The Initial Common Pathway of Inflammation, Disease, and Sudden Death

In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade

Effects of rising temperature on pelagic biogeochemistry in mesocosm systems: a comparative analysis of the AQUASHIFT Kiel experiments

A comparative analysis of data, obtained during four indoor-mesocosm experiments with natural spring plankton communities from the Baltic Sea, was conducted to investigate whether biogeochemical cycling is affected by an increase in water temperature of up to 6 °C above present-day conditions. In all experiments, warming stimulated in particular heterotrophic bacterial processes and had an accelerating effect on the temporal development of phytoplankton blooms. This was also mirrored in the build-up and partitioning of organic matter between particulate and dissolved phases. Thus, warming increased both the magnitude and rate of dissolved organic carbon (DOC) build-up, whereas the accumulation of particulate organic carbon (POC) and phosphorus (POP) decreased with rising temperature. In concert, the observed temperature-mediated changes in biogeochemical components suggest strong shifts in the functioning of marine pelagic food webs and the ocean’s biological carbon pump, hence providing potential feedback mechanisms to Earth’s climate system

Phyto- and bacterioplankton during early spring conditions in the Baltic Sea and response to short-term experimental warming

Predicted increases in sea surface temperatures are expected to shift the balance between autotrophic production and the heterotrophic degradation of organic matter toward a more heterotrophic system. For early phytoplankton spring blooms at low water temperature the impact of rising temperatures has been mainly investigated in mesocosm experiments, while field observations are scarce. During a Baltic Sea research cruise we examined early spring bloom conditions, characterized by low temperatures (0-3 degrees C), and performed on-board warming experiments to compare the responses of phyto- and bacterioplankton production to an increase in temperature. In the northern Baltic Sea, the low phytoplankton biomass indicated pre-bloom conditions. In the southern Baltic Sea, a diatom-dominated phytoplankton bloom with increased primary production (PP) occurred. Associated with this bloom were increases in bacterial production (BP) and bacterial abundance as well as shifts in bacterial community composition toward an increased proportion of Gammaproteobacteria and Bacteroidetes. However, the low BP/PP ratios (average: 1.2 +/- 0.14%) indicated weak coupling between the bacterial and phytoplankton communities. Short-term warming (6h, Delta+6 degrees C) significantly enhanced PP (mean Q(1)(0) 1.4) and especially BP (mean Q(1)(0) 2.3). Hence, the higher water temperature increased both carbon flow into the bacterial community and bacterial processing of organic matter, thereby confirming previous experimental studies. By contrast, BP/PP ratios remained relatively low after warming (average: 1.7 +/- 0.5%), unlike in previous mesocosm experiments performed at comparable temperatures and with similar plankton communities. Overall, these results imply that bacterial activities are suppressed during early phytoplankton blooms at low temperatures in the Baltic Sea and are not substantially altered by short-term warming events.Peer reviewe

Presentation_1_Phyto- and Bacterioplankton During Early Spring Conditions in the Baltic Sea and Response to Short-Term Experimental Warming.PDF

<p>Predicted increases in sea surface temperatures are expected to shift the balance between autotrophic production and the heterotrophic degradation of organic matter toward a more heterotrophic system. For early phytoplankton spring blooms at low water temperature the impact of rising temperatures has been mainly investigated in mesocosm experiments, while field observations are scarce. During a Baltic Sea research cruise we examined early spring bloom conditions, characterized by low temperatures (0–3°C), and performed on-board warming experiments to compare the responses of phyto- and bacterioplankton production to an increase in temperature. In the northern Baltic Sea, the low phytoplankton biomass indicated pre-bloom conditions. In the southern Baltic Sea, a diatom-dominated phytoplankton bloom with increased primary production (PP) occurred. Associated with this bloom were increases in bacterial production (BP) and bacterial abundance as well as shifts in bacterial community composition toward an increased proportion of Gammaproteobacteria and Bacteroidetes. However, the low BP/PP ratios (average: 1.2 ± 0.14%) indicated weak coupling between the bacterial and phytoplankton communities. Short-term warming (6 h, Δ+6°C) significantly enhanced PP (mean Q₁₀ 1.4) and especially BP (mean Q₁₀ 2.3). Hence, the higher water temperature increased both carbon flow into the bacterial community and bacterial processing of organic matter, thereby confirming previous experimental studies. By contrast, BP/PP ratios remained relatively low after warming (average: 1.7 ± 0.5%), unlike in previous mesocosm experiments performed at comparable temperatures and with similar plankton communities. Overall, these results imply that bacterial activities are suppressed during early phytoplankton blooms at low temperatures in the Baltic Sea and are not substantially altered by short-term warming events.</p

Inhibition of alpha2A-adrenoceptors ameliorates DSS-induced acute intestinal inflammation in mice

It has been hypothesized that alpha2-adrenoceptors (alpha2-ARs) may be involved in the pathomechanism of colitis, however, the results are conflicting since both aggravation and amelioration of colonic inflammation have been described in response to alpha2-AR agonists. Therefore, we aimed to analyse the role of alpha2-ARs in acute murine colitis. The experiments were carried out in wild-type (WT), alpha2A-, alpha2B- and alpha2C-AR knockout (KO) C57BL/6 mice. Colitis was induced by dextran sulfate sodium (DSS, 2 %), alpha2-AR ligands were injected intraperitoneally (i.p.). The severity of colitis was determined both macroscopically and histologically. Colonic myeloperoxidase (MPO) and cytokine levels were measured by ELISA and proteome profiler array, respectively. The non-selective alpha2-AR agonist clonidine induced a modest aggravation of DSS-induced colitis. It accelerated the disease development and markedly enhanced the weight loss of animals, but did not influence the colon shortening, tissue MPO levels or histological score. Clonidine induced similar changes in alpha2B- and alpha2C-AR KO mice, whereas it failed to affect the disease activity index (DAI) scores and caused only minor weight loss in alpha2A-AR KO animals. On the other hand, selective inhibition of alpha2A-ARs by BRL 44408 significantly delayed the development of colitis, reduced the colonic levels of MPO and the cytokines/chemokines CCL3, CXCL2, CXCL13 and G-CSF, and elevated that of TIMP-1. Here we report that activation of alpha2-ARs aggravates murine colitis, an effect mediated by the alpha2A-AR subtype, and selective inhibition of these receptors reduces the severity of gut inflammation