Remote Learning of COVID-19 Kinetic Analysis in a Physical Chemistry Laboratory Class.

The COVID-19 pandemic has affected many in-person laboratory courses across the world. The viral spreading model is complicated but parameters, such as its reproduction number, R t, can be estimated with the susceptible, infectious, or recovered model. COVID-19 data for many states and countries are widely available online. This provides an opportunity for the students to analyze its spreading kinetics remotely. Here, we reported a laboratory set up online during the third week of the spring semester of 2021 to minimize social contacts. Due to the wide interest in developing online physical chemistry and analytical laboratories during the pandemic, we would like to share this laboratory design. The method, technique, procedure, and grading are described in this report. The student participants were able to apply the kinetic techniques learned in physical chemistry to successfully analyze an ongoing real-world problem through a remote learning environment and prepare this report.

A neuronal model of Alzheimer's disease: an insight into the mechanisms of oxidative stress-mediated mitochondrial injury.

Alzheimer's disease (AD) is associated with beta-amyloid accumulation, oxidative stress and mitochondrial dysfunction. However, the effects of genetic mutation of AD on oxidative status and mitochondrial manganese superoxide dismutase (MnSOD) production during neuronal development are unclear. To investigate the consequences of genetic mutation of AD on oxidative damages and production of MnSOD during neuronal development, we used primary neurons from new born wild-type (WT/WT) and amyloid precursor protein (APP) (NLh/NLh) and presenilin 1 (PS1) (P264L) knock-in mice (APP/PS1) which incorporated humanized mutations in the genome. Increasing levels of oxidative damages, including protein carbonyl, 4-hydroxynonenal (4-HNE) and 3-nitrotyrosine (3-NT), were accompanied by a reduction in mitochondrial membrane potential in both developing and mature APP/PS1 neurons compared with WT/WT neurons suggesting mitochondrial dysfunction under oxidative stress. Interestingly, developing APP/PS1 neurons were significantly more resistant to beta-amyloid 1-42 treatment, whereas mature APP/PS1 neurons were more vulnerable than WT/WT neurons of the same age. Consistent with the protective function of MnSOD, developing APP/PS1 neurons have increased MnSOD protein and activity, indicating an adaptive response to oxidative stress in developing neurons. In contrast, mature APP/PS1 neurons exhibited lower MnSOD levels compared with mature WT/WT neurons indicating that mature APP/PS1 neurons lost the adaptive response. Moreover, mature APP/PS1 neurons had more co-localization of MnSOD with nitrotyrosine indicating a greater inhibition of MnSOD by nitrotyrosine. Overexpression of MnSOD or addition of MnTE-2-PyP(5+) (SOD mimetic) protected against beta-amyloid-induced neuronal death and improved mitochondrial respiratory function. Together, the results demonstrate that compensatory induction of MnSOD in response to an early increase in oxidative stress protects developing neurons against beta-amyloid toxicity. However, continuing development of neurons under oxidative damage conditions may suppress the expression of MnSOD and enhance cell death in mature neurons.

Inferior vena caval injury following self-inflicted abdominal stab wound.

A rare case of attempted suicidal abdominal stabbing using a shoemaker's piercing awl is reported. The patient presented with the weapon still in place. On emergency exploration, injury to the inferior vena cava and the inferior mesenteric artery were found. The case highlights the fact that major vascular injury may be present in patients of abdominal stabs with retained weapons inspite of their haemodynamic stability. It also illustrates the importance of manipulating retained weapons only after complete exposure with adequate preparation for a vascular procedure.