Pharmacology
Mechanism of action
Tetracycline inhibits protein synthesis by blocking the attachment of charged tRNA at the P site peptide chain. Tetracycline blocks the A-site so that a hydrogen bond is not formed between the amino acids. Tetracycline binds to the 30S and 50S subunit of microbial ribosomes. Thus, it prevents the formation of a peptide chain. The action is usually not inhibitory and irreversible even with the withdrawal of the drug. Mammalian cells are less vulnerable to the effect of tetracyclines, despite the fact that tetracycline binds to the small ribosomal subunit of both prokaryotes and eukaryotes (30S and 40S, respectively). This is because bacteria actively pump tetracycline in, even against a concentration gradient, whereas mammalian cells are simply not affected by the mechanisms of tetracycline within the cytoplasm. This accounts for the relatively small off-site effect of tetracycline on human cells. Mechanisms of resistance
Bacteria usually acquire resistance to tetracycline from horizontal transfer of a gene that either encodes an efflux pump or a ribosomal protection protein. Efflux pumps actively eject tetracycline from the cell, preventing the buildup of an inhibitory concentration of tetracycline in the cytoplasm. Ribosomal protection proteins interact with the ribosome and dislodge tetracycline from the ribosome, allowing for translation to continue. History
Discovery
The tetracyclines, a large family of antibiotics, were discovered by Benjamin Minge Duggar in 1948 as natural products, and first prescribed in 1948. Benjamin Duggar, working under Yellapragada Subbarow at Lederle Laboratories, discovered the first tetracycline antibiotic, chlortetracycline (Aureomycin), in 1945.
Modicon can mean:

Modicon PLC, the first programmable logic controller
Ethinylestradiol/norethisterone, an oral contraceptive formulation