Publications

BACKGROUND

Internet-based marketing has become an attractive option for promoting tobacco products due to its potential to avoid advertising restrictions. In Argentina, several cigarette brands have designed websites for the local market, which promote user participation.

OBJECTIVE

The intent of the study was to report on the use of tobacco company-sponsored websites by medical students and recently graduated physicians.

METHODS

An online self-administered survey was conducted among eligible medical students and recent graduates from the University of Buenos Aires (UBA). Sampling was from lists of email addresses of students enrolled in two required courses. Eligibility criteria were ages 18-30 years and reporting on smoking status. Questions on Internet use included accessing a tobacco brand website at least once during their lifetime and any use of tobacco promotional materials.

RESULTS

The response rate was 35.08% (1743/4969). The final sample included 1659 participants: 73.06% (1212/1659) were women and mean age was 26.6 years (SD 1.9). The majority were current medical students (55.70%, 924/1659) and 27.31% (453/1659) were current smokers. Men were more likely to report having seen a tobacco advertisement on the Internet (P=.001), to have received a tobacco promotion personally addressed to them (P=.03), to have used that promotion (P=.02), and to have accessed a tobacco-sponsored website (P=.01). Among respondents, 19.35% (321/1659) reported having accessed a tobacco-sponsored website at least once in their lifetime and almost all of them (93.8%, 301/321) accessed these sites only when it was necessary for participating in a marketing promotion. Most people logging on for promotions reported entering once a month or less (58.9%, 189/321), while 25.5% (82/321) reported accessing the tobacco industry Internet sites once a week or more. In adjusted logistic regression models, participants were more likely to have accessed a tobacco brand website if they were former smokers (OR 2.45, 95% CI 1.42-4.22) or current (OR 8.12, 95% CI 4.66-14.16), if they reported having seen a tobacco advertisement on the Internet (OR 2.44, 95% CI 1.77-3.37), received a tobacco promotion personally addressed to them (OR 5.62; 95% CI 4.19-7.55), or used one of these promotions (OR 14.05, 95% CI 9.21-21.43). Respondents were more likely to be current smokers if they received a tobacco promotion (OR 2.64, 95% CI 2.02-3.45) or if they used one of these promotions (OR 1.93, 95% CI 1.31-2.85).

CONCLUSIONS

Our study suggests that tobacco industry websites reach medical students and young physicians in a middle-income country with their marketing promotions. Current or proposed legislation to ban tobacco advertising needs to include Internet sites and related social media.

OBJECTIVE

We investigated potential interactions between human leukocyte antigen (HLA) genotype and body mass index (BMI) status in relation to the risk of developing multiple sclerosis (MS).

METHODS

We used 2 case-control studies, one with incident cases (1,510 cases, 2,017 controls) and one with prevalent cases (937 cases, 609 controls). Subjects with different genotypes and BMI were compared with regard to incidence of MS by calculating odds ratios (ORs) with 95% confidence intervals (CIs) employing logistic regression. Potential interactions between genotypes and BMI were evaluated by calculating the attributable proportion due to interaction.

RESULTS

In both cohorts, a significant interaction was observed between HLA-DRB1*15 and obesity, regardless of HLA-A*02 status. Similarly, there was a significant interaction between absence of A*02 and obesity, regardless of DRB1*15 status. In the incident cohort, obese subjects with the most susceptible genotype (carriage of DRB1*15 and absence of A*02) had an OR of 16.2 (95% CI 7.5-35.2) compared to nonobese subjects without the genetic risk factors. The corresponding OR in the prevalent study was 13.8 (95% CI 4.1-46.8).

CONCLUSIONS

We observed striking interactions between BMI status and HLA genotype with regard to MS risk. Hypothetically, a low-grade inflammatory response inherent to obesity synergizes with the adaptive, HLA molecule-restricted arm of the immune system, causing MS. Prevention of adolescent obesity may thus lower the risk of developing MS, predominantly among people with a genetic susceptibility to the disease.

Heart failure (HF) and atrial fibrillation (AF) commonly coexist and adversely affect mortality when found together. AF begets HF and HF begets AF. Rhythm restoration with antiarrhythmic drugs failed to show a mortality benefit but can be effective in improving symptoms. Nonpharmacologic treatment of AF may be of value in the HF population.

Emerging evidence indicates that myeloid cells are essential for promoting new blood vessel formation by secreting various angiogenic factors. Given that hypoxia-inducible factor (HIF) is a critical regulator for angiogenesis, we questioned whether HIF in myeloid cells also plays a role in promoting angiogenesis. To address this question, we generated a unique strain of myeloid-specific knockout mice targeting HIF pathways using human S100A8 as a myeloid-specific promoter. We observed that mutant mice where HIF-1 is transcriptionally activated in myeloid cells (by deletion of the von Hippel-Lindau gene) resulted in erythema, enhanced neovascularization in matrigel plugs, and increased production of vascular endothelial growth factor (VEGF) in the bone marrow, all of which were completely abrogated by either genetic or pharmacological inactivation of HIF-1. We further found that monocytes were the major effector producing VEGF and S100A8 proteins driving neovascularization in matrigel. Moreover, by using a mouse model of hindlimb ischemia we observed significantly improved blood flow in mice intramuscularly injected with HIF-1-activated monocytes. This study therefore demonstrates that HIF-1 activation in myeloid cells promotes angiogenesis through VEGF and S100A8 and that this may become an attractive therapeutic strategy to treat diseases with vascular defects.