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Livros sobre o tema "Nitrogen and calcium level"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 1 de fevereiro de 2022

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1

Griepink, B. The certification of the contents of calcium, ammoniacal-nitrogen, nitrate-nitrogen, and total nitrogen in a sample ofcalcium ammonium nitrate fertiliser (BCR no. 178) and uric-nitrogen, biuret and total nitrogen in a sample of urea fertiliser (BCR no. 179). Luxembourg: Commission of the European Communities, 1985.

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2

Alexander, Richard B. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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3

Bhattarai, S. P. Set size regulation by seeding density and level of nitrogen application in the nursery. Pokhara: Lumle Regional Agricultural Research Centre, 1998.

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4

Larochelle, Elaine. Comparative "in vitro" study of chemical properties of cavity liners: PH level, calcium and fluoride release measurements. [Toronto: Faculty of Dentistry, University of Toronto], 1989.

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5

Halvorson, A. R. Estimates of salinity level produced by broadcast incorporated and band-applied fertilizer. Pullman, Wash: Washington State University Cooperative Extension, 1987.

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6

Griepink, B. The certification of the contents (mass fractions) of calcium, potassium, iron, phosphorus and nitrogen in a single cell protein (CRM no.273). Luxembourg: Commission of the European Communities, 1985.

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7

Hill, R. W. Flueless gas fires - concentration of carbon monoxide, carbon dioxide and nitrogen dioxide, and particulate level produced in use. Sudbury: HSE Books, 2003.

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8

Erickson, Stephen B., Hatem Amer e Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy are renal enlargement and dilatation of the calyces, renal pelvis, and ureters. Physiologic changes include a 30% to 50% increase in glomerular filtration rate and renal blood flow; a mean decrease of 0.5 mg/dL in the creatinine level and a mean decrease of 18 mg/dL in the serum urea nitrogen level; intermittent glycosuria independent of plasma glucose; proteinuria; aminoaciduria; increased uric acid excretion; increased total body water, with osmostat resetting; 50% increase in plasma volume and cardiac output; and increased ureteral peristalsis.

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9

Lamb, Michael J. Influence of nitrogen form ratio and calcium on greenhouse and field performance of water-melon. 1990.

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10

Chandran, Kartik. Greenhouse Nitrogen Emissions from Wastewater Treatment Operations: Phase II Molecular Level Through Whole Reactor Level Characterization. IWA Publishing, 2016.

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11

A, Smith Richard, e Geological Survey (U.S.), eds. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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12

A, Smith Richard, e Geological Survey (U.S.), eds. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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13

A, Smith Richard, e Geological Survey (U.S.), eds. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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14

A, Smith Richard, e Geological Survey (U.S.), eds. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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15

A, Smith Richard, e Geological Survey (U.S.), eds. County-level estimates of nitrogen and phosphorus fertilizer use in the United States, 1945 to 1985. Reston, Va: U.S. Dept. of the Interior, U.S. Geological Survey, 1990.

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16

Stodola, Ann Wheatley. Effects of light intensity, medium pH, and supplemental calcium on bedding plant response to NH₄⁺:NO₃⁺ ratio. 1986.

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17

Temperature and pressure effects on capacitance probe cryogenic liquid level measurement accuracy. [Washington, DC]: National Aeronautics and Space Administration, 1993.

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18

Chakera, Aron, William G. Herrington e Christopher A. O’Callaghant. Disorders of plasma calcium. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0175.

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The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.

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19

Bruce, Larson, e United States. Dept. of Agriculture. Economic Research Service, eds. A direct approach for estimating nitrogen, phosphorus, and land demands at the regional level. Washington, D.C: U.S. Dept. of Agriculture, Economic Research Service, 1991.

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20

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng e Anne Bardsley. Calcium in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0018.

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Most calcium in the body is present in the skeleton, where it serves a structural role and also as a reservoir for use in other tissues. During pregnancy, calcium is accumulated in the fetal skeleton, mostly during the third trimester when bone growth is at its peak. Although this increases the demand on maternal bone stores, the calcium transfer to the fetus is balanced by increased intestinal calcium absorption in the mother, mediated by compensatory changes in vitamin D synthesis and endogenous hormone levels. Bone loss is minimized if calcium intake is maintained at 1,000#amp;#x2013;1,200 mg/day during pregnancy. This intake level builds up calcium stores in early pregnancy for increased fetal transfer in the third trimester. Additional dietary calcium is usually not required if pre-pregnancy intake is adequate, although pregnant adolescents and women carrying multiple fetuses may require supplementation.

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21

Nounamo, Laurent. Effects of growth retardant and nitrogen level on growth, development and yield of Yamhill wheat. 1985.

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22

Abhishek, Abhishek, e Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.

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23

Avila, David M. De. Effects of the level or type of protein supplementation on nitrogen utilization of ammonia-treated or untreated wheat straw diets. 1985.

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24

Linglart, Agnès, e Anne-Sophie Lambert. Approach to the patient with hypocalcaemia. Editado por Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0038.

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Calcium homeostasis is maintained through a fine balance between calcium absorption, parathyroid hormone secretion and action, vitamin D production and action, cellular compartmentalization of calcium ions, and renal function. Although the extracellular calcium level does not vary with age, the maintenance of calcium faces the significant mineral requirement of skeletal growth and bone mass acquisition during childhood. Acquired or genetic defects in any determinants of blood calcium (i.e. vitamin D, parathyroid hormone, calcium absorption, etc.) may manifest as hypocalcaemia, especially during childhood/adolescence. The discovery of hypocalcaemia in a patient should trigger two clinical responses: (1) therapy to restore the calcium level to normal and (2) investigations to determine the cause of hypo/hypercalcaemia.

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25

Australian Soil Fertility Manual. CSIRO Publishing, 2006. http://dx.doi.org/10.1071/9780643100725.

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The Australian Soil Fertility Manual is a trusted guide to the safe use and handling of fertilizers. It describes the types of agricultural soils, how they are classified and the interaction of soil, water and nutrients. It also provides an insight into how plants utilise nutrients and the role that individual nutrients play in the process of plant growth. This edition has been revised to reflect an increased emphasis on the environmental fate of nutrients and appropriate management strategies. It also has additional information on soil physical, chemical, and biological properties and discussions on the use of lime, dolomite and gypsum. New content covers liming effectiveness, nitrogen water use efficiency, regulations for handling and using fertilizers, storage and transport of security sensitive ammonium nitrate, budgeting for profitable nitrogen use and best management practice for nitrogen and phosphorus fertilizers. The chapters on potassium; calcium, magnesium and sulfur; plant nutrients and the environment; and heavy metal in fertilizers and agriculture have all been extensively revised and rewritten. This important work will be an essential text for fertilizer dealers, extension workers, consultants, teachers, farmers, horticulturists, graziers and others concerned with the profitable and environmentally safe use of plant nutrients.

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26

Williams, Erin S. Malignant Hyperthermia. Editado por Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel e Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0007.

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Malignant hyperthermia (MH) is one of the most feared syndromes in anesthesiology. Due to its rarity and adequate precautions instituted for susceptible patients, most anesthesiologist have never been involved in a case of MH. However, the lack of familiarity with the early signs of MH and quick and effective treatment can increase the potential for increased morbidity and mortality. MH involves a derangement at the molecular level at the ryanodine R1 receptor. This leads to abnormally high levels of intracellular calcium and extracellular potassium. These biochemical mechanisms lead to a hypermetabolic syndrome that if not treated early will prove deadly.

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27

Felling, Ryan J. Targets for Neuroprotection in Ischemic Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0111.

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Cerebral ischemia or hypoxia-ischemia initiate a cascade of biochemical events including impaired reuptake of glutamate into perisynaptic glia causing glutamate flooding, calcium fluxing through NMDA glutamate channels, activation of neuronal nitric oxide synthetase, and impaired mitochondrial ATP production. In animal models it is possible to block these steps and protect the brain but the temporal window of protection after the insult lasts only a few hours. Recombinant TPA is clinically protective if given within 3 hours of stroke, but other agents have not been shown to protect brain tissue after stroke. However, total body cooling has also been shown to protect the brain of term infants if initiated within 6 hours of perinatal asphyxia, and a similar level of cooling may provide protection for the brain in adults who have been resuscitated after cardiac arrest.

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28

Frise, Matthew C., e Jonathan B. Salmon. Disorders of potassium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0251.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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29

Esen, Figen. Disorders of magnesium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0252.

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Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

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30

Hausenloy, Derek, e Derek Yellon, eds. Coronary No-Reflow and Microvascular Obstruction. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0005.

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• Following an AMI, the restoration of TIMI III coronary blood flow using thrombolytic therapy or primary percutaneous coronary intervention does not guarantee actual myocardial perfusion• In 40–60% of reperfused AMI cases, myocardial perfusion is impeded at the level of the capillaries due to microvascular obstruction (MVO)- a phenomenon termed coronary no-reflow• The presence of coronary no-reflow can be detected as impaired myocardial perfusion using non-invasive imaging modalities such as nuclear myocardial perfusion scanning, myocardial contrast echocardiography or contrast-enhanced cardiac magnetic resonance imaging• The presence of microvascular obstruction post-AMI is associated with a larger infarct size, impaired LV ejection fraction, adverse LV remodelling and poorer clinical outcomes• Current treatment strategies include; vasodilator therapy such as adenosine, calcium-channel blockers, and nitrates; distal protection to prevent microemboli; and glycoprotein IIb/IIIa inhibitors• Novel treatment strategies are required to prevent and treat coronary no-reflow, thereby improving myocardial perfusion, reducing myocardial infarct size, preserving LV ejection fraction, preventing LV remodeling and improving clinical outcomes.

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31

Wolf, E. L. More about the Atmosphere, Molecules, and their Interaction with Radiation. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198769804.003.0007.

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Electric dipole radiation is possible from certain molecules (but not with diatomics like oxygen and nitrogen) to make them active in intercepting and re-radiating electromagnetic waves in the atmosphere. Molecules of the greenhouse gas variety include carbon dioxide, ozone and water, as discussed in this chapter. Molecular contributions to the greenhouse heat-trapping effect are described, including sophisticated satellite measurements. The role of molecular absorption in altering the ground-level solar spectrum absorbed by solar farms is summarized. In this chapter we provide a molecular basis for the absorption and emission from the atmosphere, first discussed in Chapter 3. This gives a better understanding of the solar spectrum as seen on Earth, that feeds photovoltaic devices as well as heating the Earth’s surface, that in turn creates winds and waves that can be harvested.

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32

Trieloff, Mario. Noble Gases. Oxford University Press, 2017. http://dx.doi.org/10.1093/acrefore/9780190647926.013.30.

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This is an advance summary of a forthcoming article in the Oxford Encyclopedia of Planetary Science. Please check back later for the full article.Although the second most abundant element in the cosmos is helium, noble gases are also called rare gases. The reason is that they are not abundant on terrestrial planets like our Earth, which is characterized by orders of magnitude depletion of—particularly light—noble gases when compared to the cosmic element abundance pattern. Indeed, such geochemical depletion and enrichment processes make noble gases so versatile concerning planetary formation and evolution: When our solar system formed, the first small grains started to adsorb small amounts of noble gases from the protosolar nebula, resulting in depletion of light He and Ne when compared to heavy noble gases Ar, Kr, and Xe: the so-called planetary type abundance pattern. Subsequent flash heating of the first small mm to cm-sized objects (chondrules and calcium, aluminum rich inclusions) resulted in further depletion, as well as heating—and occasionally differentiation—on small planetesimals, which were precursors of larger planets and which we still find in the asteroid belt today from where we get rocky fragments in form of meteorites. In most primitive meteorites, we even can find tiny rare grains that are older than our solar system and condensed billions of years ago in circumstellar atmospheres of, for example, red giant stars. These grains are characterized by nucleosynthetic anomalies and particularly identified by noble gases, for example, so-called s-process xenon.While planetesimals acquired a depleted noble gas component strongly fractionated in favor of heavy noble gases, the sun and also gas giants like Jupiter attracted a much larger amount of gas from the protosolar nebula by gravitational capture. This resulted in a cosmic or “solar type” abundance pattern, containing the full complement of light noble gases. Contrary to Jupiter or the sun, terrestrial planets accreted from planetesimals with only minor contributions from the protosolar nebula, which explains their high degree of depletion and basically “planetary” elemental abundance pattern. Indeed this depletion enables another tool to be applied in noble gas geo- and cosmochemistry: ingrowth of radiogenic nuclides. Due to heavy depletion of primordial nuclides like 36Ar and 130Xe, radiogenic ingrowth of 40Ar by 40K decay, 129Xe by 129I decay, or fission Xe from 238U or 244Pu decay are precisely measurable, and allow insight in the chronology of fractionation of lithophile parent nuclides and atmophile noble gas daughters, mainly caused by mantle degassing and formation of the atmosphere.Already the dominance of 40Ar in the terrestrial atmosphere allowed C. F v. Weizsäcker to conclude that most of the terrestrial atmosphere originated by degassing of the solid Earth, which is an ongoing process today at mid ocean ridges, where primordial helium leaves the lithosphere for the first time. Mantle degassing was much more massive in the past; in fact, most of the terrestrial atmosphere formed during the first 100 million years of Earth´s history, and was completed at about the same time when the terrestrial core formed and accretion was terminated by a giant impact that also formed our moon. However, before that time, somehow also tiny amounts of solar noble gases managed to find their way into the mantle, presumably by solar wind irradiation of small planetesimals or dust accreting to Earth. While the moon-forming impact likely dissipated the primordial atmosphere, today´s atmosphere originated by mantle degassing and a late veneer with asteroidal and possibly cometary contributions. As other atmophile elements behave similar to noble gases, they also trace the origin of major volatiles on Earth, for example, water, nitrogen, sulfur, and carbon.

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33

Frew, Anthony. Air pollution. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.

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