Radiation
For the survivors of the atomic bombing of Hiroshima and Nagasaki, who are known as the Hibakusha, no statistically demonstrable increase of birth defects/congenital malformations was found among their later conceived children, or found in the later conceived children of cancer survivors who had previously received radiotherapy. The surviving women of Hiroshima and Nagasaki who were able to conceive, though exposed to substantial amounts of radiation, later had children with no higher incidence of abnormalities/birth defects than in the Japanese population as a whole.Relatively few studies have researched the effects of paternal radiation exposure on offspring. Following the Chernobyl disaster, it was assumed in the 1990s that the germ line of irradiated fathers suffered minisatellite mutations in the DNA, which was inherited by descendants. More recently, however, the World Health Organization states, "children conceived before or after their fathers exposure showed no statistically significant differences in mutation frequencies". This statistically insignificant increase was also seen by independent researchers analyzing the children of the liquidators. Animal studies have shown that incomparably massive doses of X-ray irradiation of male mice resulted in birth defects of the offspring.In the 1980s, a relatively high prevalence of pediatric leukemia cases in children living near a nuclear processing plant in West Cumbria, UK, led researchers to investigate whether the cancer was a result of paternal radiation exposure. A significant association between paternal irradiation and offspring cancer was found, but further research areas close to other nuclear processing plants did not produce the same results.
Rhizomelic chondrodysplasia punctata is a rare developmental brain disorder characterized by systemic shortening of the proximal bones (i.e. rhizomelia), seizures, recurrent respiratory tract infections and congenital cataracts. The affected individuals have low levels of plasmalogens. Signs and symptoms
Rhizomelic chondrodysplasia punctata has the following symptoms:
Bilateral shortening of the femur
Post-natal growth problems (deficiency)
Cataracts
Intellectual disability
Possible seizures
Possible infections of respiratory tract

Genetics
This condition is a consequence of mutations in the PEX7 gene, the GNPAT gene (which is located on chromosome 1) or the AGPS gene. The condition is acquired in an autosomal recessive manner. Pathophysiology
The mechanism of rhizomelic chondrodysplasia punctata in the case of type 1 of this condition one finds that peroxisome objective is PEX7, in peroxisome assembly. There are 3 pathways that count on PEX7 and are:
AGPS (catalyzes plasmalogen biosynthesis)
PhYH (catalyzes catabolism of phytanic acid)
ACAA1 (catalyzes beta-oxidation of VLCFA - straight)

Diagnosis
The diagnosis of rhizomelic chondrodysplasia punctata can be based on genetic testing as well as radiography results, plus a physical examination of the individual. Types
Type 1 (RCDP1) is associated with PEX7 mutations; these are peroxisome biogenesis disorders where proper assembly of peroxisomes is impaired. Type 2 (RCDP2) is associated with DHAPAT mutations 
Type 3 (RCDP3) is associated with AGPS mutations

Treatment
Management of rhizomelic chondrodysplasia punctata can include physical therapy; additionally orthopedic procedures improved function sometimes in affected people. However, the prognosis is poor in this condition. See also
Plasmalogen
Peroxisomal disorder

References
Further reading


== External links ==