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Purpose: To examine heroin use and associated morbidity in young adults undergoing drug detoxification., Methods: A retrospective chart review of all persons (ages 18-25) admitted to either of the two state-funded detoxification facilities in Rhode Island was conducted between June 1998 and June 1999. Only those reporting heroin as a primary drug were included in this study (N=201)., Results: Clients were largely male (64%), and white (79%), with a mean age of 22. Of those that reported heroin as their primary drug, 62% used primarily by injection. Mean age of initiation for heroin use was 18.3 years. Twenty-two percent reported a psychiatric diagnosis, and 80% reported a substance-abusing family member. Injection, previous overdose, and a mother with a history of substance use were associated with early initiation of heroin use., Conclusions: The majority of young adults with heroin addiction undergoing detoxification began using heroin during late adolescence. Concurrence of psychiatric and medical diagnoses with heroin addiction was common, and may contribute to the severity of drug use. Efforts to identify risk factors for heroin and other injection drug use in adolescents and young adults will be critical for the design of effective interventions to prevent injection drug use and its associated morbidities.

In the United States today, half of all new HIV infections are injection drug use-associated, many of which are a result of the reuse and sharing of contaminated syringes. Thus, providing access to sterile syringes for injection drug users is an important part of preventing HIV transmission. Needle exchange programs (NEPs) have been established as one successful approach to providing sterile injection equipment. The medical literature shows that these programs are effective in decreasing both syringe sharing and HIV incidence in injection drug users. In addition, many NEPs are also beneficial because they provide other injection drug use-relevant services. There are several strategies that can be adopted in order to optimize the impact of needle exchange programs, at both the community and national levels. These include establishing NEPs in communities that need them, expanding and improving those that already exist, and implementing such programs on a larger national scale with the provision of federal funds.

The Drosophila trp gene encodes a light-activated Ca(2+) channel subunit, which is a prototypical member of a novel class of channel proteins. Previously identified trp mutants are all recessive, loss-of-function mutants characterized by a transient receptor potential and the total or near-total loss of functional TRP protein. Although retinal degeneration does occur in these mutants, it is relatively mild and slow in onset. We report herein a new mutant, Trp(P365), that does not display the transient receptor potential phenotype and is characterized by a substantial level of the TRP protein and rapid, semi-dominant degeneration of photoreceptors. We show that, in spite of its unusual phenotypes, Trp(P365) is a trp allele because a Trp(P365) transgene induces the mutant phenotype in a wild-type background, and a wild-type trp transgene in a Trp(P365) background suppresses the mutant phenotype. Moreover, amino acid alterations that could cause the Trp(P365) phenotype are found in the transmembrane segment region of the mutant channel protein. Whole-cell recordings clarified the mechanism underlying the retinal degeneration by showing that the TRP channels of Trp(P365) are constitutively active. Although several genes, when mutated, have been shown to cause retinal degeneration in Drosophila, the underlying mechanism has not been identified for any of them. The present studies provide evidence for a specific mechanism for massive degeneration of photoreceptors in Drosophila. Insofar as some human homologs of TRP are highly expressed in the brain, a similar mechanism could be a major contributor to degenerative disorders of the brain.

The trp gene of Drosophila encodes a subunit of a class of Ca(2+)-selective light-activated channels that carry the bulk of the phototransduction current. Transient receptor potential (TRP) homologs have been identified throughout animal phylogeny. In vertebrates, TRP-related channels have been suggested to mediate "store-operated Ca(2+) entry," which is important in Ca(2+) homeostasis in a wide variety of cell types. However, the mechanisms of activation and regulation of the TRP channel are not known. Here, we report on the Drosophila inaF gene, which encodes a highly eye-enriched protein, INAF, that appears to be required for TRP channel function. A null mutation in this gene significantly reduces the amount of the TRP protein and, in addition, specifically affects the TRP channel function so as to nearly shut down its activity. The inaF mutation also dramatically suppresses the severe degeneration caused by a constitutively active mutation in the trp gene. Although the reduction in the amount of the TRP protein may contribute to these phenotypes, several lines of evidence support the view that inaF mutations also more directly affect the TRP channel function, suggesting that the INAF protein may have a regulatory role in the channel function.