Flake storage effects on properties of laboratory-made flakeboards

Aspen (Populus gradidentata) and loblolly pine (Pinus taeda) flakes were prepared with tangential-grain and radial- grain faces on a laboratory disk flaker. These were gently dried in a steam-heated rotary drum dryer. Approximately 1 week after drying, surface wettability was measured on a large sample of flakes using an aqueous dye solution. Three replicate boards of each combination of flake species and face grain were then fabricated. Each of the three replicate boards was made with a different adhesive resin. The three adhesives were urea-formaldehyde, phenolic, and neat isocyanate. The procedure (wettability measurements and board fabrication) was repeated at 1 month, 6 months, and 12 months after flake preparation. Surface wettabilities were reduced as the flake surfaces aged. Tension strengths of boards perpendicular to their faces (internal bond strengths) were also reduced as flake surfaces aged, and reductions in internal bond strengths and surface wettabilities appear to be related. Bending proper- ties were, in general, not influenced by flake age. The ob- served reductions in internal bond strengths suggest that laboratory storage of flakes for much longer than 6 months is not a good practice. However, no conclusive statements can be drawn from this work concerning the influence of flake aging on board properties

Cytomegalovirus haemorrhagic enterocolitis associated with severe infection with COVID-19

We present a case of haemorrhagic enterocolitis in a patient with SARS-CoV-2 who recovered from respiratory failure after support with venovenous extracorporeal membrane oxygenation. We describe clinicopathological features consistent with the systemic coinfection/reactivation of cytomegalovirus (CMV) concurrent with COVID-19 infection and the protracted clinical course of resolution of gastrointestinal inflammation after the treatment of CMV infection. Stool PCR, abdominal CT perfusion scan and histological examination of ileal and colonic tissues excluded enterocolitis secondary to other causes of infection (common viral, bacterial and protozoal gastrointestinal pathogens), macrovascularand microvascular ischaemia and classic inflammatory bowel disease, respectively. We propose possible synergistic pathophysiologic mechanisms for enterocolitis complicating severe COVID-19 infection: (1) T lymphocyte depletion and immune response dysregulation, (2) use of immunomodulators in the management of severe COVID-19 infection and (3) high concentration of ACE-2 receptors for COVID-19 virus in the gastrointestinal tract

Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress, vagal dominance, arrhythmia and pulmonary inflammation in heart failure-prone rats

Acute exposure to ambient fine particulate matter (PM(2.5)) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiologic events precipitating these outcomes remain poorly understood but may involve inflammation, oxidative stress, arrhythmia, and autonomic nervous system imbalance. Cardiomyopathy results from cardiac injury, is the leading cause of heart failure, and can be induced in heart failure-prone rats through sub-chronic infusion of isoproterenol (ISO). To test whether cardiomyopathy confers susceptibility to inhaled PM(2.5) and can elucidate potential mechanisms, we investigated the cardiophysiologic, ventilatory, inflammatory, and oxidative effects of a single nose-only inhalation of a metal-rich PM(2.5) (580 μg/m(3), 4h) in ISO-pretreated (35 days * 1.0 mg/kg/day sc) rats. During the 5 days post-treatment, ISO-treated rats had decreased HR and BP and increased pre-ejection period (PEP, an inverse correlate of contractility) relative to saline-treated rats. Before inhalation exposure, ISO-pretreated rats had increased PR and ventricular repolarization time (QT) and heterogeneity (Tp-Te). Relative to clean air, PM(2.5) further prolonged PR-interval and decreased systolic BP during inhalation exposure; increased tidal volume, expiratory time, heart rate variability (HRV) parameters of parasympathetic tone, and atrioventricular block arrhythmias over the hours post-exposure; increased pulmonary neutrophils, macrophages, and total antioxidant status one day post-exposure; and decreased pulmonary glutathione peroxidase 8 weeks after exposure, with all effects occurring exclusively in ISO-pretreated rats but not saline-pretreated rats. Ultimately, our findings indicate that cardiomyopathy confers susceptibility to the oxidative, inflammatory, ventilatory, autonomic, and arrhythmogenic effects of acute PM(2.5) inhalation