Abnormality of DC development observed in ATM-deficient mice might explain the defect and malfunction of immune system of ATM patients and their multiple disease status.
Two complementary studies using genetically engineered murine models help to explain the association of NOD2 malfunction and mucosal disease.
It is human interests, not biological malfunctions, that explain the judgments that subordinate members have the relevant biological character.
While the molecular basis of the metabolic pathology in MADD can be explained by the malfunction of fatty acid, choline and amino acid metabolism as a result of ETF or ETFDH mutation [5], it remains unclear why individuals with MADD exhibit other defects, especially neurological defects including cortex dysplasia, encephalopathy and leukodystrophy[32], [33], [34], [35].
Our data supports a novel function of MID1 in directing mRNP complex-associated protein translation regulation to the cytoskeleton, malfunction of which would explain the observed developmental malformations in OS.
This pathogenesis can explain the evolution to RPE detachments and subsequent rips and progressive retinal malfunction.
The possibility that a fish was in the vicinity of a receiver and not detected because of transmitter malfunction can not be ruled out but this would not explain the differences in patterns between the pure species and hybrids.
In order to complement the ranking arising from CCs, we introduced a p-value for each enzyme, which is a quantitative parameter indicating the specificity of a particular enzyme knockout/malfunction to explain the metabolite alteration under consideration.
In this instance, the analogy worked in both directions: not only did the electric telegraph carry messages and regulate the social organism in the same manner that the central and peripheral nervous systems governed the body, but the telegraph was also conversely adopted by scientists and doctors as a means of explaining the functions (and malfunctions) of the nerves (Morus, 1999, 2000).
