First discovery of dolomite and magnesite in living coralline algae and its geobiological implications

Dolomite is a magnesium-rich carbonate mineral abundant in fossil carbonate reef platforms but surprisingly rare in modern sedimentary environments, a conundrum known as the "Dolomite Problem". Marine sedimentary dolomite has been interpreted to form by an unconfirmed, post-depositional diagenetic process, despite minimal experimental success at replicating this. Here we show that dolomite, accompanied by magnesite, forms within living crustose coralline alga, Hydrolithon onkodes, a prolific global tropical reef species. Chemical micro-analysis of the coralline skeleton reveals that not only are the cell walls calcitised, but that cell spaces are typically filled with magnesite, rimmed by dolomite, or both. Mineralogy was confirmed by X-ray Diffraction. Thus there are at least three mineral phases present (magnesium calcite, dolomite and magnesite) rather than one or two (magnesium calcite and brucite) as previously thought. Our results are consistent with dolomite occurrences in coralline algae rich environments in fossil reefs of the last 60 million years. We reveal that the standard method of removing organic material prior to Xray Diffraction analysis can result in a decrease in the most obvious dolomite and magnesite diffraction patterns and this may explain why the abundant protodolomite and magnesite discovered in this study has not previously been recognized. This discovery of dolomite in living coralline algae extends the range of palaeo-environments for which biologically initiated dolomite can be considered a possible source of primary dolomite.M. C. Nash, U. Troitzsch, B. N. Opdyke, J. M. Trafford, B. D. Russell and D. I. Klin

Biomineralization of dolomite and magnesite discovered in tropical coralline algae: a biological solution to the geological dolomite problem

Final revised paper can be found at Description (Link) belowDolomite is a magnesium-rich carbonate mineral abundant in fossil carbonate reef platforms but surprisingly rare in modern sedimentary environments, a conundrum known as the ''Dolomite Problem". Marine sedimentary dolomite has been interpreted to form by an unconfirmed, post-depositional diagenetic process, despite minimal experimental success at replicating this. Here we show that dolomite, accompanied by magnesite, forms within living crustose coralline alga, Hydrolithon onkodes, a prolific global tropical reef species. Chemical micro-analysis of the coralline skeleton reveals that not only are the cell walls calcitised, but that cell spaces are typically filled with magnesite, rimmed by dolomite, or both. Mineralogy was confirmed by X-ray diffraction. Thus there are at least three mineral phases present (magnesium calcite, dolomite and magnesite) rather than one or two (magnesium calcite and brucite) as previously thought. Our results are consistent with dolomite occurrences in coralline algae rich environments in fossil reefs. Instead of a theory of post-depositional dolomitisation, we present evidence revealing biomineralization that can account for the massive formations seen in the geologic record. Additionally, our findings imply that previously unrecognized dolomite and magnesite have formed throughout the Holocene. This discovery together with the scale of coralline algae dominance in past shallow carbonate environments raises the possibility that environmental factors driving this biological dolomitisation process have influenced the global marine magnesium/calcium cycle. Perhaps, most importantly, we reveal that what has been considered a geological process can be a biological process, having many implications for both disciplines.M. C. Nash, U. Troitzsch, B. N. Opdyke, J. M. Trafford, B. D. Russell and D. I. Klinehttp://hdl.handle.net/2440/6855

Muscle Fiber Viability, a Novel Method for the Fast Detection of Ischemic Muscle Injury in Rats

Acute lower extremity ischemia is a limb- and life-threatening clinical problem. Rapid detection of the degree of injury is crucial, however at present there are no exact diagnostic tests available to achieve this purpose. Our goal was to examine a novel technique - which has the potential to accurately assess the degree of ischemic muscle injury within a short period of time - in a clinically relevant rodent model. Male Wistar rats were exposed to 4, 6, 8 and 9 hours of bilateral lower limb ischemia induced by the occlusion of the infrarenal aorta. Additional animals underwent 8 and 9 hours of ischemia followed by 2 hours of reperfusion to examine the effects of revascularization. Muscle samples were collected from the left anterior tibial muscle for viability assessment. The degree of muscle damage (muscle fiber viability) was assessed by morphometric evaluation of NADH-tetrazolium reductase reaction on frozen sections. Right hind limbs were perfusion-fixed with paraformaldehyde and glutaraldehyde for light and electron microscopic examinations. Muscle fiber viability decreased progressively over the time of ischemia, with significant differences found between the consecutive times. High correlation was detected between the length of ischemia and the values of muscle fiber viability. After reperfusion, viability showed significant reduction in the 8-hour-ischemia and 2-hour-reperfusion group compared to the 8-hour-ischemia-only group, and decreased further after 9 hours of ischemia and 2 hours of reperfusion. Light- and electron microscopic findings correlated strongly with the values of muscle fiber viability: lesser viability values represented higher degree of ultrastructural injury while similar viability results corresponded to similar morphological injury. Muscle fiber viability was capable of accurately determining the degree of muscle injury in our rat model. Our method might therefore be useful in clinical settings in the diagnostics of acute ischemic muscle injury

Attenuation of Skeletal Muscle and Renal Injury to the Lower Limb following Ischemia-Reperfusion Using mPTP Inhibitor NIM-811.

INTRODUCTION: Operation on the infrarenal aorta and large arteries of the lower extremities may cause rhabdomyolysis of the skeletal muscle, which in turn may induce remote kidney injury. NIM-811 (N-metyl-4-isoleucine-cyclosporine) is a mitochondria specific drug, which can prevent ischemic-reperfusion (IR) injury, by inhibiting mitochondrial permeability transition pores (mPTP). OBJECTIVES: Our aim was to reduce damages in the skeletal muscle and the kidney after IR of the lower limb with NIM-811. MATERIALS AND METHODS: Wistar rats underwent 180 minutes of bilateral lower limb ischemia and 240 minutes of reperfusion. Four animal groups were formed called Sham (receiving vehicle and sham surgery), NIM-Sham (receiving NIM-811 and sham surgery), IR (receiving vehicle and surgery), and NIM-IR (receiving NIM-811 and surgery). Serum, urine and histological samples were taken at the end of reperfusion. NADH-tetrazolium staining, muscle Wet/Dry (W/D) ratio calculations, laser Doppler-flowmetry (LDF) and mean arterial pressure (MAP) monitoring were performed. Renal peroxynitrite concentration, serum TNF-alpha and IL-6 levels were measured. RESULTS: Less significant histopathological changes were observable in the NIM-IR group as compared with the IR group. Serum K+ and necroenzyme levels were significantly lower in the NIM-IR group than in the IR group (LDH: p<0.001; CK: p<0.001; K+: p = 0.017). Muscle mitochondrial viability proved to be significantly higher (p = 0.001) and renal function parameters were significantly better (creatinine: p = 0.016; FENa: p<0.001) in the NIM-IR group in comparison to the IR group. Serum TNF-alpha and IL-6 levels were significantly lower (TNF-alpha: p = 0.003, IL-6: p = 0.040) as well as W/D ratio and peroxynitrite concentration were significantly lower (p = 0.014; p<0.001) in the NIM-IR group than in the IR group. CONCLUSION: NIM-811 could have the potential of reducing rhabdomyolysis and impairment of the kidney after lower limb IR injury

Modellierungskonzepte der Synergetik und der Theorie der Selbstorganisation

Mnay models situated in the current research landscape of modelling and simulating social processes have roots in physics. This is visible in the name of specialties as Econophysics or Sociophysics. This chapter describes the history of knowledge transfer from physics, in particular physics of self-organization and evolution, to the social sciences. We discuss why physicists felt called to describe social processes. Across models and simulations the question how to explain the emergence of something new is the most intriguing one. We present one model approach to this problem and introduce a game -- Evolino -- inviting a larger audience to get acquainted with abstract evolution-theory approaches to describe the quest for new ideas.Comment: In German, extended first version, final version Ebeling, W., & Scharnhorst, A. (2015). Modellierungskonzepte der Synergetik und der Theorie der Selbstorganisation. In N. Braun & N. J. Saam (Eds.), Handbuch Modellbildung und Simulation in den Sozialwissenschaften (pp. 419--452). Wiesbaden: Springer Fachmedien Wiesbaden. doi:10.1007/978-3-658-01164-2 (in German

Impact of Systemic Inflammation and Autoimmune Diseases on apoA-I and HDL Plasma Levels and Functions

The cholesterol of high-density lipoproteins (HDLs) and its major proteic component, apoA-I, have been widely investigated as potential predictors of acute cardiovascular (CV) events. In particular, HDL cholesterol levels were shown to be inversely and independently associated with the risk of acute CV diseases in different patient populations, including autoimmune and chronic inflammatory disorders. Some relevant and direct anti-inflammatory activities of HDL have been also recently identified targeting both immune and vascular cell subsets. These studies recently highlighted the improvement of HDL function (instead of circulating levels) as a promising treatment strategy to reduce inflammation and associated CV risk in several diseases, such as systemic lupus erythematosus and rheumatoid arthritis. In these diseases, anti-inflammatory treatments targeting HDL function might improve both disease activity and CV risk. In this narrative review, we will focus on the pathophysiological relevance of HDL and apoA-I levels/functions in different acute and chronic inflammatory pathophysiological conditions