Diseño de perforación y voladura para mejorar el avance lineal en la Galería NW01- Nivel 2670 – Contrata Castillo Jara Teresa

La presente investigación tuvo como objetivo diseñar la perforación y voladura para mejorar el avance lineal en la galería NW01 de la contrata Castillo Jara Teresa. Esta investigación nace de la necesidad de dar solución al déficit en los metros avanzados producto de la perforación y voladura. Es por ello que se seleccionó como muestra al frente de la labor que se encuentra en la galería NW01, además se utilizó una investigación del tipo aplicativa y el diseño fue pre experimental. De la misma manera se usó a la observación y análisis documental como técnicas para el recojo de información. Por lo tanto, se obtuvo como resultado una optimización en el avance lineal del 45% y una reducción del 30% en el factor de carga. Dichos resultados han sido expuestos mediante tablas y gráficos con su respectivo análisis. Finalmente concluimos que el correcto diseño de perforación y voladura logró optimizar el avance lineal y otros parámetros producto de la perforación y voladura lo cual se vio reflejado en la reducción de costos

From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles

Titanium dioxide nanoparticles (TiO2NPs) are widely produced and used nanoparticles. Yet, TiO2NP exposure may possess toxic effects to different cells and tissues, including the brain. Recent studies significantly expanded the understanding of the molecular mechanisms underlying TiO2NP neurotoxicity implicating a number of both direct and indirect mechanisms. In view of the significant recent progress in research on TiO2NP neurotoxicity, the objective of the present study is to provide a narrative review on the molecular mechanisms involved in its neurotoxicity, with a special focus on the studies published in the last decade. The existing data demosntrate that although TiO2NP may cross blood-brain barrier and accumulate in brain, its neurotoxic effects may be mediated by systemic toxicity. In addition to neuronal damage and impaired neurogenesis, TiO2NP exposure also results in reduced neurite outgrowth and impaired neurotransmitter metabolism, especially dopamine and glutamate. TiO2NP exposure was also shown to promote α-synuclein and β-amyloid aggregation, thus increasing its toxicity. Recent findings also suggest that epigenetic effects and alterations in gut microbiota biodiversity contribute to TiO2NP neurotoxicity. Correspondingly, in vivo studies demosntrated that TiO2NPs induce a wide spectrum of adverse neurobehavioral effects, while epidemiological data are lacking. In addition, TiO2NPs were shown to promote neurotoxic effects of other toxic compounds. Here we show the contribution of a wide spectrum of molecular mechanisms to TiO2NP-induced neurotoxicity; yet, the role of TiO2NP exposure in adverse neurological outcomes in humans has yet to be fully appreciated

Neutrino Masses in the Supersymmetric Standard Model with Right-Handed Neutrinos and Spontaneous R-Parity Violation

We propose an extension of the supersymmetric standard model with right-handed neutrinos and a singlet Higgs field, and study the neutrino masses in this model. The Majorana masses for the right-handed neutrinos are generated around the supersymmetry breaking scale through the vacuum expectation value of the singlet Higgs field. This model may induce spontaneous R-parity violation via the vacuum expectation value of the right-handed sneutrino. In the case, the effective theory is similar to a bilinear R-parity violating model. There are two sources for the neutrino masses: one is this bilinear R-parity breaking effect, and the other is the ordinary seesaw effect between left- and right-handed neutrinos. Combining these two effects, the hierarchical neutrino mass pattern arises even when the neutrino Yukawa matrices are not hierarchical. We acquire appropriate masses and mixings to explain both the solar and atmospheric neutrino oscillations.Comment: 22pages, RevTeX, 3 ps figures; a reference adde

Leptogenesis and low-energy phases

In supersymmetric models, the CP asymmetry produced in the decay of the lightest right-handed neutrino, $\equiv epsilon$, can be written as a function of weak scale parameters. We introduce a way of separating epsilon into contributions from the various weak-scale phases, and study the contribution of potentially measurable neutrino phases to leptogenesis. We find that the Majorana phase phi', which could have observable effects on neutrinoless double beta decay, is important for epsilon unless there are cancellations among phases. If the phase delta can be measured at a neutrino factory, then it contributes significantly to epsilon over much of parameter space.Comment: amplified discussion, minor comments added (33 pages, 3 figures

Higgs and neutrino sector, EDM and epsilon_K in a spontaneously CP and R-parity breaking supersymmetric model

We construct an extension of the supersymmetric standard model where both CP symmetry and R-parity are spontaneously broken. We study the electroweak symmetry breaking sector of the model and find minima consistent with the experimental bounds on Higgs boson masses. Neutrino masses and mixing angles are generated through both seesaw and bilinear R-parity violation. We show that the hierarchical mass pattern is obtained, and mixings are consistent with measured values. Due to the spontaneous CP and R-parity violation, the neutrino sector is CP violating, and we calculate the corresponding phase. We further restrict the parameter space to agree with the limits on the electric dipole moment of the neutron. Finally, we study the CP violation parameter epsilon_K in the kaon system and show that we obtain results consistent with the experimental value.Comment: 13 pages, 7 figures, submitted to EPJ

Effects of R-parity Violating Couplings on CP Asymmetries in Neutral B Decays

A detailed analysis of the effects of supersymmetric models without R-parity on various CP asymmetries in neutral $B$ decays is given. We concentrate on models with Abelian horizontal symmetries that allow us to estimate the order of magnitude of the new effects. We focus on channels where the Standard Model gives clean predictions: $B_{d}\to\psi K_{S}$ and $B_{d}\to\phi K_{S}$. The two asymmetries can have a value different from $\sin2\beta.$ Moreover, they can be different from each other.Comment: 16 pages, LaTeX, minor typos corrected. Final version accepted for publication in Phys.Rev.

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570