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Abstract: Preservation of a robust circadian rhythmicity (particulsarly of the sleep/wake cycle), a proper nutrition and adequate physical exercise are key elements for healthy aging. Aging comes along with circadian alteration, e.g. a disrupted sleep and inflammation, that leads to metabolic disorders. In turn, sleep cycle disturbances cause numerous pathophysiological changes that accelerates the aging process. In the central nervous system, sleep disruption impairs several functions, among them, the clearance of waste molecules. The decrease of plasma melatonin, a molecule of unusual phylogenetic conservation present in all known aerobic organisms, plays a particular role as far as the endocrine sequels of aging. Every day, the late afternoon/nocturnal increase of melatonin synchronizes both the central circadian pacemaker located in the hypothalamic suprachiasmatic nuclei as well as myriads of peripheral cellular circadian clocks. This is called the “chronobiotic effect” of melatonin, the methoxyindole being the prototype of the endogenous family of chronobiotic agents. In addition, melatonin exerts a significant cytoprotective action by buffering free radicals and reversing inflammation via down regulation of proinflammatory cytokines, suppression of low degree inflammation and prevention of insulin resistance. Because of these properties melatonin has been advocated to be a potential therapeutic tool in COVID 19 pandemic. Melatonin administration to aged animals counteracts a significant number of senescence-related changes. In humans, melatonin is effective both as a chronobiotic and a cytoprotective agent to maintain a healthy aging. Circulating melatonin levels are consistently reduced in the metabolic syndrome, ischemic and non-ischemic cardiovascular diseases and neurodegenerative disorders like the Alzheimer's and Parkinson's diseases. The potential therapeutic value of melatonin has been suggested by a limited number of clinical trials generally employing melatonin in the 2–10 mg/day range. However, from animal studies the cytoprotective effects of melatonin need higher doses to become apparent (i.e. in the 100 mg/day range). Hence, controlled studies employing melatonin doses in this range are urgently needed.

The impact of COVID-19 on the working lives of professionals has been of much interest. Within social work, the pandemic increased workload demands, whilst the way in which work was done shifted significantly. This article uses data gathered from newly qualified social workers (NQSWs) who began their working lives during the pandemic. These first years in practice are viewed as an extension to social workers’ formal education and as a vital stage in their professional development. Survey (n = 124) and interview (n = 12) data were gathered from NQSWs across Scotland. Findings were considered through Giddens’ lens of ontological security, to explore NQSW transitions during a context of pandemic disruption and its impacts on NQSWs’ confidence and competence, as well as their sense of self and identity. Consistent with other studies, respondents were most impacted by home working and the associated isolation and separation from colleagues, particularly when engaged in emotionally charged work. Findings uncovered a trichotomy of experience, with variation in the quality and availability of some formal supports—induction, training and learning and development—and informal support. Implications for practice include a need to focus on how we support and nurture NQSWs at such a critical stage in their professional socialisation.

The COVID-19 pandemic had a profound impact on the economy, with some sectors suffering significant setbacks while others demonstrated resilience. This comprehensive dissertation analyzes the pandemic's effects on sectors, countries, investor expectations, financial support intensity, company characteristics, and stock market performance. Certain sectors, such as transportation, lodging, travel, and entertainment, experienced severe negative impacts that persisted even two years after the pandemic, resulting in declining cumulative risk-adjusted returns. Conversely, financially resilient sectors like F&B sales, electronics, and pharmaceuticals performed exceptionally well, generating cumulative riskadjusted returns ranging from 40% to 50%. Stock price reactions to resilience varied across countries. In Germany, investors responded negatively to aid announcements for more resilient companies, whereas in Greece, the reaction was positive. Except for specific countries' market value of equity and book-to-market ratio, firm-level variables had minimal impact on cumulative returns. Financial aid varied according to company characteristics. Smaller companies received more aid, while value-oriented companies received less aid compared to growth companies. Aid intensity affected profitability, cash balance, and debt. Aided firms recorded positive returns within 10-22 days of the aid announcement. The impact of financial support varied at different stages of the pandemic. Initially, higher intensity and equity support were associated with lower cumulative returns, reflecting investor pessimism. However, as the pandemic progressed, this effect reversed, suggesting an increasing recognition of the value of financial support under acute market conditions. Disclaimer: AI (Chatgpt) was used for word shortness and correctness under supervision of my advisor. Prompt conversation is available upon request. Esta dissertação analisa o impacto do apoio financeiro no desempenho do mercado de ações durante a pandemia de COVID-19. Os resultados mostram diferenças entre os setores, com os setores mais resilientes apresentando melhor desempenho. A intensidade do apoio financeiro está relacionada com as características da empresa, sendo que as empresas mais pequenas recebem mais apoio. As características das existências e os alfas da intensidade do auxílio também são examinados, destacando a influência dos fatores de mercado, dimensão e fase de crescimento nas relações observadas. A análise de curto prazo mostra retornos anormais positivos após o anúncio do suporte financeiro, com duração de 10 a 22 dias. As variáveis no nível da empresa também afetam esses retornos. Na análise de longo prazo, o suporte financeiro afeta o desempenho da empresa ao influenciar as perceções dos investidores e a importância das reservas de caixa em tempos de crise. As políticas governamentais também fortalecem a resiliência corporativa e moldam as expectativas dos investidores. O estimador de Callaway e Santana (2021) examina as tendências de pré-tratamento e o impacto da assistência financeira no valor da empresa. Os resultados mostram um efeito transitório da ajuda financeira. O trabalho contribui para o entendimento da dinâmica entre assistência financeira, resiliência empresarial e resultados de mercado durante a pandemia de COVID-19.

Podcast theme: Student ExperienceTheme episode: 6Contributors:- Sean Dynes, School of Pharmacy, Queen's University Belfast- Matthew Taylor, School of Pharmacy, Queen's University Belfast- Dr Dan Corbett, School of Pharmacy, Queen's University BelfastSummary:In this special episode of PharmaCast, we're joined by two of our MPharm Class of 2023, Sean Dynes and Matthew Taylor, who in addition to receiving their MPharm degrees this summer, have also contributed to their degree programme in a range of ways, academically and socially. In this episode of the podcast, you'll hear about the experience that Sean and Matthew have had during their time on the course, from the challenges of COVID-19 to how the course has helped them as they embark on their careers in Pharmacy.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has emerged as a serious threat to human health worldwide. The effective disinfection of surfaces contaminated with SARS-CoV-2 may help prevent its spread. The aim of this study is to determine the duration required for viral RNA elimination by 222 nm far ultraviolet light using RT-qPCR as a tool. This study investigated the effect of 222 nm UVC irradiation on SARS-CoV-2 RNA in an in vitro experiment. The results showed that the copy number of SARS-CoV-2 RNA did not change even after 300 s of 222 nm UVC irradiation at 0.1 mW/cm2, but extending the exposure to more than 600 s reduced the number of copies of SARS-CoV-2 virus significantly. However, to fully validate the results and enhance the robustness of the findings, it is crucial to increase the number of samples analyzed in future experiments.

One approach to verifying the quality of research data obtained from EHRs is auditing how complete and correct the data are in comparison with those collected by manual and controlled methods. This study analyzed data quality of an EHR-derived dataset for COVID-19 research, obtained during the pandemic at Hospital Universitario 12 de Octubre. Data were extracted from EHRs and a manually collected research database, and then transformed into the ISARIC-WHO COVID-19 CRF model. Subsequently, a data analysis was performed, comparing both sources through this convergence model. More concepts and records were obtained from EHRs, and PPV (95% CI) was above 85% in most sections. In future studies, a more detailed analysis of data quality will be carried out.

While the shock of Covid-19 has generated draconian containment policies in virtually all countries to limit the spread of the pandemic, it also brought a plethora of trade and investment policy responses that were broadly aimed at limiting cross-border commercial ties. This essay shed lights on the drivers of trade policy responses of European Free Trade Area (EFTA) members in the wake of Covid-19. I propose that while EFTA Members’ behavior by and large followed that of the European Union and its member states, Switzerland instead resorted to trade liberalizing policies. Switzerland’s reliance on imports led to supply difficulties, which was unusually affected by tourism shopping. The mobility limitations that restricted Swiss residents’ ability to buy products across the border translated into a disproportionately higher demand in the face of relatively low supply. In turn, Swiss producers requested trade barriers to be lowered and the government responded to their request. This episode highlights the importance of linkages between mobility and trade policy – showcasing how restrictions along borders can have unintended effects that ultimately shape trade policy. ISSN:1758-5880 ISSN:1758-5899

Contains recoded data for more than 25 millions of Covid-19 patients, originally published by the Mexican Government (Datos Covid19 México) between January 2020 and March 2023. A set of 26 selected variables for a total of 25,820,354 patients were recoded into an R binary file (File "come5.RData" which contains the data.frame "come5"). Names and other characteristics of the 26 variables can be seen in the R data.frame "vars.come5", which can be uploaded from the R file "vars.come5.RData". This upload also contains an R package named "CovidAssociations", which allows data mining of associations between pairs of variables in the cohort. Briefly, there are 3,899 results from different pairs of variables in 25 different sets of patients. Files and their use "CovidAssociations_1.0.tar.gz" - This file contains the R package CovidAssociations. After downloading that file to your working directory, you can install it by typing in the R command window install.packages("CovidAssociations_1.0.tar.gz", repos = NULL, type="source") After that type library(CovidAssociations) to make the package available. "CovidAssociations-manual.pdf" - Contains the PDF version of the package manual. "CovidAssocTutorial.pdf" - Contains the PDF version of a tutorial for the package. 4. "come5.RData" - This contains the data.frame with the recoded data. It is not necessary for the CovidAssociations package, but it is included if you want to perform further analyses. Having that file in your working directory you can load it and see some of their characteristics of the data.frame by typing in your R command window: load("come5.RData") # Loads the "come5" data.frame class(come5) # class (will be data.frame) dim(come5) # Number of rows (patients) and columns (variables) names(come5) # Names of the variables. 5. "vars.come5.RData" - Contains characteristics of the variables in the data.frame "come5". Having that file in your working directory you can load it and see some of their characteristics of the data frame by typing in your R command window: load("vars.come5.RData") # Loads the "vars.come5" data.frame class(vars.come5) # class (will be data.frame) dim(vars.come5) # Number of rows (patients) and columns (variables) names(vars.come5) # Names of the variables. head(vars.come5, 2) # Show the first two rows. table(vars.come5$v.class) # Classes of variables table(vars.come5$v.category) # Categories of variables Note: I am preparing for submission a manuscript entitled "Associations between variables in a cohort of Mexican Covid-19 patients". As soon as this MS is submitted, I will add the reference here. ABSTRACT FOR THE MANUSCRIPT TO BE SUBMITTED Background: Here we analyze a vast cohort comprising over 25 million COVID-19 patients collected by the Mexican Government between 2020 and 2023. The dataset contains valuable information on attributes and comorbidities, enabling us to investigate clinically relevant associations. Objective: Our objective is to unravel the intricate network of relationships between variables within the entire cohort and specific patient subsets, with a particular focus on associations involving fatalities. Methods: We employ the Odds Ratio (OR), estimated from Fisher’s test on 2×2 contingency tables, as a measure of association between variable pairs. We compute a total of 3,899 such measures by examining all possible variable pairs within 25 patient groups. The results are ordered and presented as networks, where variables are depicted as nodes (vertices) and associations at a specific OR threshold are represented as links (edges). The recoded data, along with the results and data mining functions, are publicly accessible. Results: Our findings demonstrate that hospitalization, gender, and age significantly influence disease outcomes, as do comorbidities such as pneumonia, chronic renal problems, diabetes, and hypertension. Interestingly, we observe that the associations of comorbidities are diminished in pregnant women, suggesting a pro- tective effect of pregnancy against the detrimental impact of these comorbidities on COVID-19 patients. Conclusion: Our analysis of variables in Mexican COVID-19 patients reveals a complex network of as- sociations. By visualizing these associations as networks, we provide a clear and accessible representation that enhances our understanding of the factors contributing to fatalities in this population.

Podcast theme: ResearchTheme episode: 3Contributors:- Professor Jenny McKinley, School of Natural and Built Environment, Queen's University Belfast- Professor John McGrath, School of Biological Sciences, Queen's University Belfast- Dr Deirdre Gilpin, School of Pharmacy, Queen's University Belfast- Dr Dan Corbett, School of Pharmacy, Queen's University BelfastSummary:One of the most-remembered experiences during the COVID-19 pandemic was undoubtedly the regular testing which we had to undertake whether we had symptoms of the infection or not, and before we'd see family, friends, or enter into populated environments - whilst this activity was unavoidable and absolutely necessary, it certainly wasn't enjoyable, and failed to provide us with a full picture of how the disease was spreading through the population, or the way in which it was doing so. During the pandemic, researchers at Queen's University Belfast came together to develop an innovative approach which allowed coronavirus levels to be detected via analysis of our wastewater, providing a wealth of information to public health agencies and beyond, and allowing for early and decisive action to be taken to prevent further spread. 

This Zenodo record is a permanently preserved version of a PREreview. You can view the complete PREreview at https://prereview.org/reviews/8033242. We, the students of MICI5029/5049, a Graduate Level Molecular Pathogenesis Journal Club at Dalhousie University in Halifax, NS, Canada, hereby submit a review of the following BioRxiv preprint: A human-specific motif facilitates CARD8 inflammasome activation after HIV-1 infection Jessie Kulsuptrakul, Elizabeth A. Turcotte, Michael Emerman* and Patrick S. Mitchell* doi: https://doi.org/10.1101/2022.10.04.510817 We will adhere to the Universal Principled (UP) Review guidelines proposed in: Universal Principled Review: A Community-Driven Method to Improve Peer Review. Krummel M, Blish C, Kuhns M, Cadwell K, Oberst A, Goldrath A, Ansel KM, Chi H, O'Connell R, Wherry EJ, Pepper M; Future Immunology Consortium. Cell. 2019 Dec 12;179(7):1441-1445. doi: 10.1016/j.cell.2019.11.029 SUMMARY: CARD8 is thought to sense infection stress and stimulate inflammasome formation, but precise mechanisms remain to be elucidated. HIV-1 protease (HIV-1PR) cleaves CARD8, resulting in proteasome-dependent degradation of the amino-terminal CARD8 fragment and liberation of the carboxy-terminal fragment that activates inflammasomes. Kulsuptrakul and colleagues build upon this intriguing finding to investigate evolutionary relationships between primate lentiviruses and CARD8 homologs from their host primates. They discovered that both HIV-1 and SIVcpzproteases cleave human CARD8. By contrast, chimpanzee CARD8 was not cleaved by primate lentivirus proteases. Thus, even prior to the HIV-1 pandemic, SIVcpz proteases could cleave and activate human CARD8. The authors provided evidence for CARD8-dependent inflammasome activation in an in vitro HIV-1 infection model. Complementation of CARD8 KO cells with WT human CARD8 restored inflammasome activation, whereas complementation with chimpanzee CARD8 or human CARD8 mutant constructs with substitutions that destroy the protease cleavage site did not. Together, these findings support a role for human CARD8 in activating the inflammasome upon HIV infection and suggest that, during spillover events, SIVcpz was well equipped to cleave human CARD8 and drive pathogenesis. OVERALL ASSESSMENT: This study convincingly demonstrates that human CARD8 is susceptible to cleavage and activation by diverse primate lentivirus protease enzymes, whereas chimpanzee CARD8 is not. Overall, the data is quite convincing and clearly organized and rendered for readers, and positions lentivirus proteases and host CARD8 sensors as new players in the 'genomes-in-conflict' chess match. These conclusions could be strengthened by additional evidence for CARD8-mediated inflammasome activation. STRENGTHS: The manuscript is well-written. The rationale provided for the investigation of CARD8 in the context of HIV infection is sound. The data presented is well-organized, clear and well-controlled. The primary strength is the identification and careful mapping of viral protease-mediated cleavage and activation of human CARD8, whereas the closely related chimpanzee CARD8 resists cleavage and activation. WEAKNESSES: While the manuscript was well written, the introduction was quite brief. We suggest that the authors should provide some additional information about CARD8 and inflammasomes. Does CARD8 have additional roles in the cell beyond inflammasome activation? How does CARD8 fit into the context of a diverse array of inflammasome triggers? This kind of information would really help set the stage properly. The data in Figs. 3/4 could be strengthened by additional assays to measure inflammasome activation beyond IL-1β secretion and PI staining. Options include an IL-18 ELISA, LDH release assay, HMGB1 release assay, or caspase-1 cleavage assay (western blot). The provision of a second assay to corroborate inflammasome activation is consistent with field-specific standards. DETAILED U.P. ASSESSMENT: OBJECTIVE CRITERIA (QUALITY) 1. Quality: Experiments (1–3 scale; note: 1 is best on this scale) SCORE = 1.5 · Figure by figure, do experiments, as performed, have the proper controls? [note: we use this 'figure-by-figure' section for broader detailed critiques, rather than only focusing on controls. · Fig. 1B – the cartoon introduces a 2nd PR cleavage site on CARD8 (site 88/89) that is not investigated further. Is this site relevant to this study? Do the amino acids at this site vary between humans and Old-world monkeys? The reader would benefit from some explanation about this protease cleavage site. · Fig. 1C – We wondered whether treatment with a proteasome inhibitor could prevent degradation of CARD8 protein fragments and help us better understand cleavage patterns on western blots. Moreover, could the unknown band at ~40 kDa be further characterized, and does it relate to the N-terminal cleavage product? · Figs 1D/2B - The anti-vinculin loading control western blots for Figure 1D and Figure 2B are identical. · Fig. 3 – As mentioned above, abstract-level conclusions about inflammasome activation require better support. The data in Fig. 3 could be strengthened by additional assays to measure inflammasome activation beyond IL-1β secretion and PI staining. Options include an IL-18 ELISA, LDH release assay, HMGB1 release assay, or caspase-1 cleavage assay (western blot). The provision of a second assay to corroborate inflammasome activation is consistent with field-specific standards. · Figs. 4B/4C – "Similar to our observations with VbP, we found that IL-1β secretion and cell death were significantly reduced in Pam3CSK4-primed, HIV-1LAI or HIV-1LAI-VSVG infected CARD8 KO versus WT THP-1 cells (Figure 4C). These results indicate that HIV-1-induced inflammasome activation in THP-1 cells is dependent on CARD8." - This statement requires greater support demonstrating CARD8-dependent inflammasome activation. Inflammasome activation was still evident in the CARD8 KO cells. This analysis could benefit from corroboration with a second assay, as mentioned above. We wondered whether it would be feasible to employ a reconstructed inflammasome model, as reported in this recent paper: o Qiyao Chai et al. A bacterial phospholipid phosphatase inhibits host pyroptosis by hijacking ubiquitin. Science 378, eabq0132(2022). DOI:10.1126/science.abq0132 · Fig. 4D - We were once again curious about the identity of the unknown ~40 kDa band, which is clearly present in the CARD8 KO lysates. Perhaps this could be addressed in the Discussion. Are specific analyses performed using methods that are consistent with answering the specific question? · Is there appropriate technical expertise in the collection and analysis of data presented? · Yes · Do analyses use the best-possible (most unambiguous) available methods quantified via appropriate statistical comparisons? · Yes · Are controls or experimental foundations consistent with established findings in the field? A review that raises concerns regarding inconsistency with widely reproduced observations should list at least two examples in the literature of such results. Addressing this question may occasionally require a supplemental figure that, for example, re-graphs multi-axis data from the primary figure using established axes or gating strategies to demonstrate how results in this paper line up with established understandings. It should not be necessary to defend exactly why these may be different from established truths, although doing so may increase the impact of the study and discussion of discrepancies is an important aspect of scholarship. · The provision of a second assay to corroborate inflammasome activation is consistent with field-specific standards. 2. Quality: Completeness (1–3 scale) SCORE = 2 · Does the collection of experiments and associated analysis of data support the proposed title- and abstract-level conclusions? Typically, the major (title- or abstract-level) conclusions are expected to be supported by at least two experimental systems. · The data in Figs 3/4 could be strengthened by additional assays to measure inflammasome activation beyond IL-1β secretion and PI staining. Options include an IL-18 ELISA, LDH release assay, HMGB1 release assay, or caspase-1 cleavage assay (western blot). · Are there experiments or analyses that have not been performed but if ''true'' would disprove the conclusion (sometimes considered a fatal flaw in the study)? In some cases, a reviewer may propose an alternative conclusion and abstract that is clearly defensible with the experiments as presented, and one solution to ''completeness'' here should always be to temper an abstract or remove a conclusion and to discuss this alternative in the discussion section. · Beyond additional assays for inflammasome activation, we suggest that the authors could diversify the 'priming' treatments. For example, cells could be primed with LPS, poly I:C, or GM-CSF. Demonstrating CARD8-dependent inflammasome activation in conjunction with diverse stimuli will strengthen conclusions, and take away concerns about a TLR2-specific effect. 3. Quality: Reproducibility (1–3 scale) SCORE = 1 · Figure by figure, were experiments repeated per a standard of 3 repeats or 5 mice per cohort, etc.? · Sufficient biological replicates of all assays support the author's conclusions. · Is there sufficient raw data presented to assess the rigor of the analysis? · Yes · Are methods for experimentation and analysis adequately outlined to permit reproducibility? · Yes · If a ''discovery' dataset is used, has a ''validation' cohort been assessed and/or has the issue of false discovery been addressed? · N/A 4. Quality: Scholarship (1–4 scale but generally not the basis for acceptance or rejection) SCORE = 1.5 · Has the author cited and discussed the merits of the relevant data that would argue against their conclusion? · Yes · Has the author cited and/or discussed the important works that are consistent with their conclusion and that a reader should be especially familiar when considering the work? · Yes · Specific (helpful) comments on grammar, diction, paper structure, or data presentation (e.g., change a graph style or color scheme) go in this section, but scores in this area should not be significant basis for decisions. · The following statement stimulated a lot of discussion amongst the students, who were concerned that the study doesn't really address pathogenesis: "Taken together, our work highlights how even minor, single amino acid changes can have dramatic, species-specific impacts on innate immune sensing and pathogenesis, and provides a model to explain, in part, the unique susceptibility of humans to HIV pathogenesis." · Minor points: We recommend changing the color scheme of graphs in Fig 3 to enhance readability. This could be achieved by color-coding, with one color per group (e.g. HIV-1LAI in blue and HIV-1LAI-VSVG in yellow). MORE SUBJECTIVE CRITERIA (IMPACT): 1. Impact: Novelty/Fundamental and Broad Interest (1–4 scale) SCORE= 2.5 A score here should be accompanied by a statement delineating the most interesting and/or important conceptual finding(s), as they stand right now with the current scope of the paper. A ''1'' would be expected to be understood for the importance by a layperson but would also be of top interest (have lasting impact) on the field.] How big of an advance would you consider the findings to be if fully supported but not extended? · If properly supported by corroborating assays, these findings represent a significant advance in the field without further extension. 2. Impact: Extensibility (1–4 or N/A scale) SCORE = 2.5 Has an initial result (e.g., of a paradigm in a cell line) been extended to be shown (or implicated) to be important in a bigger scheme (e.g., in animals or in a human cohort)? This criterion is only valuable as a scoring parameter if it is present, indicated by the N/A option if it simply doesn't apply. The extent to which this is necessary for a result to be considered of value is important. It should be explicitly discussed by a reviewer why it would be required. What work (scope and expected time) and/or discussion would improve this score, and what would this improvement add to the conclusions of the study? Care should be taken to avoid casually suggesting experiments of great cost (e.g., ''repeat a mouse-based experiment in humans'') and difficulty that merely confirm but do not extend (see Bad Behaviors, Box 2) · The manuscript explores human vs. chimpanzee CARD8 and diverse lentiviruses. No further extension is provided to a bigger scheme. · We did wonder whether other non-lentiviral proteases could also cleave human CARD8. This would clearly add to our understanding of selective pressures that could have influenced CARD8 evolution in primates. Coronaviruses are mentioned in the discussion. Investigating the activity of coronavirus or enterovirus proteases against CARD8 homologs from different primates would be fascinating. Some clues may already exist in the following n-terminomics studies: o Jagdeo JM, Dufour A, Klein T, Solis N, Kleifeld O, Kizhakkedathu J, Luo H, Overall CM, Jan E. N-Terminomics TAILS Identifies Host Cell Substrates of Poliovirus and Coxsackievirus B3 3C Proteinases That Modulate Virus Infection. J Virol. 2018 Mar 28;92(8):e02211-17. doi: 10.1128/JVI.02211-17. PMID: 29437971; PMCID: PMC5874412. o Pablos I, Machado Y, de Jesus HCR, Mohamud Y, Kappelhoff R, Lindskog C, Vlok M, Bell PA, Butler GS, Grin PM, Cao QT, Nguyen JP, Solis N, Abbina S, Rut W, Vederas JC, Szekely L, Szakos A, Drag M, Kizhakkedathu JN, Mossman K, Hirota JA, Jan E, Luo H, Banerjee A, Overall CM. Mechanistic insights into COVID-19 by global analysis of the SARS-CoV-2 3CLpro substrate degradome. Cell Rep. 2021 Oct 26;37(4):109892. doi: 10.1016/j.celrep.2021.109892. Epub 2021 Oct 9. PMID: 34672947; PMCID: PMC8501228. o Koudelka T, Boger J, Henkel A, Schönherr R, Krantz S, Fuchs S, Rodríguez E, Redecke L, Tholey A. N-Terminomics for the Identification of In Vitro Substrates and Cleavage Site Specificity of the SARS-CoV-2 Main Protease. Proteomics. 2021 Jan;21(2):e2000246. doi: 10.1002/pmic.202000246. Epub 2020 Nov 17. PMID: 33111431; PMCID: PMC7645863. o Luo SY, Moussa EW, Lopez-Orozco J, Felix-Lopez A, Ishida R, Fayad N, Gomez-Cardona E, Wang H, Wilson JA, Kumar A, Hobman TC, Julien O. Identification of Human Host Substrates of the SARS-CoV-2 Mpro and PLproUsing Subtiligase N-Terminomics. ACS Infect Dis. 2023 Apr 14;9(4):749-761. doi: 10.1021/acsinfecdis.2c00458. Epub 2023 Apr 3. PMID: 37011043; PMCID: PMC10081575. o Bell PA, Overall CM. No Substrate Left behind-Mining of Shotgun Proteomics Datasets Rescues Evidence of Proteolysis by SARS-CoV-2 3CLpro Main Protease. Int J Mol Sci. 2023 May 13;24(10):8723. doi: 10.3390/ijms24108723. PMID: 37240067; PMCID: PMC10218362. Competing interests The author declares that they have no competing interests.