False in Name Only-Gastroduodenal Artery Pseudoaneurysm in a Recurrently Bleeding Patient: Case Report and Literature Review.

Although the diagnosis of visceral pseudoaneurysm is unusual, it requires emergent attention due to the risk of rupture. We describe a 70-year-old man with a gastroduodenal artery pseudoaneurysm that manifested as recurrent hemorrhage. We highlight the possible etiologies, clinical presentations, diagnostic tools, and treatment options for this condition. In this instance, the patient was successfully treated by selective angioembolization. A visceral pseudoaneurysm should be considered in patients with abdominal pain and GI hemorrhage. At present, angioembolization is a first-line therapy.

Cleavage of pro-tumor necrosis factor alpha by ADAM metallopeptidase domain 17: a fluorescence-based protease assay cleaves its natural protein substrate.

A fluorescence-based Adam 17 activity assay that cleaves pro-tumor necrosis factor alpha (pro-TNFα) protein substrate has been developed. The key to the assay was site-specific labeling of a fluorescence dye to the N-terminal end of the substrate protein, which was achieved by the protein ligation method. The protease cleavage reaction was monitored by fluorescence polarization. This homogeneous assay allows reaction progress to be recorded kinetically in real time. The results were validated by gel electrophoresis and high-performance liquid chromatography. As expected, the reaction could be inhibited by an ADAM metallopeptidase domain 17 (Adam 17) active site inhibitor. Interestingly, the reaction rate of pro-TNFα cleavage by Adam 17 was also reduced by a small molecule binding to pro-TNFα protein, the substrate of the reaction. This small molecule, however, did not affect the activity of Adam 17 to its peptide substrate. These results demonstrate that this natural protein substrate-based fluorescent assay was able to identify the inhibitor binding to substrate protein in addition to that binding to the protease itself. Comparing this protein substrate with a short peptide substrate, the activity of Adam 17 showed different pH profiles. With pro-TNFα the optimal pH was approximately 7.4, whereas with the peptide substrate the optimal pH was higher than 9.0.

Nitrogen dioxide pollution increases vulnerability to COVID-19 through altered immune function.

Previous ecological studies suggest the existence of possible interplays between the exposure to air pollutants and SARS-CoV-2 infection. Confirmations at individual level, however, are lacking. To explore the relationships between previous exposure to particulate matter < 10 µm (PM10) and nitrogen dioxide (NO2), the clinical outcome following hospital admittance, and lymphocyte subsets in COVID-19 patients with pneumonia. In 147 geocoded patients, we assessed the individual exposure to PM10 and NO2 in the 2 weeks before hospital admittance. We divided subjects according to the clinical outcome (i.e., discharge at home vs in-hospital death), and explored the lymphocyte-related immune function as an index possibly affecting individual vulnerability to the infection. As compared with discharged subjects, patients who underwent in-hospital death presented neutrophilia, lymphopenia, lower number of T CD45, CD3, CD4, CD16/56 + CD3 + , and B CD19 + cells, and higher previous exposure to NO2, but not PM10. Age and previous NO2 exposure were independent predictors for mortality. NO2 concentrations were also negatively related with the number of CD45, CD3, and CD4 cells. Previous NO2 exposure is a co-factor independently affecting the mortality risk in infected individuals, through negative immune effects. Lymphopenia and altered lymphocyte subsets might precede viral infection due to nonmodifiable (i.e., age) and external (i.e., air pollution) factors. Thus, decreasing the burden of air pollutants should be a valuable primary prevention measure to reduce individual susceptibility to SARS-CoV-2 infection and mortality.

Abstractive chemisorption of O2 on Al(111).

We present experimental evidence that abstraction is a common mechanism (approximately 50%) in the dissociative chemisorption of oxygen on Al(111) at a translational energy of 0.5 eV. As a result of this mechanism, individual isolated O-atoms are observed in scanning tunneling microscopy (STM). At this translational energy ordinary dissociative chemisorption processes also occur, resulting in pairs of adatoms. The ejected O-atoms originating from the abstraction reaction are detected in the gas phase using laser spectrometry. Together, these observations provide compelling evidence for the abstraction mechanism.

Oxygen abstraction from dioxygen on the Al(111) surface.

Abstractive chemisorption in the initial oxidation of Al(111) has been experimentally verified using variable incident energy O2. Scanning tunneling microscopy images show a transition between single O-adatom reaction products to more pairs of O-adatom reaction products as the O2 incident energy is raised from 0.025 to 0.8 eV. The ejected O atoms have been detected in the gas phase with resonant enhanced multiphoton ionization. The observations that both abstractive and dissociative chemisorption are activated processes are in contrast to current adiabatic models of the absorption process.