The urban built environment and overdose mortality in New York City neighborhoods.

Accidental drug overdose continues to be a substantial cause of mortality for drug users. Characteristics of the neighborhood built environment may be important determinants of the likelihood of drug overdose mortality independent of individual-level factors. Using data from the New York City Office of the Chief Medical Examiner, we conducted a multilevel case control study using data on accidental overdose deaths as cases and non-overdose accidental deaths as controls. We used archival data from the New York City Housing and Vacancy Survey and the Mayor's Office of Operations to assess characteristics of neighborhood external (e.g. dilapidation of buildings) and internal (e.g. quality of utilities in houses) built environment. Multilevel analyses were used to assess the relations between the neighborhood built environment and the likelihood of overdose death. Six out of the eight characteristics of the external environment studied and three out of the six characteristics of the internal environment studied were significantly associated with the likelihood of fatal drug overdose in multilevel models after adjusting for individual-level (age, race, sex) and neighborhood-level (income, drug use) variables. Deterioration of the built environment, particularly the external environment, is associated with an increased likelihood of fatal accidental drug overdose. Disinvestment in social resources, psychosocial stressors, neighborhood differences in response to a witnessed overdose, and differences in vulnerability to the adverse consequences of drug use in different neighborhoods may explain the observed associations.

Genomic organization of the murine G protein beta subunit genes and related processed pseudogenes.

The functional significance of heterotrimeric guanine nucleotide binding protein (G protein) for the many physiological processes including the molecular mechanisms of drug addiction have been described. In investigating the changes of mRNA expression after acute psychostimulant administration, we previously identified a cDNA encoding a G protein beta1 subunit (Gbeta1) that was increased up to four-fold in certain brain regions after administration of psychostimulants. The mouse Gbeta1 gene (the mouse genetic symbol, GNB1) was mapped to chromosome 4, but little was known of its genetic features. To characterize the GNB1 gene further, we have cloned and analyzed the genomic structures of the mouse GNBI gene and its homologous sequences. The GNBI gene spans at least 50 kb, and consists of 12 exons and 11 introns. The exon/intron boundaries were determined and found to follow the GT/AG rule. Exons 3-11 encode the Gbeta1 protein, and the exon 2 is an alternative, resulting in putative two splicing variants. Although intron 11 is additional for GNBI compared with GNB2 and GNB3, the intron positions within the protein coding region of GNB1, GNB2 and GNB3 are identical, suggesting that GNB1 should have diverged from the ancestral gene family earlier than the genes for GNB2 and GNB3. We also found the 5'-truncated processed pseudogenes with 71-89% similarities to GNBI mRNA sequence, suggesting that the truncated cDNA copies, which have been reverse-transcribed from a processed mRNA for GNB1, might have been integrated into several new locations in the mouse genome.