Are artificial persons (or A.I.) possible in the future?Could machines think?
[1]Describe the Turing test. Describe in detail how it works and what its goal is. What counts as a pass and what does pass mean? If a woman passes the test what does Turing think that proves?
[2]Describe Functionalism and why it makes possible future artificial intelligence (see Putnamâs interview on website)
[3]Describe and explain Searleâs âChinese roomâ counterexample to functionalism and the argument it illustrates: do not forget to explain the distinction between syntax and semantics.
[4]Describe and explain at least one(more is better) reply to Searle. Make a conclusion; could machines think and have minds?
Sample Solution
. Genetics: The current epidemic of obesity clearly reflects the environmental and behavior changes during the past half century, but the genetic background remains important, especially in the severe forms of obesity. In the most recent published update, there were more than 430 genes, markers, and chromosomal regions associated or linked with human obesity phenotypes (9). The human obesity gene map reveals that loci affecting obesity related phenotypes are found on all human chromosomes except chromosome Y. The potential implication of genetic factors in the development of obesity is well demonstrated by the description of monogenic forms of human obesity. The genes implicated in these forms of obesity are summarized in Table 2. MC4R mutations are the most frequent cause of monogenic human obesity, occurring in up to 4% of early-onset and severe childhood obesity (10,11). Homozygous mutations of the leptin-melanocortin genes are often associated with other features, e.g. hypogonadotropic hypogonadism in leptin deficiency and red hair and hypocortisolism in POMC deficiency. Genetic Syndromes associated with obesity include Prader-Willi, Bardet-Biedl, Berardinelli-Seip congenital lipodystrophy, Alstrom, Borjeson-Forssman-Lehmann, Cohen, Beckwith-Wiedemann, Carpenter Syndrome>
. Genetics: The current epidemic of obesity clearly reflects the environmental and behavior changes during the past half century, but the genetic background remains important, especially in the severe forms of obesity. In the most recent published update, there were more than 430 genes, markers, and chromosomal regions associated or linked with human obesity phenotypes (9). The human obesity gene map reveals that loci affecting obesity related phenotypes are found on all human chromosomes except chromosome Y. The potential implication of genetic factors in the development of obesity is well demonstrated by the description of monogenic forms of human obesity. The genes implicated in these forms of obesity are summarized in Table 2. MC4R mutations are the most frequent cause of monogenic human obesity, occurring in up to 4% of early-onset and severe childhood obesity (10,11). Homozygous mutations of the leptin-melanocortin genes are often associated with other features, e.g. hypogonadotropic hypogonadism in leptin deficiency and red hair and hypocortisolism in POMC deficiency. Genetic Syndromes associated with obesity include Prader-Willi, Bardet-Biedl, Berardinelli-Seip congenital lipodystrophy, Alstrom, Borjeson-Forssman-Lehmann, Cohen, Beckwith-Wiedemann, Carpenter Syndrome>
