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Novel zinc biomarkers, such as the erythrocyte LA:DGLA ratio, have shown promise in pre-clinical and clinical trials and are being developed to more accurately detect dietary zinc deficiency.
Day to day requirements of vitamin d are set around 800-1000IU to maintain healthy levels which in most cases can be provided by sun exposure. Increased amounts are required for individuals who are previously diagnosed as deficient. For those of moderate deficiencies,oral supplementation can be implemented into the diet at levels of 3000-5000 IU per day for a 6- to 12-week period continued by an ongoing reduced dose of 1000- 2000 IU per day to maintain stores in the body.
Severe deficiency is treated through megadose therapy where patients are given doses around 100 000 IU to assist in raising stores faster to ensure physical health in restored to prevent further illness or disease.
Fertilisers like ammonium phosphate, calcium ammonium nitrate, urea can be supplied. Foliar spray of urea can be a quick method.
Detecting phosphorus deficiency can take multiple forms. A preliminary detection method is a visual inspection of plants. Darker green leaves and purplish or red pigment can indicate a deficiency in phosphorus. This method however can be an unclear diagnosis because other plant environment factors can result in similar discoloration symptoms. In commercial or well monitored settings for plants, phosphorus deficiency is diagnosed by scientific testing. Additionally, discoloration in plant leaves only occurs under fairly severe phosphorus deficiency so it is beneficial to planters and farmers to scientifically check phosphorus levels before discoloration occurs. The most prominent method of checking phosphorus levels is by soil testing. The major soil testing methods are Bray 1-P, Mehlich 3, and Olsen methods. Each of these methods are viable but each method has tendencies to be more accurate in known geographical areas. These tests use chemical solutions to extract phosphorus from the soil. The extract must then be analyzed to determine the concentration of the phosphorus. Colorimetry is used to determine this concentration. With the addition of the phosphorus extract into a colorimeter, there is visual color change of the solution and the degree to this color change is an indicator of phosphorus concentration. To apply this testing method on phosphorus deficiency, the measured phosphorus concentration must be compared to known values. Most plants have established and thoroughly tested optimal soil conditions. If the concentration of phosphorus measured from the colorimeter test is significantly lower than the plant’s optimal soil levels, then it is likely the plant is phosphorus deficient. The soil testing with colorimetric analysis, while widely used, can be subject to diagnostic problems as a result of interference from other present compounds and elements. Additional phosphorus detection methods such as spectral radiance and inductively coupled plasma spectrometry (ICP) are also implemented with the goal of improving reading accuracy. According to the World Congress of Soil Scientists, the advantages of these light-based measurement methods are their quickness of evaluation, simultaneous measurements of plant nutrients, and their non-destructive testing nature. Although these methods have experimental based evidence, unanimous approval of the methods has not yet been achieved.
Zinc deficiency can be classified as acute, as may occur during prolonged inappropriate zinc-free total parenteral nutrition; or chronic, as may occur in dietary deficiency or inadequate absorption.
The visual symptoms of nitrogen deficiency mean that it can be relatively easy to detect in some plant species. Symptoms include poor plant growth, and leaves that are pale green or yellow because they are unable to make sufficient chlorophyll. Leaves in this state are said to be chlorotic. Lower leaves (older leaves) show symptoms first, since the plant will move nitrogen from older tissues to more important younger ones. Nevertheless, plants are reported to show nitrogen deficiency symptoms at different parts. For example, Nitrogen deficiency of tea is identified by retarded shoot growth and yellowing of younger leaves.
However, these physical symptoms can also be caused by numerous other stresses, such as deficiencies in other nutrients, toxicity, herbicide injury, disease, insect damage or environmental conditions. Therefore, nitrogen deficiency is most reliably detected by conducting quantitative tests in addition to assessing the plants visual symptoms. These tests include soil tests and plant tissue test.
Plant tissue tests destructively sample the plant of interest. However, nitrogen deficiency can also be detected non-destructively by measuring chlorophyll content.
Chlorophyll content tests work because leaf nitrogen content and chlorophyll concentration are closely linked, which would be expected since the majority of leaf nitrogen is contained in chlorophyll molecules. Chlorophyll content can be detected with a Chlorophyll content meter; a portable instrument that measures the greenness of leaves to estimate their relative chlorophyll concentration.
Chlorophyll content can also be assessed with a chlorophyll fluorometer, which measures a chlorophyll fluorescence ratio to identify phenolic compounds that are produced in higher quantities when nitrogen is limited. These instruments can therefore be used to non-destructively test for nitrogen deficiency.
In light of the increase of vitamin D deficiency throughout Australia the federal government introduced mandatory fortification of vitamins and minerals such as vitamin D in certain foods like edible oil spreads as indicated in the: Australian Standard 2.4.2. It is mandatory for all food manufacturing companies producing table spreads like butter and margarine to have no less than 55 mg/kg of vitamin D, as a response to a growing public health requirements.
In response to recent advances, public policies are being reconsidered to ensure vitamin D is evidently being measured. With the vitamin D deficiency resurfacing the nutrient reference value guidelines were established, in turn creating the dietary vitamin D recommendations.
The dietary vitamin D guidelines are assuming limited exposure to UVB sun light are:
Infants, Children and Adults <50 years: 5 µg/day
Adults >50 - <70 years: 10 µg/day
Adults >70 years: 15 µg/day
Iron deficiency can be avoided by choosing appropriate soil for the growing conditions (e.g., avoid growing acid loving plants on lime soils), or by adding well-rotted manure or compost. If iron deficit chlorosis is suspected then check the pH of the soil with an appropriate test kit or instrument. Take a soil sample at surface and at depth. If the pH is over seven then consider soil remediation that will lower the pH toward the 6.5 - 7 range. Remediation includes: i) adding compost, manure, peat or similar organic matter (warning. Some retail blends of manure and compost have pH in the range 7 - 8 because of added lime. Read the MSDS if available. Beware of herbicide residues in manure. Source manure from a certified organic source.) ii) applying Ammonium Sulphate as a Nitrogen fertilizer (acidifying fertilizer due to decomposition of ammonium ion to nitrate in the soil and root zone) iii) applying elemental Sulphur to the soil (oxidizes over the course of months to produce sulphate/sulphite and lower pH). Note: adding acid directly e.g. sulphuric/hydrochloric/citric acid is dangerous as you may mobilize metal ions in the soil that are toxic and otherwise bound. Iron can be made available immediately to the plant by the use of iron sulphate or iron chelate compounds. Two common iron chelates are Fe EDTA and Fe EDDHA. Iron sulphate (Iron(II)_sulfate) and iron EDTA are only useful in soil up to PH 7.1 but they can be used as a foliar spray (Foliar_feeding). Iron EDDHA is useful up to PH 9 (highly alkaline) but must be applied to the soil and in the evening to avoid photodegradation. EDTA in the soil may mobilize Lead, EDDHA does not appear to.
Manganese deficiency is easy to cure and homeowners have several options when treating these symptoms. The first is to adjust the soil pH. Two materials commonly used for lowering the soil pH are aluminum sulfate and sulfur. Aluminum sulfate will change the soil pH instantly because the aluminum produces the acidity as soon as it dissolves in the soil. Sulfur, however, requires some time for the conversion to sulfuric acid with the aid of soil bacteria. If the soil pH is not a problem and there is no manganese actually in the soil then Foliar feeding for small plants and medicaps for large trees are both common ways for homeowners to get manganese into the plant.
It is hard to consider Keshan disease extremely preventable because the only way to ensure that the individual is getting enough selenium would be to test the soil in the area. However, one way that selenium intake can be improved is to increase intake of foods that are rich with selenium. Examples include onions, canned tuna, beef, cod, turkey, chicken breast, enriched pasta, egg, cottage cheese, oatmeal, white or brown rice, and garlic. If the individual lives in an area that does not have selenium enriched soil, dietary supplementation should be considered. To determine whether or not an individual is selenium deficient, blood testing is performed.
Biotinidase deficiency can be found by genetic testing. This is often done at birth as part of newborn screening in several states throughout the United States. Results are found through testing a small amount of blood gathered through a heel prick of the infant. As not all states require that this test be done, it is often skipped in those where such testing is not required. Biotinidase deficiency can also be found by sequencing the "BTD" gene, particularly in those with a family history or known familial gene mutation.
The most widely used potassium fertilizer is potassium chloride (muriate of potash). Other inorganic potassium fertilizers include potassium nitrate, potassium sulfate, and monopotassium phosphate. Potassium-rich treatments suitable for organic farming include feeding with home-made comfrey liquid, adding seaweed meal, composted bracken, and compost rich in decayed banana peels. Wood ash also has high potassium content. Adequate moisture is necessary for effective potassium uptake; low soil water reduces K uptake by plant roots. Liming acidic soils can increase potassium retention in some soils by reducing leaching; practices that increase soil organic matter can also increase potassium retention.
The European Food Safety Authority concluded that chromium is not an essential nutrient, making this the only mineral for which the United States and the European Union disagree. The proposed mechanism for cellular uptake of Cr via transferrin has been called into question. There is no proof that chromium supplementation has physiological effects on body mass or composition, and its use as a supplement may be unsafe. A 2014 systematic review concluded that chromium supplementation had no effect on glycemic control, fasting plasma glucose levels, or body weight in people with or without diabetes.
Chromium may be needed as an ingredient in total parenteral nutrition (TPN), since deficiency may occur after months of intravenous feeding with chromium-free TPN. For this reason, chromium is added to normal TPN solutions for people with diabetes, and in nutritional products for preterm infants.
In plants a micronutrient deficiency (or trace mineral deficiency) is a physiological plant disorder which occurs when a micronutrient is deficient in the soil in which a plant grows. Micronutrients are distinguished from macronutrients (nitrogen, phosphorus, sulfur, potassium, calcium and magnesium) by the relatively low quantities needed by the plant.
A number of elements are known to be needed in these small amounts for proper plant growth and development. Nutrient deficiencies in these areas can adversely affect plant growth and development. Some of the best known trace mineral deficiencies include: zinc deficiency, boron deficiency, iron deficiency, and manganese deficiency.
Correction and prevention of phosphorus deficiency typically involves increasing the levels of available phosphorus into the soil. Planters introduce more phosphorus into the soil with bone meal, rock phosphate,manure, and phosphate-fertilizers. The introduction of these compounds into the soil however does not ensure the alleviation of phosphorus deficiency. There must be phosphorus in the soil, but the phosphorus must also be absorbed by the plant. The uptake of phosphorus is limited by the chemical form in which the phosphorus is available in the soil. A large percentage of phosphorus in soil is present in chemical compounds that plants are incapable of absorbing. Phosphorus must be present in soil in specific chemical arrangements to be usable as plant nutrients. Facilitation of usable phosphorus in soil can be optimized by maintaining soil within a specified pH range. Soil acidity, measured on the pH scale, partially dictates what chemical arrangements that phosphorus forms. Between pH 6 and 7, phosphorus makes the fewest number of bonds which render the nutrient unusable to plants. At this range of acidity the likeliness of phosphorus uptake is increased and the likeliness of phosphorus deficiency is decreased. Another component in the prevention and treatment of phosphorus is the plant’s disposition to absorb nutrients. Plant species and different plants within in the same species react differently to low levels of phosphorus in soil. Greater expansion of root systems generally correlate to greater nutrient uptake. Plants within a species that have larger roots are genetically advantaged and less prone to phosphorus deficiency. These plants can be cultivated and bred as a long term phosphorus deficiency prevention method. In conjunction to root size, other genetic root adaptations to low phosphorus conditions such as mycorrhizal symbioses have been found to increase nutrient intake. These biological adaptations to roots work to maintain the levels of vital nutrients. In larger commercial agriculture settings, variation of plants to adopt these desirable phosphorus intake adaptations may be a long-term phosphorus deficiency correction method.
The diagnostic workup of a suspected iodine deficiency includes signs and symptoms as well as possible risk factors mentioned above. A 24-hour urine iodine collection is a useful medical test, as approximately 90% of ingested iodine is excreted in the urine. For the standardized 24-hour test, a 50 mg iodine load is given first, and 90% of this load is expected to be recovered in the urine of the following 24 hours. Recovery of less than 90% is taken to mean high retention, that is, iodine deficiency. The recovery may, however, be well less than 90% during pregnancy, and an intake of goitrogens can alter the test results.
If a 24-hour urine collection is not practical, a random urine iodine-to-creatinine ratio can alternatively be used. However, the 24-hour test is found to be more reliable.
A general idea of whether a deficiency exists can be determined through a functional iodine test in the form of an iodine skin test. In this test, the skin is painted with an iodine solution: if the iodine patch disappears quickly, this is taken as a sign of iodine deficiency. However, no accepted norms exist on the expected time interval for the patch to disappear, and in persons with dark skin color the disappeance of the patch may be difficult to assess. If a urine test is taken shortly after, the results may be altered due to the iodine absorbed previously in a skin test.
As always, laboratory values have to be interpreted with the lab's reference values in mind and considering all aspects of the individual clinical situation.
Serum ferritin can be elevated in inflammatory conditions; so a normal serum ferritin may not always exclude iron deficiency, and the utility is improved by taking a concurrent C-reactive protein (CRP). The level of serum ferritin that is viewed as "high" depends on the condition. For example, in inflammatory bowel disease the threshold is 100, where as in chronic heart failure (CHF) the levels are 200.
Micronutrient deficiencies affect more than two billion people of all ages in both developing and industrialized countries. They are the cause of some diseases, exacerbate others and are recognized as having an important impact on worldwide health. Important micronutrients include iodine, iron, zinc, calcium, selenium, fluorine, and vitamins A, B, B, B, B, B, and C.
Micronutrient deficiencies are associated with 10% of all children's deaths, and are therefore of special concern to those involved with child welfare. Deficiencies of essential vitamins or minerals such as Vitamin A, iron, and zinc may be caused by long-term shortages of nutritious food or by infections such as intestinal worms. They may also be caused or exacerbated when illnesses (such as diarrhoea or malaria) cause rapid loss of nutrients through feces or vomit.
Raw eggs should be avoided in those with biotin deficiency, because egg whites contain high levels of the anti-nutrient avidin. The name avidin literally means that this protein has an "avidity" (Latin: "to eagerly long for") for biotin. Avidin binds irreversibly to biotin and this compound is then excreted in the urine.
Manganese deficiency can be easy to spot in plants because, much like magnesium deficiency, the leaves start to turn yellow and undergo interveinal chlorosis. The difference between these two is that the younger leaves near the top of the plant show symptoms first because manganese is not mobile while in magnesium deficiency show symptoms in older leaves near the bottom of the plant.
Symptoms include leaves turning yellow or brown in the margins between the veins which may remain green, while young leaves may appear to be bleached. Fruit would be of poor quality and quantity. Any plant may be affected, but raspberries and pears are particularly susceptible, as well as most acid-loving plants such as azaleas and camellias.
Iodine deficiency is treated by ingestion of iodine salts, such as found in food supplements. Mild cases may be treated by using iodized salt in daily food consumption, or drinking more milk, or eating egg yolks, and saltwater fish. For a salt and/or animal product restricted diet, sea vegetables (kelp, hijiki, dulse, nori (found in sushi)) may be incorporated regularly into a diet as a good source of iodine.
The recommended daily intake of iodine for adult women is 150–300 µg for maintenance of normal thyroid function; for men it is somewhat less at 150 µg.
However, too high iodine intake, for example due to overdosage of iodine supplements, can have toxic side effects. It can lead to hyperthyroidism and consequently high blood levels of thyroid hormones (hyperthyroxinemia). In case of extremely high single-dose iodine intake, typically a short-term suppression of thyroid function (Wolff–Chaikoff effect) occurs. Persons with pre-existing thyroid disease, elderly persons, fetuses and neonates, and patients with other risk factors are at a higher risk of experiencing iodine-induced thyroid abnormalities. In particular, in persons with goiter due to iodine deficiency or with altered thyroid function, a form of hyperthyroidism called Jod-Basedow phenomenon can be triggered even at small or single iodine dosages, for example as a side effect of administration of iodine-containing contrast agents. In some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (Hashimoto's thyroiditis and Graves' disease).
Calcium deficiency can sometimes be rectified by adding agricultural lime to acid soils, aiming at a pH of 6.5, unless the subject plants specifically prefer acidic soil. Organic matter should be added to the soil to improve its moisture-retaining capacity. However, because of the nature of the disorder (i.e. poor transport of calcium to low transpiring tissues), the problem cannot generally be cured by the addition of calcium to the roots. In some species, the problem can be reduced by prophylactic spraying with calcium chloride of tissues at risk.
Plant damage is difficult to reverse, so corrective action should be taken immediately, supplemental applications of calcium nitrate at 200 ppm nitrogen, for example. Soil pH should be tested, and corrected if needed, because calcium deficiency is often associated with low pH.
Early fruit will generally have the worst systems, with them typically lessening as the season progresses. Preventative measures, such as irrigating prior to especially high temperatures and stable irrigation will minimize the occurrence.
Iron is needed for bacterial growth making its bioavailability an important factor in controlling infection. Blood plasma as a result carries iron tightly bound to transferrin, which is taken up by cells by endocytosing transferrin, thus preventing its access to bacteria. Between 15 and 20 percent of the protein content in human milk consists of lactoferrin that binds iron. As a comparison, in cow's milk, this is only 2 percent. As a result, breast fed babies have fewer infections. Lactoferrin is also concentrated in tears, saliva and at wounds to bind iron to limit bacterial growth. Egg white contains 12% conalbumin to withhold it from bacteria that get through the egg shell (for this reason, prior to antibiotics, egg white was used to treat infections).
To reduce bacterial growth, plasma concentrations of iron are lowered in a variety of systemic inflammatory states due to increased production of hepcidin which is mainly released by the liver in response to increased production of pro-inflammatory cytokines such as Interleukin-6. This functional iron deficiency will resolve once the source of inflammation is rectified; however, if not resolved, it can progress to Anaemia of Chronic Inflammation. The underlying inflammation can be caused by fever, inflammatory bowel disease, infections, Chronic Heart Failure (CHF), carcinomas, or following surgery.
Reflecting this link between iron bioavailability and bacterial growth, the taking of oral iron supplements in excess of 200 mg/day causes a relative overabundance of iron that can alter the types of bacteria that are present within the gut. There have been concerns regarding parenteral iron being administered whilst bacteremia is present, although this has not been borne out in clinical practice. A moderate iron deficiency, in contrast, can provide protection against acute infection, especially against organisms that reside within hepatocytes and macrophages, such as malaria and tuberculosis. This is mainly beneficial in regions with a high prevalence of these diseases and where standard treatment is unavailable.
Measurements of a child’s growth provide the key information for the presence of malnutrition, but weight and height measurements alone can lead to failure to recognize kwashiorkor and an underestimation of the severity of malnutrition in children.