive and oblique loads, good mechanical behaviour was observed. The decrease in bone quality determines a worse stress distribution, and the cortical bone is overloaded. An efficient distribution of the forces may increase the implants' longevity.

CXCR3 regulates CD4+ T cell cardiotropism in pressure overload-induced cardiac dysfunction.

Heart failure (HF) is associated in humans and mice with increased circulating levels of CXCL9 and CXCL10, chemokine ligands of the CXCR3 receptor, predominantly expressed on CD4+ Th1 cells. Chemokine engagement of receptors is required for T cell integrin activation and recruitment to sites of inflammation. Th1 cells drive adverse cardiac remodeling in pressure overload-induced cardiac dysfunction, and mice lacking the integrin ligand ICAM-1 show defective T cell recruitment to the heart. Here, we show that CXCR3+ T cells infiltrate the heart in humans and mice with pressure overload-induced cardiac dysfunction. Genetic deletion of CXCR3 disrupts CD4+ T cell heart infiltration and prevents adverse cardiac remodeling. We demonstrate that cardiac fibroblasts and cardiac myeloid cells that include resident and infiltrated macrophages are the source of CXCL9 and CXCL10, which mechanistically promote Th1 cell adhesion to ICAM-1 under shear conditions in a CXCR3-dependent manner. To our knowledge, our findings identify a previously unrecognized role for CXCR3 in Th1 cell recruitment into the heart in pressure overload-induced cardiac dysfunction.

Sialomucin CD43 regulates T helper type 17 cell intercellular adhesion molecule 1 dependent adhesion, apical migration and transendothelial migration.

T helper type 17 lymphocytes (Th17 cells) infiltrate the central nervous system (CNS), induce inflammation and demyelination and play a pivotal role in the pathogenesis of multiple sclerosis. Sialomucin CD43 is highly expressed in Th17 cells and mediates adhesion to endothelial selectin (E-selectin), an initiating step in Th17 cell recruitment to sites of inflammation. CD43-/- mice have impaired Th17 cell recruitment to the CNS and are protected from experimental autoimmune encephalomyelitis (EAE), the mouse model of multiple sclerosis. However, E-selectin is dispensable for the development of EAE, in contrast to intercellular and vascular cell adhesion molecules (ICAM-1 and VCAM-1). We report that CD43-/- mice have decreased demyelination and T-cell infiltration, but similar up-regulation of ICAM-1 and VCAM-1 in the spinal cord, compared with wild-type (WT) mice, at the initiation of EAE. CD43-/- Th17 cells have impaired adhesion to ICAM-1 under flow conditions in vitro, despite having similar expression of LFA-1, the main T-cell ligand for ICAM-1, as WT Th17 cells. Regardless of the route of integrin activation, CD43-/- Th17 cell firm arrest on ICAM-1 was comparable to that of WT Th17 cells, but CD43-/- Th17 cells failed to optimally apically migrate on immobilized ICAM-1-coated coverslips and endothelial cells, and to transmigrate under shear flow conditions in an ICAM-1-dependent manner. Collectively, these findings unveil novel roles for CD43, facilitating adhesion of Th17 cells to ICAM-1 and modulating apical and transendothelial migration, as mechanisms potentially responsible for Th17 cell recruitment to sites of inflammation such as the CNS.

Non-apoptotic Fas (CD95) Signaling on T Cells Regulates the Resolution of Th2-Mediated Inflammation.

Fas (CD95/APO-1) and its ligand (FasL/CD95L) promote the resolution of type 2 lung inflammation and eosinophilia. We previously found that Fas-deficiency on T cells, but not eosinophils, delayed resolution of inflammation. However, Fas can signal both cell death and have a positive signaling function that can actually activate cells. In this study, we investigated whether Fas-induced death or Fas-activated signaling pathways promote resolution of allergic lung inflammation. By increasing T cell survival through two Fas-independent pathways, using Bim-deficient T cells or Bcl-xL overexpressing T cells, no differences in resolution of Th2-mediated inflammation was observed. Furthermore, Th2 cells were inherently resistant to Fas-mediated apoptosis and preferentially signaled through non-apoptotic pathways following FasL treatment. Utilizing Fas-mutant mice deficient in apoptotic but sufficient for non-apoptotic Fas signaling pathways, we demonstrate that non-apoptotic Fas signaling in T cells drives resolution of Th2-mediated airway inflammation. Our findings reveal a previously unknown role for non-apoptotic Fas signaling on Th2 cells in the induction of resolution of type 2 inflammation.

Alpha-synuclein mitochondrial interaction leads to irreversible translocation and complex I impairment.

α-synuclein is involved in both familial and sporadic Parkinson's disease. Although its interaction with mitochondria has been well documented, several aspects remains unknown or under debate such as the specific sub-mitochondrial localization or the dynamics of the interaction. It has been suggested that α-synuclein could only interact with ER-associated mitochondria. The vast use of model systems and experimental conditions makes difficult to compare results and extract definitive conclusions. Here we tackle this by analyzing, in a simplified system, the interaction between purified α-synuclein and isolated rat brain mitochondria. This work shows that wild type α-synuclein interacts with isolated mitochondria and translocates into the mitochondrial matrix. This interaction and the irreversibility of α-synuclein translocation depend on incubation time and α-synuclein concentration. FRET experiments show that α-synuclein localizes close to components of the TOM complex suggesting a passive transport of α-synuclein through the outer membrane. In addition, α-synuclein binding alters mitochondrial function at the level of Complex I leading to a decrease in ATP synthesis and an increase of ROS production.

Th1 effector T cells selectively orchestrate cardiac fibrosis in nonischemic heart failure.

Despite emerging data indicating a role for T cells in profibrotic cardiac repair and healing after ischemia, little is known about whether T cells directly impact cardiac fibroblasts (CFBs) to promote cardiac fibrosis (CF) in nonischemic heart failure (HF). Recently, we reported increased T cell infiltration in the fibrotic myocardium of nonischemic HF patients, as well as the protection from CF and HF in TCR-α-/- mice. Here, we report that T cells activated in such a context are mainly IFN-γ+, adhere to CFB, and induce their transition into myofibroblasts. Th1 effector cells selectively drive CF both in vitro and in vivo, whereas adoptive transfer of Th1 cells, opposite to activated IFN-γ-/- Th cells, partially reconstituted CF and HF in TCR-α-/- recipient mice. Mechanistically, Th1 cells use integrin α4 to adhere to and induce TGF-ß in CFB in an IFN-γ-dependent manner. Our findings identify a previously unrecognized role for Th1 cells as integrators of perivascular CF and cardiac dysfunction in nonischemic HF.

Effectiveness of flossing loops in the control of the gingival health.

BACKGROUND: One of the key factor in the good condition of periodontal tissues is their daily hygiene. Oral hygiene techniques such brushing and a good interdental hygiene by correct flossing are very important. The aim of this study is to compare the use of dental floss in a loop vs traditional floss in the control of Loe-Silness Gingival Index (IG), Turesky´s Plaque Index (IPT), Gingival Bleeding Index (IS) and the values of interleukin 6 (IL-6) and interleukin 8 (IL-8). MATERIAL AND METHODS: A comparative study of 40 patients in which each patient was his own control, using during 45 days each one of the devices (new loop floss and conventional floss) of interdental hygiene analysed. Data for Loe-Silness Gingival Index (IG), Turesky´s Plaque Index (IPT), Gingival Bleeding Index (IS) and the values of interleukin 6 (IL-6) and interleukin 8 (IL-8)were collected and measured in every visit for every type of interdental hygiene device. RESULTS: Our data indicates that the rate of Turesky´s Plaque Index presented statistically significant differences between groups (loop: 1.66 ± 0.8; traditional: 1.12 ± 0.8; p<0.0001). The rest of the indices studied showed no statistically significant differences. CONCLUSIONS: The creation of new dental floss designs try to make their use easier and more sensitive, and plaque removal more effective. The loop design can facilitate interdental hygiene, reaching similar effectiveness than traditional floss, improving some indicators, such as Turesky´s Plaque Index. Key words:Dental floss, bacterial plaque, loop floss, plaque index, periodontal diseases.