91 research outputs found

    Holography in asymptotically flat space-times and the BMS group

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    In a previous paper (hep-th/0306142) we have started to explore the holographic principle in the case of asymptotically flat space-times and analyzed in particular different aspects of the Bondi-Metzner-Sachs (BMS) group, namely the asymptotic symmetry group of any asymptotically flat space-time. We continue this investigation in this paper. Having in mind a S-matrix approach with future and past null infinity playing the role of holographic screens on which the BMS group acts, we connect the IR sectors of the gravitational field with the representation theory of the BMS group. We analyze the (complicated) mapping between bulk and boundary symmetries pointing out differences with respect to the AdS/CFT set up. Finally we construct a BMS phase space and a free hamiltonian for fields transforming w.r.t BMS representations. The last step is supposed to be an explorative investigation of the boundary data living on the degenerate null manifold at infinity.Comment: 31 pages, several changes in section 3 and 7 and references update

    Mollicutes antibiotic resistance profile and presence of genital abnormalities in couples attending an infertility clinic.

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    OBJECTIVE: The present study aimed to identify Mollicutes infection in the reproductive system. We also examined the microbiological, biochemical, and antimicrobial profiles of Mollicutes infection, which are potentially associated with clinical reproductive abnormalities causing infertility in couples. METHODS: Thirty-seven couples who were attending an infertility clinic were enrolled. Detection of genital mycoplasmas was performed in cervicovaginal samples or male urethral swabs. Microbiological culture and biochemical and antimicrobial profiles were characterized using a Mycoplasma kit. The results were associated with reproductive abnormalities, as assessed by medical specialists from the infertility clinic. RESULTS: Up to 28.3% of all biological samples (n = 74) showed positive cultures. Bacterial isolates were Ureaplasma urealyticum (71.4%), Mycoplasma hominis (9.5%), or coinfections (19%). Most Mollicutes showed significant resistance to fluoroquinolones, macrolides, and tetracycline; and showed susceptibility to doxycycline, josamycin, and pristinamycin. The presence of resistant strains to any antibiotic was significantly associated with genital abnormalities (χ2 test, relative risk = 11.38 [95% confidence interval: 5.8-22.9]), particularly in women. The highest statistical association was found for macrolide-resistant strains. CONCLUSION: The microbiological antibiotic resistance profile is epidemiologically associated with abnormalities of the reproductive system in couples attending an infertility clinic

    A Primary Prevention Clinical Risk Score Model for Patients With Brugada Syndrome (BRUGADA-RISK)

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    OBJECTIVES: The goal of this study was to develop a risk score model for patients with Brugada syndrome (BrS). BACKGROUND: Risk stratification in BrS is a significant challenge due to the low event rates and conflicting evidence. METHODS: A multicenter international cohort of patients with BrS and no previous cardiac arrest was used to evaluate the role of 16 proposed clinical or electrocardiogram (ECG) markers in predicting ventricular arrhythmias (VAs)/sudden cardiac death (SCD) during follow-up. Predictive markers were incorporated into a risk score model, and this model was validated by using out-of-sample cross-validation. RESULTS: A total of 1,110 patients with BrS from 16 centers in 8 countries were included (mean age 51.8 ± 13.6 years; 71.8% male). Median follow-up was 5.33 years; 114 patients had VA/SCD (10.3%) with an annual event rate of 1.5%. Of the 16 proposed risk factors, probable arrhythmia-related syncope (hazard ratio [HR]: 3.71; p < 0.001), spontaneous type 1 ECG (HR: 3.80; p < 0.001), early repolarization (HR: 3.42; p < 0.001), and a type 1 Brugada ECG pattern in peripheral leads (HR: 2.33; p < 0.001) were associated with a higher risk of VA/SCD. A risk score model incorporating these factors revealed a sensitivity of 71.2% (95% confidence interval: 61.5% to 84.6%) and a specificity of 80.2% (95% confidence interval: 75.7% to 82.3%) in predicting VA/SCD at 5 years. Calibration plots showed a mean prediction error of 1.2%. The model was effectively validated by using out-of-sample cross-validation according to country. CONCLUSIONS: This multicenter study identified 4 risk factors for VA/SCD in a primary prevention BrS population. A risk score model was generated to quantify risk of VA/SCD in BrS and inform implantable cardioverter-defibrillator prescription

    Molecular definition of group 1 innate lymphoid cells in the mouse uterus

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    Determining the function of uterine lymphocytes is challenging because of the rapidly changing nature of the organ in response to sex hormones and, during pregnancy, to the invading fetal trophoblast cells. Here we provide the first genome-wide transcriptome atlas of mouse uterine group 1 innate lymphoid cells (g1 ILCs) at mid-gestation. The composition of g1 ILCs fluctuates throughout reproductive life, with Eomes-veCD49a+ ILC1s dominating before puberty and specifically expanding in second pregnancies, when the expression of CXCR6, a marker of memory cells, is upregulated. Tissue-resident Eomes+CD49a+ NK cells (trNK), which resemble human uterine NK cells, are most abundant during early pregnancy, and showcase gene signatures of responsiveness to TGF-β, connections with trophoblast, epithelial, endothelial and smooth muscle cells, leucocytes, as well as extracellular matrix. Unexpectedly, trNK cells express genes involved in anaerobic glycolysis, lipid metabolism, iron transport, protein ubiquitination, and recognition of microbial molecular patterns. Conventional NK cells expand late in gestation and may engage in crosstalk with trNK cells involving IL-18 and IFN-γ. These results identify trNK cells as the cellular hub of uterine g1 ILCs at mid-gestation and mark CXCR6+ ILC1s as potential memory cells of pregnancy.This work was funded by a Wellcome Trust Investigator Award 200841/Z/16/Z, the Centre for Trophoblast Research (CTR), and the Cambridge NIHR BRC Cell Phenotyping Hub to FC, the Associazione Italiana Ricerca per la Ricerca sul Cancro (AIRC) - Special Project 5x1000 no. 9962, AIRC IG 2017 Id.19920 and AIRC 2014 Id. 15283 to LM, and Ministero della Salute RF-2013, GR-2013-02356568 to PV. IF was funded by a CTR PhD fellowship

    Escucha México, Estrategias Gráficas y Cultura Auditiva. Otoño 2022

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    Este reporte del PAP Escucha México, perteneciente al trabajo realizado durante el periodo de Otoño 2022, cuenta con información detallada sobre los resultados alcanzados en cada uno de los proyectos que integran esta organización en el período anteriormente establecido. Para este proceso en específico, se buscó enfocar la mayor cantidad de esfuerzos posibles a que el 4to Encuentro Internacional de Cultura Auditiva se desarrollara de la mejor forma posible, sin descuidar el trabajo que se siguió realizando en el resto de proyectos. Como resumen general, todos presentaron resultados positivos, pues se tuvo presencia importante en redes sociales, mejor que en periodos anteriores, además de que se combinaron esfuerzos para que el 4to Encuentro tuviera una difusión adecuada y alcanzara a la mayor cantidad de personas posibles, lo que a su vez resultó en eventos llenos de gente interesada en aprender sobre Cultura Auditiva y Discapacidad, ejes temáticos centrales de este PAP.ITESO, A.C

    Clonal heterogeneity and rates of specific chromosome gains are risk predictors in childhood high-hyperdiploid B-cell acute lymphoblastic leukemia

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    B-cell acute lymphoblastic leukemia (B-ALL) is the commonest childhood cancer. High hyperdiploidy (HHD) identifies the most frequent cytogenetic subgroup in childhood B-ALL. Although hyperdiploidy represents an important prognostic factor in childhood B-ALL, the specific chromosome gains with prognostic value in HHD-B-ALL remain controversial, and the current knowledge about the hierarchy of chromosome gains, clonal heterogeneity and chromosomal instability in HHD-B-ALL remains very limited. We applied automated sequential-iFISH coupled with single-cell computational modeling to identify the specific chromosomal gains of the eight typically gained chromosomes in a large cohort of 72 primary diagnostic (DX, n = 62) and matched relapse (REL, n = 10) samples from HHD-B-ALL patients with either favorable or unfavorable clinical outcome in order to characterize the clonal heterogeneity, specific chromosome gains and clonal evolution. Our data show a high degree of clonal heterogeneity and a hierarchical order of chromosome gains in DX samples of HHD-B-ALL. The rates of specific chromosome gains and clonal heterogeneity found in DX samples differ between HHD-B-ALL patients with favorable or unfavorable clinical outcome. In fact, our comprehensive analyses at DX using a computationally defined risk predictor revealed low levels of trisomies +18+10 and low levels of clonal heterogeneity as robust relapse risk factors in minimal residual disease (MRD)-negative childhood HHD-B-ALL patients: relapse-free survival beyond 5 years: 22.1% versus 87.9%, P < 0.0001 and 33.3% versus 80%, P < 0.0001, respectively. Moreover, longitudinal analysis of matched DX-REL HHD-B-ALL samples revealed distinct patterns of clonal evolution at relapse. Our study offers a reliable prognostic sub-stratification of pediatric MRD-negative HHD-B-ALL patients

    Epithelial-immune cell interplay in primary Sjogren syndrome salivary gland pathogenesis

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    In primary Sjogren syndrome (pSS), the function of the salivary glands is often considerably reduced. Multiple innate immune pathways are likely dysregulated in the salivary gland epithelium in pSS, including the nuclear factor-kappa B pathway, the inflammasome and interferon signalling. The ductal cells of the salivary gland in pSS are characteristically surrounded by a CD4(+) T cell-rich and B cell-rich infiltrate, implying a degree of communication between epithelial cells and immune cells. B cell infiltrates within the ducts can initiate the development of lymphoepithelial lesions, including basal ductal cell hyperplasia. Vice versa, the epithelium provides chronic activation signals to the glandular B cell fraction. This continuous stimulation might ultimately drive the development of mucosa-associated lymphoid tissue lymphoma. This Review discusses changes in the cells of the salivary gland epithelium in pSS (including acinar, ductal and progenitor cells), and the proposed interplay of these cells with environmental stimuli and the immune system. Current therapeutic options are insufficient to address both lymphocytic infiltration and salivary gland dysfunction. Successful rescue of salivary gland function in pSS will probably demand a multimodal therapeutic approach and an appreciation of the complicity of the salivary gland epithelium in the development of pSS. Salivary gland dysfunction is an important characteristic of primary Sjogren syndrome (pSS). In this Review, the authors discuss various epithelial abnormalities in pSS and the mechanisms by which epithelial cell-immune cell interactions contribute to disease development and progression
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