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In order to describe the role of sedimentary processes for the phosphorus (P) cycle in the open Baltic Proper, P deposition and reflux were quantified for the predominately anoxic sediments of the Eastern Gotland Basin. The study is based on investigations of 53 surface sediment samples and pore water samples from 8 sediment cores. The average P deposition rate was estimated at 0.20 g±0.18 g m−2 yr−1, the fluctuation being due to variable bulk sediment deposition rates. P refluxes were estimated by applying Fick’s First Law of Diffusion. A fairly good positive correlation between sedimentary P deposition and P release was obtained. P release from sediments by diffusion exceeds net P deposition by a factor of 2. This suggests that 2/3 of the deposited gross P is recycled in the sediments and released back into the water column; only 1/3 remains in the sediment permanently. A budget calculation demonstrates that the released dissolved inorganic phosphorus (DIP) accounts for the observed increase in DIP concentrations in the deep water during periods of stagnation, which is noticeable even at the surface P concentrations. Under such conditions and with the present remediation conditions it is not possible to freely manage P concentrations in the water column on short time scales.
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Helicobacter pylori infection in pathogenesis of gastroesophageal reflux disease

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Gastroesophageal reflux disease (GERD) refers to the very common and constantly increasing conditions where reflux of gastric contents into the esophagus leads to development of characteristic symptoms. The esophagus, LES and stomach can be envisioned as single functional unit controlled by neuro-hormonal factors. The abnormalities that contribute to GERD can start in any component of this unit, resulting particularly from disturbances in their control system. It is extremely important to identify factors and mechanisms leading to functional failure of this system so that causative therapy can be effectively applied. The key-role has been attributed to parasympathetic dysfunction, which may adversely affect motor activity of this area by increasing transient LES relaxation number and impairing LES pressure, esophageal acid clearance and motility of the proximal stomach. Recently, numerous investigations have been performed to elucidate the role of Helicobacter pylori (Hp) infection in GERD pathogenesis with the most concern given to its potency to increase gastric acid secretion. However, it appeared that this infection leads to much more complex changes in gastric mucosa including modification of afferent neural signals and specific gastric hormones release. Plasma ghrelin level is low in subjects infected and increases significantly after eradication. Since ghrelin, beside potency to increase gastric secretion has strong prokinetic action on LES functional unit, this phenomenon together with impaired vagal control may contribute to the Hp infection or eradication - related GERD development. Thus, ghrelin and vagal activity could be the missing links that partially explains relationship between GERD and Hp infection.
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