Integrated Seismic Risk Assessment in Nepal

As Nepal is at high risk of earthquakes, the district-wide (VDC/Municipality level) study has been performed for vulnerability assessment of seismic-hazard, and the hazard-risk study is incorporated with social conditions as it has become a crucial issue in recent years. There is an interrelationship between hazards, physical risk, and the social characteristics of populations which are significant for policy-makers and individuals. Mapping the spatial variability of average annual loss (seismic risk) and social vulnerability discretely does not reflect the true nature of parameters contributing to the earthquake risk, so when the integrated risk is mapped, such combined spatial distribution becomes more evident. The purpose of this paper is to compute the risk analysis from the exposure model of the country using OpenQuake and then integrate the results with socio-economic parameters. The methodology of seismic-risk assessment and the way of combining the results of the physical risk and socio-economic data to develop an integrated vulnerability score of the regions has been described. This study considers all 75 districts and corresponding VDC/Municipalities using the available census. The combined vulnerability score has been developed and presented by integrating earthquake risk and social vulnerability aspects of the country and represented in form of the map produced using ArcGIS 10. The knowledge and information of the relationship between earthquake hazards and the demographic characteristics of the population in the vulnerable area are imperative to mitigate the local impact of earthquakes. Therefore, we utilize social vulnerability study as part of a comprehensive risk management framework to recuperate and recover from natural disasters.

Perspectives on Primary Blast Injury of the Brain: Translational Insights Into Non-inertial Low-Intensity Blast Injury

Most traumatic brain injuries (TBIs) during military deployment or training are clinically “mild” and frequently caused by non-impact blast exposures. Experimental models were developed to reproduce the biological consequences of high-intensity blasts causing moderate to severe brain injuries. However, the pathophysiological mechanisms of low-intensity blast (LIB)-induced neurological deficits have been understudied. This review provides perspectives on primary blast-induced mild TBI models and discusses translational aspects of LIB exposures as defined by standardized physical parameters including overpressure, impulse, and shock wave velocity. Our mouse LIB-exposure model, which reproduces deployment-related scenarios of open-field blast (OFB), caused neurobehavioral changes, including reduced exploratory activities, elevated anxiety-like levels, impaired nesting behavior, and compromised spatial reference learning and memory. These functional impairments associate with subcellular and ultrastructural neuropathological changes, such as myelinated axonal damage, synaptic alterations, and mitochondrial abnormalities occurring in the absence of gross- or cellular damage. Biochemically, we observed dysfunctional mitochondrial pathways that led to elevated oxidative stress, impaired fission-fusion dynamics, diminished mitophagy, decreased oxidative phosphorylation, and compensated cell respiration-relevant enzyme activity. LIB also induced increased levels of total tau, phosphorylated tau, and amyloid β peptide, suggesting initiation of signaling cascades leading to neurodegeneration. We also compare translational aspects of OFB findings to alternative blast injury models. By scoping relevant recent research findings, we provide recommendations for future preclinical studies to better reflect military-operational and clinical realities. Overall, better alignment of preclinical models with clinical observations and experience related to military injuries will facilitate development of more precise diagnosis, clinical evaluation, treatment, and rehabilitation.

Calculating earthquake damage building by building: the case of the city of Cologne, Germany

The creation of building exposure models for seismic risk assessment is frequently challenging due to the lack of availability of detailed information on building structures. Different strategies have been developed in recent years to overcome this, including the use of census data, remote sensing imagery and volunteered graphic information (VGI). This paper presents the development of a building-by-building exposure model based exclusively on openly available datasets, including both VGI and census statistics, which are defined at different levels of spatial resolution and for different moments in time. The initial model stemming purely from building-level data is enriched with statistics aggregated at the neighbourhood and city level by means of a Monte Carlo simulation that enables the generation of full realisations of damage estimates when using the exposure model in the context of an earthquake scenario calculation. Though applicable to any other region of interest where analogous datasets are available, the workflow and approach followed are explained by focusing on the case of the German city of Cologne, for which a scenario earthquake is defined and the potential damage is calculated. The resulting exposure model and damage estimates are presented, and it is shown that the latter are broadly consistent with damage data from the 1978 Albstadt earthquake, notwithstanding the differences in the scenario. Through this real-world application we demonstrate the potential of VGI and open data to be used for exposure modelling for natural risk assessment, when combined with suitable knowledge on building fragility and accounting for the inherent uncertainties.

International Pesticide Operator Safety Meeting 2021: hand-held application scenarios in low- and middle-income countries

An international web meeting on the topic of operator safety for pesticide operators was held on 20–21 September 2021. The meeting provided an opportunity for experts from regulatory agencies, pesticide industry, the Food and Agriculture Organization (FAO), and other organizations to discuss operator safety in low- and middle-income countries (LMIC). The meeting focused on risk assessment and risk mitigation, the first steps to address operator safety. The key message at the meeting was the need for an operator exposure model that includes common hand-held scenarios used in LMIC and consistent personal protective equipment communication. The experts supported a transparent collaborative process that will enable us to build on the past efforts.

A model for measuring distruption risk in the prefabrication supply chain

Use of prefabrication in construction projects is increasing due to the benefits in cost, time, quality, and safety. However, utilizing prefabrication introduces uncertainties inherent with the supply chain of the process. These uncertainties, if not managed, can disrupt the prefabrication process and result in schedule delays and cost overruns. This study proposes a model to measure disruption risks in the prefabrication process. The model was used in measuring the disruption risks of prefabrication of headwalls in patients’ rooms for a healthcare project as a pilot study. The risk model could successfully identify the disruption risks originating anywhere in the supply chain based on input information such as required material quantity, batch sizes of material deliveries, production rates, and batch sizes of transporting the headwall units. Using the model, the project team identified two uncertainties that could lead to possible disruptions: the start of the prefabrication processes and the required production rate to meet the on-site schedule. This is a first step to developing a risk exposure model that can prove valuable to the risk managers to analyse and manage the impact of disruptions. This will help the risk managers in making informed decisions about where to focus their limited resources.

Sex-dependent changes in murine striatal dopamine release, sleep, and behavior during spontaneous Δ-9-tetrahydrocannabinol abstinence

Withdrawal symptoms are observed upon cessation of cannabis use in humans. Although animal studies have examined withdrawal symptoms following exposure to delta-9-tetrahydrocannabinol (THC), difficulties in obtaining objective measures of spontaneous withdrawal using paradigms that mimic cessation of use in humans have slowed research. The neuromodulator dopamine (DA) is known to be affected by chronic THC treatment and plays a role in many behaviors related to human THC withdrawal symptoms. These symptoms include sleep disturbances that often drive relapse, and emotional behaviors, e.g., irritability and anhedonia. We examined THC withdrawal-induced changes in striatal DA release and the extent to which sleep disruption and behavioral maladaptation manifest during withdrawal in a mouse chronic cannabis exposure model. Using a THC treatment regimen known to produce tolerance we measured electrically elicited DA release in acute brain slices from different striatal subregions during early and late THC abstinence. Long-term polysomnographic recordings from mice were used to assess vigilance state and sleep architecture before, during, and after THC treatment. We additionally assessed how behaviors that model human withdrawal symptoms are altered by chronic THC treatment in early and late abstinence. We detected altered striatal DA release, sleep disturbances that mimic clinical observations, and behavioral maladaptation in mice following tolerance inducing THC treatment. Sex differences were observed in nearly all metrics. Altered striatal DA release, sleep and affect-related behaviors associated with spontaneous THC abstinence were more consistently observed in male mice. To our knowledge these findings provide the first model of directly translatable non-precipitated cannabis withdrawal symptoms, in particular, sleep disruption.

Characterization and Lifetime Dietary Risk Assessment of Eighteen Pyrrolizidine Alkaloids and Pyrrolizidine Alkaloid N-Oxides in New Zealand Honey

Pyrrolizidine alkaloids (PAs) are a large group of botanical toxins of concern, as they are considered genotoxic carcinogens, with long-term dietary exposure presenting an elevated risk of liver cancer. PAs can contaminate honey through honeybees visiting the flowers of PA-containing plant species. A program of monitoring New Zealand honey has been undertaken over several years to build a comprehensive dataset on the concentration, regional and seasonal distribution, and botanical origin of 18 PAs and PA N-oxides. A bespoke probabilistic exposure model has then been used to assess the averaged lifetime dietary risk to honey consumers, with exposures at each percentile of the model characterized for risk using a margin of exposure from the Joint World Health Organization and United Nations Food and Agriculture Organization Expert Committee on Food Additives (JECFA) Benchmark Dose. Survey findings identify the typical PA types for New Zealand honey as lycopsamine, echimidine, retrorsine and senecionine. Regional and seasonal variation is evident in the types and levels of total PAs, linked to the ranges and flowering times of certain plants. Over a lifetime basis, the average exposure an individual will receive through honey consumption is considered within tolerable levels, although there are uncertainties over high and brand-loyal consumers, and other dietary contributors. An average lifetime risk to the general population from PAs in honey is not expected. However, given the uncertainties in the assessment, risk management approaches to limit or reduce exposures through honey are still of value.

Novel Bioactive Adhesive Monomer CMET Promotes Odontogenic Differentiation and Dentin Regeneration

This study aimed to evaluate the in vitro effect of the novel bioactive adhesive monomer CMET, a calcium salt of 4-methacryloxyethyl trimellitate acid (4-MET), on human dental pulp stem cells (hDPSCs) and its capacity to induce tertiary dentin formation in a rat pulp injury model. Aqueous solutions of four tested materials [4-MET, CMET, Ca(OH)2, and mineral trioxide aggregate (MTA)] were added to the culture medium upon confluence, and solvent (dH2O) was used as a control. Cell proliferation was assessed using the Cell Counting Kit-8 assay, and cell differentiation was evaluated by real-time quantitative reverse transcription-polymerase chain reaction. The mineralization-inducing capacity was evaluated using alizarin red S staining and an alkaline phosphatase activity assay. For an in vivo experiment, a mechanical pulp exposure model was prepared on Wistar rats; damaged pulp was capped with Ca(OH)2 or CMET. Cavities were sealed with composite resin, and specimens were assessed after 14 and 28 days. The in vitro results showed that CMET exhibited the lowest cytotoxicity and highest odontogenic differentiation capacity among all tested materials. The favorable outcome on cell mineralization after treatment with CMET involved p38 and c-Jun N-terminal kinases signaling. The nuclear factor kappa B pathway was involved in the CMET-induced mRNA expression of odontogenic markers. Similar to Ca(OH)2, CMET produced a continuous hard tissue bridge at the pulp exposure site, but treatment with only CMET produced a regular dentinal tubule pattern. The findings suggest that (1) the evaluated novel bioactive adhesive monomer provides favorable biocompatibility and odontogenic induction capacity and that (2) CMET might be a very promising adjunctive for pulp-capping materials.