ΔFosB plays a crucial role in the development of drug addictions, since its overexpression in D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for most of the behavioral and neural adaptations that arise from addiction. Once ΔFosB is sufficiently overexpressed, it induces an addictive state that becomes increasingly more severe with further increases in ΔFosB expression. It has been implicated in addictions to alcohol, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and substituted amphetamines, among others.ΔJunD, a transcription factor, and G9a, a histone methyltransferase enzyme, both directly oppose the induction of ΔFosB in the nucleus accumbens (i.e., they oppose increases in its expression). Sufficiently overexpressing ΔJunD in the nucleus accumbens with viral vectors can completely block many of the neural and behavioral alterations seen in chronic drug use (i.e., the alterations mediated by ΔFosB). ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. Since both natural rewards and addictive drugs induce expression of ΔFosB (i.e., they cause the brain to produce more of it), chronic acquisition of these rewards can result in a similar pathological state of addiction. ΔFosB is the most significant factor involved in both amphetamine addiction and amphetamine-induced sex addictions, which are compulsive sexual behaviors that result from excessive sexual activity and amphetamine use. These sex addictions (i.e., drug-induced compulsive sexual behaviors) are associated with a dopamine dysregulation syndrome which occurs in some patients taking dopaminergic drugs, such as amphetamine or methamphetamine.
Seal finger, also known as sealers finger and spekkfinger (from the Norwegian for "blubber"), is an infection that afflicts the fingers of seal hunters and other people who handle seals, as a result of bites or contact with exposed seal bones; it has also been contracted by exposure to untreated seal pelts. The State of Alaska Section of Epidemiology defines it as "a finger infection associated with bites, cuts, or scratches contaminated by the mouths, blood, or blubber of certain marine mammals".It can cause cellulitis, joint inflammation, and swelling of the bone marrow; untreated, the course of "seal finger" is slow and results often in thickened contracted joint. Historically, seal finger was treated by amputation of the affected digits once they became unusable. It was first described scientifically in 1907.The precise nature of the organism responsible for seal finger is unknown, as it has resisted culturing because most cases are promptly treated with antibiotics; however, as seal finger can be treated with tetracycline or similar antibiotics, the causative organism is most likely bacterial, or possibly fungal; in 1998, Baker, Ruoff, and Madoff showed that the organism is most likely a species of Mycoplasma called Mycoplasma phocacerebrale. This Mycoplasma was isolated in an epidemic of seal disease occurring in the Baltic Sea. Notes
External links
Working with Marine Mammals and Your Health, NOAA brochure on zoonoses, including seal finger. (requires Acrobat Reader (via archive.org))