Pentose Phosphate Pathway
Phosphate Transport Proteins
Receptor, IGF Type 2
Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)
Phosphotransferases (Alcohol Group Acceptor)
Molecular Sequence Data
Glucosephosphate Dehydrogenase Deficiency
Phosphoric Monoester Hydrolases
Amino Acid Sequence
Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)
Sodium-Phosphate Cotransporter Proteins
Magnetic Resonance Spectroscopy
Polyisoprenyl Phosphate Monosaccharides
Transferases (Other Substituted Phosphate Groups)
Polyisoprenyl Phosphate Sugars
Phosphotransferases (Phosphate Group Acceptor)
Carbamoyl-Phosphate Synthase (Ammonia)
Glucosamine 6-Phosphate N-Acetyltransferase
Chromatography, High Pressure Liquid
Sodium-Phosphate Cotransporter Proteins, Type IIa
Sodium-Phosphate Cotransporter Proteins, Type III
Sequence Homology, Amino Acid
Electrophoresis, Polyacrylamide Gel
PHEX Phosphate Regulating Neutral Endopeptidase
Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)
Sodium-Phosphate Cotransporter Proteins, Type IIb
Guanosine Diphosphate Mannose
Phosphorus Metabolism Disorders
Dolichol Monophosphate Mannose
Phosphoric Diester Hydrolases
Rats, Inbred Strains
Zinc Phosphate Cement
Chromatography, Ion Exchange
Chromatography, Thin Layer
Biological Transport, Active
A novel interaction mechanism accounting for different acylphosphatase effects on cardiac and fast twitch skeletal muscle sarcoplasmic reticulum calcium pumps. (1/8540)In cardiac and skeletal muscle Ca2+ translocation from cytoplasm into sarcoplasmic reticulum (SR) is accomplished by different Ca2+-ATPases whose functioning involves the formation and decomposition of an acylphosphorylated phosphoenzyme intermediate (EP). In this study we found that acylphosphatase, an enzyme well represented in muscular tissues and which actively hydrolyzes EP, had different effects on heart (SERCA2a) and fast twitch skeletal muscle SR Ca2+-ATPase (SERCA1). With physiological acylphosphatase concentrations SERCA2a exhibited a parallel increase in the rates of both ATP hydrolysis and Ca2+ transport; in contrast, SERCA1 appeared to be uncoupled since the stimulation of ATP hydrolysis matched an inhibition of Ca2+ pump. These different effects probably depend on phospholamban, which is associated with SERCA2a but not SERCA1. Consistent with this view, the present study suggests that acylphosphatase-induced stimulation of SERCA2a, in addition to an enhanced EP hydrolysis, may be due to a displacement of phospholamban, thus to a removal of its inhibitory effect. (+info)
The Golgi apparatus plays a significant role in the maintenance of Ca2+ homeostasis in the vps33Delta vacuolar biogenesis mutant of Saccharomyces cerevisiae. (2/8540)The vacuole is the major site of intracellular Ca2+ storage in yeast and functions to maintain cytosolic Ca2+ levels within a narrow physiological range. In this study, we examined how cellular Ca2+ homeostasis is maintained in a vps33Delta vacuolar biogenesis mutant. We found that growth of the vps33Delta strain was sensitive to high or low extracellular Ca2+. This strain could not properly regulate cytosolic Ca2+ levels and was able to retain only a small fraction of its total cellular Ca2+ in a nonexchangeable intracellular pool. Surprisingly, the vps33Delta strain contained more total cellular Ca2+ than the wild type strain. Because most cellular Ca2+ is normally found within the vacuole, this suggested that other intracellular compartments compensated for the reduced capacity to store Ca2+ within the vacuole of this strain. To test this hypothesis, we examined the contribution of the Golgi-localized Ca2+ ATPase Pmr1p in the maintenance of cellular Ca2+ homeostasis. We found that a vps33Delta/pmr1Delta strain was hypersensitive to high extracellular Ca2+. In addition, certain combinations of mutations effecting both vacuolar and Golgi Ca2+ transport resulted in synthetic lethality. These results indicate that the Golgi apparatus plays a significant role in maintaining Ca2+ homeostasis when vacuolar biogenesis is compromised. (+info)
Regulation of AMP deaminase from chicken erythrocytes. A kinetic study of the allosteric interactions. (3/8540)The allosteric properties of AMP deaminase [EC 184.108.40.206] from chicken erythrocytes have been qualitatively and quantitatively accounted for by the concerted transition theory of Monod et al., on the assumption that this enzyme has different numbers of binding sites for each ligand. Theoretical curves yield a satisfactory fit for all experimental saturation functions with respect to activation by alkali metals and inhibition by Pi, assuming that the numbers of binding sites for AMP, alkali metals, and Pi are 4, 2, and 4, respectively. The enzyme was inhibited by concentrations of ATP and GTP below 0.1 and 0.25 mM, respectively, whereas activation of the enzyme was observed at ATP and GTP concentrations above 0.4 and 1.5 mM, respectively. These unusual kinetics with respect to ATP and GTP could be also accounted for by assuming 2 inhibitory and 4 activating sites for each ligand. (+info)
Myocardial oxygenation during high work states in hearts with postinfarction remodeling. (4/8540)BACKGROUND: Postinfarction left ventricular remodeling (LVR) is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more severe in animals that develop overt congestive heart failure (CHF). During high work states, further HEP loss occurs, which suggests demand-induced ischemia. This study tested the hypothesis that inadequate myocyte oxygen availability is the basis for these HEP abnormalities. METHODS AND RESULTS: Myocardial infarction was produced by left circumflex coronary artery ligation in swine. Studies were performed in 20 normal animals, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatine (PCr)/ATP was determined with 31P NMR and deoxymyoglobin (Mb-delta) with 1H NMR in myocardium remote from the infarct. Basal PCr/ATP tended to be decreased in postinfarct hearts, and this was significant in animals with CHF. Infusion of dobutamine (20 microg x kg-1 x min-1 IV) caused doubling of the rate-pressure product in both normal and LVR hearts and resulted in comparable significant decreases of PCr/ATP in both groups. This decrease in PCr/ATP was not associated with detectable Mb-delta. In CHF hearts, rate-pressure product increased only 40% in response to dobutamine; this attenuated response also was not associated with detectable Mb-delta. CONCLUSIONS: Thus, the decrease of PCr/ATP during dobutamine infusion is not the result of insufficient myocardial oxygen availability. Furthermore, in CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamine occurred in the absence of myocardial hypoxia, indicating that the HEP and contractile abnormalities were not the result of insufficient oxygen availability. (+info)
Effects of phosphate intake on distribution of type II Na/Pi cotransporter mRNA in rat kidney. (5/8540)BACKGROUND: Renal phosphate (Pi) reabsorption is regulated by dietary Pi intake, as well as in other ways. Changes in Pi reabsorption are associated with the modulation of sodium/Pi cotransporter type II (NaPi-2) protein abundance in the brush border membrane (BBM) of proximal tubules (PTs) and of renal NaPi-2 mRNA levels. In this study, we address whether the NaPi-2 protein and NaPi-2 mRNA distribution patterns in the renal cortex vary in parallel with changes of dietary Pi intake. METHODS: We investigated in cryosections of perfusion-fixed rat kidneys by in situ hybridization (ISH) and immunohistochemistry (IHC) the distribution patterns of NaPi-2 mRNA and of NaPi-2 protein one week, two hours, and four hours after changes in dietary Pi intake. RESULTS: NaPi-2 mRNA and NaPi-2 protein were present in PTs exclusively. In rats adapted to one week of high Pi intake, signals for NaPi-2 mRNA and NaPi-2 protein in cortical PTs were weak, except in the convoluted parts of PTs of juxtamedullary nephrons. After one week of low Pi intake, the ISH and IHC signals for NaPi-2 were high in PT segments in all cortical levels. The switch from a chronic high to a low Pi intake within two and four hours induced no increase and a slight increase, respectively, in the NaPi-2 mRNA signal in PTs of midcortical and of superficial nephrons, whereas in the BBM of these nephrons, NaPi-2 protein was markedly up-regulated. Two and four hours after switching from low to high Pi intake, the overall high ISH signal for NaPi-2 mRNA was unchanged, whereas NaPi-2 protein staining was drastically down-regulated in the BBM of PTs from superficial and midcortical nephrons. CONCLUSIONS: The marked changes in NaPi-2 protein abundance in the BBM, following altered dietary Pi intake, precede corresponding changes at the RNA level by several hours. Thus, the early adaptation to altered Pi intake involves mRNA-independent mechanisms. The up- or down-regulation of NaPi-2 protein abundance in the BBM and NaPi-2 mRNA in PT affects mainly midcortical and superficial nephrons. (+info)
Biochemical indices of osteomalacia in pregnant Asian immigrants in Britain. (6/8540)Serum calcium, phosphate and alkaline phosphatase, and urinary calcium excretion were examined during the second trimester of uncomplicated normal pregnancy in Asian immigrants to Britain and in local Caucasians. The mean serum calcium was significantly lower in Asians than in Caucasians, and the mean serum alkaline phosphatase was significantly higher in Asians. The geometric mean of the urinary calcium excretion was highly significantly lower in Asians than in Caucasians. The variances of the serum calcium, serum alkaline phosphatase, and urine calcium excretion did not differ significantly in the two populations. This indicates that there is a shift in values of immigrant Asians as a group compared with Caucasians. A comparison with figures obtained on normal nonpregnant persons of both suggests that the shift is not an inherent feature of the Asian population. (+info)
Bound forms of Ca taken up by the synaptic plasma membrane. (7/8540)Temperature dependent Ca-binding by the synaptic plasma membrane was increased in the presence of ATP and Mg++. Apparent Km for ATP was about 2.8 X 10(-5) M and optimal concentration of Mg++ was 2 mM in the presence of 2 mM ATP. After preincubation with nonradioactive Ca++, ATP and Mg++ to attain a steady state, addition of 45Ca resulted in remarkable labelling of the membrane, indicating rapid turnover of most of the membrane bound Ca. The presence of oxalate (60 mM) greatly increased Ca up-take on prolonged incubation. The Ca uptake in presence and absence of oxalate had similar substrate specificity and was similarly influenced by various monovalent cations. Furthermore, activities for Ca-uptake in the presence and absence of oxalate could not be separated by sucrose density gradient centrifugation of the synaptic plasma membrane fraction. Accordingly, it was considered that Ca++ in the medium was taken up by surface of the membrane, ATP- and temperature-dependently and then transferred into a cavity where the Ca-oxalate complex is formed. (+info)
Mutations of Arg198 in sarcoplasmic reticulum Ca2+-ATPase cause inhibition of hydrolysis of the phosphoenzyme intermediate formed from inorganic phosphate. (8/8540)Arg198 of sarcoplasmic reticulum Ca2+-ATPase was substituted with lysine, glutamine, glutamic acid, alanine, and isoleucine by site-directed mutagenesis. Kinetic analysis was performed with microsomal membranes isolated from COS-1 cells which were transfected with the mutated cDNAs. The rate of dephosphorylation of the ADP-insensitive phosphoenzyme was determined by first phosphorylating the Ca2+-ATPase with 32Pi and then diluting the sample with non-radioactive Pi. This rate was reduced substantially in the mutant R198Q, more strongly in the mutants R198A and R1981, and most strongly in the mutant R198E, but to a much lesser extent in R198K. The reduction in the rate of dephosphorylation was consistent with the observed decrease in the turnover rate of the Ca2+-ATPase accompanied by the steady-state accumulation of the ADP-insensitive phosphoenzyme formed from ATP. These results indicate that the positive charge and high hydrophilicity of Arg198 are critical for rapid hydrolysis of the ADP-insensitive phosphoenzyme. (+info)
The condition is inherited in an X-linked recessive pattern, meaning that the gene for G6PD deficiency is located on the X chromosome and affects males more frequently than females. Females may also be affected but typically have milder symptoms or may be carriers of the condition without experiencing any symptoms themselves.
G6PD deficiency can be caused by mutations in the G6PD gene, which can lead to a reduction in the amount of functional enzyme produced. The severity of the condition depends on the specific nature of the mutation and the degree to which it reduces the activity of the enzyme.
Symptoms of G6PD deficiency may include jaundice (yellowing of the skin and eyes), fatigue, weakness, and shortness of breath. In severe cases, the condition can lead to hemolytic anemia, which is characterized by the premature destruction of red blood cells. This can be triggered by certain drugs, infections, or foods that contain high levels of oxalic acid or other oxidizing agents.
Diagnosis of G6PD deficiency typically involves a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing symptoms and preventing complications through dietary modifications, medications, and avoidance of triggers such as certain drugs or infections.
Overall, G6PD deficiency is a relatively common genetic disorder that can have significant health implications if left untreated. Understanding the causes, symptoms, and treatment options for this condition is important for ensuring appropriate care and management for individuals affected by it.
Causes of Hyperphosphatemia:
There are several possible causes of hyperphosphatemia, including:
1. Kidney disease or failure: The kidneys regulate the levels of phosphate in the blood, and if they are not functioning properly, phosphate levels can become elevated.
2. Resistance to parathyroid hormone (PTH): PTH is a hormone that helps regulate calcium and phosphate levels in the body. If there is resistance to PTH, phosphate levels can become elevated.
3. Vitamin D deficiency: Vitamin D is important for the absorption of phosphate from food in the gut. A deficiency in vitamin D can lead to an excessive amount of phosphate in the blood.
4. Certain medications: Some medications, such as certain antacids and nutritional supplements, can contain high levels of phosphate and cause hyperphosphatemia.
5. Poor dietary habits: Consuming a diet that is high in phosphate-rich foods, such as meat and processed foods, can lead to elevated phosphate levels in the blood.
Symptoms of Hyperphosphatemia:
The symptoms of hyperphosphatemia can vary depending on the severity of the condition, but may include:
1. Bone pain or weakness
3. Nausea and vomiting
4. Weakness in the muscles
5. Rickets (in children)
6. Osteoporosis (in adults)
7. Kidney damage or failure
Diagnosis of Hyperphosphatemia:
Hyperphosphatemia is typically diagnosed through blood tests that measure the level of phosphate in the blood. Other tests may also be performed to assess kidney function and rule out other potential causes of elevated phosphate levels. These tests may include:
1. Serum creatinine test: This test measures the level of creatinine, a waste product that is produced by the muscles and removed from the blood by the kidneys. Elevated levels of creatinine can indicate kidney damage or failure.
2. Urine test: A urine test may be performed to check for proteinuria (excess protein in the urine), which can be a sign of kidney damage.
3. Parathyroid hormone (PTH) test: This test measures the level of PTH, a hormone that regulates calcium and phosphate levels in the blood. Elevated levels of PTH can indicate hyperparathyroidism, a condition in which the parathyroid glands produce too much PTH.
4. 24-hour urine phosphate test: This test measures the amount of phosphate excreted in the urine over a 24-hour period.
Treatment of Hyperphosphatemia:
The treatment of hyperphosphatemia depends on the underlying cause of the condition. Here are some possible treatment options:
1. Phosphate-binding agents: These medications, such as sevelamer and lanthanum carbonate, bind to phosphate in the gut and prevent it from being absorbed into the bloodstream.
2. Calcium supplements: Calcium can help to lower phosphate levels by binding to it and removing it from the bloodstream.
3. Dietary changes: A dietitian can work with you to develop a meal plan that limits phosphate-rich foods, such as meat, dairy products, and processed foods, while emphasizing fruits, vegetables, and whole grains.
4. Dialysis: In cases where the condition is caused by kidney failure, dialysis may be necessary to remove excess phosphate from the blood.
5. Surgery: In cases where the condition is caused by a parathyroid adenoma or hyperplasia, surgery may be necessary to remove the affected gland(s).
It's important to note that hyperphosphatemia can lead to complications such as mineral bone disease, which can cause weakened bones, bone pain, and an increased risk of fractures. Therefore, it's important to work with your healthcare provider to manage the condition and prevent these complications.
Causes of Hypophosphatemia
There are several possible causes of hypophosphatemia, including:
1. Malnutrition or a poor diet that is deficient in phosphorus.
2. Gastrointestinal disorders such as celiac disease, inflammatory bowel disease, or gastrointestinal surgery.
3. Kidney problems such as chronic kidney disease, renal tubular acidosis, or distal renal tubular phosphate loss.
4. Hormonal imbalances such as hypoparathyroidism (underactive parathyroid glands) or hyperparathyroidism (overactive parathyroid glands).
5. Medications such as diuretics, antacids, and certain antibiotics.
6. Chronic alcoholism.
7. Genetic disorders such as X-linked hypophosphatemic rickets or familial hypophosphatemic rickets.
Symptoms of Hypophosphatemia
The symptoms of hypophosphatemia can vary depending on the severity and duration of the condition, but may include:
1. Weakness, fatigue, or muscle cramps.
2. Bone pain or joint stiffness.
3. Difficulty healing from injuries or infections.
4. Numbness or tingling sensations in the extremities.
5. Seizures or other neurological symptoms.
6. Respiratory problems such as shortness of breath or difficulty breathing.
7. Heart arrhythmias or cardiac failure.
Diagnosis and Treatment of Hypophosphatemia
Hypophosphatemia can be diagnosed through blood tests that measure the levels of phosphate in the blood. Treatment for hypophosphatemia typically involves correcting any underlying causes, such as stopping medications that may be causing the condition or treating underlying medical conditions.
In some cases, treatment may involve supplements to increase phosphate levels in the blood. Vitamin D and calcium supplements may also be prescribed to help maintain bone health. In severe cases of hypophosphatemia, hospitalization may be necessary to manage symptoms and prevent complications.
Prognosis and Complications of Hypophosphatemia
The prognosis for hypophosphatemia is generally good if the underlying cause is identified and treated promptly. However, untreated hypophosphatemia can lead to a number of complications, including:
1. Osteomalacia or osteoporosis.
2. Rickets in children.
3. Weakened immune system.
4. Increased risk of infections.
5. Nerve damage or neuropathy.
6. Cardiovascular problems such as heart arrhythmias or cardiac failure.
7. Respiratory failure.
8. Kidney damage or kidney failure.
It is important to seek medical attention if symptoms persist or worsen over time, as hypophosphatemia can lead to serious complications if left untreated.
Hypophosphatemia is a condition characterized by low levels of phosphate in the blood. It can be caused by a variety of factors and may present with symptoms such as weakness, bone pain, and respiratory problems. Treatment typically involves correcting any underlying causes and supplements to increase phosphate levels in the blood.
Early detection and treatment are important to prevent complications of hypophosphatemia, which can include osteomalacia or osteoporosis, nerve damage, cardiovascular problems, respiratory failure, and kidney damage. If you suspect you may have hypophosphatemia, it is important to seek medical attention as soon as possible to receive proper diagnosis and treatment.
There are several types of phosphorus metabolism disorders, including:
1. Hypophosphatemia: This is a condition characterized by low levels of phosphorus in the blood. It can be caused by a variety of factors, such as malnutrition, kidney disease, or hormonal imbalances. Symptoms of hypophosphatemia can include fatigue, weakness, and bone pain.
2. Hyperphosphatemia: This is a condition characterized by high levels of phosphorus in the blood. It can be caused by conditions such as kidney disease or excessive intake of phosphorus-containing foods. Symptoms of hyperphosphatemia can include nausea, vomiting, and an increased risk of kidney stones.
3. Fanconi syndrome: This is a rare genetic disorder that affects the body's ability to absorb and utilize phosphorus. It is characterized by low levels of phosphorus in the blood, as well as other symptoms such as rickets, bone pain, and an increased risk of fractures.
4. X-linked hypophosphatemic tumor-induced osteomalacia (XLH): This is a rare genetic disorder that affects males and is characterized by low levels of phosphorus in the blood and an increased risk of bone fractures. It is caused by mutations in the TNS1 gene, which codes for a protein involved in phosphorus metabolism.
5. Tumor-induced osteomalacia (TIO): This is a rare disorder that is caused by tumors that produce excessive amounts of a hormone called fibroblast growth factor 23 (FGF23). This hormone interferes with the body's ability to absorb phosphorus, leading to low levels of phosphorus in the blood and an increased risk of bone fractures.
6. Chronic kidney disease: In advanced stages of chronic kidney disease, the kidneys may not be able to effectively remove excess phosphorus from the blood, leading to hyperphosphatemia.
7. Heart disease: High levels of phosphorus in the blood can increase the risk of heart disease, including conditions such as atherosclerosis and heart failure.
8. Kidney damage: Prolonged exposure to high levels of phosphorus in the blood can damage the kidneys and increase the risk of kidney disease.
It is important to note that these are just a few examples of conditions that can cause hyperphosphatemia, and there may be other causes as well. If you suspect that you or someone you know has hyperphosphatemia, it is important to consult with a healthcare professional for proper diagnosis and treatment.
There are two main types of galactosemia:
1. Classical galactosemia: This is the most severe form of the disorder, and it is characterized by a complete lack of the enzyme galactose-1-phosphate uridylyltransferase (GALT). Without GALT, galactose builds up in the blood and tissues, leading to serious health problems.
2. Dialectical galactosemia: This form of the disorder is less severe than classical galactosemia, and it is characterized by a partial deficiency of GALT. People with dialectical galactosemia may experience some symptoms, but they are typically milder than those experienced by people with classical galactosemia.
Symptoms of galactosemia can include:
* Jaundice (yellowing of the skin and eyes)
* Poor feeding in infants
* Developmental delays
If left untreated, galactosemia can lead to a range of complications, including:
* Liver disease
* Kidney disease
* Increased risk of infections
* Delayed growth and development
The diagnosis of galactosemia is typically made through a combination of physical examination, medical history, and laboratory tests. Treatment for the disorder typically involves a strict diet that limits or eliminates galactose-containing foods, such as milk and other dairy products. In some cases, medication may also be prescribed to help manage symptoms.
Overall, early diagnosis and treatment of galactosemia are important for preventing or minimizing the risk of complications associated with this condition.
The symptoms of familial hypophosphatemic rickets typically appear during infancy or early childhood and may include:
* Bowed legs
* Delayed closure of the fontanelles (soft spots on the skull)
* Difficulty walking or standing
* Growth retardation
* Increased risk of fractures
* Thickening of the bones (hyperostosis)
* Tooth decay and gum disease (dental caries and periodontal disease)
If left untreated, familial hypophosphatemic rickets can lead to severe complications such as:
* Permanent skeletal deformities
* Increased risk of bone fractures
* Dental problems
* Growth retardation
* Intellectual disability
* Death in rare cases
The diagnosis of familial hypophosphatemic rickets is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include measurements of serum phosphate levels, urinary phosphate excretion, and assessment of bone density using imaging techniques such as X-rays or computed tomography (CT) scans. Genetic testing can identify mutations in the PHEX gene that confirm the diagnosis.
Treatment for familial hypophosphatemic rickets typically involves a combination of dietary modifications and medication. Dietary modifications may include increasing phosphate intake through supplements or high-phosphate foods, while medications such as vitamin D analogues and bisphosphonates can help to improve bone density and reduce the risk of fractures. In severe cases, surgery may be necessary to correct skeletal deformities.
In conclusion, familial hypophosphatemic rickets is a rare genetic disorder that affects the development of bones and teeth, leading to a range of symptoms including bowed legs, thickened skin, and dental problems. The diagnosis is based on a combination of clinical findings, laboratory tests, and genetic analysis, while treatment involves a combination of dietary modifications and medication. With appropriate management, individuals with familial hypophosphatemic rickets can lead active and productive lives, although some may experience ongoing health issues throughout their lifetime.
Favism is characterized by a sudden and severe anemia, often triggered by exposure to certain foods or medications that contain a chemical called quinine. Quinine is found in the bark of the cinchona tree, which is used to make antimalarial drugs. In individuals with favism, quinine can cause red blood cells to rupture and die prematurely, leading to anemia and other complications.
Symptoms of favism usually begin within 24 hours of exposure to quinine and may include fatigue, jaundice, dark urine, and a low platelet count. In severe cases, favism can lead to life-threatening complications such as kidney failure and cardiac arrest.
Favism is most commonly found in individuals of Mediterranean or African descent, particularly those from Greece, Italy, Turkey, and the Middle East. It is estimated that approximately 10% of these populations carry the G6PD deficiency that causes favism.
There is no cure for favism, but certain medications and dietary changes can help manage symptoms and prevent complications. Individuals with favism are advised to avoid consuming foods or medications containing quinine, and may require regular monitoring of their red blood cell count and other clinical parameters.
In conclusion, favism is a rare genetic disorder that affects the metabolism of hemoglobin and can cause sudden and severe anemia in certain populations. It is important to be aware of this condition and take necessary precautions to prevent complications, particularly when consuming certain foods or medications containing quinine.
Symptoms of nephrocalcinosis may include nausea, vomiting, abdominal pain, frequent urination, and blood in the urine. Diagnosis is typically made through imaging tests such as X-rays, CT scans, or ultrasound, and blood tests to determine calcium levels and kidney function.
Treatment for nephrocalcinosis depends on the underlying cause of the condition and may include medications to lower calcium levels, dietary changes to reduce calcium intake, and in severe cases, dialysis or kidney transplantation may be necessary. It is important to seek medical attention if symptoms persist or worsen over time, as early detection and treatment can help prevent long-term damage to the kidneys.
There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:
1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.
Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
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Sodium Phosphate - PubMed
- Long-term occupational exposure to two flame retardants (tris(1,3-dichloro-2-propyl)phosphate, TDCP, and triphenyl phosphate, TPP) did not produce adverse health effects. (cdc.gov)
- There have been a few cases of allergic reactions to consumer products that contain triphenyl phosphate (TPP), but a study that examined several hundred people exposed to plastics and glues that contained TPP or TCP did not find any allergic reactions. (cdc.gov)
- Triphenyl phosphate / published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization. (who.int)
- Evaluates risks to human health and the environment posed by the production and use of triphenyl phosphate, a compound widely used as a flame retardant in phenolic and phenylene-oxide-based resins for the manufacture of electrical and automobile components. (who.int)
- Triphenyl phosphate is also used as a non-flammable plasticizer in cellulose acetate for photographic films, and as a component of hydraulic fluids and lubricant oils. (who.int)
- A review of data on effects on organisms in the environment concentrates on risks to the aquatic environment, concluding that triphenyl phosphate is the most acutely toxic of te various triaryl phosphates to fish, shrimp, and daphnids. (who.int)
- The book notes that triphenyl phosphate exhibits low toxicity in short-term studies, is not mutagenic, and has not been shown, in several well-designed studies, to cause delayed neuropathy or other neurotoxic changes. (who.int)
- The chemical name for clindamycin phosphate is Methyl 7-chloro-6,7,8-trideoxy-6-(1-methyl- trans -4-propyl-L-2-pyrrolidinecarboxamido)-1-thio-L- threo - α-D- galacto -octopyranoside 2-(dihydrogen phosphate). (nih.gov)
- UNSW scientists show that dihydrogen phosphate anions actually bind to one another when their negative charges suggest they shouldn't. (edu.au)
- Scientists at UNSW Sydney, together with collaborators from Western Sydney University and The Netherlands, were surprised to find that dihydrogen phosphate anions - vital inorganic ions for cellular activity - bind with other dihydrogen phosphate anions despite being negatively charged. (edu.au)
- The same team also made a molecule that could 'grab' these dihydrogen phosphate anions and depending on what coloured light was shone on them, either increase or inhibit their movement in solution. (edu.au)
- Associate Professor Jon Beves from UNSW's School of Chemistry says chemists have always known dihydrogen phosphate was 'a bit weird' and hard to study in solution, but until now nobody knew what was really happening. (edu.au)
- The hydrogen bonds between dihydrogen phosphate anions seem to be surprisingly strong. (edu.au)
Amounts of phosphate3
- Serum phosphate levels should be regularly monitored and appropriate amounts of phosphate should be added to the infusions to maintain normal serum phosphate levels. (nih.gov)
- Most foods contain small amounts of phosphate esters and you may be exposed by eating contaminated food. (cdc.gov)
- Most foods have been found to contain trace amounts of phosphate ester flame retardants due to their wide use in plastics and presence in the environment. (cdc.gov)
- Oral phosphate binders are used to decrease the highly efficient gastrointestinal absorption of phosphorus. (medscape.com)
- Lanthanum carbonate is a noncalcium, nonaluminum phosphate binder indicated for the reduction of high phosphorus levels in patients with end-stage renal disease. (medscape.com)
- Phosphorus in the form of organic and inorganic phosphate has a variety of important biochemical functions in the body and is involved in many significant metabolic and enzyme reactions in almost all organs and tissues. (nih.gov)
- This site is aimed at guiding decisions and providing recommendations on the use of phosphate rock (PR) as fertilizer, predict their cost-effectiveness as a source of phosphorus for crop productivity and its long-term sustainability and environmental consequences of using soluble P and phosphate rocks. (iaea.org)
- Soft rock phosphate, also known as colloidal phosphate, is a natural untreated source of phosphorus and calcium. (groworganic.com)
Hydroxyapatite and tricalcium1
- This paper deals with most common types of the calcium phosphate materials such as hydroxyapatite and tricalcium phosphate which are currently used in dental and medical fields. (bvsalud.org)
Prednisolone sodium ph8
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Calcium Phosphate Cement3
- We have sought to improve calcium phosphate cement by developing a method for seeding bone cells into the cement. (nist.gov)
- Calcium phosphate cement (CPC) is a dry white powder of calcium phosphate salts that when mixed with water will react to form microcrystalline hydroxyapatite (HA) in about 30 min. (nist.gov)
- Objective: to perform a histological analysis of nylon, carbon, and polypropylene fiber-enriched calcium phosphate cement (CPC) for use as bone substitute in the femur or rats. (bvsalud.org)
- Phosphate in the extracellular fluid is primarily in inorganic form and plasma levels may vary somewhat with age. (nih.gov)
- The ratio of disodium phosphate and monosodium phosphate in the extracellular fluid is 4 to 1 (80% to 20%) at the normal pH of 7.4. (nih.gov)
- They are used when there is an abnormally high blood phosphate level ( hyperphosphatemia ) which can be caused by impaired renal phosphate excretion or increased extracellular fluid phosphate loads. (drugs.com)
- The Centers for Disease Control and Prevention (CDC) issued a health safety alert to inform the public that commercially available non-pharmaceutical chloroquine phosphate, such as that used in aquariums, is not safe and does not provide protection from COVID-19 infection. (ihs.gov)
- The Issue: There have been two cases where people ingested chloroquine phosphate used in aquariums in an attempt to prevent COVID-19 infection. (ihs.gov)
- Chloroquine phosphate, when used without a prescription and supervision of a healthcare provider, can cause serious health consequences, including death. (ihs.gov)
- Clinicians and public health officials should discourage the public from misusing non-pharmaceutical chloroquine phosphate. (ihs.gov)
- Within 30 minutes of taking chloroquine phosphate, the man in his 60s experienced "immediate effects" and had to be admitted to a nearby Banner Health hospital, the medical system in Arizona said in a press release Monday. (nypost.com)
High in phosphate2
- Sodium Phosphates Injection, USP, 3 mmol/mL (millimoles/mL), is a sterile, nonpyrogenic, concentrated solution containing a mixture of monobasic sodium phosphate and dibasic sodium phosphate in Water for Injection. (nih.gov)
- PiT-2 protein uses positively charged sodium atoms ( ions ) to transport phosphate in out and of cell membranes. (nih.gov)
- Be careful not to confuse phosphate salts with substances such as organophosphates, or with tribasic sodium phosphates and tribasic potassium phosphates, which are very poisonous. (medicinenet.com)
- Sodium phosphate tablets ( OsmoPrep , Visicol, Salix Pharmaceuticals, Raleigh, NC) are FDA-approved for cleansing the colon before a colonoscopy . (medicinenet.com)
- Over-the-counter sodium phosphate solutions and enemas may also be used for bowel cleansing before medical procedures. (medicinenet.com)
- Taking sodium or potassium phosphate by mouth is effective for preventing or treating low phosphate levels in the blood. (medicinenet.com)
- Sodium phosphate is an FDA-permitted over-the-counter (OTC) ingredient for the treatment of constipation . (medicinenet.com)
- Some early research suggests that taking sodium phosphate by mouth four times daily for 6 days might increase athletic performance in male cyclists. (medicinenet.com)
- Limited research shows that giving sodium and potassium phosphates intravenously (by IV) over 24 hours prevents refeeding syndrome when restarting nutrition in people who are severely malnourished or starved. (medicinenet.com)
- Phosphate concentrations have not been measured in breastmilk after large maternal doses of sodium phosphate, such a 30 gram oral dose for pre-procedural bowel evacuation. (nih.gov)
- It is probably not necessary to suspend breastfeeding after the use of oral sodium phosphate solutions given once or twice for bowel evacuation before a procedure. (nih.gov)
- Sodium Phosphate P 32. (nih.gov)
- Phosphate salts are taken by mouth for treating blood phosphate levels that are too low and blood calcium levels that are too high, and for preventing kidney stones . (medicinenet.com)
- Drinking water may contain phosphate esters due to leakage from plastics or industrial waste water discharge. (cdc.gov)
- Avoid installation or use of materials that are known to contain phosphate esters-based flame retardants in indoor environments to minimize exposure via air. (cdc.gov)
- Indoor air can contain phosphate ester flame retardants from certain plastics, adhesives, foams, or electronics. (cdc.gov)
- Acetazolamide is particularly efficient in promoting renal phosphate excretion. (medscape.com)
- Diuretics lower phosphate serum levels by enhancing renal excretion. (medscape.com)
- This agent increases the excretion of phosphate. (medscape.com)
- As NaHCO3 delivery to the collecting duct increases, the renal excretion of phosphate increases. (medscape.com)
- The polymer forms ionic and hydrogen bonds with phosphates and bile acids to promote fecal excretion. (medscape.com)
- Glucose 6 phosphate dehydrogenase (G6PD) deficiency is a hereditary condition in which red blood cells break down (hemolysis) when the body is exposed to certain foods, drugs, infections or stress. (nih.gov)
- G6PD deficiency occurs when a person is missing or does not have enough of an enzyme called glucose-6-phosphate dehydrogenase. (medlineplus.gov)
- Glucose-6-phosphate dehydrogenase deficiency results from variants (also called mutations) in the G6PD gene. (nih.gov)
- If variants in the G6PD gene reduce the amount of glucose-6-phosphate dehydrogenase or alter its structure, this enzyme can no longer play its protective role. (nih.gov)
- However, many females with one altered copy of this gene have glucose-6-phosphate dehydrogenase deficiency similar to affected males because the X chromosome with the normal copy of the G6PD gene is turned off through a process called X-inactivation . (nih.gov)
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy in humans affecting about 400 million people worldwide (1,2). (who.int)
- Glucose-6-phosphate dehydrogenase in western Islamic Republic of Iran) to [G6PD] deficiency is a common X-linked find the prevalence of G6PD deficiency. (who.int)
- 6-phosphate dehydrogenase (G6PD) of Physicians and Surgeons Pakistan , deficiency. (who.int)
- What are Phosphate binders? (drugs.com)
- Phosphate binders are used to decrease the absorption of phosphate from food in the digestive tract. (drugs.com)
- Phosphate binders react with phosphate to form an insoluble compound, making it unable to be absorbed from the gastrointestinal tract. (drugs.com)
- When taken regularly with meals, phosphate binders lower the concentration of phosphate in serum. (drugs.com)
- In an analysis of Medicare beneficiaries on dialysis, patients prescribed sucroferric oxyhydroxide (Velphoro) had lower hospital admission rates compared with patients who received four other phosphate binders (7.97 per 100 member months), according to Kristain Lindemann, of Fresenius Health Partners in Waltham, Massachusetts, and colleagues. (medpagetoday.com)
- All patients included had intact parathyroid levels under 600 pg/mL, and had phosphate binders prescribed between 2016 and 2018. (medpagetoday.com)
- The solution is intended as an alternative to potassium phosphate to provide phosphate ion (PO 4 3- ) for addition to large volume infusion fluids for intravenous use. (nih.gov)
- FARMVILLE, N.C. , March 31, 2023 /PRNewswire/ -- CMP Pharma announced today that in order to mitigate drug shortage concerns, the FDA's CDER Office of Compliance has granted a shelf life extension for CMP Development LLC Potassium Phosphates Injection (NDA 212121). (prnewswire.com)
- CMP Pharma's Potassium Phosphates Injection is appropriate for pediatric patients 12 years of age and older who weigh at least 40 kg and adults weighing at least 45 kg. (prnewswire.com)
- CMP consistently has supply of potassium phosphates available for you and your patient's needs. (prnewswire.com)
- CMP Pharma's FDA-approved Potassium Phosphates Injection can be ordered using NDC 46287-024-10 (10 X 15 mL single-dose glass vial). (prnewswire.com)
- Healthcare providers sometimes give potassium phosphate intravenously (by IV) for treating low phosphate and high calcium levels in the blood, and for preventing low phosphate in patients who are being tube-fed. (medicinenet.com)
- Taking potassium phosphate by mouth might help prevent calcium kidney stones from forming in patients with high urine levels of calcium. (medicinenet.com)
- Early research suggests that taking potassium phosphate intravenously (by IV) does not improve a diabetes complication in which the body produces too many blood acids called ketones. (medicinenet.com)
- Plasma phosphate is believed to be filterable by the renal glomeruli, and the major portion of filtered phosphate (greater than 80%) is actively reabsorbed by the tubules. (nih.gov)
- Neuropsychiatric events: Patients with influenza, including those receiving oseltamivir phosphate capsules, particularly pediatric patients, may be at an increased risk of confusion or abnormal behavior early in their illness. (nih.gov)
- Intravenously infused phosphate not taken up by the tissues is excreted almost entirely in the urine. (nih.gov)
- It occurs when a person is missing or has low levels of the enzyme glucose-6-phosphate dehydrogenase. (nih.gov)
- In affected individuals, a defect in an enzyme called glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely. (nih.gov)
- This gene provides instructions for making an enzyme called glucose-6-phosphate dehydrogenase. (nih.gov)
- Studies found that TDCP, tris(2-chloroethyl) phosphate (TCEP), TCP, and tri-n-butyl phosphate (TnBP) can easily pass from the stomach and intestines into the blood stream after oral exposure to these chemicals. (cdc.gov)
- Phosphate esters are added to consumer and industrial products in order to reduce flammability. (cdc.gov)
- Some phosphate esters will deposit on wet and dry surfaces and others will be broken down by water. (cdc.gov)
- The Department of Health and Human Services (DHHS) and the EPA have not classified the carcinogenic potential of the phosphate esters. (cdc.gov)
- Generally, most phosphate esters are poorly soluble in water and adsorb strongly to soils. (cdc.gov)
- Ingesting food contaminated with phosphate esters is the primary source of exposure. (cdc.gov)
- Hydraulic fluid is the primary source of phosphate esters in outdoor air. (cdc.gov)
- Drinking water contaminated with phosphate esters due to leaching from plastics or industrial waste water discharge is another potential exposure route. (cdc.gov)
- Hydraulic fluid spills or industrial waste water used for agriculture can result in the presence of phosphate esters in soil. (cdc.gov)
- This fact sheet answers the most frequently asked health questions (FAQs) about phosphate ester flame retardants. (cdc.gov)
- The general population is primarily exposed to phosphate ester flame retardants by eating contaminated food. (cdc.gov)
- Phosphate ester flame retardants are human-made chemicals that are typically liquids at room temperature, although some are solids. (cdc.gov)
- What happens to phosphate ester flame retardants when they enter the environment? (cdc.gov)
- How might I be exposed to phosphate ester flame retardants? (cdc.gov)
- How can phosphate ester flame retardants affect my health? (cdc.gov)
- How likely are phosphate ester flame retardants to cause cancer? (cdc.gov)
- There is not enough information available to determine with certainty whether or not phosphate ester flame retardants produce cancer in humans. (cdc.gov)
- No studies have been conducted to examine the toxicity of phosphate ester flame retardants in children. (cdc.gov)
- How can families reduce the risk of exposure to phosphate ester flame retardants? (cdc.gov)
- Phosphate ester flame retardants are human-made chemicals added to consumer and industrial products for the purpose of reducing flammability. (cdc.gov)
- Phosphate ester flame retardants are composed of a group of chemicals with similar properties but slightly different structures. (cdc.gov)
- Phosphate ester flame retardants are released to the environment from industrial sources and disposal of consumer products containing flame retardants. (cdc.gov)
- Phosphate ester flame retardants can change chemical composition in the environment. (cdc.gov)
- Young children may be at a higher risk of exposure since they are more likely to put phosphate ester flame retardant treated materials in their mouths. (cdc.gov)
- Currently, we do not know much about phosphate ester flame retardants and the body. (cdc.gov)
- There is no information on how these chemicals leave your body, but based on studies in animals, phosphate ester flame retardants may be broken down in the body and the breakdown product may be eliminated in the urine. (cdc.gov)
- Neither phosphate ester flame retardants nor their breakdown products seemed to accumulate in the body based on studies in animals. (cdc.gov)
- Few studies have looked at the health effects of exposure to phosphate ester flame retardants. (cdc.gov)
- Clindamycin phosphate is a water soluble ester of the semi-synthetic antibiotic produced by a 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the parent antibiotic lincomycin. (nih.gov)
- In composite bioceramics world, many researchers have focused their interest on the development of biphasic calcium phosphate (BCP) ceramics, especially with hydroxyapatite (HA: Ca 10 (PO 4 ) 6 (OH) 2 ) and tricalcium phosphate (TCP: Ca 3 (PO 4 ) 2 ). (hindawi.com)
- Cylindrical biphasic calcium phosphate ceramic samples (BCP) are put together by mixing dry HA and β -TCP (MERCK, Darmstadt, Germany). (hindawi.com)
- These highlights do not include all the information needed to use OSELTAMIVIR PHOSPHATE CAPSULES safely and effectively. (nih.gov)
- See full prescribing information for OSELTAMIVIR PHOSPHATE CAPSULES. (nih.gov)
- Serious skin/hypersensitivity reactions such as Stevens-Johnson Syndrome, toxic epidermal necrolysis and erythema multiforme: Discontinue oseltamivir phosphate capsules and initiate appropriate treatment if allergic-like reactions occur or are suspected. (nih.gov)
- Avoid administration of LAIV within 2 weeks before or 48 hours after oseltamivir phosphate capsules use, unless medically indicated. (nih.gov)
- Phosphate salts refers to many different combinations of the chemical phosphate with salts and minerals . (medicinenet.com)
- People use phosphate salts for medicine. (medicinenet.com)
- Phosphate salts are also used for improving exercise performance, as an antacid for gastroesophageal reflux disease ( GERD ), and as a laxative for emptying the bowels before surgery. (medicinenet.com)
- Phosphate salts and calcium are applied to sensitive teeth to reduce pain . (medicinenet.com)
- Rectally, phosphate salts are used as a laxative to clean the bowels before surgery or intestinal tests. (medicinenet.com)
- Phosphate salts can act as laxatives by causing more fluid to be drawn into the intestines and stimulating the gut to push out its contents faster. (medicinenet.com)
- However, most evidence shows that taking phosphate salts by mouth does not improve exercise performance. (medicinenet.com)
- More evidence is needed to rate phosphate salts for these uses. (medicinenet.com)
- OSHA previously had an 8-hour TWA PEL of 1 ppm for dibutyl phosphate. (cdc.gov)
- There are no published reports of toxic reactions caused by exposure to dibutyl phosphate. (cdc.gov)
- However, in a personal communication to the ACGIH, Mastromatteo reported that workers exposed to relatively low levels of dibutyl phosphate developed respiratory tract irritation and headache (Mastromatteo 1964a, as cited in ACGIH 1986/Ex. (cdc.gov)
- Calcium phosphate materials are similar to bone in composition and in having bioactive and osteoconductive properties. (bvsalud.org)
- It also includes a decision support system (DSS) integrating soil, crop, phosphate rock and site factors to predict their relative agronomic effectiveness and economic utilization, so that valuable information can be provided to resource managers including policy makers and farmers. (iaea.org)
- It is essential for building soil phosphate levels for long-term plant productivity and for preventing calcium deficient soils. (groworganic.com)
- Academy of Sciences of the United States phosphate dehydrogenase phenotypes of America , 1988, 85:5171-5. (who.int)
- This agent is a polymeric phosphate binder for oral administration. (medscape.com)
- Sucroferric oxyhydroxide is an iron-based, calcium-free phosphate binder. (medscape.com)
- Ferric citrate is a phosphate binder. (medscape.com)
- The type of phosphate binder utilized in dialysis patients may affect rate of hospitalizations, researchers reported. (medpagetoday.com)
- Choice of phosphate binder may help to reduce hospital admissions and overall costs of medical care. (medpagetoday.com)
- The most common medical problem associated with glucose-6-phosphate dehydrogenase deficiency is hemolytic anemia, which occurs when red blood cells are destroyed faster than the body can replace them. (nih.gov)
- In people with glucose-6-phosphate dehydrogenase deficiency, hemolytic anemia is most often triggered by bacterial or viral infections or by certain drugs (such as some antibiotics and medications used to treat malaria). (nih.gov)
- This agent normalizes phosphate concentrations in patients on dialysis. (medscape.com)
- Phosphate, present in large amounts in erythrocytes and other tissue cells, plays a significant intracellular role in the synthesis of high energy organic phosphates. (nih.gov)
- The project is expected to produce 300,000tpa of organic phosphate fertiliser. (mining-technology.com)
- He says the work his team carried out used an organic solvent called dimethyl sulfoxide and he imagines future studies would look at whether phosphate behaves in the same way in water, where all biological chemistry takes place. (edu.au)
- Use of a phosphate rectal enema by a nursing mother would require no special precautions. (nih.gov)
- Adverse health effects seen in humans after exposure to tri-o-cresyl phosphate (TCP) indicate that this substance can enter the body and pass into the bloodstream. (cdc.gov)
- An organophosphate oxoanion that is a trianion arising from deprotonation of the phosphate and carboxylic acid functions of N -acetylmuramic acid 6-phosphate. (ebi.ac.uk)
- Nicotinamide adenine dinucleotide phosphate ( NADP + , in older notation TPN ) is used in anabolic reactions, such as fatty acid and nucleic acid synthesis, which require NADPH as a reducing agent. (bionity.com)
- However, tris (1,3-dichloro-2-propyl) phosphate (TDCP) had been found in human tissues and body fluids, so we know that this substance can enter the body possibly by inhaling aerosols or dusts or ingesting contaminated food or water. (cdc.gov)
- When Do Symptoms of Class I glucose-6-phosphate dehydrogenase deficiency Begin? (nih.gov)
- Class I glucose-6-phosphate dehydrogenase deficiency is a genetic disease, which means that it is caused by one or more genes not working correctly. (nih.gov)
- Glucose-6-phosphate dehydrogenase deficiency is a genetic disorder that affects red blood cells, which carry oxygen from the lungs to tissues throughout the body. (nih.gov)
- Glucose-6-phosphate dehydrogenase deficiency is also a significant cause of mild to severe jaundice in newborns. (nih.gov)
- An estimated 400 million people worldwide have glucose-6-phosphate dehydrogenase deficiency. (nih.gov)
- Chemical reactions involving glucose-6-phosphate dehydrogenase produce compounds that prevent reactive oxygen species from building up to toxic levels within red blood cells. (nih.gov)
- A reduction in the amount of functional glucose-6-phosphate dehydrogenase appears to make it more difficult for this parasite to invade red blood cells. (nih.gov)
- Glucose-6-phosphate dehydrogenase deficiency occurs most frequently in areas of the world where malaria is common. (nih.gov)
- Glucose-6-phosphate dehydrogenase is inherited in an X-linked pattern. (nih.gov)
- Incidence and molecular polymerase-chain-reaction amplification analysis of glucose-6-phosphate dehyd- of the entire coding region from genomic rogenase deficiency in the province of DNA. (who.int)
- Genetic of glucose-6-phosphate dehydrogenase blood disorders survey in the Sultanate deficiency in the Fars province of Iran. (who.int)
- Following multiple topical applications of clindamycin phosphate at a concentration equivalent to 10 mg clindamycin per mL in an isopropyl alcohol and water solution, very low levels of clindamycin are present in the serum (0-3 ng/mL) and less than 0.2% of the dose is recovered in urine as clindamycin. (nih.gov)
- It lowers serum phosphate to near normal levels in hemodialysis patients as effectively as calcium acetate without inducing hypercalcemia or increased aluminum levels. (medscape.com)
- It has been suggested that patients receiving TPN receive 20 mEq phosphate (13 mmol phosphate)/1000 kcal from dextrose. (nih.gov)
- Aluminum phosphate and calcium phosphate are FDA-permitted ingredients used in antacids. (medicinenet.com)
- Although clindamycin phosphate is inactive in vitro , rapid in vivo hydrolysis converts this compound to the antibacterially active clindamycin. (nih.gov)
- The DAPR website also has a database of phosphate rocks containing the chemical properties of the rocks and their solubility values. (iaea.org)