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The resurgence of the May 2021 COVID-19 wave in India not only pointed to the explosive speed with which SARS-CoV-2 can spread in vulnerable populations if unchecked, but also to the gross misreading of the status of the pandemic when decisions to reopen the economy were made in March 2021. In this combined modelling and scenario-based analysis, we isolated the population and policy-related factors underlying the May 2021 viral resurgence by projecting the growth and magnitude of the health impact and demand for hospital care that would have arisen if the spread was not impeded, and by evaluating the intervention options best able to curb the observed rapidly developing contagion. We show that only by immediately re-introducing a moderately high level of social mitigation over a medium-term period alongside a swift ramping up of vaccinations could the country be able to contain and ultimately end the pandemic safely. We also show that delaying the delivery of the 2nd dose of the Astra Zeneca vaccine, as proposed by the Government of India, would have had only slightly more deleterious impacts, supporting the government's decision to vaccinate a greater fraction of the population with at least a single dose as rapidly as possible. Our projections of the scale of the virus resurgence based on the observed May 2021 growth in cases and impacts of intervention scenarios to control the wave, along with the diverse range of variable control actions taken by state authorities, also exemplify the importance of shifting from the use of science and knowledge in an ad hoc reactive fashion to a more effective proactive strategy for assessing and managing the risk of fast-changing hazards, like a pandemic. We show that epidemic models parameterized with data can be used in combination with plausible intervention scenarios to enable such policy-making.

Ischaemic Hepatitis (IH) or Hypoxic Hepatitis (HH) also known as centrilobular liver cell necrosis is an acute liver injury characterized by a rapid increase in serum aminotransferase. The liver injury typically results from different underlying medical conditions such as cardiac failure, respiratory failure and septic shock in which the liver becomes damaged due to deprivation of either blood or oxygen. IH is a potentially lethal condition that is often preventable if diagnosed timely. The role of mechanisms that cause IH is often not well understood, making it difficult to diagnose or accurately quantify the patterns of related biomarkers. In most patients, currently, the only way to determine a case of IH is to rule out all other possible conditions for liver injuries. A better understanding of the liver's response to IH is necessary to aid in its diagnosis, measurement, and improve outcomes. The goal of this study is to identify mechanisms that can alter associated biomarkers for reducing the density of damaged hepatocytes, and thus reduce the chances of IH. We develop a mathematical model capturing dynamics of hepatocytes in the liver through the rise and fall of associated liver enzymes aspartate transaminase (AST), alanine transaminase (ALT) and lactate dehydrogenase (LDH) related to the condition of IH. The model analysis provides a novel approach to predict the level of biomarkers given variations in the systemic oxygen in the body. Using IH patient data in the US, novel model parameters are described and then estimated for the first time to capture real-time dynamics of hepatocytes in the presence and absence of IH condition. The results may allow physicians to estimate the extent of liver damage in an IH patient based on their enzyme levels and receive faster treatment on a real-time basis.

When attempting to statistically distinguish between a null and an alternative hypothesis, many researchers in the life and social sciences turn to binned statistical analysis methods, or methods that are simply based on the moments of a distribution (such as the mean, and variance). These methods have the advantage of simplicity of implementation, and simplicity of explanation. However, when null and alternative hypotheses manifest themselves in subtle differences in patterns in the data, binned analysis methods may be insensitive to these differences, and researchers may erroneously fail to reject the null hypothesis when in fact more sensitive statistical analysis methods might produce a different result when the null hypothesis is actually false. Here, with a focus on two recent conflicting studies of contagion in mass killings as instructive examples, we discuss how the use of unbinned likelihood methods makes optimal use of the information in the data; a fact that has been long known in statistical theory, but perhaps is not as widely appreciated amongst general researchers in the life and social sciences.In 2015, Towers et al published a paper that quantified the long-suspected contagion effect in mass killings. However, in 2017, Lankford & Tomek subsequently published a paper, based upon the same data, that claimed to contradict the results of the earlier study. The former used unbinned likelihood methods, and the latter used binned methods, and comparison of distribution moments. Using these analyses, we also discuss how visualization of the data can aid in determination of the most appropriate statistical analysis methods to distinguish between a null and alternate hypothesis. We also discuss the importance of assessment of the robustness of analysis results to methodological assumptions made (for example, arbitrary choices of number of bins and bin widths when using binned methods); an issue that is widely overlooked in the literature, but is critical to analysis reproducibility and robustness.When an analysis cannot distinguish between a null and alternate hypothesis, care must be taken to ensure that the analysis methodology itself maximizes the use of information in the data that can distinguish between the two hypotheses. The use of binned methods by Lankford & Tomek (2017), that examined how many mass killings fell within a 14 day window from a previous mass killing, substantially reduced the sensitivity of their analysis to contagion effects. The unbinned likelihood methods used by Towers et al (2015) did not suffer from this problem. While a binned analysis might be favorable for simplicity and clarity of presentation, unbinned likelihood methods are preferable when effects might be somewhat subtle.

Several past studies have found that media reports of suicides and homicides appear to subsequently increase the incidence of similar events in the community, apparently due to the coverage planting the seeds of ideation in at-risk individuals to commit similar acts.Here we explore whether or not contagion is evident in more high-profile incidents, such as school shootings and mass killings (incidents with four or more people killed). We fit a contagion model to recent data sets related to such incidents in the US, with terms that take into account the fact that a school shooting or mass murder may temporarily increase the probability of a similar event in the immediate future, by assuming an exponential decay in contagiousness after an event.We find significant evidence that mass killings involving firearms are incented by similar events in the immediate past. On average, this temporary increase in probability lasts 13 days, and each incident incites at least 0.30 new incidents (p = 0.0015). We also find significant evidence of contagion in school shootings, for which an incident is contagious for an average of 13 days, and incites an average of at least 0.22 new incidents (p = 0.0001). All p-values are assessed based on a likelihood ratio test comparing the likelihood of a contagion model to that of a null model with no contagion. On average, mass killings involving firearms occur approximately every two weeks in the US, while school shootings occur on average monthly. We find that state prevalence of firearm ownership is significantly associated with the state incidence of mass killings with firearms, school shootings, and mass shootings.