Background Worldwide, both the incidence and death rates of pancreatic cancer are increasing. Evaluation of pancreatic cancer burden and its global, regional, and national patterns is crucial to policy making and better resource allocation for controlling pancreatic cancer risk factors, developing early detection methods, and providing faster and more effective treatments. Methods Vital registration, vital registration sample, and cancer registry data were used to generate mortality, incidence, and disability-adjusted life-years (DALYs) estimates. We used the comparative risk assessment framework to estimate the proportion of deaths attributable to risk factors for pancreatic cancer: smoking, high fasting plasma glucose, and high body-mass index. All of the estimates were reported as counts and age-standardised rates per 100 000 person-years. 95% uncertainty intervals (UIs) were reported for all estimates. Findings In 2017, there were 448 000 (95% UI 439 000-456 000) incident cases of pancreatic cancer globally, of which 232 000 (210 000-221 000; 51•9%) were in males. The age-standardised incidence rate was 5•0 (4•9-5•1) per 100 000 person-years in 1990 and increased to 5•7 (5•6-5•8) per 100 000 person-years in 2017. There was a 2•3 times increase in number of deaths for both sexes from 196 000 (193 000-200 000) in 1990 to 441 000 (433 000-449 000) in 2017. There was a 2•1 times increase in DALYs due to pancreatic cancer, increasing from 4•4 million (4•3-4•5) in 1990 to 9•1 million (8•9-9•3) in 2017. The age-standardised death rate of pancreatic cancer was highest in the highincome super-region across all years from 1990 to 2017. In 2017, the highest age-standardised death rates were observed in Greenland (17•4 [15•8-19•0] per 100 000 person-years) and Uruguay (12•1 [10•9-13•5] per 100 000 personyears). These countries also had the highest age-standardised death rates in 1990. Bangladesh (1•9 [1•5-2•3] per 100 000 person-years) had the lowest rate in 2017, and São Tomé and Príncipe (1•3 [1•1-1•5] per 100 000 personyears) had the lowest rate in 1990. The numbers of incident cases and deaths peaked at the ages of 65-69 years for males and at 75-79 years for females. Age-standardised pancreatic cancer deaths worldwide were primarily attributable to smoking (21•1% [18•8-23•7]), high fasting plasma glucose (8•9% [2•1-19•4]), and high body-mass index (6•2% [2•5-11•4]) in 2017. Interpretation Globally, the number of deaths, incident cases, and DALYs caused by pancreatic cancer has more than doubled from 1990 to 2017. The increase in incidence of pancreatic cancer is likely to continue as the population ages. Prevention strategies should focus on modifiable risk factors. Development of screening programmes for early detection and more effective treatment strategies for pancreatic cancer are needed. Funding Bill & Melinda Gates Foundation.

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We proposed a new model of DNA structure, which allows rearrangement of monomers in the polymer chain backbone according to mathematical laws. On the basis of the analysis of structural organization of DNA we concluded that rearrangements of monomers should also occur during the formation of the molecular structure of other polymers (RNA and proteins).

The kinetics of DNA synthesis in the mitotic cycle of mouse corneal epithelial cells was studied after a single γ-irradiation of cells in a dose of 4 Gy at different S-phase points. Normally, corneal epitheliocyte S phase consists of S1 and S2 phases separated by an interval during which no DNA is synthesized. The duration of each phase was lengthened after single irradiation due to reparation of injuries in the cells at the expense of the time normally occupied by g1 period of the mitotic cycle. The first event during reparation is excision of damaged complex from the DNA molecule; this complex consists of labeled daughter fragment and matrix site of DNA chain that was used for the synthesis of the daughter fragment. Presumably, the entire reparation process in the cell consists of two stages: "reparative" synthesis and "additional" synthesis. The reparative synthesis, in turn, includes two stages: de novo synthesis of matrix fragment in the DNA chain at the site of the gap formation and de novo synthesis of the daughter fragment after the synthesis of the new matrix fragment is over.