FTIR Study of Copper Agglomeration during Atomic Layer Deposition of Copper

The growth of of metallic copper by atomic layer deposition (ALD) using copper(I) di-sec-butylacetamidinate $([Cu(^sBu-amd)]_2)$ and molecular hydrogen $(H_2)$ on $SiO_2/Si$ surfaces has been studied. The mechanisms for the initial surface reaction and chemical bonding evolutions with each ALD cycle are inferred from in situ Fourier transform infrared spectroscopy (FTIR) data. Spectroscopic evidence for Cu agglomeration on $SiO_2$ is presented involving the intensity variations of the $SiO_2$ LO/TO phonon modes after chemical reaction with the Cu precursor and after the $H_2$ precursor cycle. These intensity variations are observed over the first 20 ALD cycles at 185°C.Chemistry and Chemical Biolog

In-situ Infrared Characterization During Atomic Layer Deposition of Lanthanum Oxide

Mechanisms of atomic layer deposition (ALD) growth of lanthanum oxide on H-terminated Si(111) using lanthanum tris(N,N′-diisopropylacetamidinate) (La(iPr-MeAMD)3) are investigated using infrared (IR) absorption spectroscopy. The reactivity of this amidinate precursor is high, with almost all surface Si−H bonds consumed after 5 ALD cycles at 300 °C. Gas phase IR spectra show that, although most of the precursor (La(iPr-MeAMD)3) remains intact, a strong feature at 1665 cm−1, characteristic of a hydrogenated and dissociated free ligand with localized electrons in the N−CN bonds, is present. Such partial precursor dissociation in the gas phase is due to hydrolysis by traces of water vapor remaining in the reactor, even after purging. As a result, some Si−O−La bonds are formed upon reaction with the surface during the first La(iPr-MeAMD)3 pulse, prior to any water pulse. During film growth, acetate/carbonate and hydroxyl impurities are incorporated into the film. Annealing to 500 °C in dry N2 removes these impurities but fosters the growth of interfacial SiO2. Deposition at 300 °C leads to decomposition of adsorbed ligands, as evidenced by the formation of cyanamide or carbodiimide vibrational bands (or both) at 1990 and 2110 cm−1, respectively. Despite this decomposition, ideal self-limited ALD growth is maintained because the decomposed ligands are removed by the subsequent water pulse. Growth of pure lanthanum oxide films is often characterized by nonuniform film thickness if purging is not complete because of reversible absorption of water by the La2O3 film. Uniform ALD growth can be maintained without a rigorous dry purge by introducing alternating trimethylaluminum (TMA)/D2O ALD cycles between La/D2O cycles.Chemistry and Chemical Biolog

FTIR study of copper agglomeration during atomic layer deposition of copper

ABSTRACT The growth of of metallic copper by atomic layer deposition (ALD) using copper(I) di-secbutylacetamidinate ([Cu

Chlorination of hydrogen-terminated silicon (111) surfaces

Infrared absorption spectroscopy was used to investigate the chlorination of hydrogen-terminated Si(111) surfaces by three different methods: (a) exposure to a saturated solution of phosphorus pentachloride (PCl5) in chlorobenzene; (b) exposure to chlorine gas, Cl2(g), and (c) exposure to Cl2(g) under UV illumination. X-ray photoelectron spectroscopy and first principles model (clusters) calculations were used to explore the structure and dynamics of these surfaces. The infrared spectra exhibited sharp chlorine-related vibrations at 586 and 527 cm^–1. The narrow full width at half maximum of these vibrations for all three preparation methods indicated that all functionalization schemes produced a nearly complete monolayer of Cl with little surface roughening or introduction of step edges. The 527 cm^–1 mode was at a much higher frequency than might be expected for the bending vibration of Si monochloride. Theoretical calculations show, however, that this vibration involves the displacement of the top Si atom parallel to the surface, subject to a relatively stiff potential, shifting its frequency to a value fairly close to that of the Si–Cl stretching mode on a Si(111) surface

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome

Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial

Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome