Michelle Rodgers entered The Golden Spike Bar and Grill on a Friday night at approximately 10:30pm. At the door, she was stopped briefly by the bar’s security guard. The guard, Luis Sargota, inspected Michelle’s photo ID, as he had been trained to do during the one-hour orientation class he attended on his first day of work.
The photo ID presented by Michelle showed her age to be 21 years and three months. The photo on the picture was clearly her own. She was not asked to remove the ID from her wallet. Michelle entered the bar and, over a period of three hours, consumed five fuzzy navel drinks, each containing approximately 1.5 ounces of 80 proof alcohol served with fruit juice.
Upon leaving the bar at 1:30am, Michelle was involved in a traffic accident that seriously injured a man who was driving home from working the late shift at a local factory. The family of the injured man sued Michelle and the Golden Spike when it was discovered that Michelle was, in fact, only 20 years old, and thus was not of legal drinking age.
The attorney for the Golden Spike maintained that the bar acted responsibly , in that it trained its security guards to check for ID prior to allowing admission to the bar, and that Ms. Rodgers had presented a falsified ID card, which the bar could not have reasonably known was false. In addition, the security guard stated that Ms. Rodgers “looked” at least 21 when she entered the bar. Thus, the bar was not guilty of knowingly serving minors.
- Is the bar responsible for illegally serving Ms. Rodgers? Was she served excessively?
- Since the security guard did not serve alcohol, do you think a jury would find one hour of orientation sufficient in his training?
- What could the owners of the Golden Spike do in the future to prevent a reoccurrence such as this?
Sample Solution
environments. Neglected children are nine times more likely to become obese than other children (8). Food provides comfort and therefore that eating serves as a compensatory mechanism for children who have survived traumatic experiences or who live in difficult environments. 3. 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. TABLE 2>
environments. Neglected children are nine times more likely to become obese than other children (8). Food provides comfort and therefore that eating serves as a compensatory mechanism for children who have survived traumatic experiences or who live in difficult environments. 3. 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. TABLE 2>
