BackgroundPopulation ageing is an increasingly severe global issue. And this has been posing challenges for public health policies and medical resource allocation There are various features of population ageing in different regions worldwide.MethodsAll data were obtained from the health data of World Bank Open Data. Quantile linear regression was used to subtly measure the common variation tendency and strength of the global ageing rate and ageing population. The Bayesian space-time hierarchy model (BSTHM) was employed to assess the detailed spatial temporal evolution of ageing rate and ageing population in global 195 countries and regions.ResultsAnnual growth of the ageing (65 and above) rate occurred on six continents: Europe (0.1532%), Oceania (0.0873%), Asia (0.0834%), South America (0.0723%), North America (0.0673%) and Africa (0.0069%). The coefficient of variation of the global ageing rate increased from 0.54 in 1960 to 0.69 in 2017. The global ageing rate and ageing population increased over this period, correlating positively with their quantiles. Most countries (37/39) in Europe belong to the top level with regard to the ageing rate, including the countries with the greatest degree of ageing—Sweden, Germany, Austria, Belgium and the UK—whose spatial relative risks of ageing are 3.180 (3.113–3.214), 3.071 (3.018–3.122), 2.951 (2.903–3.001), 2.932 (2.880–2.984) and 2.917 (2.869–2.967), respectively. Worldwide, 44 low ageing areas which were distributed mainly in Africa (26 areas) and Asia (15 areas) experienced a decreasing trend of ageing rates. The local trends of ageing population in the 195 areas increased.ConclusionsThe differentiation of global population ageing is becoming increasingly serious. Globally, all 195 areas showed an increasing local ageing trend in absolute terms, although there were 44 low-ageing areas that experienced a decreasing local trend of ageing rate. The statistical results may provide some baseline reference for developing public health policies in various countries or regions, especially in less-developed areas.
The relentless adaptability of pathogen populations is a major obstacle to effective disease control measures. Increasing evidence suggests that gene transcriptional polymorphisms are a strategy deployed by pathogens to evade host immunity. However, the underlying mechanisms of transcriptional plasticity remain largely elusive. Here we found that the soybean root rot pathogen Phytophthora sojae evades the soybean Resistance gene Rps1b through transcriptional polymorphisms in the effector gene Avr1b that occur in the absence of any sequence variation. Elevated levels of histone H3 Lysine27 tri-methylation (H3K27me3) were observed at the Avr1b locus in a naturally occurring Avr1b-silenced strain but not in an Avr1b-expressing strain, suggesting a correlation between this epigenetic modification and silencing of Avr1b. To genetically test this hypothesis, we edited the gene, PsSu(z)12, encoding a core subunit of the H3K27me3 methyltransferase complex by using CRISPR/Cas9, and obtained three deletion mutants. H3K27me3 depletion within the Avr1b genomic region correlated with impaired Avr1b gene silencing in these mutants. Importantly, these mutants lost the ability to evade immune recognition by soybeans carrying Rps1b. These data support a model in which pathogen effector transcriptional polymorphisms are associated with changes in chromatin epigenetic marks, highlighting epigenetic variation as a mechanism of pathogen adaptive plasticity.
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