Organisms, including humans, fish-eating birds, and fish-eating mammals such as otters and cetaceans (i.e. whales and dolphins) that consume fish from the top of the aquatic food chain receive the methylmercury that has accumulated through this process, plus the toxins in their habitat. Fish and other aquatic species are the main source of human methylmercury exposure.The concentration of mercury in any given fish depends on the species of fish, the age and size of the fish and the type of water body in which it is found. In general, fish-eating fish such as shark, swordfish, marlin, larger species of tuna, walleye, largemouth bass, and northern pike, have higher levels of methylmercury than herbivorous fish or smaller fish such as tilapia and herring. Within a given species of fish, older and larger fish have higher levels of methylmercury than smaller fish. Fish that develop in water bodies that are more acidic also tend to have higher levels of methylmercury. Biological impact
Human health effects
Ingested methylmercury is readily and completely absorbed by the gastrointestinal tract. It is mostly found complexed with free cysteine and with proteins and peptides containing that amino acid. The methylmercuric-cysteinyl complex is recognized by amino acids transporting proteins in the body as methionine, another essential amino acid. Because of this mimicry, it is transported freely throughout the body including across the blood–brain barrier and across the placenta, where it is absorbed by the developing fetus. Also for this reason as well as its strong binding to proteins, methylmercury is not readily eliminated.
SMC1A, SMC3 and RAD21 proteins are structural components of the cohesin ring complex. NIPBL is involved in the loading of the cohesin ring onto chromosomes, and HDAC8 deacylates SMC3 to facilitate its function. The cohesin pathway is involved in cohesion of sister chromatids during mitosis, DNA repair, chromosome segregation and the regulation of developmental gene expression. Defects in these functions are theorised to underlie some of the features of CdLS. In particular, defective DNA repair may underlie the features of premature aging. Diagnosis
The diagnosis of CdLS is primarily based on clinical findings by a clinical geneticist; and in some cases may be confirmed through laboratory testing. Treatment
Often, an interdisciplinary approach is recommended to treat the issues associated with CdLS. A team for promoting the childs well-being often includes speech, occupational and physical therapists, teachers, physicians, and parents.Cornelia de Lange syndrome (CdLS) affects many different systems of the body, medical management is often provided by a team of doctors and other healthcare professionals. Treatment for this condition varies based on the signs and symptoms present in each person.