Actual causes of death in Alaska.
Ontology highlight
ABSTRACT:
SUBMITTER: Cueva K
PROVIDER: S-EPMC7480475 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Despite numerous public health advancements over the last century, we continue to under-invest in prevention and public health efforts. As a result, one of the most challenging aspects of public health is prioritizing the use of limited resources. Building on the foundation of previous researchers, the goal of this exploratory study was to provide current estimates for the actual causes of death, media attention, policy focus, and research funding in the United States. In addition, we sought to calculate and compare media attention, policy attention, and research funding trends to better assess the nation's prioritization of health issues. Using a systematic approach, we searched available databases, including Media Cloud, Nexis Uni, Congress.gov, and the Department of Health and Human Services Tracking Accountability in Government Grants System from January 1, 2010-December 31, 2019 and compared how the actual causes of death in the United States align with health-related media attention, policy attention, and federal spending. Overall, our findings suggest that our priorities are not well-aligned with the actual causes of death. Certain actual causes appear to be consistently misaligned across media, legislative, and financial sectors (e.g., tobacco). This work highlights the importance of multiple strategies-media coverage, national legislation, and government spending-as indicators of public health attention and priorities. These results may inform discussions about how to best allocate U.S. public health resources to better align with the actual causes of death.
| S-EPMC7358349 | biostudies-literature
Project description:BackgroundTo isolate progress against cancer from changes in competing causes of death, population cancer registries have traditionally reported cancer prognosis (net measures). But clinicians and cancer patients generally want to understand actual prognosis (crude measures): the chance of surviving, dying from the specific cancer and from competing causes of death in a given time period.ObjectiveTo compare cancer and actual prognosis in the United States for four leading cancers-lung, breast, prostate, and colon-by age, comorbidity, and cancer stage and to provide templates to help patients, clinicians, and researchers understand actual prognosis.MethodUsing population-based registry data from the Surveillance, Epidemiology, and End Results (SEER) Program, we calculated cancer prognosis (relative survival) and actual prognosis (five-year overall survival and the "crude" probability of dying from cancer and competing causes) for three important prognostic determinants (age, comorbidity [Charlson-score from 2012 SEER-Medicare linkage dataset] and cancer stage at diagnosis).ResultFor younger, healthier, and earlier stage cancer patients, cancer and actual prognosis estimates were quite similar. For older and sicker patients, these prognosis estimates differed substantially. For example, the five-year overall survival for an 85-year-old patient with colorectal cancer is 54% (cancer prognosis) versus 22% (actual prognosis)-the difference reflecting the patient's substantial chance of dying from competing causes. The corresponding five-year chances of dying from the patient's cancer are 46% versus 37%. Although age and comorbidity lowered actual prognosis, stage at diagnosis was the most powerful factor: The five-year chance of colon cancer death was 10% for localized stage and 83% for distant stage.ConclusionBoth cancer and actual prognosis measures are important. Cancer registries should routinely report both cancer and actual prognosis to help clinicians and researchers understand the difference between these measures and what question they can and cannot answer. We encourage them to use formats like the ones presented in this paper to communicate them clearly.
| S-EPMC4841170 | biostudies-literature
Project description:ObjectivesCumulative incidence of lung cancer deaths (LC-CID) is an important metric to understand cancer prognosis and to determine treatment options. However, credible estimates of LC-CID rely on accurate cause-of-death coding in death certificates. Results from lung cancer screening trials estimated 15% under-reporting and 1% over-reporting of lung cancer deaths due to misclassification. This study investigated the impact of cause-of-death misclassification on the estimation of LC-CID.Materials and methodsPatients with stage I/II non-small cell lung cancer (NSCLC) from the Surveillance, Epidemiology, and End Results registry were included. LC-CID was estimated using the competing-risk approach in two ways: (1) reporting observed estimates that ignore potential cause-of-death misclassification and (2) correcting for plausible misclassification rates reported in the literature (15% under-reporting and 1% over-reporting). Bias was quantified as the difference between observed and corrected 10-year LC-CIDs: positive values indicated that observed LC-CID overestimated true LC-CID, whereas negative values indicated the opposite.ResultsAmong 66,179 patients, the impact of over-reporting on 10-year LC-CID was negligible across all age groups. In contrast, under-reporting resulted in substantial underestimation of 10-year LC-CID. The biases increased as age increased due to higher LC-CIDs: 10-year LC-CIDs among stage I patients 18-44, 45-59, 60-74 and ≥75 years were 25%, 32%, 41%, and 50%, respectively, and the corresponding biases given the plausible misclassification rates were -4.4%, -5.6%, -7.1%, and -8.6%. Because the observed LC-CIDs among patients with stage II disease were higher than those with stage I disease, the biases were greater among stage II patients, up to -12.5% in the oldest age group.ConclusionsIn lung cancer, LC-CID may be severely underestimated due to under-reporting of lung cancer deaths, particularly among older patients or those with late-stage disease. Future studies that involve such subpopulations should present the corrected LC-CIDs based on plausible misclassification rates alongside the observed LC-CIDs.
| S-EPMC6650158 | biostudies-literature
Project description:Finding actual causes of unmanned aerial vehicle (UAV) failures can be split into two main tasks: building causal models and performing actual causality analysis (ACA) over them. While there are available solutions in the literature to perform ACA, building comprehensive causal models is still an open problem. The expensive and time-consuming process of building such models, typically performed manually by domain experts, has hindered the widespread application of causality-based diagnosis solutions in practice. This study proposes a methodology based on natural language processing for automating causal model generation for UAVs. After collecting textual data from online resources, causal keywords are identified in sentences. Next, cause-effect phrases are extracted from sentences based on predefined dependency rules between tokens. Finally, the extracted cause-effect pairs are merged to form a causal graph, which we then use for ACA. To demonstrate the applicability of our framework, we scrape online text resources of Ardupilot, an open-source UAV controller software. Our evaluations using real flight logs show that the generated graphs can successfully be used to find the actual causes of unwanted events. Moreover, our hybrid cause-effect extraction module performs better than a purely deep-learning based tool (i.e., CiRA) by 32% in precision and 25% in recall in our Ardupilot use case.
| S-EPMC10880731 | biostudies-literature
Project description:Relict woolly mammoth (Mammuthus primigenius) populations survived on several small Beringian islands for thousands of years after mainland populations went extinct. Here we present multiproxy paleoenvironmental records to investigate the timing, causes, and consequences of mammoth disappearance from St. Paul Island, Alaska. Five independent indicators of extinction show that mammoths survived on St. Paul until 5,600 ± 100 y ago. Vegetation composition remained stable during the extinction window, and there is no evidence of human presence on the island before 1787 CE, suggesting that these factors were not extinction drivers. Instead, the extinction coincided with declining freshwater resources and drier climates between 7,850 and 5,600 y ago, as inferred from sedimentary magnetic susceptibility, oxygen isotopes, and diatom and cladoceran assemblages in a sediment core from a freshwater lake on the island, and stable nitrogen isotopes from mammoth remains. Contrary to other extinction models for the St. Paul mammoth population, this evidence indicates that this mammoth population died out because of the synergistic effects of shrinking island area and freshwater scarcity caused by rising sea levels and regional climate change. Degradation of water quality by intensified mammoth activity around the lake likely exacerbated the situation. The St. Paul mammoth demise is now one of the best-dated prehistoric extinctions, highlighting freshwater limitation as an overlooked extinction driver and underscoring the vulnerability of small island populations to environmental change, even in the absence of human influence.
| S-EPMC4995940 | biostudies-literature
Project description:Background:The purpose of our study was to characterize the causes of death among cancer patients as a function of objectives: (i) calendar year, (ii) patient age, and (iii) time after diagnosis. Patients and methods:US death certificate data in Surveillance, Epidemiology, and End Results Stat 8.2.1 were used to categorize cancer patient death as being due to index-cancer, nonindex-cancer, and noncancer cause from 1973 to 2012. In addition, data were characterized with standardized mortality ratios (SMRs), which provide the relative risk of death compared with all persons. Results:The greatest relative decrease in index-cancer death (generally from?>?60% to?<?30%) was among those with cancers of the testis, kidney, bladder, endometrium, breast, cervix, prostate, ovary, anus, colorectum, melanoma, and lymphoma. Index-cancer deaths were stable (typically?>40%) among patients with cancers of the liver, pancreas, esophagus, and lung, and brain. Noncancer causes of death were highest in patients with cancers of the colorectum, bladder, kidney, endometrium, breast, prostate, testis;?>40% of deaths from heart disease. The highest SMRs were from nonbacterial infections, particularly among?<50-year olds (e.g. SMR?>1,000 for lymphomas, P?<?0.001). The highest SMRs were typically within the first year after cancer diagnosis (SMRs 10-10,000, P?<?0.001). Prostate cancer patients had increasing SMRs from Alzheimer's disease, as did testicular patients from suicide. Conclusion:The risk of death from index- and nonindex-cancers varies widely among primary sites. Risk of noncancer deaths now surpasses that of cancer deaths, particularly for young patients in the year after diagnosis.
| S-EPMC5834100 | biostudies-literature
Project description:Withaferin A (WA), a major chemical component of an Indian herb Withania somnifera, induces cell death (apoptosis/necrosis) in a variety of tumor cells, but its molecular mechanism remains elusive. We report that WA induces cell death selectively in high-grade prostate (PC-3 and DU-145) and tongue (SAS) cancer cells but not in normal human fibroblast (TIG-1) and low-grade prostate cancer (LNCaP) cells. To identify genes whose expression levels were up- or down-regulated in prostate cancer cells following WA treatment, we examined the transcriptome profiles of mRNA prepared from TIG-1, LNCaP, PC-3 and DU-145 cells using Agilent’s Whole Human Genome Microarray.
2015-08-02 | E-GEOD-55728 | biostudies-arrayexpress
Project description:ImportanceA recent increase in patients presenting with nonfatal opioid overdoses has focused clinical attention on characterizing their risks of premature mortality.ObjectiveTo describe all-cause mortality rates, selected cause-specific mortality rates, and standardized mortality rate ratios (SMRs) of adults during their first year after nonfatal opioid overdose.Design, setting, and participantsThis US national longitudinal study assesses a cohort of patients aged 18 to 64 years who were Medicaid beneficiaries and experienced nonfatal opioid overdoses. The Medicaid data set included the years 2001 through 2007. Death record information was obtained from the National Death Index. Data analysis occurred from October 2017 to January 2018.Main outcomes and measuresCrude mortality rates per 100 000 person-years were determined in the first year after nonfatal opioid overdose. Standardized mortality rate ratios (SMR) were estimated for all-cause and selected cause-specific mortality standardized to the general population with respect to age, sex, and race/ethnicity.ResultsThe primary cohort included 76 325 adults and 66 736 person-years of follow-up. During the first year after nonfatal opioid overdose, there were 5194 deaths, the crude death rate was 778.3 per 10 000 person-years, and the all-cause SMR was 24.2 (95% CI, 23.6-24.9). The most common immediate causes of death were substance use-associated diseases (26.2%), diseases of the circulatory system (13.2%), and cancer (10.3%). For every cause examined, SMRs were significantly elevated, especially with respect to drug use-associated diseases (SMR, 132.1; 95% CI, 125.6-140.0), HIV (SMR, 45.9; 95% CI, 39.5-53.0), chronic respiratory diseases (SMR, 41.1; 95% CI, 36.0-46.8), viral hepatitis (SMR, 30.6; 95% CI, 22.9-40.2), and suicide (SMR, 25.9; 95% CI, 22.6-29.6), particularly including suicide among females (SMR, 47.9; 95% CI, 39.8-52.3).Conclusions and relevanceIn a US national cohort of adults who had experienced a nonfatal opioid overdose, a marked excess of deaths was attributable to a wide range of substance use-associated, mental health, and medical conditions, underscoring the importance of closely coordinating the substance use, mental health, and medical care of this patient population.
| S-EPMC6143082 | biostudies-literature
Project description:BackgroundFamilial hypercholesterolemia (FH) is a codominant autosomal disease characterized by high low-density lipoprotein cholesterol (LDLc) and a high risk of premature cardiovascular disease (CVD). The molecular bases have been well defined, and effective lipid lowering is possible. This analysis aimed to study the current major causes of death of genetically defined heterozygous familial hypercholesterolemia (heFH).MethodsA case‒control study was designed to analyse life-long mortality in a group of heFH and control families. Data from first-degree family members of cases and controls (nonconsanguineous cohabitants), including deceased relatives, were collected from a questionnaire and review of medical records. Mortality was compared among heFH patients, nonheFH patients, and nonconsanguineous family members.ResultsA total of 813 family members were analysed, 26.4% of whom were deceased. Among the deceased, the mean age of death was 69.3 years in heFH individuals, 73.5 years in nonheFH individuals, and 73.2 years in nonconsanguineous individuals, without significant differences. CVD was the cause of death in 59.7% of heFH individuals, 37.7% of nonheFH individuals, and 37.4% of nonconsanguineous individuals (P = 0.012). These differences were greater after restricting the analyses to parents. The hazard ratio of dying from CVD was 2.85 times higher (95% CI, (1.73-4.69) in heFH individuals than in individuals in the other two groups (non-FH and nonconsanguineous), who did not differ in their risk.ConclusionsCVD mortality in heFH individuals is lower and occurs later than that described in the last century but is still higher than that in non-FH individuals. This improved prognosis of CVD risk is not associated with changes in non-CVD mortality.
| S-EPMC9344778 | biostudies-literature