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Background: Online assessments are the need of the hour during the prevailing pandemic situation to continue the educational activities and at the same time ensuring the safety of the students and faculty. All Higher Educational Institutions must take the necessary steps to design an effective assessment model to assess the various levels of student competency. Here, we analyzed the responses of the students after the conduct of the online practical assessment (OPrA) in Biochemistry.Methods: The blueprint of the OPrA was prepared by the faculty referring to the various levels and domains of Bloom’s taxonomy. Four components were chosen for the online assessment: digital spotters, enumerating the steps of objective structured practical examination, interpretation of quantitative estimation, and case discussion. Detailed instruction was provided to the students and the breakout room option in the Zoom platform was chosen for assessment. About 12-13 students were assessed by each faculty in separate breakout rooms over 15-20 minutes on all four components. Feedback on the conduct of the examination was collected from the students and faculty anonymously and analyzed. Results: Among 200 students who submitted their responses, 20% of them had previous experience of attending the OPrA. They differed in their opinion from the rest of the students on five aspects; time allotted for the assessment (P-value=0.02, χ2=5.07), students using unfair means during the online viva (P-value=0.02, χ2=5.57), their computing skills (P-value=0.001, χ2=19.82), their performance (P-value=0.001, χ2=8.84), and overall conduct of the examination (P-value=0.001, χ2=15.55). Conclusion: OPrA tools may be designed referring to Bloom’s taxonomy and prior exposure to the online tools may be beneficial for the students.

Simple Summary Aim of this review is to provide an overview on (a) Fructosamine-3-Kinase (FN3K) and its role in regulating Nuclear Factor Erythorid-2-Related Factor-2 (Nrf2); (b) the role of glycation and deglycation mechanisms in modulating the functional properties of proteins, in particular, the Nrf2; (c) the dual role of Nrf2 in the prevention and treatment of cancers. Since controlling the glycation of Nrf2 is one of the key mechanisms determining the fate of a cell; whether to get transformed into a cancerous one or to stay as a normal one, it is important to regulate Nrf2 and deglycating FN3K using pharmacological agents. Inhibitors of FN3K are being explored currently to modulate Nrf2 activity thereby control the cancers. Abstract Glycated stress is mediated by the advanced glycation end products (AGE) and the binding of AGEs to the receptors for advanced glycation end products (RAGEs) in cancer cells. RAGEs are involved in mediating tumorigenesis of multiple cancers through the modulation of several downstream signaling cascades. Glycated stress modulates various signaling pathways that include p38 mitogen-activated protein kinase (p38 MAPK), nuclear factor kappa–B (NF-κB), tumor necrosis factor (TNF)-α, etc., which further foster the uncontrolled proliferation, growth, metastasis, angiogenesis, drug resistance, and evasion of apoptosis in several cancers. In this review, a balanced overview on the role of glycation and deglycation in modulating several signaling cascades that are involved in the progression of cancers was discussed. Further, we have highlighted the functional role of deglycating enzyme fructosamine-3-kinase (FN3K) on Nrf2-driven cancers. The activity of FN3K is attributed to its ability to deglycate Nrf2, a master regulator of oxidative stress in cells. FN3K is a unique protein that mediates deglycation by phosphorylating basic amino acids lysine and arginine in various proteins such as Nrf2. Deglycated Nrf2 is stable and binds to small musculoaponeurotic fibrosarcoma (sMAF) proteins, thereby activating cellular antioxidant mechanisms to protect cells from oxidative stress. This cellular protection offered by Nrf2 activation, in one way, prevents the transformation of a normal cell into a cancer cell; however, in the other way, it helps a cancer cell not only to survive under hypoxic conditions but also, to stay protected from various chemo- and radio-therapeutic treatments. Therefore, the activation of Nrf2 is similar to a double-edged sword and, if not controlled properly, can lead to the development of many solid tumors. Hence, there is a need to develop novel small molecule modulators/phytochemicals that can regulate FN3K activity, thereby maintaining Nrf2 in a controlled activation state.