External examination and autopsy findings are often non-specific, and the available laboratory tests are often inconclusive or controversial. The purpose of an investigation is generally to distinguish whether the death was due to immersion or whether the body was immersed postmortem. The mechanism in acute drowning is hypoxemia and irreversible cerebral anoxia due to submersion in liquid.Drowning would be considered a possible cause of death if the body was recovered from a body of water, near a fluid that could plausibly have caused drowning, or found with the head immersed in a fluid. A medical diagnosis of death by drowning is generally made after other possible causes of death have been excluded by a complete autopsy and toxicology tests. Indications of drowning are seldom completely unambiguous and may include bloody froth in the airway, water in the stomach, cerebral edema and petrous or mastoid hemorrhage. Some evidence of immersion may be unrelated to the cause of death, and lacerations and abrasions may have occurred before or after immersion or death.Diatoms should normally never be present in human tissue unless water was aspirated. Their presence in tissues such as bone marrow suggests drowning; however, they are present in soil and the atmosphere, and samples may easily be contaminated. An absence of diatoms does not rule out drowning, as they are not always present in water. A match of diatom shells to those found in the water may provide supporting evidence of the place of death.
Absorption refers to the overall process happening in the intestine in lieu of normal digestive breakdown of proteins, while reabsorption refers to the process occurring in the renal proximal tubule to reclaim amino and imino acids that have been filtered out of the blood via the glomerulus.These forms of transport require energy, as the products being transported are usually moving against a higher concentration gradient. This process, called active transport, get its energy from ATP and other ATP-related cotransport systems that produce energy, like the sodium-potassium pump. Mechanism
The primary defect associated with iminoglycinuria is a homozygous (recessive) mutation of the SLC36A2 (PAT2) gene. One of several membrane transport proteins in the solute carrier family of amino acid transporters, PAT2 is the high-affinity renal transporter of glycine, proline and hydroxyproline found to be defective in both alleles when iminoglycinuria is present in an individual. This is in contrast to the fact that when only one PAT2 allele is defective, hyperglycinuria will be present instead of iminoglycinuria. These findings delineate iminoglycinuria as the homozygous form of hyperglycinuria, with the former having a higher degree of urinary excretion of glycine and imino acids correlating to mutations in both alleles.Another mutation suspected to convey the iminoglycinuria phenotype may be found in the SLC36A1 (PAT1) gene. Identified as the low-affinity intestinal transporter of glycine and imino acids, PAT1 works in cooperation with the renal sodium-hydrogen exchanger NHE3 (SLC9A3).