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Control of phase formation of (AlxGa1 - X)2O3thin films on c-plane Al2O3

In this paper, the growth of orthorhombic and monoclinic (Al x Ga1 - x )2O3 thin films on (00.1) Al2O3 by tin-assisted pulsed laser deposition is investigated as a function of oxygen pressure p(O2) and substrate temperature Tg. For certain growth conditions, defined by Tg = 580°C and p(O2) = 0.016 mbar, the orthorhombic ?-polymorph is stabilized. For Tg = 540°C and p(O2) = 0.016 mbar, the ?-, and the ß-, as well as the spinel ?-polymorph coexist, as illustrated by XRD 2?-?-scans. Further employed growth parameters result in thin films with a monoclinic ß-gallia structure. For all polymorphs, p(O2) and Tg affect the formation and desorption of volatile suboxides, and thereby the growth rate and the cation composition. For example, low oxygen pressures lead to low growth rates and enhanced Al incorporation. This facilitates the structural engineering of polymorphic, ternary (Al,Ga)2O3 via selection of the relevant process parameters. Transmission electron microscopy (TEM) studies of a ? - (Al0.13Ga0.87)2O3 thin film reveal a more complex picture compared to that derived from x-ray diffraction measurements. Furthermore, this study presents the possibility of controlling the phase formation, as well as the Al-content, of thin films based on the choice of their growth conditions. © 2020 The Author(s). Published by IOP Publishing Ltd

Airborne cultivable microflora and microbial transfer in farm buildings and rural dwellings

Exposure to environments rich in microorganisms such as farms has been shown to protect against the development of childhood asthma and allergies. However, it remains unclear where, and how, farm and other rural children are exposed to microbes. Furthermore, the composition of the microbial flora is poorly characterised. We tested the hypothesis that farm children are exposed indoors to substantial levels of viable microbes originating from animal sheds and barns. We also expected that environmental microbial flora on farms and in farm homes would be more complex than in the homes of rural control children

Dissecting the role of the gut microbiome and fecal microbiota transplantation in radio- and immunotherapy treatment of colorectal cancer

Colorectal cancer (CRC) is one of the most commonly diagnosed cancers and poses a major burden on the human health worldwide. At the moment, treatment of CRC consists of surgery in combination with (neo)adjuvant chemotherapy and/or radiotherapy. More recently, immune checkpoint blockers (ICBs) have also been approved for CRC treatment. In addition, recent studies have shown that radiotherapy and ICBs act synergistically, with radiotherapy stimulating the immune system that is activated by ICBs. However, both treatments are also associated with severe toxicity and efficacy issues, which can lead to temporary or permanent discontinuation of these treatment programs. There's growing evidence pointing to the gut microbiome playing a role in these issues. Some microorganisms seem to contribute to radiotherapy-associated toxicity and hinder ICB efficacy, while others seem to reduce radiotherapy-associated toxicity or enhance ICB efficacy. Consequently, fecal microbiota transplantation (FMT) has been applied to reduce radio- and immunotherapy-related toxicity and enhance their efficacies. Here, we have reviewed the currently available preclinical and clinical data in CRC treatment, with a focus on how the gut microbiome influences radio- and immunotherapy toxicity and efficacy and if these treatments could benefit from FMT

Cigarette smoke extract induced exosome release is mediated by depletion of exofacial thiols and can be inhibited by thiol-antioxidants

Introduction: Airway epithelial cells have been described to release extracellular vesicles (EVs) with pathological properties when exposed to cigarette smoke extract (CSE). As CSE causes oxidative stress, we investigated whether its oxidative components are responsible for inducing EV release and whether this could be prevented using the thiol antioxidants N-acetyl-L-cysteine (NAC) or glutathione (GSH). Methods: BEAS-2B cells were exposed for 24 h to CSE, H2O2, acrolein, 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB), bacitracin, rutin or the anti-protein disulfide isomerase (PDI) antibody clone RL90; with or without NAC or GSH. EVs in media were measured using CD63(+)CD81(+) bead-coupled flow cytometry or tunable resistive pulse sensing (TRPS). For characterization by Western Blotting, cryo-transmission electron microscopy and TRPS, EVs were isolated using ultracentrifugation. Glutathione disulfide and GSH in cells were assessed by a GSH reductase cycling assay, and exofacial thiols using Flow cytometry. Results: CSE augmented the release of the EV subtype exosomes, which could be prevented by scavenging thiol-reactive components using NAC or GSH. Among thiol-reactive CSE components, H2O2 had no effect on exosome release, whereas acrolein imitated the NAC-reversible exosome induction. The exosome induction by CSE and acrolein was paralleled by depletion of cell surface thiols. Membrane impermeable thiol blocking agents, but not specific inhibitors of the exofacially located thiol-dependent enzyme PDI, stimulated exosome release. Summary/conclusion: Thiol-reactive compounds like acrolein account for CSE-induced exosome release by reacting with cell surface thiols. As acrolein is produced endogenously during inflammation, it may influence exosome release not only in smokers, but also in ex-smokers with chronic obstructive pulmonary disease. NAC and GSH prevent acrolein-and CSE-induced exosome release, which may contribute to the clinical benefits of NAC treatment

Circulating desmosine levels do not predict emphysema progression but are associated with cardiovascular risk and mortality in COPD.

Elastin degradation is a key feature of emphysema and may have a role in the pathogenesis of atherosclerosis associated with chronic obstructive pulmonary disease (COPD). Circulating desmosine is a specific biomarker of elastin degradation. We investigated the association between plasma desmosine (pDES) and emphysema severity/progression, coronary artery calcium score (CACS) and mortality. pDES was measured in 1177 COPD patients and 110 healthy control subjects from two independent cohorts. Emphysema was assessed on chest computed tomography scans. Aortic arterial stiffness was measured as the aortic-femoral pulse wave velocity. pDES was elevated in patients with cardiovascular disease (p<0.005) and correlated with age (rho=0.39, p<0.0005), CACS (rho=0.19, p<0.0005) modified Medical Research Council dyspnoea score (rho=0.15, p<0.0005), 6-min walking distance (rho=−0.17, p<0.0005) and body mass index, airflow obstruction, dyspnoea, exercise capacity index (rho=0.10, p<0.01), but not with emphysema, emphysema progression or forced expiratory volume in 1 s decline. pDES predicted all-cause mortality independently of several confounding factors (p<0.005). In an independent cohort of 186 patients with COPD and 110 control subjects, pDES levels were higher in COPD patients with cardiovascular disease and correlated with arterial stiffness (p<0.05). In COPD, excess elastin degradation relates to cardiovascular comorbidities, atherosclerosis, arterial stiffness, systemic inflammation and mortality, but not to emphysema or emphysema progression. pDES is a good biomarker of cardiovascular risk and mortality in COPD

Circulating desmosine levels do not predict emphysema progression but are associated with cardiovascular risk and mortality in COPD

Elastin degradation is a key feature of emphysema and may have a role in the pathogenesis of atherosclerosis associated with chronic obstructive pulmonary disease (COPD). Circulating desmosine is a specific biomarker of elastin degradation. We investigated the association between plasma desmosine (pDES) and emphysema severity/progression, coronary artery calcium score (CACS) and mortality. pDES was measured in 1177 COPD patients and 110 healthy control subjects from two independent cohorts. Emphysema was assessed on chest computed tomography scans. Aortic arterial stiffness was measured as the aortic–femoral pulse wave velocity. pDES was elevated in patients with cardiovascular disease (p&lt;0.005) and correlated with age (rho=0.39, p&lt;0.0005), CACS (rho=0.19, p&lt;0.0005) modified Medical Research Council dyspnoea score (rho=0.15, p&lt;0.0005), 6-min walking distance (rho=−0.17, p&lt;0.0005) and body mass index, airflow obstruction, dyspnoea, exercise capacity index (rho=0.10, p&lt;0.01), but not with emphysema, emphysema progression or forced expiratory volume in 1 s decline. pDES predicted all-cause mortality independently of several confounding factors (p&lt;0.005). In an independent cohort of 186 patients with COPD and 110 control subjects, pDES levels were higher in COPD patients with cardiovascular disease and correlated with arterial stiffness (p&lt;0.05). In COPD, excess elastin degradation relates to cardiovascular comorbidities, atherosclerosis, arterial stiffness, systemic inflammation and mortality, but not to emphysema or emphysema progression. pDES is a good biomarker of cardiovascular risk and mortality in COPD.Elastin degradation is a hallmark of emphysema and may have a role in the pathogenesis of atherosclerosis with COPD http://ow.ly/Y9Gs

Publisher Correction:Voices of biotech leaders (Nature Biotechnology, (2021), 39, 6, (654-660), 10.1038/s41587-021-00941-4)

In the version of this article initially published, an author name was given as Abasi Ene Abong. The correct name is Abasi Ene-Obong. Also, the affiliation for Sebastian Giwa was given as Elevian, Pagliuca Harvard Life Lab, Allston, MA, USA. The correct affiliations are Biostasis Research Institute, Berkeley, CA, USA; Sylvatica Biotech, North Charleston, SC, USA; and Humanity Bio, Kensington, CA, USA. An affiliation for Jeantine Lunshof was given as Department of Genetics, Harvard Medical School, Boston, MA, USA. The correct affiliation is Wyss Institute for Biological Engineering, Harvard University, Boston, MA, USA. The errors have been corrected in the PDF and HTML versions of the article

Voices of biotech leaders

Nature Biotechnology asks a selection of leaders from across biotech to look at the future of the sector and make some predictions for the coming years

Voices of biotech leaders

Nature Biotechnology asks a selection of leaders from across biotech to look at the future of the sector and make some predictions for the coming years.</p