Pathways

Gadoteridol is indicated for use with magnetic resonance imaging (MRI) in order to visualize lesions with disrupted blood-brain barrier and/or abnormal vascularity in the brain, spine, and associated tissues in adult and pediatric patients, including term neonates. It is also indicated for visualization of lesions in the head and neck in adult patients. Gadoteridol provides contrast enhancement of the brain, spine and surrounding tissues resulting in improved visualization (compared with unenhanced MRI) of lesions with abnormal vascularity or those thought to cause a disruption of the normal blood brain barrier. Gadoteridol can also be used for whole body contrast enhanced MRI including the head, neck, liver, breast, musculoskeletal system and soft tissue pathologies. n MRI, visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoteridol shortens the T1 relaxation time in tissues where it accumulates. Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoteridol in lesions such as neoplasms, abscesses, and subacute infarcts.

Gadoversetamide is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Gadoversetamide passes through the liver and is then excreted from the body mainly through the kidney.

Gadoversetamide is an MRI contrast agent used for MRI diagnostic procedures to provide increased enhancement and visualization of lesions of the brain, spine and liver, including tumors. Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. MR images are based primarily on proton density and proton relaxation dynamics. MR instruments are sensitive to two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). Paramagnetic agents contain one or more unpaired electrons that enhance the T1 and T2 relaxation rates of protons in their molecular environment. In MRI, visualization of normal and pathological brain, spinal and hepatic tissue depends in part on variations in the radio frequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoversetamide shortens the T1 and T2 relaxation times in tissues where it accumulates. At the recommended dose, the effect is primarily on T1 relaxation time, and produces an increase in signal intensity (brightness). Gadoversetamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in CNS lesions that may have a normal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoversetamide in lesions such as neoplasms, abscesses, and subacute infarcts. Diethylenetriamine pentaacetate (DTPA) and its derivatives, which are commonly used as organic ligands in gadolinium-based contrast agents (GBCAs), are designed to form stable complexes with gadolinium ions (Gd3+). These complexes enhance the contrast in medical imaging, particularly in magnetic resonance imaging (MRI). When these GBCAs are administered for imaging, they are primarily eliminated from the body through renal excretion, and a significant portion of them is excreted largely unchanged.

Gadoxetic acid is a gadolinium-based contrast agent used in magnetic resonance imaging (MRI) to help characterize lesions in the liver. Gadoxetate disodium is an amphipathic compound in which gadoxetate is hydrophillic and its moiety, the ethoxybenyzl group, is lipophillic. Consequently, gadoxetate disodium has a biphasic mode of action in which it first distributes into the extracellular space after bolus injection and then hepatocytes selectively takes up the drug. When gadoxetate disodium is placed in an external magnetic field, a large magnetic moment is produced. As a result, a magnetic field is induced around the tissue. The water protons in the vicinity are disrupted such that the change the proton density and spin characteristics are detected and visualized by a device.

Escherichia coli can solely use D-galactonate as a carbon and energy source. The initial step, after the transport of galactonic acid into the cell is the dehydration of D-galactonate to 2-dehydro-3-deoxy-D-galactonate by D-galactonate dehydratase. Subsequent phosphorylation by 2-dehydro-3-deoxygalactonate kinase and aldol cleavage by 2-oxo-3-deoxygalactonate 6-phosphate aldolase produces pyruvate and D-glyceraldehyde-3-phosphate, which enter central metabolism. Galactitol can also be utilized by E. coli K-12 as the sole source of carbon and energy. Each enters the cell via a specific phosphotransferase system, so the first intracellular species is D-galactitol-1-phosphate or D-galactitol-6-phosphate, which are identical. This sugar alcohol phosphate becomes the substrate for a dehydrogenase that oxidizes its 2-alcohol group to a keto group. Galactitol-1-phosphate is dehydrogenated to tagatose-6-phosphate which is then acted on by a kinase and an aldose and eventually is converted to glycolysis intermediates.

Escherichia coli can solely use D-galactonate as a carbon and energy source. The initial step, after the transport of galactonic acid into the cell is the dehydration of D-galactonate to 2-dehydro-3-deoxy-D-galactonate by D-galactonate dehydratase. Subsequent phosphorylation by 2-dehydro-3-deoxygalactonate kinase and aldol cleavage by 2-oxo-3-deoxygalactonate 6-phosphate aldolase produces pyruvate and D-glyceraldehyde-3-phosphate, which enter central metabolism. Galactitol can also be utilized by E. coli K-12 as the sole source of carbon and energy. Each enters the cell via a specific phosphotransferase system, so the first intracellular species is D-galactitol-1-phosphate or D-galactitol-6-phosphate, which are identical. This sugar alcohol phosphate becomes the substrate for a dehydrogenase that oxidizes its 2-alcohol group to a keto group. Galactitol-1-phosphate is dehydrogenated to tagatose-6-phosphate which is then acted on by a kinase and an aldose and eventually is converted to glycolysis intermediates.

Galactolipids are a type of glycolipid whose sugar group is galactose. They are the main part of plant photosynthetic membrane lipids where they substitute phospholipids to conserve phosphate for other essential processes . Their synthesis is localized to the chloroplast membranes (membrane-associated enzymes are coloured dark green in the image). First, UDP-galactose:DAG galactosyltransferase catalyzes the conversion of a 1,2-diacyl-sn-glycerol into a 1,2-diacyl-3-O-(beta-D-galactopyranosyl)-sn-glycerol. This compound has two different fates. The first subpathway consists of a single reaction catalyzed by UDP-galactose:MGDG galactosyltransferase whereby 1,2-diacyl-3-O-(beta-D-galactopyranosyl)-sn-glycerol is converted into an alpha,beta-digalactosyldiacylglycerol. This enzyme requires a magesium ion as a cofactor. The second pathway consists of three successive reactions catalyzed by the same enzyme. Galactolipid:galactolipid galactosyltransferase uses a 1,2-diacyl-3-O-(beta-D-galactopyranosyl)-sn-glycerol to first convert another 1,2-diacyl-3-O-(beta-D-galactopyranosyl)-sn-glycerol into a 1,2-diacyl-3-O-[beta-D-galactosyl-(1→6)-beta-D-galactosyl]-sn-glycerol then into a trigalactosyldiacylglycerol and finally into a tetragalactosyldiacylglycerol.