Defects development

We now proceed as we did for the stoichiometric case, namely to develop defect- concentration equations for the non-stoichiometric case. Consider the effect of Anti-Frenkel defect production. From Table 2-1, we get Kaf with its associated equation, kAF In Table 2-2, we use Kxi for X-interstitial sites. Combining these, we get ... 

Caspase-1 Yes Normal development Defects in death receptor-mediated apoptosis, resistant to lipopolysaccaharide (LPS)-induced endotoxic shock Normal [57-59]... 

Caspase-12 Yes Normal development Defective endoplasmic reticulum-mediated apoptosis, reduced neuronal apoptosis by /3-amyloid Normal [72]... 

The human body consists of cells built up of chains and networks of different types of protein and lipid molecules. For younger persons, these chains and networks are very perfect and orderly but as he grows old (although slowly but spontaneously, i.e., irreversibly) the structure develops defects or disorders signifying an increase in entropy. This particular example needs to be accepted only figuratively as it is difficult to derive a mathematical correlation. 

After treatment with activated carbon, a product may in time develop defects of quality such as color and odor reversion. Or again,... 

Cyanoalanine is an unusual amino acid derived from cysteine that is produced in the seeds of Lathyris odoratus. Animals consuming these seeds develop defects in their collagen. In humans the disease is associated with consumption of / -cyanoalanine is called Ehlers-Danlos syndrome and it manifests itself as curvature of the spine and heart problems. 

SNL Develops Defect-Free Thin Film Membranes for Hydrogen Senaration and Isolation... 

Deletion of the CXCR5 gene yields a phenotype in which the animals do not develop inguinal lymph nodes and do develop defective follicles and germinal centers in the spleen and Peyer s patches (3,41). Receptor-deficient B lymphocytes are able to migrate into T-lymphocyte-rich peripheral and interfollicular areas, but are unable to migrate farther, into the deeper B-lymphocyte-rich follicles (3). 

BMP15 (9210) Xpll.2 ODG2, POF4, GDF9B May be involved in oocyte maturation and follicular development defects in the gene are the cause of ovarian dysgenesis type 2... 

Hardcastle Z. et al. 1998. The Shh signaling pathway in tooth development defects in G112 and G113 mutants. Development 125(15) 2803-2811. 

The correct level of the active metabolites of vitamin A which control the nuclear receptor signalling pathway is required for appropriate embryonic development. Too much or too little of the receptor ligands is equally harmful for the embryo. It has been well documented that when there is an excess of vitamin A or its metabolites during embryonic development, defects occur in the CNS. An excess of RA causes specific defects of the anterior hindbrain whereby anterior rhombomeres can be lost or respecified to more posterior areas or it can cause poste-riorization of the whole CNS, whereby forebrain structures are lost [36, 50, 86-88]. More recently, Maden et al. describe defects that arise in the central nervous system of quail embryos when they develop in the absence of vitamin A [50]. There are three defects in these embryos (1) the posterior hindbrain is completely missing (2) the neural tube fails to extend neurites out into the periphery (3) the neural crest cells die. 

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