Steel slag amendment impacts on soil microbial communities and activities of rice (Oryza sativa L.).

With the increase in iron/steel production, the higher volume of by-products (slag) generated necessitates its efficient recycling. Because the Linz-Donawitz (LD) slag is rich in silicon (Si) and other fertilizer components, we aim to evaluate the impact of the LD slag amendment on soil quality (by measuring soil physicochemical and biological properties), plant nutrient uptake, and strengthens correlations between nutrient uptake and soil bacterial communities. We used 16 S rRNA illumine sequencing to study soil bacterial community and APIZYM assay to study soil enzymes involved in C, N, and P cycling. The LD slag was applied at 2 Mg ha-1 to Japonica and Indica rice cultivated under flooded conditions. The LD slag amendment significantly improved soil pH, plant photosynthesis, soil nutrient availability, and the crop yield, irrespective of cultivars. It significantly increased N, P, and Si uptake of rice straw. The slag amendment enhanced soil microbial biomass, soil enzyme activities and enriched certain bacterial taxa featuring copiotrophic lifestyles and having the potential role for ecosystem services provided to the benefit of the plant. The study evidenced that the short-term LD slag amendment in rice cropping systems is useful to improve soil physicochemical and biological status, and the crop yield.

[Dynamic alteration of microRNA in high phosphorus induced calcification of vascular smooth muscle cell].

OBJECTIVE: To study the change of microRNA during the early stage of high phosphorus induced vascular smooth muscle cell (VSMC) calcification and its related mechanism. METHODS: The in vitro calcification model was created through stimulating VSMC cell line A7r5 with high Pi (2.6 mmol/L) for 7 d. The calcification was validated through ocresolphthalein complexone colorimetry to detect the cellular calcium content, real-time PCR to measure the calcification-related gene expression and alizarin red staining to observe the formation of calcium nodules. Based on the cell calcification model, microRNA microarray array was applied to screen the profiles of microRNA expression in VSMC following high Pi stimulation for different periods (0, 3 and 12 h). The array data were analyzed by TAM tool to explore the activated signaling pathway. RESULTS: The calcium content of A7r5 cells induced by high Pi was increased 9.6 times high as cells without Pi treatment (P<0.05). VSMC contractile phenotype genes (SM-α actin, SM22) were down-regulated (P<0.05), while calcification-related genes (BMP2, MSX2, Runx2) were up-regulated (P<0.05) in VSMC stimulated by high Pi. The calcium nodules were obviously formed in cells after 7 d high Pi treatment. In microarray experiment, 680 individual microRNAs were detected in high Pi-treated VSMCs at different time points (0, 3 and 12 h). Among these genes, miR-183, miR-664 and miR-9* were increased whereas miR-542-5P, let-7f and miR-29a were decreased in time-dependent manners. Twenty-six kinds of signaling pathways, including cell apoptosis, differentiation and proliferation, were significantly activated. All these activated pathways were associated with calcification. CONCLUSION: This study implies that microRNA changed in high Pi-induced VSMCs may involve in the process of calcification.

Phosphate: from stardust to eukaryotic cell cycle control.

Phosphorus is a pivotal element in all biochemical systems: it serves to store metabolic energy as ATP, it forms the backbone of genetic material such as RNA and DNA, and it separates cells from the environment as phospholipids. In addition to this "big hits", phosphorus has recently been shown to play an important role in other important processes such as cell cycle regulation. In the present review, we briefly summarize the biological processes in which phosphorus is involved in the yeast Saccharomyces cerevisiae before discussing our latest findings on the role of this element in the regulation of DNA replication in this eukaryotic model organism. We describe both the role of phosphorus in the regulation of G1 progression by means of the Cyclin Dependent Kinase (CDK) Pho85 and the stabilization of the cyclin Cln3, as well as the role of other molecule composed of phosphorus-the polyphosphate-in cell cycle progression, dNTP synthesis, and genome stability. Given the eminent role played by phosphorus in life, we outline the future of phosphorus in the context of one of the main challenges in human health: cancer treatment. [Int Microbiol 19(3):133-141 (2016)].

A primary phosphorus-deficient skeletal phenotype in juvenile Atlantic salmon Salmo salar: the uncoupling of bone formation and mineralization.

To understand the effect of low dietary phosphorus (P) intake on the vertebral column of Atlantic salmon Salmo salar, a primary P deficiency was induced in post-smolts. The dietary P provision was reduced by 50% for a period of 10 weeks under controlled conditions. The animal's skeleton was subsequently analysed by radiology, histological examination, histochemical detection of minerals in bones and scales and chemical mineral analysis. This is the first account of how a primary P deficiency affects the skeleton in S. salar at the cellular and at the micro-anatomical level. Animals that received the P-deficient diet displayed known signs of P deficiency including reduced growth and soft, pliable opercula. Bone and scale mineral content decreased by c. 50%. On radiographs, vertebral bodies appear small, undersized and with enlarged intervertebral spaces. Contrary to the X-ray-based diagnosis, the histological examination revealed that vertebral bodies had a regular size and regular internal bone structures; intervertebral spaces were not enlarged. Bone matrix formation was continuous and uninterrupted, albeit without traces of mineralization. Likewise, scale growth continues with regular annuli formation, but new scale matrix remains without minerals. The 10 week long experiment generated a homogeneous osteomalacia of vertebral bodies without apparent induction of skeletal malformations. The experiment shows that bone formation and bone mineralization are, to a large degree, independent processes in the fish examined. Therefore, a deficit in mineralization must not be the only cause of the alterations of the vertebral bone structure observed in farmed S. salar. It is discussed how the observed uncoupling of bone formation and mineralization helps to better diagnose, understand and prevent P deficiency-related malformations in farmed S. salar.

[Bone and Nutrition. A novel function of phosphorus].

Phosphorus is an essential nutrient for bone formation by forming hydroxyapatite with calcium. Simultaneously, phosphorus is also a component of high energy bond of ATP, nucleic acids, and phospholipids. Recent studies have demonstrated that excess or lack of dietary phosphorus intake may cause vascular dysfunction, cardiac hypertrophy, and impaired glucose tolerance. Here, we introduce recent findings about the effects of high or low dietary phosphorus intake on several organs except for bone.

[Vascular Calcification - Pathological Mechanism and Clinical Application - . Role of vascular smooth muscle cells in vascular calcification].

Vascular calcification is commonly seen with aging, chronic kidney disese (CKD), diabetes, and atherosclerosis, and is closely associated with cardiovascular morbidity and mortality. Vascular calcification has long been regarded as the final stage of degeneration and necrosis of arterial wall and a passive, unregulated process. However, it is now known to be an active and tightly regulated process involved with phenotypic transition of vascular smooth muscle cells (VSMC) that resembles bone mineralization. Briefly, calcium deposits of atherosclerotic plaque consist of hydroxyapatite and may appear identical to fully formed lamellar bone. By using a genetic fate mapping strategy, VSMC of the vascular media give rise to the majority of the osteochondrogenic precursor- and chondrocyte-like cells observed in the calcified arterial media of MGP (- / -) mice. Osteogenic differentiation of VSMC is characterized by the expression of bone-related molecules including bone morphogenetic protein (BMP) -2, Msx2 and osteopontin, which are produced by osteoblasts and chondrocytes. Our recent findings are that (i) Runx2 and Notch1 induce osteogenic differentiation, and (ii) advanced glycation end-product (AGE) /receptor for AGE (RAGE) and palmitic acid promote osteogenic differentiation of VSMC. To understand of the molecular mechanisms of vascular calcification is now under intensive research area.

Phosphorus sequestration in the form of polyphosphate by microbial symbionts in marine sponges.

Marine sponges are major habitat-forming organisms in coastal benthic communities and have an ancient origin in evolution history. Here, we report significant accumulation of polyphosphate (polyP) granules in three common sponge species of the Caribbean coral reef. The identity of the polyP granules was confirmed by energy-dispersive spectroscopy (EDS) and by the fluorescence properties of the granules. Microscopy images revealed that a large proportion of microbial cells associated with sponge hosts contained intracellular polyP granules. Cyanobacterial symbionts cultured from sponges were shown to accumulate polyP. We also amplified polyphosphate kinase (ppk) genes from sponge DNA and confirmed that the gene was expressed. Based on these findings, we propose here a potentially important phosphorus (P) sequestration pathway through symbiotic microorganisms of marine sponges. Considering the widespread sponge population and abundant microbial cells associated with them, this pathway is likely to have a significant impact on the P cycle in benthic ecosystems.

Mineral and antioxidant management of transition dairy cows.

Transition management needs to be fully integrated to be effective. We discuss and demonstrate this concept in the context of a study that used these principles. The roles of calcium, magnesium, phosphorus and dietary anion cation difference in influencing the pathophysiology and incidence of hypocalcemia are highlighted. Recent understandings of the pivotal role of skeleton in metabolism are reviewed. Micronutrient mineral and vitamin needs are addressed in the context of exposure of periparturient cattle to oxidative stress and inflammatory disorders. This article provides a series of practical approaches to improving transition diets.

Low phosphorus status might contribute to the onset of obesity.

Overweight and obesity are becoming global health problems. Although genetics certainly plays a role, weight gain is ultimately the result of a failure in the balance between energy expenditure and energy intake. Obesity during the past few decades was paralleled with several changes in dietary habits favouring low phosphorus consumption. This is believed to compromise adenosine triphosphate (ATP) production that is involved in the regulation of energy metabolism. Ingestion of high-carbohydrate-low phosphorus food is known to increase insulin release, to simultaneously stimulate peripheral uptake of phosphorus and the phosphorylation of many compounds. This creates a competition for phosphorus that compromises its availability for ATP production, possibly translated into low diet-induced thermogenesis. Moreover, reduced hepatic ATP production is believed to be transmitted through neural afferents to the central nervous system, resulting in an increase in food intake. On the other hand, the positive relation between phosphorus and red blood cell 2,3-diphosphoglycerate, which reduces oxygen affinity to haemoglobin, would be expected to reduce the capacity for physical activity. In line with that, plasma phosphorus status was reported to be inversely related to body weight. Adequate intakes of phosphorus are thus potentially protective against rising obesity epidemic across the globe.

[Calcium pros and cons significance and risk of phosphorus supplementation. The necessity of phosphorus supplementation for hypophosphatemia].

Phosphate plays a vital role forming the high-energy band within ATP. The pathophysiological results of phosphate deficiency are inadequate supplies of energy-rich phosphates and, in particular, inhibition of glyceraldehyde-3- phosphate dehydrogenase, which occupies a key position in glycolysis. The effect of this on the central nervous system, muscle and erythrocyte energy metabolism is to reduce ATP and 2,3-diphosphoglycerate levels, leading to left-hand displacement of the oxygen-hemoglobin dissociation curve with decreased peripheral oxygen uptake and transport. Therefore, detection and treatment of acute hypophosphatemia is important in many hospitalized patients particularly in ICU patients. Severe hypophosphatemia is also associated with a number of neuromuscular and cardiovascular sequelae, in which phosphate supplementation leads to improved symptoms and clinical parameters. In clinical practice it is common on administering 0.4 mmol (12 mg) phosphate/kg per day, and to adjust this on the basis of the serum phosphate analysis.

Alterations in phosphorus, calcium and PTHrP contribute to defects in dental and dental alveolar bone formation in calcium-sensing receptor-deficient mice.

To determine whether the calcium-sensing receptor (CaR) participates in tooth formation and dental alveolar bone development in mandibles in vivo, we examined these processes, as well as mineralization, in 2-week-old CaR-knockout (CaR(-/-)) mice. We also attempted to rescue the phenotype of CaR(-/-) mice by genetic means, in mice doubly homozygous for CaR and 25-hydroxyvitamin D 1alpha-hydroxylase [1alpha(OH)ase] or parathyroid hormone (Pth). In CaR(-/-) mice, which exhibited hypercalcemia, hypophosphatemia and increased serum PTH, the volumes of teeth and of dental alveolar bone were decreased dramatically, whereas the ratio of the area of predentin to total dentin and the number and surface of osteoblasts in dental alveolar bone were increased significantly, as compared with wild-type littermates. The normocalcemia present in CaR(-/-);1alpha(OH)ase(-/-) mice only slightly improved the defects in dental and alveolar bone formation observed in the hypercalcemic CaR(-/-) mice. However, these defects were completely rescued by the additional elimination of hypophosphatemia and by an increase in parathyroid hormone-related protein (PTHrP) expression in the apical pulp, Hertwig's epithelial root sheath and mandibular tissue in CaR(-/-); Pth(-/-) mice. Therefore, alterations in calcium, phosphorus and PTHrP contribute to defects in the formation of teeth and alveolar bone in CaR-deficient mice. This study indicates that CaR participates in the formation of teeth and in the development of dental alveolar bone in mandibles in vivo, although it appears to do so largely indirectly.

[Vascular calcification in chronic kidney disease]. / La calcificazione vascolare nel paziente con insufficienza renale cronica.

Patients affected by chronic kidney disease (CKD) suffer by secondary hyperparathyroidism and hyperphosphatemia. The new KDIGO guidelines identify a new definition in CKD-MBD (Mineral Bone Disorder), in which vascular calcification plays a central role. In fact, CKD patients that present vascular calcification have highest risk of cardiovascular morbility and mortality. Recently, it has been elucidated that the control of phosphate is one of the major problems for the nephrology community. Furthermore, new markers, such as FGF-23, have been identified as inducers of vascular calcification and cardiovascular disease in CKD. Therefore, the use of calcium-free phosphate-binders may reduce the risk of cardiovascular disease by reducing both serum phosphate and FGF-23 levels.

Fibroblast growth factor 23 (FGF23) and the kidney.

Phosphate homeostasis in humans is a complex phenomenon involving the interplay of several different organs and circulating hormones. Among the latter, parathyroid hormone (PTh), and vitamin D3 (Vit D3) were thought to be the main regulators of serum phosphate concentration since they mediated the intestinal, renal and bone responses that follow fluctuations in serum phosphate levels. The study of three rare disorders - tumor-induced osteomalacia (TIo), autosomal dominant hypophosphatemic rickets (ADhr) and X-linked hypophosphatemic rickets (XLh) - has offered a completely new insight into phosphate metabolism by unraveling the role of a group of peptides that can directly affect serum phosphate concentration by increasing urinary phosphate excretion. fibroblast growth factor-23 (fGf-23) is the most extensively studied ''phosphatonin''. The production, mechanism of action, effects in various target tissues, and its role in common clinical disorders are the focus of this review.

Pathogenesis of bone and mineral related disorders in chronic kidney disease: key role of hyperphosphatemia.

This paper reviews the pathogenesis of hyperphosphataemia and its role in the regulation of parathyroid hormone synthesis and parathyroid cell proliferation in chronic kidney disease. The association between hyperphosphaemia and vascular calcification, and the interventions that can be used to control plasma phosphate are also discussed.

Vascular calcification: lessons from scientific models.

Patients with chronic kidney disease have increased cardiovascular mortality from a combination of increased atherosclerotic disease, left ventricular hypertrophy and increased prevalence of vascular calcification (VC). Previously VC was thought to be a passive process which involved the deposition of calcium and phosphate into the vessel wall. However, recent studies have shown that VC is a highly regulated, cell-mediated process similar to bone formation, in that it is associated with expression of bone-related proteins, such as type I collagen and alkaline phosphatase. Animal and in vitro models of VC have shown that a multitude of factors including phosphate, matrix gla protein (MGP) and fetuin are involved in regulating VC. Certain factors induce calcification whereas others inhibit the process. Despite these insights, it is still not fully known how VC is regulated and a treatment for VC remains elusive. Ongoing research will hopefully elucidate these mechanisms and thereby produce targets for future therapeutic intervention. This review will highlight some of the scientific models of VC and how they have increased the understanding of this complex process.

The mechanism of phosphorus as a cardiovascular risk factor in CKD.

Hyperphosphatemia and vascular calcification have emerged as cardiovascular risk factors among those with chronic kidney disease. This study examined the mechanism by which phosphorous stimulates vascular calcification, as well as how controlling hyperphosphatemia affects established calcification. In primary cultures of vascular smooth muscle cells derived from atherosclerotic human aortas, activation of osteoblastic events, including increased expression of bone morphogenetic protein 2 (BMP-2) and the transcription factor RUNX2, which normally play roles in skeletal morphogenesis, was observed. These changes, however, did not lead to matrix mineralization until the phosphorus concentration of the media was increased; phosphorus stimulated expression of osterix, a second critical osteoblast transcription factor. Knockdown of osterix with small interference RNA (siRNA) or antagonism of BMP-2 with noggin prevented matrix mineralization in vitro. Similarly, vascular BMP-2 and RUNX2 were upregulated in atherosclerotic mice, but significant mineralization occurred only after the induction of renal dysfunction, which led to hyperphosphatemia and increased aortic expression of osterix. Administration of oral phosphate binders or intraperitoneal BMP-7 decreased expression of osterix and aortic mineralization. It is concluded that, in chronic kidney disease, hyperphosphatemia stimulates an osteoblastic transcriptional program in the vasculature, which is mediated by osterix activation in cells of the vascular tunica media and neointima.

Osteoblast autonomous Pi regulation via Pit1 plays a role in bone mineralization.

The complex pathogenesis of mineralization defects seen in inherited and/or acquired hypophosphatemic disorders suggests that local inorganic phosphate (P(i)) regulation by osteoblasts may be a rate-limiting step in physiological bone mineralization. To test whether an osteoblast autonomous phosphate regulatory system regulates mineralization, we manipulated well-established in vivo and in vitro models to study mineralization stages separately from cellular proliferation/differentiation stages of osteogenesis. Foscarnet, an inhibitor of NaP(i) transport, blocked mineralization of osteoid formation in osteoblast cultures and local mineralization after injection over the calvariae of newborn rats. Mineralization was also down- and upregulated, respectively, with under- and overexpression of the type III NaP(i) transporter Pit1 in osteoblast cultures. Among molecules expressed in osteoblasts and known to be related to P(i) handling, stanniocalcin 1 was identified as an early response gene after foscarnet treatment; it was also regulated by extracellular P(i), and itself increased Pit1 accumulation in both osteoblast cultures and in vivo. These results provide new insights into the functional role of osteoblast autonomous P(i) handling in normal bone mineralization and the abnormalities seen in skeletal tissue in hypophosphatemic disorders.

Effects of iron and phosphorus on Microcystis physiological reactions.

OBJECTIVE: To observe the effects of iron and phosphorus on Microcystis physiological reactions. METHODS: The experimental conditions were chosen as the light dark cycles of 16 h 8 h, 12 h 12 h, and 8 h 16 h. The cell change of morphology and life history, cell number, cell color, and cell area of Microcystis were analyzed quantitatively. According to the resource competition and Monod equation, Microcystis kinetics of phosphorus and iron were also examined. RESULTS: The longer light time caused more special cell division, slower growth rate, and easier change of bigger cell area. The color of alga was changed from green to brown. Ks and micromax of phosphorus absorption were 0.0352 mircomol x L(-l) and 0.493 d(-1), respectively. Those of iron absorption were 0.00323 micromol x L(-1) and 0.483 d(-1). CONCLUSION: Microcystis bloom is more dominant than other algae.