a. Sn2/E2 mixture (secondary; strong nucleophile) b. Mostly Sn2 with some E2 (primary; strong nucleophile) c. E2 (secondary and very hindered, blocking Sn2) d. Sn1/E1 mixture (tertiary; water indicates it\'s going Sn1/E1) a. cyanide b. alcohol c. ester Solution a. Sn2/E2 mixture (secondary; strong nucleophile) b. Mostly Sn2 with some E2 (primary; strong nucleophile) c. E2 (secondary and very hindered, blocking Sn2) d. Sn1/E1 mixture (tertiary; water indicates it\'s going Sn1/E1) a. cyanide b. alcohol c. ester.

1. Macrophages: These cells regulate inflammatory responses to bacteria and antigens that breach
the gastrointestinal barrier, protect the mucosa against harmful pathogens, and scavenge dead
cells and foreign debris. NK (Natural killer cells) cells: NK cells and NK-derived IFN- function
in regulating the intestinal inflammatory response to Salmonella. Along with other types of
lymphocytes, produced IFN- in response to the bacteria in vitro. Then the IFN--regulated
chemokines induced by Salmonella in the gut are likely to play important roles in the
inflammatory response to the infection. Complement proteins: A family of glycoproteins
secreted by specialized types of epithelial cells, called Goblet cells. In addition to the mucins,
cells in the gastrointestinal tract secrete several types of antimicrobial peptides, which are small
amphipathic proteins that function like peptide antibiotics by disrupting the integrity of the
bacterial cell membrane. The production and release of antimicrobial peptides and mucins by the
epithelial cells of the gut represents a major barrier against microbial invasion and an important
part of the innate immune response. Tumor necrosis factor: TNF-a and nitric oxide, which are
produced as components of the intestinal epithelial cell proinflammatory program in the early
period after bacterial invasion, play an important role in the later induction and regulation of the
epithelial cell apoptotic program. (Apoptosis in response to bacterial infection may function to
delete infected and damaged epithelial cells and restore epithelial cell growth regulation and
epithelial integrity that are altered during the course of enteric infection. The delay in onset of
epithelial cell apoptosis after bacterial infection may be important both to the host and the
invading pathogen since it provides sufficient time for epithelial cells to generate signals
important for the activation of mucosal inflammation and concurrently allows invading bacteria
time to adapt to the intracellular environment before invading deeper mucosal layers).
Solution
Macrophages: These cells regulate inflammatory responses to bacteria and antigens that breach
the gastrointestinal barrier, protect the mucosa against harmful pathogens, and scavenge dead
cells and foreign debris. NK (Natural killer cells) cells: NK cells and NK-derived IFN- function
in regulating the intestinal inflammatory response to Salmonella. Along with other types of
lymphocytes, produced IFN- in response to the bacteria in vitro. Then the IFN--regulated
chemokines induced by Salmonella in the gut are likely to play important roles in the
inflammatory response to the infection. Complement proteins: A family of glycoproteins
secreted by specialized types of epithelial cells, called Goblet cells. In addition to the mucins,
cells in the gastrointestinal tract secrete several types of antimicrobial peptides, which are small
amphipathic proteins that function like peptide antibiotics by disrupting the integrity of the
bacterial cell membrane. The production and release of antimicrobial peptides and mucins by the
epithelial cells of the gut represents a major barrier against microbial invasion and an important

2. part of the innate immune response. Tumor necrosis factor: TNF-a and nitric oxide, which are
produced as components of the intestinal epithelial cell proinflammatory program in the early
period after bacterial invasion, play an important role in the later induction and regulation of the
epithelial cell apoptotic program. (Apoptosis in response to bacterial infection may function to
delete infected and damaged epithelial cells and restore epithelial cell growth regulation and
epithelial integrity that are altered during the course of enteric infection. The delay in onset of
epithelial cell apoptosis after bacterial infection may be important both to the host and the
invading pathogen since it provides sufficient time for epithelial cells to generate signals
important for the activation of mucosal inflammation and concurrently allows invading bacteria
time to adapt to the intracellular environment before invading deeper mucosal layers).