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Base excision repair (BER) operates mainly on small DNA adduct complexes such as irreversibly alkylated DNA bases, and is carried out by DNA glycosylases which catalyse the hydrolysis of N-glycosylic bonds linking damaged bases to the deoxyribose-phosphate backbone of DNA Subsequently, sites lacking their bases are removed by speci c endonucleases, and the resynthesis and ligation of the excised region Nucleotide excision repair (NER) involves the removal of whole nucleotides including bases and deoxyribose-phosphate backbone of DNA, and thus excised fragments are usually oligonucleotide fragments rather than free bases As in base excision repair, the resulting gap is lled by repair synthesis using the alternate strand as template and ligation However, nucleotide excision repair is more complex than base excision repair and involves many more gene products Nucleotide excision repair is considered to repair DNA at different rates, thus allowing fast preferential repair of active cells (Harvey, 1995).

In addition to BER and NER, several other pathways for DNA repair exist, including direct reversal by photoreactivation of pyrimidine dimers, alkyltransferases, purine insertion and the ligation of strand breaks The ef ciency of DNA repair processes will depend to a large degree on the development of DNA adducts and associated damage (Espina & Weis, 1995) Chemical agents with proliferation or inhibitive capabilities have been shown to in uence the repair capacity of cells, by modulating the balance between repair and replication (Barrett, 1995) Ef ciency of repair will not only depend on various physical factors such as position in the DNA sequence, chemical stability of adduct complex, and accessibility to repair complexes, but there is also apparent intrinsic variability depending on species and exposure (Anderson & Harrison, 1990).

However, in practice the number of hidden layer neurons may necessarily be large, thus contradicting the desire to use small hidden layers to better avoid over tting and overtraining To gain further insights into the innerworkings of a three-layer MLF, let wk = (wk1 , , wkr ) denote the vector of weights between the input layer and the kth-hidden neuron It follows that yj = g sj bj , where bj denotes the bias of the jth output neuron, where.

organization. Given this fact, there may be serious impediments for the achievement of learning by the organization, since information flow, particularly when the news is not good, may be severely constricted. This may be the fault of the individuals themselves, who believe that rather than report bad news, with a little additional work on their part it can be turned into good news. Also, they instinctively understand that bad news is often not well received at the top. Were they so inclined to send bad news upward, they also understand that senior management usually adopts an orientation that requires that bad news be accompanied by proposed solutions in the same package thus more disincentive to send the bad news upward. Once middle management is in receipt of the bad news, they also have a tendency not to report it upward. Accordingly, it goes forward, if at all, in smaller, manageable pieces. Thus they contend, does upper management receive bad news in incremental bites, usually with firm assurances that those below have the situation under control and will have it resolved promptly. The net effect of these dynamics is that those at the bottom of the ladder, where the problem was first surfaced, remain ignorant and frustrated by the fact that bad news was reported and top management apparently is doing nothing about it. Argyris and Schon see this as a classis example of problems in organizational learning and define the issue as follows:

Data for example has indicated that DNA damage may be cumulative in oocytes, leading to the hypothesis that organisms with long synchronous periods of gametogenesis may be more vulnerable to chronic exposure, based on reduced repair capacities In the mouse, data suggests that DNA repair is not active in postmeiotic cells (Russell et al, 1990), and thus a precedent exists for low DNA repair capacities in gametogenic stages of some organisms Studies that explore the effect of long-term, low-level exposures to mutagens on gametes would require direct assessments of the kinetics of absorbed dose and of DNA repair in gametes The lability of repair systems, and the extent to which they may be associated with long-term exposure, have been relatively neglected in marine organisms (Wirgin & Waldman, 1998), and yet will have major impacts on the evolution of tolerance and long-term evolutionary impacts of genotoxicity.

Most studies concerning repair systems have been carried out in the bacteria Escherichia coli and the yeast Saccharomyces cerevisiae Studies on aquatic organisms are rare, though.