Actomyosin is a smooth muscle protein found throughout the body. In the intestinal barrier's epithelial cells, actomyosin proteins form cables called the Actin Network.

Gastrointestinal microfilaments of the Actomyosin Network are critical for apical junctional complex biogenesis and function. The apical junctional complex, made up in part by tight junction proteins zonulin and occludin, is responsible for preventing antigen invasion and preservation of the biochemical homeostasis within the gastrointestinal tract. The Actomyosin Network can signal tight junction contractions and give structure to their assembly.

Acylcarnitine is a crucial molecule in the body, playing a significant role in the metabolism of fatty acids. Essentially, it acts as a transporter that helps move fatty acids into the mitochondria, the energy powerhouses of our cells, where they can be broken down and used for energy production. The process begins when fatty acids bind to carnitine, forming acylcarnitine, which can then cross the mitochondrial membrane. Once inside the mitochondria, the fatty acids are released from carnitine and undergo a process called beta-oxidation, which ultimately generates ATP, the energy currency of cells. Measuring levels of acylcarnitines in the blood can provide valuable insights into metabolic health. Abnormal levels may indicate metabolic disorders such as fatty acid oxidation defects, which can lead to energy production issues and accumulation of toxic substances in the body. Therefore, understanding and monitoring acylcarnitine levels is important for diagnosing and managing various metabolic conditions.

The ADAMTS13 activity and inhibitor assays are useful for the diagnosis of congenital or acquired form of TTP.

ADAMTS13 is a plasma protein responsible for regulating the interaction of platelets with von Willebrand factor (VWF) and physiologic proteolytic cleavage of ultra large (UL) VWF multimers at the Tyr(1605)- Met(1606) bond in the A2 domain of VWF. Reduced or absent ADAMTS13 activity can retain UL VWF that can trigger intravascular platelet aggregation and microthrombi causing clinical symptoms or signs of thrombotic thrombocytopenic purpura (TTP).

Measurement of ADAMTS13 activity and its inhibitor is crucial in the diagnosis of TTP, potentially fatal thrombotic microangiopathy (TMA) syndrome and further differentiation of congenital (Upshaw-Schulman syndrome) versus acquired (e.g. autoimmune-related disorder) etiology.

Adenovirus serotypes 40 and 41 cause acute gastroenteritis (inflammation of the stomach and intestines) primarily in children.

Adenoviruses are non-enveloped DNA viruses.

Adenovirus is a cause of acute gastroenteritis in infants, young children, the elderly and immuno-compromised patients. The Adenovirus serotypes most frequently associated with gastroenteritis are Adenovirus 40 and 41.

Adenovirus gastroenteritis generally causes watery diarrhea lasting one to two weeks.

ADH stands for antidiuretic hormone also known as vasopressin. ADH primarily acts in the kidney to resorb water. Vasopressin can also be administered to raise blood pressure.

Adipate, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipate, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Carnitine is needed to move fatty acids into the mitochondria where they are converted to energy using vitamin B2.

If carnitine is sufficient long-chain fatty acids go through beta-oxidation in the mitochondria.

When insufficient levels of carnitine or vitamin B2 slow down this process, other parts of the cellular machinery take over and make adipate and suberate.

A similar block in another pathway causes high ethylmalonate. Since most of our bodies’ energy is produced from the burning of fatty acids, our muscles and brain suffer when this cellular energy pathway is blocked. Anything that interferes with the normal fatty acid oxidation may reveal high levels of these metabolites.

Adipate, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Carnitine is needed to move fatty acids into the mitochondria where they are converted to energy using vitamin B2.

If carnitine is sufficient long-chain fatty acids go through beta-oxidation in the mitochondria.

When insufficient levels of carnitine or vitamin B2 slow down this process, other parts of the cellular machinery take over and make adipate and suberate.

A similar block in another pathway causes high ethylmalonate. Since most of our bodies’ energy is produced from the burning of fatty acids, our muscles and brain suffer when this cellular energy pathway is blocked. Anything that interferes with the normal fatty acid oxidation may reveal high levels of these metabolites.

Dietary fatty acids are metabolized into fuel sources using beta-oxidation. Fatty acid conversion into Acetyl-CoA requires transport across the mitochondrial membrane via the carnitine shuttle. When beta-oxidation is impaired, fats are metabolized using an alternate pathway called omega-oxidation. Omega-oxidation results in elevated levels of dicarboxylic acids such as adipic acid and suberic acid. Impaired beta-oxidation occurs in carnitine deficiency or enzymatic dysfunction due to lack of nutrient cofactors. Vitamin B2 and magnesium play a role in optimizing beta-oxidation.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Dietary fatty acids are metabolized into fuel sources using beta-oxidation. Fatty acid conversion into Acetyl-CoA requires transport across the mitochondrial membrane via the carnitine shuttle. When beta-oxidation is impaired, fats are metabolized using an alternate pathway called omega-oxidation. Omega-oxidation results in elevated levels of dicarboxylic acids such as adipic acid and suberic acid. Impaired beta-oxidation occurs in carnitine deficiency or enzymatic dysfunction due to lack of nutrient cofactors. Vitamin B2 and magnesium play a role in optimizing beta-oxidation.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.

Adipic Acid, together with Suberate and Ethylmalonate are all functional markers for deficiency of carnitine.