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Marine heatwaves (MHWs) can cause thermal stress in marine organisms, experienced as extreme 'pulses' against the gradual trend of anthropogenic warming. When thermal stress exceeds organismal capacity to maintain homeostasis, organism survival becomes time-limited and can result in mass mortality events. Current methods of detecting and categorizing MHWs rely on statistical analysis of historic climatology and do not consider biological effects as a basis of MHW severity. The re-emergence of ectotherm thermal tolerance landscape models provides a physiological framework for assessing the lethal effects of MHWs by accounting for both the magnitude and duration of extreme heat events. Here, we used a simulation approach to understand the effects of a suite of MHW profiles on organism survival probability across (1) three thermal tolerance adaptive strategies, (2) interannual temperature variation and (3) seasonal timing of MHWs. We identified survival isoclines across MHW magnitude and duration where acute (short duration-high magnitude) and chronic (long duration-low magnitude) events had equivalent lethal effects on marine organisms. While most research attention has focused on chronic MHW events, we show similar lethal effects can be experienced by more common but neglected acute marine heat spikes. Critically, a statistical definition of MHWs does not accurately categorize biological mortality. By letting organism responses define the extremeness of a MHW event, we can build a mechanistic understanding of MHW effects from a physiological basis. Organism responses can then be transferred across scales of ecological organization and better predict marine ecosystem shifts to MHWs.

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Over the last decades, mass mortality events have become increasingly common across taxa with sometimes devastating effects on population biomass. In the aquatic environment, fish are sensitive to mass mortality events, particularly at the early life stages that are crucial for population dynamics. However, it has recently been shown for fish, that a single mass mortality event in early life typically does not lead to population collapse. Moreover, the frequency and intensity of extreme events that can cause mass mortality, such as marine heatwaves, are increasing. Here, we show that increasing frequency and intensity of mass mortality events may lead to population collapse. Since the drivers of mass mortality events are diverse, and often linked to climate change, it is challenging to predict the frequency and severity of future mass mortality events. As an alternative, we quantify the probability of population collapse depending on the frequency and intensity as well as the duration of mass mortality events. Based on 39 fish species, we show that the probability of collapse typically increases with increasing frequency, intensity, and duration of the mortality events. In addition, we show that the collapse depends on key traits such as natural mortality, recruitment variation, and density dependence. The presented framework provides quantitative estimates of the sensitivity of fish species to these increasingly common extreme events, which paves the way for potential mitigation actions to alleviate adverse impacts on harvested fish populations across the globe.

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This study introduces a comprehensive method for quantifying mass mortality events in freshwater wildlife, exemplified by the ecological disaster in the Odra River in 2022. Our approach integrates field observations, statistical analysis, and ecological assessment to measure the impact of such events on various aquatic species. Key steps include systematic counting of deceased organisms, assessing population declines, and evaluating the ecological repercussions of invasive species. Utilizing the R programming language, we developed a framework that is adaptable to similar ecological crises in different aquatic environments. This methodology facilitates a detailed understanding of the scale and implications of mass mortality events, thereby contributing to effective environmental management and conservation efforts. •The analysis and modeling methods of the disaster are presented in the R programming language.•Exclusively open-source software was used for the analysis.•The analysis includes detailed data on the disaster's impact on various species.

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In 2011 and 2015, four mass mortalities of Prussian carp (Carassius gibelio) were observed in a recreational freshwater lake and open freshwater in the western part of the Netherlands. Cyprinid herpesvirus 2 (CyHV-2) infection was suspected in these cases, based on presumptive gross diagnosis. To elucidate the cause of the mass mortalities diagnostic PCR assays were performed for CyHV-2, based on the helicase gene. Furthermore, the viral isolates were genotyped by sequencing the enlarged marker A and marker B sequences. Diagnostic PCR revealed that three of four samples were positive for CyHV-2, indicating these three mass mortalities were associated with CyHV-2 infection. The marker A sequence from one of the isolates found in this study was identical to those from different locations such as Asia and Middle East, suggesting a link among the isolates. This is the first detailed report on mass mortalities of Prussian carp associated with CyHV-2 infection in natural aquatic environments in the Netherlands. Since 2015, additionally, in total three CyHV-2 associated outbreaks of Dutch Prussian carp were seen in 2016 and 2020. These outbreaks in Prussian carp from lakes and open water suggest that the virus has been spreading in natural freshwaters in the Netherlands.

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Recent bacteriological investigations of freshwater mussel mortality events in the southeastern United States have identified a variety of bacteria and differences in bacterial communities between sick and healthy mussels. In particular, Yokenella regensburgei and Aeromonas spp. have been shown to be associated with moribund mussels, although it remains unclear whether these bacteria are causes or consequences of disease. To further understand the role of bacteria in mussel epizootics, we investigated mortality events that occurred in the upper Midwest in the Embarrass River (Wisconsin) and the Huron River (Michigan). For comparison, we also studied mussels from an unaffected population in the St. Croix River (Wisconsin). Diverse bacterial genera were identified from these sites, including Y. regensburgei from moribund mussels in the Embarrass River (Wisconsin). This bacterium has also been consistently isolated during ongoing mortality events in the Clinch River (Virginia). Subsequently, we developed and validated molecular assays for the detection of Yokenella to use in future investigations of mussel mortality events and to identify environmental reservoirs of this bacterium.

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The Mediterranean Sea hosts a population of fin whale (Balaenoptera physalus), the only species of Mysticete regularly occurring in the basin. Observed and inferred mortality suggests that the population is likely declining. Accordingly, understanding the causes of mortality and assessing the health status is pivotal to the survival of this endangered population. While such studies are inherently difficult for a highly roaming species with a pelagic distribution, mortality events provide the opportunity to investigate biological and epidemiological traits linked to these events, and evaluate the footprint of human activity, especially when long-term data series exist. We present a comprehensive spatial-temporal overview of fin whale mortality events along the Italian coast encompassing four centuries (1624-2021). Time series analysis was used to highlight structural changes in the evolution of mortality through time, while spatial-temporal patterns in the distribution of mortality events were assessed through emerging hot spot analysis methods. Recent mortality events (1964-2021) were further explored to evaluate, where possible, the primary causes of mortality and to identify anthropogenic threats of conservation concerns. This long-term survey offers the basis for an understanding of the health status of this B. physalus population and provides much-needed information for developing an effective management and conservation plan for the species in the region.

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Introduction: Studies found that the impact of dysglycemia on microvascular, macrovascular events and mortality outcomes were different between the younger vs. older population. We aimed to investigate the age-specific association of prediabetes with clinical outcomes including type 2 diabetes (T2DM), hypertension, chronic kidney disease (CKD), cardiovascular disease (CVD), and mortality. Materials and methods: A total of 5,970 Iranians (3,829 women) aged ≥30 years, without T2DM, were included. The age-specific (<60 and ≥60 years; minimum p-value for interaction = 0.001) multivariable-adjusted Cox regression was done to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) of the impaired glucose status including impaired fasting glucose (IFG) vs. normal fasting glucose (NFG), impaired glucose tolerance (IGT) vs. normal glucose tolerance (NGT), and IFG&IGT vs. NFG/NGT with each outcome. Results: Among individuals aged ≥60 years, the prevalence of impaired glucose status (IFG, IGT, or both) was about 2 times higher compared to those aged <60. Age-specific association between prediabetes and incident hypertension was found for those aged <60 years; [HR (95% CI); IFG: 1.38 (1.16-1.65), IGT: 1.51 (1.26-1.81), and IFG&IGT: 1.62 (1.21-2.12)]. For CVD, in all impaired glycemic states, those aged <60 were at higher significant risk [IFG: 1.39 (1.09-1.77), IGT: 1.53 (1.19-1.97), and IFG&IGT: 1.60 (1.14-2.25)]. Stratified analyses showed similar associations for IFG and IGT with non-CV mortality 1.71 (1.04-2.80) and 2.12 (1.30-3.46), respectively, and for all-cause mortality among those aged <60 years [IFG: 1.63 (1.08-2.45) and IGT: 1.82 (1.20-2.76)]. In both age groups, all glycemic status groups were significantly associated with T2DM but not with CKD and CV mortality. Conclusions: The high prevalence of prediabetes particularly among the elderly population, limited resources, and the observed significant age differences in the impact of prediabetes states on different clinical outcomes calls for multicomponent intervention strategies by policy health makers, including lifestyle and possible pharmacological therapy, with the priority for the young Iranian population.

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Marine biotoxins have been frequently implicated in morbidity and mortality events in numerous species of birds worldwide. Nevertheless, their effects on seabirds have often been overlooked and the associated ecological impact has not been extensively studied. On top of that, the number of published studies confirming by analyses the presence of marine biotoxins from harmful algal blooms (HABs) in seabirds, although having increased in recent years, is still quite low. This review compiles information on studies evidencing the impact of HAB toxins on marine birds, with a special focus on the effects of paralytic and amnesic shellfish toxins (PSTs and ASTs). It is mainly centered on studies in which the presence of PSTs and/or ASTs in seabird samples was demonstrated through analyses. The analytical techniques commonly employed, the tissues selected and the adjustments done in protocols for processing seabird matrixes are summarized. Other topics covered include the role of different vectors in the seabird intoxications, information on clinical signs in birds affected by PSTs and ASTs, and multifactorial causes which could aggravate the syndromes. Close collaboration between seabird experts and marine biotoxins researchers is needed to identify and report the potential involvement of HABs and their toxins in the mortality events. Future studies on the PSTs and ASTs pharmacodynamics, together with the establishment of lethal doses in various seabird species, are also necessary. These studies would aid in the selection of the target organs for toxins analyses and in the postmortem intoxication diagnoses.

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The IOC-ICES-PICES Harmful Algal Event Database (HAEDAT) was used to describe the diversity and spatiotemporal distribution of harmful algal events along the Atlantic margin of Europe from 1987 - 2018. The majority of events recorded are caused by Diarrhetic Shellfish Toxins (DSTs). These events are recorded annually over a wide geographic area from southern Spain to northern Scotland and Iceland, and are responsible for annual closures of many shellfish harvesting areas. The dominant causative dinoflagellates, members of the morphospecies 'Dinophysis acuminata complex' and D. acuta, are common in the waters of the majority of countries affected. There are regional differences in the causative species associated with PST events; the coasts of Spain and Portugal with the dinoflagellates Alexandrium minutum and Gymnodinium catenatum, north west France/south west England/south Ireland with A. minutum, and Scotland/Faroe Islands/Iceland with A. catenella. This can influence the duration and spatial scale of PST events as well as the toxicity of shellfish. The diatom Pseudo-nitzschia australis is the most widespread Domoic Acid (DA) producer, with records coming from Spain, Portugal, France, Ireland and the UK. Amnesic Shellfish Toxins (ASTs) have caused prolonged closures for the scallop fishing industry due to the slow depuration rate of DA. Amendments to EU shellfish hygiene regulations introduced between 2002 and 2005 facilitated end-product testing and sale of adductor muscle. This reduced the impact of ASTs on the scallop fishing industry and thus the number of recorded HAEDAT events. Azaspiracids (AZAs) are the most recent toxin group responsible for events to be characterised in the ICES area. Events associated with AZAs have a discrete distribution with the majority recorded along the west coast of Ireland. Ciguatera Poisoning (CP) has been an emerging issue in the Canary Islands and Madeira since 2004. The majority of aquaculture and wild fish mortality events are associated with blooms of the dinoflagellate Karenia mikimotoi and raphidophyte Heterosigma akashiwo. Such fish killing events occur infrequently yet can cause significant mortalities. Interannual variability was observed in the annual number of HAEDAT areas with events associated with individual shellfish toxin groups. HABs represent a continued risk for the aquaculture industry along the Atlantic margin of Europe and should be accounted for when considering expansion of the industry or operational shifts to offshore areas.

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The octocoral, Paramuricea clavata, is a habitat-forming anthozoan with a key ecological role in rocky benthic and biodiversity-rich communities in the Mediterranean and Eastern Atlantic. Shallow populations of P. clavata in the North-Western Mediterranean are severely affected by warming-induced mass mortality events (MMEs). These MMEs have differentially impacted individuals and populations of P. clavata (i.e., varied levels of tissue necrosis and mortality rates) over thousands of kilometers of coastal areas. The eco-evolutionary processes, including genetic factors, contributing to these differential responses remain to be characterized. Here, we sequenced a P. clavata individual with short and long read technologies, producing 169.98 Gb of Illumina paired-end and 3.55 Gb of Oxford Nanopore Technologies (ONT) reads. We obtained a de novo genome assembly accounting for 607 Mb in 64,145 scaffolds. The contig and scaffold N50s are 19.15 Kb and 23.92 Kb, respectively. Despite of the low contiguity of the assembly, its gene completeness is relatively high, including 75.8% complete and 9.4% fragmented genes out of the 978 metazoan genes contained in the metazoa_odb9 database. A total of 62,652 protein-coding genes have been annotated. This assembly is one of the few octocoral genomes currently available. This is undoubtedly a valuable resource for characterizing the genetic bases of the differential responses to thermal stress and for the identification of thermo-resistant individuals and populations. Overall, having the genome of P. clavata will facilitate studies of various aspects of its evolutionary ecology and elaboration of effective conservation plans such as active restoration to overcome the threats of global change.

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BACKGROUND: This study provides biochemical and molecular genetic characteristics of P. multocida isolated from dead saigas in 1988, 2010-2015 on the territory of the Republic of Kazakhstan. RESULTS: Bacteriological samples taken from carcasses of saiga antelope during mortality events recorded in West Kazakhstan in both 2010 and 2011 and in Kostanay in 2012 and 2015 confirmed the presence of P. multocida, according to morphological and biochemical characterisation. Only in the event of 2015 was the agent proven to be the causative agent of the disease observed, haemorrhagic septicaemia. In the other mortality events it is not certain if the organism was a primary aetiology or an incidental finding as confirmatory pathological investigation was not undertaken. The implemented phylogenetic analysis of ribosomal RNA 16S gene allowed us to identify Pasteurella strains isolated in 2010-2015 as P. multocida subspecies multocida. Capsular typing by PCR showed that the studied strains isolated from dead saiga in 2010, 2011, 2012 and 2015 belonged to serotype B. MLST analysis showed that these strains of P. multocida are of the capsule type B and form one clonal grouping with isolates ST64, ST44, ST45, ST46, ST44, ST47 which isolated from cases of hemorrhagic septicemia of animals in Hungary, Burma, Sri Lanka, Pakistan and Spain. Sixteen virulence genes of the five strains of P. multocida, isolated from saigas were studied using multiplex PCR. ptfA, ompA, ompH, oma87, plpB, fimA, hsf-2, pfhA, exbB, tonB, hgbA, fur, nanB, nanH and pmHAS genes were detected in all strains. The toxA gene was not identified in the studied strains. The phylogenies of these isolates is compared across saiga populations and years and the 2015 isolate was compared to that of an isolate from a disease outbreak in 1988 and the findings suggest that these isolated bacteria are stable commensals, opportunistically pathogenic, being phylogenetically uniform with very little genetic variation notable over the last 4 decades. CONCLUSION: Isolation, phenotypic and genetic characterization of the P. multocida isolates inform understanding of the epidemiology of infection in saigas and predict virulent potential of these opportunistic bacteria.

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Objective: To estimate the association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular events as well as all-cause mortality events. Methods: During 2009- 2010, out of the 11 623 individuals, 1 000 participants aged 35-64 years, were recruited and divided into 12 age-groups, to have received a study on CVD risk factors. Information on the risk factors of cardiovascular diseases was also collected. Fasting blood sample was gathered for all the participants, with hs-CRP tested. Participants in 7 out of the 12 sites were followed, with 6.21 years (36 075 person-years) as the median follow-up period. Cardiovascular and all-cause mortality events were collected. A total of 6 177 participants had been followed after excluding participants who had baseline infections, or did not take hs-CRP test/physical examination at the baseline. Finally, 5 984 participants were included for analysis. Participants were categorized into three groups based on the hs-CRP (mg/L) values: <1, 1-3 and >3, respectively. Cox proportional hazards regression model was used to analyze the relationships between hs-CRP with cardiovascular events or all-cause mortality events, after adjusting for confounding factors. Results: Mean age of the participants was 50.2 years. The incidence rates of cardiovascular disease events were 3.6/1 000 person-years, 7.1/1 000 person-years,and 10.4/1 000 person-years among three groups and 3.0/1 000 person-years, 5.7/1 000 person-years, 9.1/1 000 person-years for all-cause mortality events, respectively. After adjusting for confounding factors, the hazard risks (HR) for cardiovascular events were 1.33 (95%CI: 0.95-1.84) in the hs-CRP 1-3 mg/L group and 1.76 (95%CI: 1.20-2.60) in the hs-CRP>3 mg/L group when comparing with the hs-CRP<1 mg/L group (trend test P=0.003). The HRs for all-cause mortality events were 1.76 (95%CI: 1.23-2.54) and 2.64 (95%CI: 1.74-4.01) (trend test P<0.001), respectively. Conclusion: Hs-CRP appeared an independent predictor for cardiovascular events and all-cause mortality events.

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Objective: To estimate the association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular events as well as all-cause mortality events. Methods: During 2009- 2010, out of the 11 623 individuals, 1 000 participants aged 35-64 years, were recruited and divided into 12 age-groups, to have received a study on CVD risk factors. Information on the risk factors of cardiovascular diseases was also collected. Fasting blood sample was gathered for all the participants, with hs-CRP tested. Participants in 7 out of the 12 sites were followed, with 6.21 years (36 075 person-years) as the median follow-up period. Cardiovascular and all-cause mortality events were collected. A total of 6 177 participants had been followed after excluding participants who had baseline infections, or did not take hs-CRP test/physical examination at the baseline. Finally, 5 984 participants were included for analysis. Participants were categorized into three groups based on the hs-CRP (mg/L) values: <1, 1-3 and >3, respectively. Cox proportional hazards regression model was used to analyze the relationships between hs-CRP with cardiovascular events or all-cause mortality events, after adjusting for confounding factors. Results: Mean age of the participants was 50.2 years. The incidence rates of cardiovascular disease events were 3.6/1 000 person-years, 7.1/1 000 person-years,and 10.4/1 000 person-years among three groups and 3.0/1 000 person-years, 5.7/1 000 person-years, 9.1/1 000 person-years for all-cause mortality events, respectively. After adjusting for confounding factors, the hazard risks (HR) for cardiovascular events were 1.33 (95%CI: 0.95-1.84) in the hs-CRP 1-3 mg/L group and 1.76 (95%CI: 1.20-2.60) in the hs-CRP>3 mg/L group when comparing with the hs-CRP<1 mg/L group (trend test P=0.003). The HRs for all-cause mortality events were 1.76 (95%CI: 1.23-2.54) and 2.64 (95%CI: 1.74-4.01) (trend test P<0.001), respectively. Conclusion: Hs-CRP appeared an independent predictor for cardiovascular events and all-cause mortality events.

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Objective To estimate the association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular events as well as all-cause mortality events.Methods During 2009-2010,out of the 11 623 individuals,1 000 participants aged 35-64 years,were recruited and divided into 12 age-groups,to have received a study on CVD risk factors.Information on the risk factors of cardiovascular diseases was also collected.Fasting blood sample was gathered for all the participants,with hs-CRP tested.Participants in 7 out of the 12 sites were followed,with 6.21 years (36 075 personyears) as the median follow-up period.Cardiovascular and all-cause mortality events were collected.A total of 6 177 participants had been followed after excluding participants who had baseline infections,or did not take hs-CRP test/physical examination at the baseline.Finally,5 984 participants were included for analysis.Participants were categorized into three groups based on the hs-CRP (mg/L) values:＜ 1,1-3 and ＞3,respectively.Cox proportional hazards regression model was used to analyze the relationships between hs-CRP with cardiovascular events or all-cause mortality events,after adjusting for confounding factors.Results Mean age of the participants was 50.2 years.The incidence rates of cardiovascular disease events were 3.6/1 000 person-years,7.1/1 000 person-years,and 10.4/1 000 person-years among three groups and 3.0/1 000 person-years,5.7/1 000 person-years,9.1/1 000 person-years for all-cause mortality events,respectively.After adjusting for confounding factors,the hazard risks (HR) for cardiovascular events were 1.33 (95％CI:0.95-1.84) in the hs-CRP 1-3 mg/L group and 1.76 (95％CI:1.20-2.60) in the hs-CRP＞3 mg/L group when comparing with the hs-CRP＜ 1 mg/L group (trend test P=0.003).The HRs for all-cause mortality events were 1.76 (95％CI:1.23-2.54) and 2.64 (95％CI:1.74-4.01) (trend test P＜0.001),respectively.Conclusion Hs-CRP appeared an independent predictor for cardiovascular events and all-cause mortality events.

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Mass mortality events caused by pulse anthropogenic or environmental perturbations (e.g., extreme weather, toxic spills or epizootics) severely reduce the abundance of a population in a short time. The frequency and impact of these events are likely to increase across the globe. Studies on how such events may affect ecological communities of interacting species are scarce. By combining a multispecies Gompertz model with a Bayesian state-space framework, we quantify community-level effects of a mass mortality event in a single species. We present a case study on a community of fish and zooplankton in the Barents Sea to illustrate how a mass mortality event of different intensities affecting the lower trophic level (krill) may propagate to higher trophic levels (capelin and cod). This approach is especially valuable for assessing community-level effects of potential anthropogenic-driven mass mortality events, owing to the ability to account for uncertainty in the assessed impact due to uncertainty about the ecological dynamics. We hence quantify how the assessed impact of a mass mortality event depends on the degree of precaution considered. We suggest that this approach can be useful for assessing the possible detrimental outcomes of toxic spills, for example oil spills, in relatively simple communities such as often found in the Arctic, a region under increasing influence of human activities due to increased land and sea use.

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Marine mammals in the past mass mortality events may have been susceptible to infection because their immune systems were suppressed through the bioaccumulation of environmental pollutants such as polychlorinated biphenyls (PCBs). We compiled mortality event data sets of 33 marine mammal species, and employed a Finely-Advanced Transboundary Environmental model (FATE) to model the exposure of the global fish community to PCB congeners, in order to define critical exposure levels (CELs) of PCBs above which mass mortality events are likely to occur. Our modelling approach enabled us to describe the mass mortality events in the context of exposure of higher-trophic consumers to PCBs and to identify marine pollution 'hotspots' such as the Mediterranean Sea and north-western European coasts. We demonstrated that the CELs can be applied to quantify a chemical pollution Planetary Boundary, under which a safe operating space for marine mammals and humanity can exist.

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