Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

The R. rickettsii IFA - IgG marker on a Rickettsiosis panel is a crucial diagnostic tool for identifying infection with Rickettsia rickettsii, the bacterium responsible for Rocky Mountain spotted fever (RMSF), a potentially severe tick-borne illness. This serological test detects Immunoglobulin G (IgG) antibodies that the immune system produces specifically in response to an R. rickettsii infection. IgG antibodies are part of the body's later immune response, typically developing a few weeks after initial exposure to the pathogen and potentially persisting for years, thus indicating either past exposure or chronic infection.

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An "Indeterminate" result (if result falls in orange reference range) in the R. rickettsii IFA - IgG test indicates that the detected levels of IgG antibodies against Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever (RMSF), are unclear and do not conclusively fall within the defined positive or negative ranges. This ambiguous result can be due to several reasons. It might suggest that the antibody levels are at a borderline range, possibly indicating an early immune response where the antibodies are just starting to develop and have not reached a level high enough to be considered positive. Alternatively, it could be a sign of declining antibody levels from a past infection that is resolving or has already resolved, where the antibodies are present but at diminishing levels. An indeterminate result can also arise from technical issues in the test procedure or cross-reactivity with antibodies from other similar infections. In such cases, further evaluation is necessary, often including a clinical assessment of symptoms, patient history, and possibly additional diagnostic tests, such as a repeat IgG test after some time or other serological tests like IgM testing. This indeterminate outcome highlights the complexity of diagnosing RMSF based solely on serological testing and underscores the importance of a comprehensive clinical assessment to accurately determine the infection status.

The R. typhi IFA - IgG marker on a Rickettsiosis panel is a specialized diagnostic tool used for the detection of IgG antibodies against Rickettsia typhi, the causative agent of murine typhus. This serological assay plays a critical role in the diagnosis of the disease, particularly in epidemiological settings where murine typhus is prevalent. IgG antibodies are a key component of the adaptive immune response, typically developing within a few weeks following exposure to a pathogen and persisting for an extended period, thereby indicating past exposure or a possible chronic infection.

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An "Indeterminate" result (a result that falls within the orange reference range) in the R. typhi IFA - IgG test signifies that the levels of IgG antibodies against Rickettsia typhi, the bacterium responsible for murine typhus, are ambiguous and do not clearly fall into the positive or negative categories. This uncertain result can occur for several reasons. It may indicate that the antibody levels are at a borderline, possibly suggesting an early stage of the immune response where antibodies are just starting to develop but haven't reached a definitive positive level. Alternatively, it could be a sign of declining antibody levels from a past infection that is resolving or has already resolved, where the antibodies are present but at diminishing levels. Technical factors within the test itself or cross-reactivity with antibodies from other similar pathogens can also contribute to an indeterminate result. In such cases, further evaluation is often necessary, including a clinical assessment of symptoms, patient history, and possibly additional diagnostic tests, such as a repeat IgG test after some time or IgM testing. This indeterminate outcome emphasizes the need for a comprehensive approach in diagnosing murine typhus, considering serological results alongside the broader clinical picture to accurately determine the infection status.

The rheumatoid arthritis (RA) latex turbid test is a laboratory test that’s used to help your doctor diagnose rheumatoid arthritis and other autoimmune diseases.

T-Cell-Specific Protein RANTES is chemotactic for T-cells, human eosinophils and basophils and plays an active role in recruiting leukocytes into inflammatory sites. It also activates the release of proteins from eosinophils such as eosinophilic cationic protein. It changes the density of eosinophils and makes them hypodense, which is thought to represent a state of generalized cell activation and is associated most often with diseases such as asthma and allergic rhinitis.

The rapid plasma reagin (RPR) is a test used to screen for syphilis. The RPR test measures IgM and IgG antibodies to lipoidal material released from damaged host cells as well as to lipoprotein-like material, and possibly cardiolipin released from the treponemes.