BackgroundLifetime stroke risk has been calculated in a limited number of selected populations. We determined lifetime risk of stroke globally and at the regional and country level.MethodsUsing Global Burden of Disease Study estimates of stroke incidence and the competing risks of non-stroke mortality, we estimated the cumulative lifetime risk of ischemic stroke, hemorrhagic stroke, and total stroke (with 95% uncertainty intervals [UI]) for 195 countries among adults over 25 years) for the years 1990 and 2016 and according to the GBD Study Socio-Demographic Index (SDI).ResultsThe global estimated lifetime risk of stroke from age 25 onward was 24.9% (95% UI: 23.5–26.2): 24.7% (23.3–26.0) in men and 25.1% (23.7–26.5) in women. The lifetime risk of ischemic stroke was 18.3% and of hemorrhagic stroke was 8.2%. The risk of stroke was 23.5% in high SDI countries, 31.1% in high-middle SDI countries, and 13.2% in low SDI countries with UIs not overlapping for these categories. The greatest estimated risk of stroke was in East Asia (38.8%) and Central and Eastern Europe (31.7 and 31.6 %%), and lowest in Eastern Sub-Saharan Africa (11.8%). From 1990 to 2016, there was a relative increase of 8.9% in global lifetime risk.ConclusionsThe global lifetime risk of stroke is approximately 25% starting at age 25 in both men and women. There is geographical variation in the lifetime risk of stroke, with particularly high risk in East Asia, Central and Eastern Europe.

A cardioacceleratory peptide, CAP2b, identified originally in the lepidopteran Manduca sexta, stimulates fluid secretion by Malpighian tubules of the dipteran Drosophila melanogaster. High-performance liquid chromatography analyses of adult D. melanogaster reveal the presence of a CAP2b-like peptide, that coelutes with M. sexta CAP2b and synthetic CAP2b and that has CAP2b-like effects on the M. sexta heart. CAP2b accelerates fluid secretion in tubules stimulated by adenosine 3',5'-cyclic monophosphate (cAMP) but has no effect on tubules stimulated by guanosine 3',5'-cyclic monophosphate (cGMP), implying that it acts through the latter pathway. By contrast, the action of leucokinin is additive to both cAMP and cGMP but not to thapsigargin, suggesting that leucokinin acts by the elevation of intracellular calcium. CAP2b stimulation elevates tubule cGMP levels but not those of cAMP. By contrast, leucokinin has no effect on levels of either cyclic nucleotide. Both CAP2b and cGMP increase transepithelial potential difference, suggesting that stimulation of vacuolar-adenosinetriphosphatase action underlies the corresponding increases in fluid secretion. Overall, the results show that a Drosophila CAP2b-related peptide acts to stimulate fluid secretion by Malpighian tubules through the cGMP-signaling pathway.

SUMMARYWhen agitated, Atlantic hagfish (Myxine glutinosa) produce large quantities of slime that consists of hydrated bundles of protein filaments and membrane-bound mucin vesicles from numerous slime glands. When the slime exudate contacts seawater, the thread bundles unravel and the mucin vesicles swell and rupture. Little is known about the mechanisms of vesicle rupture in seawater and stabilization within the gland, although it is believed that the vesicle membrane is permeable to most ions except polyvalent anions. We hypothesized that the most abundant compounds within the slime gland exudate have a stabilizing effect on the mucin vesicles. To test this hypothesis, we measured the chemical composition of the fluid component of hagfish slime exudate and conducted functional assays with these solutes to test their ability to keep the vesicles in a condensed state. We found K + concentrations that were elevated relative to plasma, and Na + , Cl -and Ca 2+ concentrations that were considerably lower. Our analysis also revealed high levels of methylamines such as trimethylamine oxide (TMAO), betaine and dimethylglycine, which had a combined concentration of 388 mmol l -1 in the glandular fluid. In vitro rupture assays demonstrated that both TMAO and betaine had a significant effect on rupture, but neither was capable of completely abolishing mucin swelling and rupture, even at high concentrations. This suggests that some other mechanism such as the chemical microenvironment within gland mucous cells, or hydrostatic pressure is responsible for stabilization of the vesicles within the gland.

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+concentration and a 0.3-0.6·pH unit increase on the cutaneous surface of R. marmoratus. In air-exposed fish, the calculated cutaneous partial pressure (P NH 3 3) was 608-1251· Torr, representing a 33-to 75-fold increase over control (immersed) fish. The P NH 3 3 on the cutaneous surface water film was more than sufficient to account for the rate of NH 3 volatilization under terrestrial conditions. Together, these data indicate that during air exposure, R. marmoratus utilize the cutaneous surface as a key site of NH 3 volatilization.