Numerical modeling of the filament-assisted diamond growth environment

A numerical model of the filament-assisted diamond growth environment has been developed and used to calculate temperature, velocity, and species concentration profiles, accounting both for transport and detailed chemical kinetics. The computed hydrocarbon concentrations agree well with previously measured values, when allowance is made for 3D effects not included in our model. Upper-bound, diffusion-limited film growth rates for various assumed growth species have been computed, and it has been found no hydrocarbon species other than CH3, C2H2, or CH4 can account for measured diamond growth rates. The effect of thermal diffusion on H-atom profiles has been examined, and found to be only 10%. Although the environment is far from thermodynamic equilibrium, several reactions are close to partial equilibrium throughout the region from the filament to the substrate. It is also shown that homogeneous H-atom recombination is too slow to explain the experimentally observed decrease in the concentration of H with increasing initial methane concentration

Pressure effects on the transition temperature and the magnetic field penetration depth in the pyrochlore superconductor RbOs_2O_6

We report magnetization measurements under high hydrostatic pressure in the newly discovered pyrochlore superconductor RbOs_2O_6 (T_c\simeq6.3K at p=0). A pronounced and {\it positive} pressure effect (PE) on T_c with dT_c/dp =0.090(1)K/kbar was observed, whereas no PE on the magnetic penetration depth \lambda was detected. The relative pressure shift of T_c [ dlnT_c/dp \simeq 1.5%/kbar] is comparable with the highest values obtained for highly underdoped high-temperature cuprate superconductors. Our results suggest that RbOs_2O_6 is an adiabatic BCS-type superconductor.Comment: 11 pages, 4 figure

SU(3) Mixing for Excited Mesons

The SU(3)-flavor symmetry breaking and the quark-antiquark annihilation mechanism are taken into account for describing the singlet-octet mixing for several nonets assigned by Particle Data Group(PDG). This task is approached with the mass matrix formalism

Adenosine mediates functional and metabolic suppression of peripheral and tumor-infiltrating CD8⁺ T cells.

Several mechanisms are present in the tumor microenvironment (TME) to impair cytotoxic T cell responses potentially able to control tumor growth. Among these, the accumulation of adenosine (Ado) contributes to tumor progression and represents a promising immunotherapeutic target. Ado has been shown to impair T cell effector function, but the role and mechanisms employed by Ado/Ado receptors (AdoRs) in modulating human peripheral and tumor-infiltrating lymphocyte (TIL) function are still puzzling. CD8 <sup>+</sup> T cell cytokine production following stimulation was quantified by intracellular staining and flow cytometry. The cytotoxic capacity of tumor infiltrating lymphocytes (TILs) was quantified by the chromium release assay following co-culture with autologous or anti-CD3-loaded tumor cell lines. The CD8 <sup>+</sup> T cell metabolic fitness was evaluated by the seahorse assay and by the quantification of 2-NBDG uptake and CD71/CD98 upregulation upon stimulation. The expression of AdoRs was assessed by RNA flow cytometry, a recently developed technology that we validated by semiquantitative RT-PCR (qRT-PCR), while the impact on T cell function was evaluated by the use of selective antagonists and agonists. The influence of Ado/AdoR on the PKA and mTOR pathways was evaluated by phosphoflow staining of p-CREB and p-S6, respectively, and validated by western blot. Here, we demonstrate that Ado signaling through the A2A receptor (A2AR) in human peripheral CD8 <sup>+</sup> T cells and TILs is responsible for the higher sensitivity to Ado-mediated suppression of T central memory cells. We confirmed that Ado is able to impair peripheral and tumor-expanded T cell effector functions, and we show for the first time its impact on metabolic fitness. The Ado-mediated immunosuppressive effects are mediated by increased PKA activation that results in impairment of the mTORC1 pathway. Our findings unveil A2AR/PKA/mTORC1 as the main Ado signaling pathway impairing the immune competence of peripheral T cells and TILs. Thus, p-CREB and p-S6 may represent useful pharmacodynamic and efficacy biomarkers of immunotherapies targeting Ado. The effect of Ado on T cell metabolic fitness reinforces the importance of the adenosinergic pathway as a target for next-generation immunotherapy

Intestinal function and transit associate with gut microbiota dysbiosis in cystic fibrosis

Background: Most people with cystic fibrosis (pwCF) suffer from gastrointestinal symptoms and are at risk of gut complications. Gut microbiota dysbiosis is apparent within the CF population across all age groups, with evidence linking dysbiosis to intestinal inflammation and other markers of health. This pilot study aimed to investigate the potential relationships between the gut microbiota and gastrointestinal physiology, transit, and health. Study design: Faecal samples from 10 pwCF and matched controls were subject to 16S rRNA sequencing. Results were combined with clinical metadata and MRI metrics of gut function to investigate relationships. Results: pwCF had significantly reduced microbiota diversity compared to controls. Microbiota compositions were significantly different, suggesting remodelling of core and rarer satellite taxa in CF. Dissimilarity between groups was driven by a variety of taxa, including Escherichia coli, Bacteroides spp., Clostridium spp., and Faecalibacterium prausnitzii. The core taxa were explained primarily by CF disease, whilst the satellite taxa were associated with pulmonary antibiotic usage, CF disease, and gut function metrics. Species-specific ordination biplots revealed relationships between taxa and the clinical or MRI-based variables observed. Conclusions: Alterations in gut function and transit resultant of CF disease are associated with the gut microbiota composition, notably the satellite taxa. Delayed transit in the small intestine might allow for the expansion of satellite taxa resulting in potential downstream consequences for core community function in the colon