INTRODUCTION: Transcobalamin II deficiency is one of the rare causes of inherited vitamin B12 disorders in which the patients have characteristically normal or high vitamin B12 levels related to the transport defect of vitamin B12 into the cell, ending up with intracellular cobalamin depletion and high homocysteine and methylmalonic acid levels ...
Holotranscobalamin, cobalamin-saturated transcobalamin, is the minor fraction of circulating cobalamin (vitamin B12), which is available for cellular uptake and hence is physiologically relevant. Currently, no method allows simple, direct quantification of holotranscobalamin. We now report on the identification and characterization of a monoclonal antibody with a unique specificity for holotranscobalamin. The specificity and affinity of the monoclonal antibodies were determined using surface plasmon resonance and recombinant transcobalamin as well as by immobilizing the antibodies on magnetic microspheres and using native transcobalamin in serum. The epitope of the holotranscobalamin specific antibody was identified using phage display and comparison to a de novo generated three-dimensional model of transcobalamin using the program Rosetta. A direct assay for holotrnscobalamin in the ELISA format was developed using the specific antibody and compared to the commercial assay HoloTC RIA. An antibody
Vitamin B12 (cobalamin) deficiency is prevalent worldwide and causes megaloblastic anemia and neurologic deficits. While the anemia can be treated, the neurologic deficits can become refractive to treatment as the disease progresses. Therefore, timely intervention is critical for a favorable outcome. Moreover, the metabolic basis for the neuro-pathologic changes and the role of cobalamin deficiency in the pathology still remains unexplained. Using a transcobalamin receptor / CD320 knockout mouse that lacks the receptor for cellular uptake of transcobalamin bound cobalamin, we aimed to determine whether cobalamin deficiency in the central nervous system produced functional neurologic deficits in the mouse that would parallel those observed in humans ...
In agreement with previous studies,1, 6 we found an almost 50% decline in the concentration of cobalamins during late pregnancy (Table 1). A small increase in MMA was observed during pregnancy and post partum (Table 1) but we question whether this is caused by an increased metabolic rate during pregnancy and lactation rather than a sign of vitamin B12 deficiency. Only two women (holoTC: 33-43 pmol/L and 39-48 pmol/L) had a MMA above the upper limit of the reference intervals (,0.28 μmol/L) at all four time points during pregnancy and post partum. None of the women had a MMA ,0.75 μmol/L, the diagnostic level for vitamin B12 deficiency,7 at any time during pregnancy and post partum. These results suggest that the vitamin B12 status during pregnancy remains unchanged and that a sufficient amount of cobalamin was available for transportation into the cells despite the decreased level of total plasma cobalamins.. Interestingly, the decline in cobalamins during pregnancy was not reflected in holoTC ...
The unsaturated binding capacities (UBBC) of individual vitamin B12- binding proteins in plasma were measured by a two-step procedure. Transcobalamin II (TC II) was separated by precipitation with ammonium sulfate; the "R"-type binders remaining soluble were then divided into two components by bath separation with anion exchange on DEAE- cellulose. The two R components were designated alpha1-R (TC 1) and alpha2-R (third binder, fetal binder, PV binder, TC III). Ten normal sera were studied by this technique giving a separation into TC III and total plasma R identical to that obtained simultaneously by gel filtration. The mean UBBC of TC II was 969 plus or minus 204 pg of 57 Co B12 per ml of serum. The mean contamination of the precipitated TC III with plasma R was 3%. The UBBCs of alpha 2-R and alpha 1-R were 127 plus or minus 42 and 40 plus or minus 12 pg/ml, respectively. The mean contamination of the R fraction by TC II was 14% as evaluated by gel filtration. By isoelectric focusing it was ...
Commercially available 1000 μg cyanocobalamin administered IM as 1 mL from a vial containing 1000 μg/mL drug administered by study personnel, in the research clinic, in the morning, in the fasted state and at least 1 hour prior to the morning meal on study Days 1, 3, 7, 10, 14, 21, 30, 60 and 90 ...
As was the case for the first ChemMedChem December, 2007 cover issue (posted previously), the cover story in this month’s issue is a communication by myself and members and collaborators of the Robert Doyle Group here at Syracuse University. In this case, the work for the cover image actually went into computational research published in the associated article (instead of just a pretty cover image to complement the associated article, which was the intent of the previous cover).. The image below shows the Transcobalamin II (TCII) protein (in teal ribbons, with a bound cyanocobalamin (B12) shown in red. The PDB code for this complex is 2BB5) sitting within the surface-accessible fragment of the gigantic insulin receptor (PDB code 2DTG. The cell membrane would be at the bottom of this image, with the remainder of the complete protein sitting both within the cell membrane and then into the cytoplasm). Saving the lead-up to this structure generation for the associated published ...
The cover picture shows three views of a vitamin B12-insulin conjugate bound to transcobalamin II, docked in the insulin receptor (IR). This study reveals how the structure of an orally deliverable insulin changes in solution after vitamin B12 conjugation and its effect on IR binding capacity. The results demonstrate that chemical modification of insulin by linking relatively large pendant groups does not interfere with IR recognition. For more details, see the Full Paper by T. J. Fairchild, R. P. Doyle, et al. on p. 421 ff. ...
In the first study of its kind, we have found that men with the highest levels of plasma folate measured just before PSA-based diagnosis of localized prostate cancer were more likely to exceed an a priori PSAV threshold of 2 ng/mL/y during subsequent follow-up. However, this positive association was not observed for PSAV as a continuous measure and was not robust to sensitivity analysis. Plasma concentrations of vitamin B12, tHcy, and B12 bound to haptocorrin and transcobalamin were not associated with postdiagnosis PSAV. PSAV is a potential prognostic marker in men with localized prostate cancer undergoing active monitoring (8, 9). Hence, our findings may be important in the context of current controversies over the potentially harmful long-term effects of folic acid and vitamin B12 fortification (5, 14).. We previously reported that circulating folate was positively associated with prostate cancer risk in prospective cohort studies (based mainly on clinically detected cases) but not in the ...
Transcobalamin (TC) er et protein på 45,5 kDa som finnes i blodbanen til pattedyr. TC transporterer de to kofaktorene til vitamin B12, metyl- og 5 -deoksyadenosyl-cobalamin, til kroppens celler etter opptak fra tarm. Man ...
Looking for online definition of transcobalamins in the Medical Dictionary? transcobalamins explanation free. What is transcobalamins? Meaning of transcobalamins medical term. What does transcobalamins mean?
Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 (cobalamin) later on in the ileum of the small intestine. In humans, the gastric intrinsic factor protein is encoded by the GIF gene. Haptocorrin (also known as HC, R protein, and transcobalamin I, TCN1) is another glycoprotein secreted by the salivary glands which binds to vitamin B12. Vitamin B12 is acid sensitive and in binding to transcobalamin I it can safely pass through the acidic stomach to the duodenum. In the less acidic environment of the small intestine, pancreatic enzymes digest the glycoprotein carrier and vitamin B12 can then bind to intrinsic factor. This new complex is then absorbed by the epithelial cells (enterocytes) of the ileum. Inside the cells, B12 dissociates once again and binds to another protein, transcobalamin II (TCN2); the new complex can then exit the epithelial cells to be carried ...
Treatment with the anti-diabetic drug metformin is followed by a decline in plasma cobalamin, but it is unsettled whether this denotes an impaired cobalamin status. This study has explored changes in the markers of cobalamin status in women with Polycystic Ovary Syndrome treated with metformin (1.5-2.5 g per day) (n = 29) or placebo (n = 23) for six months. Serum samples were collected before and after two, four, and six months of treatment. We found serum cobalamin to decline and reach significant lower levels after six months of treatment (p = 0.003). Despite the decline in serum cobalamin, we observed no reductions in the physiological active part of cobalamin bound to transcobalamin (holotranscobalamin), or increase in the metabolic marker of cobalamin status, methylmalonic acid. Instead, the non-functional part of circulating cobalamin bound to haptocorrin declined (p = 0.0009). Our results have two implications: The data questions whether metformin treatment induces an impaired cobalamin status
SUMMARY: Euglena gracilis pellicle, separated by sucrose density gradient centrifugation, had a high cobalamin (Cb1) binding activity. Of the Cb1 binding protein 65% was solubilized from E. gracilis pellicle by using 0.1% SDS/2 M-urea and the residual 35% by using 1% (w/v) SDS. Both of the Cb1 binding protein fractions showed a broad pH dependence for the binding of Cb1. No evidence for the involvement of SH-groups or metal ions in Cb1 binding was obtained. The K s values for cyanocobalamin of the proteins solubilized with 0.1% SDS/2 M-urea and with 1% SDS were 0.22 and 0.19 nM, respectively. The M r of a Cb1 binding polypeptide of each protein was estimated to be 38000 by SDS-PAGE. The Cb1 binding protein solubilized with 0.1% SDS/2 M-urea was purified to homogeneity. Inhibition experiments on Cb1 uptake in E. gracilis cells, using an antibody against the Cb1 binding protein solubilized with 0.1% SDS/2 M-urea, showed that the Cb1 binding proteins solubilized with 0.1% SDS/2 M-urea and 1% SDS take part
Did you get a course of B12 loading doses? If you are low, you often need a LOT of B12, such as 5 shots in one week followed by three shots a week for two weeks, then two shots a week for two weeks, then weekly or monthly depending on your own needs. Nearly all of the B12 you receive in a shot is processed out of your body within 48 hours with some remaining in your blood and liver. If your stores in the liver are low to begin with, it will take some time to top them up. This is why a regime of both shots and sublinguals can be good - you need an injected form of hydroxocobalamin, of which processing involves a pathway that includes the liver, so youre replenishing liver stores. Adding some methylcobalamin sublinguals provides a lot of directly available B12. Also if your thyroid function is low (whether temporarily or chronically) it will deplete vitamin and mineral stores. You can ask for your holotranscobalamin (also called transcobalamin II) to be tested. That will show you how much of the ...
OBJECTIVES: To investigate the relationship between markers of vitamin B(12) status and brain volume loss per year over a 5-year period in an elderly population. METHODS: A prospective study of 107 community-dwelling volunteers aged 61 to 87 years without cognitive impairment at enrollment. Volunteers were assessed yearly by clinical examination, MRI scans, and cognitive tests. Blood was collected at baseline for measurement of plasma vitamin B(12), transcobalamin (TC), holotranscobalamin (holoTC), methylmalonic acid (MMA), total homocysteine (tHcy), and serum folate. RESULTS: The decrease in brain volume was greater among those with lower vitamin B(12) and holoTC levels and higher plasma tHcy and MMA levels at baseline. Linear regression analysis showed that associations with vitamin B(12) and holoTC remained significant after adjustment for age, sex, creatinine, education, initial brain volume, cognitive test scores, systolic blood pressure, ApoE epsilon4 status, tHcy, and folate. Using the upper (for
Detecting disorders of Vitamin B12 and/or folic acid by determining the levels of holotranscobalamin II (A); homocysteine (B); methylmalonic acid (C) and optionally cystathionine (D).
For the seven-year study, researchers took blood samples from 271 Finnish people age 65 to 79 who did not have dementia at the start of the study. During that time, 17 people developed Alzheimers disease. Blood samples were tested for levels for homocysteine, an amino acid associated with vitamin B12, and for levels of the active portion of the vitamin, called holotranscobalamin. Too much homocysteine in the blood has been linked to negative effects on the brain, such as stroke. However, higher levels of vitamin B12 can lower homocysteine.. The study found that for each micromolar increase in the concentration of homocysteine, the risk of Alzheimers disease increased by 16 percent, whereas each picomolar increase in concentration of the active form of vitamin B12 reduced risk by two percent. The results stayed the same after taking into account other factors, such as age, gender, education, smoking status, blood pressure and body mass index. The addition of folate did not appear to raise or ...
use strict; use warnings; my @processed; while (my $a_line = ,DATA,) { chomp $a_line; if ($a_line =~ /^,/) { #this is a header, keep as is push @processed, $a_line; } else { # This is a dna seq, process # Translate each three-base codon into amino acid, # and append to a protein my $protein = ; my $len = length($a_line) -2; for(my $i=0; $i , $len ; $i += 3) { my $codon = substr($a_line, $i,3); $protein .= codon2aa($codon); } push @processed, $protein; } } #now display what we have processed print $_, \n for @processed; # codon2aa # # A subroutine to translate a DNA 3-character codon to an amino acid sub codon2aa { my($codon) = @_; if ( $codon =~ /GC./i) { return A } # Alanine elsif ( $codon =~ /TG[TC]/i) { return C } # Cysteine elsif ( $codon =~ /GA[TC]/i) { return D } # Aspartic Acid elsif ( $codon =~ /GA[AG]/i) { return E } # Glutamic Acid elsif ( $codon =~ /TT[TC]/i) { return F } # Phenylalanine elsif ( $codon =~ /GG./i) { return G } # Glycine elsif ( $codon =~ /CA[TC]/i) ...
The first crystal structure of the vitamin B12-binding protein from a three-component O-demethylase enzyme system is reported. During O-demethylation methyl groups are transferred from phenyl methyl ethers to tetrahydrofolate via methyl-B12 intermediates. This study describes the identification and the structural and spectroscopic analysis of a cobalamin-binding protein (termed CobDH) implicated in O-demethylation by the organohalide-respiring bacterium Desulfitobacterium hafniense DCB-2. The 1.5 Å resolution crystal structure of CobDH is presented in the cobalamin-bound state and reveals that the protein is composed of an N-terminal helix-bundle domain and a C-terminal Rossmann-fold domain, with the cobalamin coordinated in the base-off/His-on conformation similar to other cobalamin-binding domains that catalyse methyl-transfer reactions. EPR spectroscopy of CobDH confirms cobalamin binding and reveals the presence of a cob(III)alamin superoxide, indicating binding of oxygen to the fully ...
Adult, Aged, Biological Markers/blood, Diarrhea/blood, Female, Homocystine/blood, Humans, Male, Methylmalonic Acid/blood, Middle Aged, Rectal Neoplasms/*blood/*radiotherapy/surgery, Transcobalamins/metabolism, Vitamin B 12/*blood, Vitamin B 12 Deficiency/etiology ...
Coβ-4-ethylphenyl-cob(III) alamin (EtPhCbl) is an organometallic analogue of vitamin B12 (CNCbl) which binds to transcobalamin (TC), a plasma protein that facilitates the cellular uptake of cobalamin (Cbl). In vitro assays with key enzymes do not convert EtPhCbl to the active coenzyme forms of Cbl suggesting that administration of EtPhCbl may cause cellular Cbl deficiency. Here, we investigate the in vivo effect of EtPhCbl in mice and its ability, if any, to induce Cbl deficiency. We show that EtPhCbl binds to mouse TC and we examined mice that received 3.5 nmol/24h EtPhCbl (n=6), 3.5 nmol/24h CNCbl (n=7) or NaCl (control group) (n=5) through osmotic mini-pumps for four weeks. We analyzed plasma, urine, liver, spleen, submaxillary glands and spinal cord for Cbl and markers of Cbl deficiency including methylmalonic acid (MMA) and homocysteine (tHcy). Plasma MMA (mean±SEM) was elevated in animals treated with EtPhCbl (1.01±0.12 µmol/L) compared to controls (0.30±0.02 µmol/L) and CNCbl ...
By Nayak, Tapan K Hathaway, Helen J; Ramesh, Chinnasamy; Arterburn, Jeffrey B; Dai, Donghai; Sklar, Larry A; Norenberg, Jeffrey P; Prossnitz, Eric R Breast and endometrial cancers are the most common invasive malignancies in women, with more than 217,000 new diagnoses per year in the United States. These cancers are often classified into 2 subtypes based on the expression of the classical estrogen receptor. In this study, we describe a new structural class of neutraf tridentate ^sup 99m^Tc(I)-estradiol-pyridin-2-yl hydrazine derivatives for potential use in breast and endometrial cancer imaging. Methods: The ^sup 99m^Tc(I)-estradiol-pyridin-2-yl hydrazine derivative was synthesized via the Sonogashira cross- coupling reaction and radiolabeled via the tricarbonyl approach. Radiochemical purity was assessed by high-performance liquid chromatography. Cell-binding studies were performed with human breast adenocarcinoma MCF-7 cells. The in vivo biodistribution of the ^sup 99m^Tc(I) derivative was ...
Imerslund-Gräsbeck syndrome, is a rare autosomal recessive, familial form of vitamin B12 deficiency caused by malfunction of the "Cubam" receptor located in the terminal ileum. This receptor is composed of two proteins, amnionless (AMN), and cubilin. A defect in either of these protein components can cause this syndrome. This is a rare disease, with a prevalence about 1 in 200,000, and is usually seen in patients of European ancestry. Vitamin B12 is an important vitamin needed for bone marrow functioning, the deficit of which causes decreased marrow output and anemia. Vitamin B12 has two forms, one of which, along with folate, is important in DNA synthesis. Vitamin B12 is sensitive to acid deformation in the stomach, so a molecule called haptocorrin (R-factor), protects it in the stomach. In the small bowel, a molecule named intrinsic factor (IF), allows vitamin B12 to be absorbed in the ileum. IGS is caused by a mutation in the receptors located in the terminal portion of ileum. This is a very ...
The GI Panel is a blood test performed on a FASTED animal (no food for 12 hours) to help evaluate the function of the gastrointestinal tract. The GI Panel includes the following values; Cobalamin (Vitamin B12): Cobalamin is absorbed in the ileum (a specific section of the small intestine). A decreased cobalamin level can be seen…
Grifitov eksperiment, koji je objavio Frederik Grifit 1928,[1] je bio prvi eksperiment koji je sugerisao da bakterije imaju sposobnost transfera genetičke informacije putem procesa poznatog kao transformacija.[2][3] Grifit je koristio dve vrste bakterija pneumokoka (Streptococcus pneumoniae) koje inficiraju miševe: tip III-S (glatku) i tip II-R (grubu) vrstu. III-S vrsta se prekriva polisaharidnim kapsulom koja je štiti od imunskog sistema domaćina. Rezultat toga je smrt domaćina. II-R vrsta nema tu zaštitnu kapsulu, te je imunski sistem domaćina uništava. Nemački bakteriolog, Fred Nojfeld, je otkrio tri tipa pneumokoka (Tupivu I, II, i III), kao i način za njihovu identifikaciju in vitro.[4] Do vremena Grifitovog eksperimenta, bakteriolozi su smatrali da su tipovi fiksni i nepromenljivi, iz jedne generacije u drugu. U ovom eksperimentu, bakterije III-S vrste su ubijene toplotom, i njihovi ostaci su dodati u II-R vrstu bakterija. Dok ni jedna od ovih komponenti samostalno nije nanosila ...
CBL兔单克隆抗体[YE323](ab32027)可与人样本反应并经WB, IP, ICC, Flow Cyt实验严格验证,被5篇文献引用。所有产品均提供质保服务,中国75%以上现货。
PA may be suspected when a patients blood smear shows large, fragile, immature erythrocytes, known as megaloblasts. A diagnosis of PA first requires demonstration of megaloblastic anemia by conducting a full blood count and blood smear, which evaluates the mean corpuscular volume (MCV), as well the mean corpuscular hemoglobin concentration (MCHC). PA is identified with a high MCV (macrocytic anemia) and a normal MCHC (normochromic anemia).[38] Ovalocytes are also typically seen on the blood smear, and a pathognomonic feature of megaloblastic anemias (which include PA and others) is hypersegmented neutrophils.[18]. Serum vitamin B12 levels are used to detect its deficiency, but they do not distinguish its causes. Vitamin B12 levels can be falsely high or low and data for sensitivity and specificity vary widely. Normal serum levels may be found in cases of deficiency where myeloproliferative disorders, liver disease, transcobalamin II deficiency, or intestinal bacterial overgrowth are present. ...
Heres a simplified explanation of the Exercise metabolic pathway:. 1. The Pilates Exercises in food is bound to animal proteins, and your body has to free it. To cleave Exercise from protein, your stomach contains specialized cells in its lining called parietal cells that secrete hydrochloric acid and an enzyme called pepsin.. 2. Your stomachs parietal cells also produce intrinsic factor (IF), a critical protein that makes its way into your intestine to be available for a later step in the Exercise absorption pathway.. 3. Next, other proteins called R-binders ferry the Exercise into your small intestine.. 4. In the intestine, intrinsic factor is bound to the Exercise (with the help of enzymes called pancreatic proteases) and carries it to the last section of the small intestine, the ileum. The cells that line the ileum contain receptors that grab onto the Exercise-IF complex, pulling it into the bloodstream. 5. In the bloodstream, another protein, transcobalamin II, transports Pilates ...
During fetal life and infancy, an adequate cobalamin status is important for normal growth and central nervous system development. A metabolic profile consistent with impaired cobalamin status is prevalent in breast-fed infants. Whether this profile reflects immature organ systems or cobalamin deficiency has not been clarified.. Low levels of cobalamin, elevated levels of total homocysteine (tHcy), cystathionine and/or methylmalonic acid (MMA) in the blood are measures of impaired cobalamin status.. The purpose of this randomized, controlled study is to determine if cobalamin supplementation may influence the metabolic profile related to cobalamin status in infants.. Six weeks old infants will be randomly assigned to receive either an intramuscular injection with 400 µg cobalamin or no intervention. Concentrations of cobalamin and folate in serum, and total homocysteine (tHcy), methylmalonic acid (MMA) and cystathionine in plasma will be determined at inclusion and at the age of 4 months. A ...
Cobalamin is a complex organic molecule containing a tetrapyrole corrin ring that is similar in structure to heme but that has a divalent cobalt atom in its center instead of an iron atom. Like heme iron, this cobalt atom binds to two ligands. One is a benzimidazole nucleotide, whereas the other can be either a methyl group (found in methylcobalamin) or an adenosyl group (found in adenosylcobalamin). Cobalamin is present in all foods of animal origin including meat, fish, and dairy products. Food cobalamin is tightly bound to proteins. Following ingestion, some cobalamin in food is transferred to human haptocorrin in saliva. As depicted in Figure 6-1, the low pH of the gastric juice facilitates efficient release and transfer of the remaining food cobalamin to haptocorrin. After transit to the duodenum, the increase in pH enables the transfer of cobalamin from haptocorrin to intrinsic factor, a transport protein secreted by gastric parietal cells. The cobalamin-intrinsic factor complex resists ...
Harvard Pilgrim has developed a new medical policy for Vitamin B12 screening and testing. Effective for dates of service beginning October 1, 2016, Harvard Pilgrim does not consider routine vitamin B12 screening and testing in healthy, asymptomatic adults medically necessary and will not offer reimbursement for this testing in these cases. Harvard Pilgrim will offer coverage of medically necessary vitamin B12 screening and testing for members who are clinically symptomatic or considered high-risk for deficiency due to certain medical conditions. For a complete list of the conditions in which vitamin B12 screening and testing is considered medically necessary, please refer to the Vitamin B12 Screening and Testing Medical Policy. In addition, Harvard Pilgrim considers the testing of methylmalonic acid (MMA) medically necessary for the diagnosis of vitamin B12 deficiency when vitamin B12 levels are borderline-low or low.. However, the testing of holo-transcobalamin as a marker of vitamin B12 is ...
Because cobalamin deficiency is routinely treated with parenteral cobalamin, we investigated the efficacy of oral therapy. We randomly assigned 38 newly diagnosed cobalamin deficient patients to receive cyanocobalamin as either 1 mg intramuscularly on days 1, 3, 7, 10, 14, 21, 30, 60, and 90 or 2 mg orally on a daily basis for 120 days. Therapeutic effectiveness was evaluated by measuring hematologic and neurologic improvement and changes in serum levels of cobalamin (normal, 200 to 900 pg/mL) methylmalonic acid (normal, 73 to 271 nmol/L), and homocysteine (normal, 5.1 to 13.9 mmol/L). Five patients were subsequently found to have folate deficiency, which left 18 evaluable patients in the oral group and 15 in the parenteral group. Correction of hematologic and neurologic abnormalities was prompt and indistinguishable between the 2 groups. The mean pretreatment values for serum cobalamin, methylmalonic acid, and homocysteine were, respectively, 93 pg/mL, 3,850 nmol/L, and 37.2 mmol/L in the oral ...
In this study, they demonstrated that vitamin B treatment reduced grey matter atrophy (shrinkage) 7-fold in the areas specifically vulnerable to the Alzheimers process.. In the placebo group, higher levels of homocysteine were associated with faster grey matter atrophy, but this is largely prevented by the B vitamins Folic acid, B6, and B12.. Homocysteine is a metabolite and an amino acid involved I an important metabolic pathway. It is however not healthy to have high homocysteine levels.. An earlier study found that higher folate levels were associated with a better cognitive function, and better performance on psychomotor speed regardless of homocysteine levels (deLau LM, et.al.,2007).. The 1092 participants did not have dementia and were between 60 and 90 years of age. They underwent extensive cognitive testing and brain imaging.. When 51 patients with Alzheimers disease and 65 cognitively screened controls were studied, blood holotranscobalamin which is the active fraction of blood B12, ...
... is a blood-clotting disorder that results in excessive or prolonged bleeding after an injury or surgery. Factor II is one of 13 proteins involved in proper formation of blood clots. Blood clots are needed to heal wounds, form scabs, and stop bleeding. When factor I levels are low or absent, the blood does not clot correctly, leading to excessive bleeding. Factor II deficiency runs in families and affect both males and females equally. The main symptom of factor II deficiency is excessive and abnormal bleeding. This may occur after childbirth, surgery, trauma, and with menstruation (periods). Bleeding can also occur in the muscles, joints, the mouth, the gut, or, infrequently, the brain. Easy bruising and nosebleeds are also common. Factor II deficiency can be diagnosed by a physician using blood tests. Treatment for factor II deficiency is largely based on controlling bleeding and treating any underlying conditions that contribute to excessive bleeding. When necessary, ...
Cobalamin (Cbl, vitamin B(12)) is a bacterial organic compound and an essential coenzyme in mammals, which take it up from the diet. This occurs by the combined action of the gastric intrinsic factor (IF) and the ileal endocytic cubam receptor formed by the 460-kilodalton (kDa) protein cubilin and the 45-kDa transmembrane protein amnionless. Loss of function of any of these proteins ultimately leads to Cbl deficiency in man. Here we present the crystal structure of the complex between IF-Cbl and the cubilin IF-Cbl-binding-region (CUB(5-8)) determined at 3.3 A resolution. The structure provides insight into how several CUB (for complement C1r/C1s, Uegf, Bmp1) domains collectively function as modular ligand-binding regions, and how two distant CUB domains embrace the Cbl molecule by binding the two IF domains in a Ca(2+)-dependent manner. This dual-point model provides a probable explanation of how Cbl indirectly induces ligand-receptor coupling. Finally, the comparison of Ca(2+)-binding CUB domains and
Gaining a better understanding of plasminogens role in maintaining health; becoming informed about congenital deficiency and who is affected.
A congenital deficiency of either one of the basics or coa the family proteins results and the accumulation of community intermediates in lysosomes, leading to a lysosomal fishing disease.
Cobalamins are derivatives of vitamin B12 that serve as cofactors in various enzymatic reactions involving either radicals or supernucleophilic intermediates
Discover Lifes page about the biology, natural history, ecology, identification and distribution of Discover Life -- CSCA_TCN00001630
caactaacc taaagcaca actgtcagt ggattgtca agtgctttg ttgatattt tttgtaaat aaagcgttt aatcaacaa agggcatgt ccaacatga ctgcaccca acaacaaga agcacgcca gctcaaccg agagctcct ccggctcaa gcgactctt ccagctcca gctcttcgt caagcggtt ccgactcgt cctcatcca gcgatagcg aatcgtcca gttcgcaag aatccacca aacaacaat ccggatccg aattaaaaa agagcgcaa cgatccaga aaaacccgc gcaaaagct cagacagcc tcaaaaccg gcacttcca agtcatcag accccaaac cggccccta aacccaaaa cccaagccc ccaaaaccg ggaaacaac cggccaaaa ccaccatct actcgtcgg aagatgacg acaaaccta aacctagcg cgaagcgca aaagcacag caaagccta aaagcagcg ccacgatca cgcctaaag ccgccacta agccgctgc ctaaaccgg ccgttaaaa acgtgcaaa ataagggcg ccaaaggga aggaaccac cgaagaagg tggtcggga aaaacgcaa agaatgatt ccgccaaca agaaaaaaa gcattttct cgccggaaa atagctccg aatccgacg atgcggcca agaagagtc ggccgaagc ccgcgccac ctaaacccc ggcccaagg ctgcggcca gaacggtcg agaagccca aacctgtgg agaagaagc ccgaaaaac cggcgccta aatctaagg ccgtggtca gttctgcga gttcggcta cgtcctcaa ccgcctcta gtagcagct ctgatagtg agagtagcg ccgaatcgt ccagcacta ctcggaaaa tgagcgata aaaaaatta ...
gttttagtc ggacttttg ctatccagt ctggttgaa tgaggtgtc attcttttt gattgtgac tgtaggtcg atatacttg cgatagttt gtcaacaca caatacacg ttacatatt aatggagaa tctccgatt ctacatccg gtcgaatat ttcacaatt tgccttgtc atcggggga atttggcaa agaaagtgt gttaaaacg cttggatgt ccaaatgaa gactttcga accacgcat tttttaaac ctttgacca cattgtgcc aatttttat ttttggaat ttttcacct gatgtttac ttgcacctg aaaagggcc atcctacaa tcggtgaac gtcgcccca ctatcacgg ttagtcgct ggtaggctt ggcggaggc caaccatcg ctcatggtt gtacaacag accgctgac cggccgcag acctaccaa gaatttccc agtgatgtg atctaagct gctatttcg agtgcggtg atcgactga cgatcacga tgatactca tcgttctgg tgtttgtgg cgtgtgtga attggactt tagcacagt gtcccgaag gaataaccg ggaattgta ccatccgac ataatgaaa cgtcgccga aaccgcccc tgctccaag caatgaaca tgctcgctg aagatgacg accacaaag ggcgagctc ttaatttta caatgaccg aatcgaaca acacacatg acgaacatg gagacctta gcgatgtca ccatcaacg aagatgaag aagaacatg acaaaatca cagctcata atgtcaccg tttgctcaa aaggaggtt tgacgtacg aagaaggag aaaaattag aaatcggct gcgaatcga cgtgcacgt gccgaaacg ggaagatgc aatgtgaag atagatgtg ttaaaccga ...
The aims of this study were to document the levels of cobalamin, folate, methylmalonic acid (MMA) and total homocysteine (tHcy) in serum and their relations to symptoms, clinical findings, and other factors in order to improve the possibilities of detecting early deficiency of vitamin B12 or folate, and to study the effects of cobalamin and folic acid treatment over a three-year period.. The study population consisted of a 20% random sample of persons 70 years or older living in Älvkarleby in mid-Sweden. They were invited to a survey and 224 (88.4%) persons responded. Data were obtained by questionnaire, laboratory investigations and physical examination for the period 1993 - 1999.. In a multivariate analysis performed at baseline, serum MMA and tHcy were significantly and independently correlated to age, serum cobalamin, and creatinine levels, and tHcy also to sex and serum folate. Neither serum cobalamin, folate, MMA nor tHcy had any significant correlation to haemoglobin or mean red cell ...
Vitamin B-12) We have previously described 10 patients with multiple sclerosis (MS) and unusual vitamin B12 deficiency. We have therefore studied vitamin B12 metabolism in 29 consecutive cases of MS, 17 neurological controls, and 31 normal subjects. Patients with MS had significantly lower serum vitamin B12 levels and significantly higher unsaturated R-binder capacities than neurological and normal controls, and they were significantly macrocytic compared with normal controls. Nine patients with MS had serum vitamin B12 levels less than 147 pmol/L and, in the absence of anemia, this subgroup was significantly macrocytic and had significantly lower red blood cell folate levels than neurological and normal controls. Nine patients with MS had raised plasma unsaturated R-binder capacities, including three patients with very high values. There is a significant association between MS and disturbed vitamin B12 metabolism. Vitamin B12 deficiency should always be looked for in patients with MS. The ...
Vitamin B12 is an essential cofactor that is integral to methylation processes important in reactions related to DNA and cell metabolism, thus a deficiency may lead to disruption of DNA and cell metabolism and thus have serious clinical consequences.1 Intracellular conversion of vitamin B12 to two active coenzymes, adenosylcobalamin in mitochondria and methylcobalamin in the cytoplasm, is necessary for the homeostasis of methylmalonic acid and homocysteine, respectively.2 3 Methylmalonic acid is converted into succinyl-CoA, of which vitamin B12 is a cofactor for the reaction. Homocysteine is biosynthesised from methionine then resynthesised into methionine or converted into amino acid cysteine. Vitamin B12 (also referred to as cobalamin) deficiency is relatively common, with important and variable clinical consequences. This review presents a concise summary of the most up to date evidence on how to diagnose and manage vitamin B12 deficiency. ...
... , Min-Chien Tu, Chung-Ping Lo, Ching-Feng Huang, Yen-Hsuan Hsu, Tzu-Lan Wang
... abnormalities. with nutritional Cbl deficiency were included in the study. There were 5 females and 2 males. The mean age was 11??2.30 (range 6C13) months. All individuals experienced general muscular hypotonia and 4 experienced growth retardation. Neuromotor growth retardation was found in 4 of the children who experienced previously demonstrated normal neuromotor development for age. The mean Cbl level was 83.8??27.6 (45.6C114)?pg/mL. The mean Cbl level of the mothers was 155??56.6 (88C258)?pg/mL. Six of the individuals experienced anemia and 1 Laninamivir manufacture experienced thrombocytopenia. Mean corpuscular volume value was 91.5??12.2?fL. Following treatment, the muscle mass tonus of the individuals improved, the anemia and growth retardation decreased, and the lost neuromotor abilities were recovered. Severe nutritional Cbl deficiency is an important nutritional disease where complications ...
How much of Vitamin B-12, also called cobalamin is present in Veal, composite of trimmed retail cuts, separable fat, cooked in details, quantity how high or low Vitamin B-12, also called cobalamin nutrient content it has.
... 1000 mcg / mL Intramuscular or Subcutaneous Injection Single Dose Vial 1 mL, 25/Pack Westward 00143962125
Vitamin B-12, a family of compounds called cobalamins, is one of eight essential B-complex vitamins. Foods or dietary supplements might contain several types of cobalamins, but your body converts dietary B-12 into two active forms -- methylcobalamin and 5-deoxyadenosyl cobalamin -- and uses these forms to maintain ...