Thiamine Pyrophosphate
Thiamine Monophosphate
Thiamine Triphosphate
Pyrithiamine
Wernicke Encephalopathy
Beriberi
Pyruvate Decarboxylase
Korsakoff Syndrome
Anemia, Megaloblastic
Alcohol Amnestic Disorder
Encephalomalacia
Phosphotransferases (Phosphate Group Acceptor)
Pyruvate Dehydrogenase Complex
Membrane Transport Proteins
Riboflavin
Defective high-affinity thiamine transporter leads to cell death in thiamine-responsive megaloblastic anemia syndrome fibroblasts. (1/735)
We have investigated the cellular pathology of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness. Cultured diploid fibroblasts were grown in thiamine-free medium and dialyzed serum. Normal fibroblasts survived indefinitely without supplemental thiamine, whereas patient cells died in 5-14 days (mean 9.5 days), and heterozygous cells survived for more than 30 days. TRMA fibroblasts were rescued from death with 10-30 nM thiamine (in the range of normal plasma thiamine concentrations). Positive terminal deoxynucleotide transferase-mediated dUTP nick end-labeling (TUNEL) staining suggested that cell death was due to apoptosis. We assessed cellular uptake of [3H]thiamine at submicromolar concentrations. Normal fibroblasts exhibited saturable, high-affinity thiamine uptake (Km 400-550 nM; Vmax 11 pmol/min/10(6) cells) in addition to a low-affinity unsaturable component. Mutant cells lacked detectable high-affinity uptake. At 30 nM thiamine, the rate of uptake of thiamine by TRMA fibroblasts was 10-fold less than that of wild-type, and cells from obligate heterozygotes had an intermediate phenotype. Transfection of TRMA fibroblasts with the yeast thiamine transporter gene THI10 prevented cell death when cells were grown in the absence of supplemental thiamine. We therefore propose that the primary abnormality in TRMA is absence of a high-affinity thiamine transporter and that low intracellular thiamine concentrations in the mutant cells cause biochemical abnormalities that lead to apoptotic cell death. (+info)Cloning and characterization of the thiD/J gene of Escherichia coli encoding a thiamin-synthesizing bifunctional enzyme, hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase. (2/735)
A 1.7 kb DNA fragment isolated from an E. coli genomic library was able to complement the thiamin requirement of strains carrying the thiM, thiJ and thiD mutations. The three genes encode hydroxyethylthiazole kinase, hydroxymethylpyrimidine (HMP) kinase and phosphomethylpyrimidine (HMP-p) kinase, respectively. Sequence analysis revealed that the 1.7 kb fragment contained two ORFs of 708 bp and 801 bp. The former ORF complemented the thiM mutation and the latter ORF both the thiJ and thiD mutations. The latter ORF was cloned into the expression vector pET3a, and the encoded protein was purified through three successive column chromatographies. The purified protein was able to convert HMP to its monophosphate and the monophosphate to its pyrophosphate. These results suggest that the two distinct enzyme activities, HMP kinase and HMP-P kinase, are indeed a bifunctional enzyme encoded by a single gene, designated thiDIJ. (+info)Efficient sequence analysis of the six gene products (7-74 kDa) from the Escherichia coli thiamin biosynthetic operon by tandem high-resolution mass spectrometry. (3/735)
The 10(5) resolving power and MS/MS capabilities of Fourier-transform mass spectrometry provide electrospray ionization mass spectra containing >100 molecular and fragment ion mass values of high accuracy. Applying these spectra to the detection and localization of errors and modifications in the DNA-derived sequences of proteins is illustrated with the thiCEFSGH thiamin biosynthesis operon from Escherichia coli. Direct fragmentation of the multiply-charged intact protein ions produces large fragment ions covering the entire sequence; further dissociation of these fragment ions provides information on their sequences. For ThiE (23 kDa), the entire sequence was verified in a single spectrum with an accurate (0.3 Da) molecular weight (Mr) value, with confirmation from MS/MS fragment masses. Those for ThiH (46 kDa) showed that the Mr value (1 Da error) represented the protein without the start Met residue. For ThiF (27 kDa), MS/MS localized a sequence discrepancy to a 34 residue peptide. The first 107 residues of ThiC (74 kDa) were shown to be correct, with C-terminal heterogeneity indicated. For ThiG (predicted Mr = 34 kDa), ESI/FTMS showed two components of 7,310.74 (ThiS) and 26,896.5 Da (ThiG); MS/MS uncovered three reading frame errors and a stop codon for the first protein. MS/MS ions are consistent with 68 fragments predicted by the corrected ThiS/ThiG DNA sequences. (+info)Overexpression of recombinant proteins with a C-terminal thiocarboxylate: implications for protein semisynthesis and thiamin biosynthesis. (4/735)
A facile and rapid method for the production of protein C-terminal thiocarboxylates on DNA-encoded polypeptides is described. This method, which relies on the mechanism of the cleavage reaction of intein-containing fusion proteins, can produce multi-milligram quantities of protein C-terminal thiocarboxylate quickly and inexpensively. The utility of this method for protein semisynthesis and implications for studies on the biosynthesis of thiamin are discussed. (+info)Dietary thiamin level influences levels of its diphosphate form and thiamin-dependent enzymic activities of rat liver. (5/735)
This study was prompted by our incomplete understanding of the mechanism responsible for the clinical benefits of pharmacological doses of thiamin in some patients with maple syrup urine disease (MSUD) and the question of whether thiamin diphosphate (TDP), a potent inhibitor of the activity of the protein kinase that phosphorylates and inactivates the isolated branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex, affects the activity state of the complex. Rats were fed a chemically-defined diet containing graded levels of thiamin (0, 0.275, 0.55, 5.5, and 55 mg thiamin/kg diet). Maximal weight gain was attained over a 3-wk period only in rats fed diets with 5.5 and 55 mg thiamin/kg. Feeding rats the thiamin-free diet for just 2 d caused loss of nearly half of the TDP from liver mitochondria. Three more days caused over 70% loss, an additional 3 wk, over 90%. Starvation for 2 d had no effect, suggesting a mechanism for conservation of TDP in this nutritional state. Mitochondrial TDP was higher in rats fed pharmacological amounts of thiamin (55 mg thiamin/kg diet) than in rats fed adequate thiamin for maximal growth. Varying dietary thiamin had marked but opposite effects on the activities of alpha-ketoglutarate dehydrogenase (alpha-KGDH) and BCKDH. Thiamin deficiency decreased alpha-KGDH activity, increased BCKDH activity, and increased the proportion of BCKDH in the active, dephosphorylated, state. Excess dietary thiamin had the opposite effects. TDP appears to be more tightly associated with alpha-KGDH than BCKDH in thiamin-deficient rats, perhaps denoting retention of alpha-KGDH activity at the expense of BCKDH activity. Thus, thiamin deficiency and excess cause large changes in mitochondrial TDP levels that have a major influence on the activities of the keto acid dehydrogenase complexes. (+info)Thiamine repression and pyruvate decarboxylase autoregulation independently control the expression of the Saccharomyces cerevisiae PDC5 gene. (6/735)
The Saccharomyces cerevisiae gene PDC5 encodes the minor isoform of pyruvate decarboxylase (Pdc). In this work we show that expression of PDC5 but not that of PDC1, which encodes the major isoform, is repressed by thiamine. Hence, under thiamine limitation both PDC1 and PDC5 are expressed. PDC5 also becomes strongly expressed in a pdc1delta mutant. Two-dimensional gel electrophoresis of whole protein extracts shows that thiamine limitation stimulates the production of THI gene products and of Pdc5p. Deletion of PDC1 only stimulates production of Pdc5p. We conclude that the stimulation of PDC5 expression in a pdc1delta mutant is not due to a response to thiamine limitation. (+info)Rereplication phenomenon in fission yeast requires MCM proteins and other S phase genes. (7/735)
The fission yeast Schizosaccharomyces pombe can be induced to perform multiple rounds of DNA replication without intervening mitoses by manipulating the activity of the cyclin-dependent kinase p34(cdc2). We have examined the role in this abnormal rereplication of a large panel of genes known to be involved in normal S phase. The genes analyzed can be grouped into four classes: (1) those that have no effect on rereplication, (2) others that delay DNA accumulation, (3) several that allow a gradual increase in DNA content but not in genome equivalents, and finally, (4) mutations that completely block rereplication. The rereplication induced by overexpression of the CDK inhibitor Rum1p or depletion of the Cdc13p cyclin is essentially the same and requires the activity of two minor B-type cyclins, cig1(+) and cig2(+). In particular, the level, composition, and localization of the MCM protein complex does not alter during rereplication. Thus rereplication in fission yeast mimics the DNA synthesis of normal S phase, and the inability to rereplicate provides an excellent assay for novel S-phase mutants. (+info)Characterization and hormonal modulation of immunoreactive thiamin carrier protein secreted by adult rat Leydig cells in vitro. (8/735)
Leydig cells isolated from adult rats and maintained under defined conditions in culture secrete a protein of molecular weight (Mr) 70 000 which is immunologically similar to chicken thiamin carrier protein (TCP). Synthesis of immunoreactive TCP by these cells is demonstrated by immunoprecipitation of [35S]methionine incorporated, newly synthesized proteins with monoclonal and polyclonal antibodies to chicken TCP. The amount of immunoreactive TCP secreted into the culture supernatant is quantitated by using a specific radioimmunoassay. Under the influence of LH, secretion of immunoreactive TCP is enhanced 3-fold and can be inhibited by up to 70% with aromatase inhibitor (1,4,6-androstatrien-3,17-dione). Cyclic AMP acts as a second messenger in the sequence of events involved in LH-induced elevation of immunoreactive TCP in Leydig cells. The effects of exogenous estradiol-17beta and diethylstilbestrol are comparable in terms of stimulation of secretion of immunoreactive TCP by these cells. Tamoxifen brought about a 70% decrease in the elevated levels of immunoreactive TCP. These results suggest that estrogen mediates immunoreactive TCP induction in hormonally stimulated adult rat Leydig cells. (+info)The symptoms of WE can vary depending on the severity of the deficiency, but common manifestations include:
1. Confusion and disorientation
2. Memory loss and difficulty learning new information
3. Difficulty with coordination and balance
4. Loss of muscle tone and weakness in the arms and legs
5. Disturbances in vision, hearing, and taste
6. Nausea and vomiting
7. Abnormalities in heart rate and blood pressure
8. Increased risk of seizures and coma
If left untreated, WE can lead to more severe complications such as Wernicke-Korsakoff Syndrome (WKS), a condition that involves the loss of brain tissue and memory loss. Treatment for WE typically involves thiamine supplements and addressing any underlying causes of the deficiency. In severe cases, hospitalization may be necessary to monitor and treat complications.
The symptoms of beriberi include weakness, fatigue, loss of appetite, nausea, vomiting, diarrhea, and heart failure. In severe cases, it can cause paralysis, psychosis, and even death. Beriberi is most commonly seen in areas where polished rice is a major part of the diet, as thiamine is lost during the processing of rice.
Treatment of beriberi involves replacing the missing thiamine through dietary supplements or injections. Prevention includes ensuring adequate intake of thiamine-rich foods, such as whole grains, legumes, and leafy greens, and avoiding the consumption of polished rice.
Beri-beri is a significant public health issue in many developing countries, where access to nutritious food may be limited and poverty and malnutrition are widespread. It is also an important reminder of the importance of proper nutrition in maintaining good health.
The key symptoms of Korsakoff syndrome are:
* Memory loss: Sufferers experience difficulty in forming new memories, which can result in short-term memory loss. They may not remember recent events or conversations, and may have trouble recalling information they learned recently.
* Confabulation: Individuals with Korsakoff syndrome may fill in memory gaps with fabricated information, leading to confabulation (false memories). This can result in inaccurate or distorted recollections of past events.
* Dissociation: The condition can lead to dissociative symptoms such as depersonalization (feeling detached from oneself) and derealization (feeling detached from the world around them).
Korsakoff syndrome is a serious condition that requires prompt medical attention, particularly if it is caused by severe alcoholism or malnutrition. Treatment typically involves addressing the underlying cause of the disorder, such as stopping alcohol consumption and correcting any nutritional deficiencies. In some cases, medication may be prescribed to manage symptoms like anxiety or depression.
The condition is often seen in people who have a history of chronic alcoholism, although it can also occur in individuals with other conditions that affect the brain and central nervous system. Korsakoff syndrome can significantly impact an individual's ability to function in daily life, particularly if left untreated.
Symptoms of megaloblastic anemia may include fatigue, weakness, shortness of breath, pale skin, and weight loss. The condition is typically diagnosed through a physical examination, blood tests (including a complete blood count and blood chemistry tests), and possibly a bone marrow biopsy.
Treatment for megaloblastic anemia usually involves addressing the underlying cause of the condition, such as vitamin B12 or folate supplements. In some cases, medications to stimulate the production of red blood cells may be prescribed. If left untreated, megaloblastic anemia can lead to complications such as heart problems and increased risk of infections.
The disorder is caused by the damage of brain cells due to the deficiency of thiamine (Vitamin B1) which is essential for proper brain functioning. The condition can be divided into two main categories:
1. Wernicke's Encephalopathy: This is the acute form of the disorder where the individual experiences confusion, ataxia (loss of coordination), and oculomotor dysfunction (abnormal eye movements).
2. Korsakoff's Psychosis: This is the chronic form of the disorder where the individual experiences memory loss and confabulation (making up memories).
Symptoms of Alcohol Amnestic Disorder include:
* Memory loss for events that occurred both short-term and long-term
* Difficulty learning new information
* Confusion and disorientation
* Slurred speech and difficulty with coordination
* Increased risk of seizures
Diagnosis of the disorder is based on a combination of medical history, physical examination, and laboratory tests such as blood tests to check for thiamine deficiency. Treatment typically involves abstinence from alcohol, thiamine supplements, and supportive care to manage symptoms.
Prognosis for Alcohol Amnestic Disorder varies depending on the severity of the condition and the individual's response to treatment. In general, the earlier the diagnosis and treatment, the better the prognosis. However, if left untreated, the condition can lead to permanent brain damage and even death.
It is important to note that Alcohol Amnestic Disorder is preventable by avoiding excessive alcohol consumption and ensuring adequate thiamine intake through a balanced diet or supplements. Early detection and treatment can help to reduce the risk of long-term cognitive impairment and improve overall outcomes.
Encephalomalacia can be caused by a variety of factors, including:
1. Traumatic brain injury: A blow to the head or other form of trauma can cause the brain to become bruised or damaged, leading to encephalomalacia.
2. Infection: Certain infections, such as meningitis or encephalitis, can damage brain tissue and lead to encephalomalacia.
3. Stroke or other forms of ischemia: A lack of blood flow to the brain can cause damage to brain tissue and lead to encephalomalacia.
4. Neurodegenerative diseases: Conditions such as Alzheimer's disease, Parkinson's disease, and Huntington's disease can cause progressive degeneration of brain tissue over time.
5. Toxins: Exposure to certain toxins, such as lead or other heavy metals, can damage brain tissue and lead to encephalomalacia.
Symptoms of encephalomalacia may include:
1. Cognitive decline
2. Memory loss
3. Confusion
4. Difficulty with coordination and balance
5. Weakness or paralysis of certain muscle groups
6. Seizures
7. Vision problems
8. Hearing loss
Encephalomalacia is typically diagnosed through a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment depends on the underlying cause of the condition and may include medication, surgery, or other forms of therapy. In some cases, encephalomalacia may be a chronic and progressive condition, while in others it may resolve with treatment.
Thiamine
Thiamine oxidase
Thiamine monophosphate
Thiamine-triphosphatase
Thiamine pyrophosphate
Thiamine deficiency
Thiamine triphosphate
Thiamine kinase
Thiamine transporter
Thiamine diphosphokinase
Thiamine-diphosphate kinase
Adenosine thiamine triphosphate
Thiamine-phosphate diphosphorylase
Thiamine-phosphate kinase
Thiamine transporter 2
Adenosine thiamine diphosphate
Thiamine transporter 1
Mitochondrial thiamine pyrophosphate carrier
Thiamine responsive megaloblastic anemia syndrome
Biotin-thiamine-responsive basal ganglia disease
Allithiamine
4-Amino-5-hydroxymethyl-2-methylpyrimidine
Thiochrome
Allicin
Sulbutiamine
Hydroxymethylpyrimidine kinase
Phosphomethylpyrimidine kinase
Nutritional neuroscience
Chloroquine
Heterocyclic amine
Deaths Associated with Thiamine-Deficient
Total Parenteral Nutrition
ciprofloxacin otic and thiamine pyrophosphate oral Drug Interactions - RxList
Thiamine HCl
Hydrocortisone-Ascorbic Acid-Thiamine Use Associated with Lower Mortality in Pediatric Septic Shock
Thiamine Prices - U.S. & International | PharmacyChecker.com
Thiamine (Vitamin B1) : MedlinePlus Drug Information
Thiamin Pyrophosphokinase | Harvard Catalyst Profiles | Harvard Catalyst
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Deficiency14
- For the two patients on whom autopsies were performed, examination of the brain showed lesions diagnostic of acute thiamine deficiency: necrosis and petechial hemorrhages in each mammillary body, hypothalamic neovascularization, and petechial hemorrhage with gliosis and engorgement of parenchymal periaqueductal blood vessels near the third and fourth ventricles. (cdc.gov)
- Editorial Note: Each of these three patients developed lactic acidosis within 5 weeks of initiation of treatment with thiamine-deficient TPN, as did four patients reported previously with lactic acidosis secondary to iatrogenic thiamine deficiency (1,2). (cdc.gov)
- In other reports of thiamine deficiency attributed to IV therapy containing insufficient or no thiamine supplementation, the deficiency was manifested by Wernicke's encephalopathy without lactic acidosis. (cdc.gov)
- In one study, deficiency was detected after approximately 6 weeks without thiamine (7). (cdc.gov)
- The case studies reported here suggest that fatal deficiency can develop in as few as 3 weeks without thiamine intake. (cdc.gov)
- Measuring whole blood or erythrocyte transketolase activity, with and without addition of thiamine diphosphate, is the most reliable method of detecting thiamine deficiency (9). (cdc.gov)
- People most at risk for thiamine deficiency are older adults, those who are dependent on alcohol, or who have HIV/AIDS, diabetes, malabsorption syndrome (problems absorbing food), or have had bariatric surgery (an operation that helps you lose weight by making changes to your digestive system). (medlineplus.gov)
- Therapeutic in case of thiamin deficiency: therapy is urgent, should bypass the intestinal tract, and consists of parenteral administration of thiamin (intramuscular or intravenous) as 50-100 mg/day for 7-14 days, followed by oral thiamin therapy. (allnutritionals.com)
- In clinical disorders related to thiamin deficiency. (allnutritionals.com)
- Prophylactic in persons susceptible to thiamin deficiency: More moderate doses may be prudent for cancer patients in need of nourishment. (allnutritionals.com)
- thiamine deficiency. (hormonesmatter.com)
- cellular energy, producing biochemical changes which are similar to clinical thiamine deficiency. (hormonesmatter.com)
- This could basically be referred to as "functional" thiamine deficiency. (hormonesmatter.com)
- SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency? (hormonesmatter.com)
Vitamin B15
- Vitamin B1 or Thiamine is an essential nutrient required for energy metabolism. (whathelps.com)
- There are possible interactions between Vitamin B1 (Thiamine) and other supplements and drugs. (whathelps.com)
- You may want to focus on treating a specific side effect of Vitamin B1 (Thiamine). (whathelps.com)
- Our user data reports Vitamin B1 (Thiamine) used in conjunction with the following conditions. (whathelps.com)
- The chemical reactions and pathways resulting in the formation of thiamine (vitamin B1), and related compounds. (planteome.org)
Pyrophosphate5
- ciprofloxacin otic will decrease the level or effect of thiamine pyrophosphate oral by suppressing bacteria in the stomach that may assist with drug absorption. (rxlist.com)
- ciprofloxacin otic will decrease the level or effect of thiamine pyrophosphate oral by altering intestinal flora. (rxlist.com)
- An enzyme that catalyzes the formation of thiamine pyrophosphate from ATP and thiamine. (harvard.edu)
- Enterohemorrhagic Escherichia coli infection inhibits colonic thiamin pyrophosphate uptake via transcriptional mechanism. (escholarship.org)
- This same study also found reduced serum levels of the active form of thiamine - thiamine pyrophosphate (TPP). (hormonesmatter.com)
Anti-thiamine factors2
- Coffee, tea are high in anti-thiamine factors. (medscape.com)
- but some have anti-thiamine factors and are high in what are called oxalates. (hormonesmatter.com)
Excretion2
- In a study of healthy young men ingesting less than or equal to0.2 mg thiamine daily, urinary excretion of thiamine stopped within 18 days (8). (cdc.gov)
- thiamine excretion. (hormonesmatter.com)
Supplementation1
- read about thiamine and dysautonomia before starting, and learn how thiamine supplementation in a person long deficient can cause refeeding syndrome. (hormonesmatter.com)
Vitamins2
- Thiamine is in a class of medications called vitamins. (medlineplus.gov)
- Thiamine supplements are available alone and in combination with other vitamins. (medlineplus.gov)
Renal1
- bumetanide decreases levels of thiamine by increasing renal clearance. (medscape.com)
Clinical2
- Each died within 5 weeks of receiving TPN without thiamine and had had a clinical course strongly suggestive of acute beriberi. (cdc.gov)
- thiamine testing), clinical response to thiamine treatment has been confirmatory. (hormonesmatter.com)
Carbohydrate1
- and a chronically malnourished 22-year-old man with ulcerative colitis who developed Wernicke's encephalopathy 5 days after colectomy and 17 days after beginning a TPN regimen providing 300 g of carbohydrate (50 g on the last 3 days) and 3.2 mg of thiamine daily (6). (cdc.gov)
MeSH1
- Thiamin Pyrophosphokinase" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
Toxicity1
- Oral thiamin: no toxicity. (allnutritionals.com)
Enzyme1
- Butterworth, R. F., Kril, J. J. & Harper, C. G. (1993) Thiamine-dependent enzyme changes in the brains of alcoholics: relationship to the Wernicke-Korsakoff syndrome. (allnutritionals.com)
Search1
- Results of search for 'su:{Thiamine. (who.int)
Capsule1
- Thiamine comes as a tablet, capsule, and solution (liquid drops) to take by mouth. (medlineplus.gov)
Fruits2
- There are quite a number of fruits rich in thiamin, and most of this list will provide a significant portion of your recommended daily values. (soupersage.com)
- We calculated the top fruits for thiamin by both their common measurement as well as in 200 calories, including by gender daily requirements. (soupersage.com)
Intestinal6
- azithromycin will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
- clarithromycin will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
- erythromycin base will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
- amikacin will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
- cefadroxil will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
- cefamandole will decrease the level or effect of thiamine by altering intestinal flora. (medscape.com)
Sulfur1
- Got the name "thiamine" due to the presence of sulfur in its molecule. (meldonium-mildronate.com)
Products2
- Thiamine, one of the components in the multivitamin products, is essential for two enzymes needed for aerobic metabolism: pyruvate dehydrogenase and ga-ketoglutarate dehydrogenase. (cdc.gov)
- tell your doctor and pharmacist if you are allergic to thiamine, any other medications, or any of the ingredients in thiamine products. (medlineplus.gov)
Treatment1
- Can thiamine treatment reduce potato virus Y on potatoes? (oregonstate.edu)
Reports1
- Intravenous thiamin: only a few reports of toxic reactions, resulting mainly in an anaphylactic reaction. (allnutritionals.com)
Dietary1
- Thiamine (vitamin B 1 ) is used as a dietary supplement when the amount of thiamine in the diet is not enough. (medlineplus.gov)
Mechanism1
- thiamine increases effects of atracurium by unspecified interaction mechanism. (medscape.com)
People2
- This graph shows the total number of publications written about "Thiamin Pyrophosphokinase" by people in Harvard Catalyst Profiles by year, and whether "Thiamin Pyrophosphokinase" was a major or minor topic of these publication. (harvard.edu)
- Below are the most recent publications written about "Thiamin Pyrophosphokinase" by people in Profiles. (harvard.edu)
Loss1
- Thiamine is used to treat beriberi (tingling and numbness in feet and hands, muscle loss, and poor reflexes caused by a lack of thiamine in the diet) and to treat and prevent Wernicke-Korsakoff syndrome (tingling and numbness in hands and feet, memory loss, confusion caused by a lack of thiamine in the diet). (medlineplus.gov)
Unknown1
- the duration of availability of thiamine reserves is unknown. (cdc.gov)
Found1
- Thiamin is found in large amounts in lean pork, legumes and yeast. (allnutritionals.com)
Daily6
- In 1 cup, raisin has 0.18mg of thiamin, or about 17% of daily values for women and 15% for men. (soupersage.com)
- 1 cup of jackfruit contains 0.17mg of thiamin, or about 16% of daily values for women and 14% for men. (soupersage.com)
- 1 cup of pineapple contains 0.13mg of thiamin, or about 12% of daily values for women and 11% for men. (soupersage.com)
- 1 cup of grapefruit contains 0.1mg of thiamin, or about 9% of daily values for women and 8% for men. (soupersage.com)
- In 1 melon, cantaloupe has 0.33mg of thiamin, or about 30% of daily values for women and 28% for men. (soupersage.com)
- 1 cup of watermelon contains 0.05mg of thiamin, or about 5% of daily values for women and 4% for men. (soupersage.com)
Enter1
- In the absence of thiamine, pyruvate cannot enter the Krebs cycle, resulting in pyruvate accumulation and conversion to lactate (Figure 1). (cdc.gov)
Similar1
- They contain thiamine, which enhances memory - similar to the herb gingko biloba. (naturalwellnessacademy.org)
Levels1
- caffeine decreases levels of thiamine by inhibition of GI absorption. (medscape.com)
Major1
- Thiamine was absent from the TPN fluids given these patients during a nationwide shortage of intravenous (IV) multivitamins resulting from substantially reduced production by one of the two major domestic manufacturers of multivitamins in June 1988. (cdc.gov)
Process2
- Link to all annotated objects annotated to thiamine-containing compound biosynthetic process. (planteome.org)
- Link to all direct and indirect annotations to thiamine-containing compound biosynthetic process. (planteome.org)
Large1
- 1 large fig has 0.04mg of thiamin, or about 3% for adults. (soupersage.com)