Publications

OBJECTIVE

While flavoured cigarettes were prohibited in the USA in 2009, flavoured little cigars and cigarillos (LCCs) remain on the market. We describe the evolving strategies used by tobacco companies to encourage uptake of flavoured LCCs and industry research findings on consumer perceptions of flavoured LCC products.

METHODS

Analysis of internal tobacco industry documents was triangulated with data from tobacco advertisement archives, national newspapers, trade press and the internet.

RESULTS

Flavoured LCC products were associated with young and inexperienced tobacco users, women and African-Americans. Internal industry studies confirmed that menthol and candy-like flavours (eg, vanilla and cherry) increased LCC appeal to starters by masking the heavy cigar taste, reducing throat irritation and making LCC smoke easier to inhale. To appeal to new users, manufacturers also reduced the size of cigars to make them more cigarette-like, introduced filters and flavoured filter tips, emphasised mildness and ease of draw in advertising, and featured actors using little cigars in television commercials. RJ Reynolds tried to capitalise on the popularity of menthol cigarettes among African-Americans and marketed a menthol little cigar to African-Americans.

CONCLUSIONS

Tobacco companies engaged in a calculated effort to blur the line between LCCs to increase the appeal to cigarette smokers, and the use of flavours facilitated these efforts. Bans on flavoured cigarettes should be expanded to include flavoured LCCs, and tobacco use prevention initiatives should include LCCs.

Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4(+) T-cell subsets, regulatory T cells, CD8(+) T cells, B cells, and monocytes. We find that ∼90% of causal variants are non-coding, with ∼60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10-20% directly alter recognizable transcription factor binding motifs. Rather, most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.

Gastroenteritis is a clinical illness of humans and other animals that is characterized by vomiting and diarrhea and caused by a variety of pathogens, including viruses. An increasing number of viral species have been associated with gastroenteritis or have been found in stool samples as new molecular tools have been developed. In this work, a DNA microarray capable in theory of parallel detection of more than 100 viral species was developed and tested. Initial validation was done with 10 different virus species, and an additional 5 species were validated using clinical samples. Detection limits of 1 × 10(3) virus particles of Human adenovirus C (HAdV), Human astrovirus (HAstV), and group A Rotavirus (RV-A) were established. Furthermore, when exogenous RNA was added, the limit for RV-A detection decreased by one log. In a small group of clinical samples from children with gastroenteritis (n = 76), the microarray detected at least one viral species in 92% of the samples. Single infection was identified in 63 samples (83%), and coinfection with more than one virus was identified in 7 samples (9%). The most abundant virus species were RV-A (58%), followed by Anellovirus (15.8%), HAstV (6.6%), HAdV (5.3%), Norwalk virus (6.6%), Human enterovirus (HEV) (9.2%), Human parechovirus (1.3%), Sapporo virus (1.3%), and Human bocavirus (1.3%). To further test the specificity and sensitivity of the microarray, the results were verified by reverse transcription-PCR (RT-PCR) detection of 5 gastrointestinal viruses. The RT-PCR assay detected a virus in 59 samples (78%). The microarray showed good performance for detection of RV-A, HAstV, and calicivirus, while the sensitivity for HAdV and HEV was low. Furthermore, some discrepancies in detection of mixed infections were observed and were addressed by reverse transcription-quantitative PCR (RT-qPCR) of the viruses involved. It was observed that differences in the amount of genetic material favored the detection of the most abundant virus. The microarray described in this work should help in understanding the etiology of gastroenteritis in humans and animals.